Differential Diagnosis in Dermatology

DERMATOLOGY FOURTH EDITION
DIFFERENTIAL DIAGNOSIS IN
“Brilliant... Take for granted the superb colour photographs, the comprehensive and
readable text, the clinical accuracy and acumen of the authors... what’s special is the
DIFFERENTIAL DIAGNOSIS
diagnostically and educationally helpful structure. This book understands that most of us do
not have photographic memories, and panic when we don’t immediately recognise a skin
lesion. Provided we can establish a few simple features of the rash – where it is, what colour,
how long it has been there, surface characteristics – we turn to the appropriate algorithm,
IN DERMATOLOGY
look at the picture for confirmation and come up with the right answer. It is such a relief I
could burst into tears of gratitude.”
Postgraduate Education for General Practice, on the First Edition
FOURTH EDITION
Revised and updated for its Fourth Edition with specially added images of pigmented skins,
the key aim of Differential Diagnosis in Dermatology remains the same – to allow primary
care physicians to diagnose quickly and confidently with the patient present. Chapters are
divided into different body areas and contain over 750 illustrations, combining excellent
clinical photography with practical text and clear diagrams throughout.
By looking inside the front cover at the intuitive “How To” guide and using the index RICHARD ASHTON, BARBARA LEPPARD and HYWEL COOPER
AND HYWEL COOPER
RICHARD ASHTON, BARBARA LEPPARD
of algorithms found at the back, diagnosis can be effectively reached by identifying the
relevant clinical features. High quality images of white and pigmented skins illustrate each
condition, with a concise description of the clinical features and treatment options.
Other titles of related interest

An Atlas of African Dermatology
Barbara Leppard
EMQs in Ophthalmology, Dermatology and ENT:
An essential revision guide with comprehensive answers
Mukhtar Bizrah and Manaf Khatib
The Pictorial Atlas of Common Genito-urinary Medicine
Shiv Pareek
K28636
ISBN: 978-1-90936-872-9
6000 Broken Sound Parkway, NW 90000
Suite 300, Boca Raton, FL 33487
711 Third Avenue
New York, NY 10017 9 78 1 909 368729
an informa business 2 Park Square, Milton Park
Abingdon, Oxon OX14 4RN, UK w w w. c rc p r e s s . c o m
How to use this book
This book has been written to aid in the diagnosis of an unknown SITE INDEX
rash or lesion, and we encourage you to use it while examining
the patient. You will need to describe the rash or lesions using the Chapter 6 Chapters 4, 5 & 9 Chapter 3
system outlined here. Ears p. 159 Face & bald scalp Hairy scalp
1. Site Mouth p. 142 pp. 97, 111, 261 p. 69
Tongue p. 150
2. Erythematous (blanches on pressure) or Non-erythematous Lips p. 152
3. Acute (<2 weeks’ duration) or Chronic (>2 weeks’ duration) Chapters 7,
4. Surface features (see Chapter 1 for definitions): 8&9
normal/smooth (i.e. same as surrounding skin) or scaly, Chapter 10 Trunk & limbs
hyperkeratotic, warty, crust, exudate, excoriated Flexures p. 335 pp. 165,
195, 261
5. Type of lesion(s) (see Chapter 1 for definitions): Chapter 13
flat lesions – macules and patches Hands p. 404
raised lesions – papules, plaques and nodules
fluid-filled lesions – vesicles, bullae and pustules
surface broken – erosions, ulcers and fissures Chapter 11
Genitalia p. 351 Chapter 14
And if non-erythematous, describe the Chapter 12 Nails p. 435
6. Colour: Lower legs
due to blood – pink, red, purple, mauve p. 371
due to pigment – brown, black, blue
due to lack of blood/pigment – white Chapter 14 Chapter 13
Nails Feet
other colours – yellow, orange, grey p. 435 p. 419
This will enable you to go to the algorithm that gives the differential diagnosis for
the clinical features that you have elicited. You can find the index of algorithms on
the inside back cover or at the beginning of each chapter. Diagnoses in the dark blue
boxes are more common and likely to be seen in General Practice. Other diagnoses not
highlighted are rare, and may need a specialist to diagnose correctly.
Examples of how to describe the clinical
features of lesions or rashes
1. Site: dorsum hand 1. Site: face 1. Site: trunk

2. Erythematous 2. Non-erythematous 2. Erythematous
3. Chronic 3. Chronic 3. Chronic
4. Surface: scale 4. Surface: normal 4. Surface: crust
5. Raised lesion: plaques 5. Flat lesion: patch 5. Lesions: bullae and erosions
6. Colour: white
GO TO algorithm on p. 407 GO TO algorithm on p. 255
GO TO algorithm on p. 281
For all the patients from whom we have learnt so much over the years
and to all those who we hope will benefit from this book in the future
Differential Diagnosis in Dermatology
Fourth Edition
Richard Ashton
Consultant Dermatologist Portsmouth NHS Trust,
Nobles Hospital, Isle of Man
Barbara Leppard
Retired Consultant Dermatologist, Southampton University NHS Trust
Hywel Cooper
Consultant Dermatologist, Portsmouth NHS Trust
Boca Raton London New York
CRC Press is an imprint of the

Taylor & Francis Group, an informa business
CRC Press
Taylor & Francis Group
6000 Broken Sound Parkway NW, Suite 300
Boca Raton, FL 33487-2742
© 2014 by Richard Ashton, Barbara Leppard and Hywel Cooper
CRC Press is an imprint of Taylor & Francis Group, an Informa business
No claim to original U.S. Government works

Version Date: 20160307
International Standard Book Number-13: 978-1-4987-8473-3 (eBook - PDF)
This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any
legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them
and do not necessarily reflect the views/opinions of the publishers. The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supple-
ment to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in
medical science, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ and device
or material manufacturers’ printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book. This book does not indicate whether a particular treatment is
appropriate or suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately. The authors and
publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material
has not been acknowledged please write and let us know so we may rectify in any future reprint.
Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including
photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers.
For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright.com/) or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers,
MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment
has been arranged.
Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe.
Visit the Taylor & Francis Web site at
http://www.taylorandfrancis.com
and the CRC Press Web site at
http://www.crcpress.com
Contents
Preface to the fourth edition vi
1 Introduction to dermatological diagnosis 1
2 Introduction to dermatological treatment 23
3 Hair and hairy scalp 69
4 Acute erythematous rash on the face 97
5 Chronic erythematous rash on the face 111
6 Mouth, tongue, lips and ears 141
7 Acute erythematous rash on the trunk and limbs 165
8 Chronic erythematous lesions on trunk and limbs 195
9 Non-erythematous lesions 261
10 Flexures: axilla, groin, natal cleft, sub-mammary folds 335
11 Genitalia including pubic, perianal and perineal areas 351
12 Lower legs 371
13 Hands and feet 403
14 Nails 435
List of drugs and associated drug reactions 459

Emollient products: how and when to use 462
Wash and bath emollient products: how and when to use 463
Classification of topical steroids by potency 464
Index of algorithms 465
Preface to the fourth edition
In a review of the first edition of Differential Diagnosis in The third edition incorporated treatment into the text and this
Dermatology in Postgraduate Education for General Practice, the new edition has brought that up to date, particularly with the new
reviewer wrote: biologic treatments. We have invited our colleague Hywel Cooper
to keep the text and treatments up to date, and we have included
Brilliant! Take for granted the superb colour photographs, the many new photographs, especially of rashes in black and Asian
comprehensive and readable text, the clinical accuracy and skin.
acumen of the authors. What’s special is the diagnostically
We would like to thank several colleagues for their help in
and educationally helpful structure. This book understands
keeping us up to date, especially Dr Steven Hayes (dermoscopy
that most of us haven’t got photographic memories, and panic
for general practitioners), Dr Adam Haworth (patch testing and
when we don’t immediately recognise a skin lesion. Provided
lasers), Dr Suzanna Hoey (vascular birthmarks), Dr Jennifer Jones
we can establish a few simple features of the rash – where it is,
(scalp), Liz Jones (emollients), Mr Tim Mellor (lasers), Dr Raj Patel
what colour, how long it has been there, surface characteristics
(genitalia) and Denise Woodd (wound dressings and leg ulcers)
– we turn to the appropriate algorithm, look at the picture for
and all the patients who have allowed us to use their photographs
confirmation and come up with the right answer. It is such a
in this book.
relief I could burst into tears of gratitude.
Richard Ashton
We hope we haven’t changed any of that, and that this new
Barbara Leppard
edition is equally user-friendly. It is designed for the primary care
September 2014
physician to use with the patient sitting in front of him or her.
1
Introduction to dermatological
diagnosis
1
Basic biology of the skin
The epidermis 2
The dermis 2
Diagnosis of skin disease
History of presenting complaint 3
Past, family and social history 4
Previous treatment 4
Describing skin lesions
1. Sites involved 4
2. Number of lesions 4
3. Distribution 5
4. Arrangement 6
5. Surface palpation 7
6. Deep palpation 7
7. Type of lesion 8
8. Surface features and texture 11
9. Colour of lesion 14
10. Border of lesion or rash 16
11. Shape of lesion 17
Special investigations
Wood’s light 18
Dermoscopy 18
Bacteriology 20
Mycology 20
Skin biopsy 20
Prick testing 21
Patch testing 21
2 / INTRODUCTION TO DIAGNOSIS
BASIC BIOLOGY OF THE SKIN

THE EPIDERMIS
As the outside layer of the skin, the function of the epidermis
is to produce keratin and melanin. Pathology in the epidermis
produces a rash or a lesion with abnormal scale, change in
pigmentation, or loss of surface integrity (exudate or erosion).
Keratin
Keratin is the end product of maturation of the epidermal cells; its
function is to make the skin waterproof.
Melanin
Melanin is produced by melanocytes in the basal layer. Packets
of melanin (melanosomes) are transferred from the melanocytes
through their dendritic processes into the surrounding epidermal
cells (see Fig. 1.02). Melanosomes protect the nucleus from the
harmful effects of ultraviolet radiation; without this protection
skin cancer may develop. Fig. 1.01 The structure of the skin
THE DERMIS
The bulk of the dermis is made up of connective tissue: collagen,
which gives the skin its strength, and elastic fibres, which allow it
to stretch. Here are also the blood vessels, lymphatics, cutaneous
nerves and the skin appendages (hair follicles, sebaceous glands
and sweat glands). Diseases of the dermis usually result in change
in elevation of the skin (i.e. papules, nodules, atrophy), and if the
pathology is restricted to the dermis, then there will be no surface
changes such as scale, crust or exudate. Loss or necrosis of the
dermis results in an ulcer (as opposed to an erosion, which is due
to loss of epidermis alone).
Fig. 1.02 Melanocyte in basal layer inserting melanosomes into keratinocytes

HISTORY TAKING / 3
DIAGNOSIS OF SKIN DISEASE Table 1.01 Skin types
The diagnosis of skin disease is made by following the same Type 1: Always burns, never tans
Type 2: Always burns, tans minimally
general principles as in any other branch of medicine. Begin by Type 3: Sometimes burns, tans gradually
taking a history. This is followed by careful physical examination. Type 4: Rarely burns, tans well
If at this stage the diagnosis has not been made, further Type 5: Asian skin
investigations can be carried out. Very often the non-dermatologist Type 6: Black skin
tends to look at a rash or skin lesion and ‘guess’ the diagnosis.
Those with fair skin (types 1 and 2) are more liable to develop skin cancers.
This is quite unnecessary. In this section we have outlined a
scheme to enable you to make the correct diagnosis.
(see Table 1.01). In rashes on the face and backs of the hands, ask
HISTORY OF PRESENTING COMPLAINT about relationship to sun exposure. The important questions to
Duration of individual lesions ask are regarding the time interval after sun exposure before the
How long has/have the lesion/s been present? This is the most rash occurs and whether the patient gets the rash through window
important question in the history. Acute lesions present for less glass on a sunny day. In solar urticaria‚ the rash occurs within
than 2 weeks need to be distinguished from chronic ones. 5 minutes of sun exposure and is gone in an hour. In polymorphic
light eruption (see p. 100)‚ the rash occurs several hours after
Do the lesions come and go? Do they occur at the same site or
sun exposure and lasts several days. In porphyria (which is very
at different sites? This question is particularly important if the
rare, see p. 408) the rash occurs within a few minutes and lasts
diagnosis of urticaria or herpes simplex is being considered.
several days. Rashes that occur through window glass are due to
Urticaria (see p. 171) can be diagnosed by a history of lesions
ultraviolet A rays and will need a sunblock containing titanium
coming and going within a 24-hour period. To establish the
dioxide or zinc oxide (see p. 39).
transitory nature of urticarial weals, draw a line around a weal
and ask the patient to return the next day. You will see that the site Ask about irritants on the skin in hand dermatitis (see p. 414), e.g.
and shape will have changed. Herpes simplex (see p. 108–9) and detergents and oils, and about working practices and hobbies.
fixed drug eruptions (see p. 181) last around 7–14 days and usually Are the hands protected by rubber gloves or in direct contact with
reoccur at the same site. irritants?
Relationship to physical agents Itching

A past history of living or working in a hot climate may be Itching is a nuisance to the patient but may not help you in
the clue you need for the diagnosis of skin cancer. Determine making a diagnosis. Severe itching, especially at night bad enough
the patient’s skin response to sun exposure. Six skin types are to prevent sleep, should make you think of scabies (see p. 248) or
recognised, depending how well a patient develops a skin tan rarely dermatitis herpetiformis (see p. 246).
PAST, FAMILY AND SOCIAL HISTORY DESCRIBING SKIN LESIONS

Past history Look first and identify:
Has the patient had a rash before and, if so, was it the same as 1. sites involved
now? If eczema is present, a history of infantile eczema, asthma or 2. number of lesions
hay fever may suggest a diagnosis of atopic eczema. 3. distribution
4. arrangement.
Family history
Feel the lesions by:
Does anyone else in the family have a skin problem and is it
5. surface palpation – with fingertips
the same as the patient’s? This will indicate either that the skin
6. deep palpation – by squeezing between finger and thumb.
disease is genetically determined, e.g. atopic eczema, ichthyosis or
psoriasis, or that it is contagious, e.g. scabies, impetigo. Describe a typical lesion under the following headings:
7. type of lesion
Social history 8. surface features and texture
This should include family relationships and work practices that 9. colour of lesion – including erythematous or
may give you a clue as to the cause of the problem. For instance, in non-erythematous
cases of hand dermatitis, does the condition improve at weekends 10. border of lesion or rash
or when away on holiday? 11. shape of lesion.
PREVIOUS TREATMENT Check other sites, e.g. scalp, nails, mouth and genitalia.
What topical agents have been used and did they help? Establish 1. SITES INVOLVED
whether these are ointments or creams, because the base may
Describe body areas involved.
be as important as the active agent. Remember that topical local
anaesthetics, antibiotics and antihistamines may induce a contact 2. NUMBER OF LESIONS
allergic dermatitis. A drug history is important if a drug-induced
rash is considered, e.g. if there is a sudden onset of a widespread
rash. If the patient has been on the drug for more than 2 months,
the likelihood of it being the cause of the rash is low.
Single Fig. 1.03 Lymphoma Multiple Fig. 1.04 Lichen planus

DISTRIBUTION / 5
3. DISTRIBUTION
Symmetrical Fig. 1.05 Psoriasis Asymmetrical Fig. 1.06 Tinea corporis on buttocks Unilateral Fig. 1.07 Herpes zoster
Involving both sides of body to a similar extent; usually due Involving predominantly one side of the body, usually due Restricted to one side of body only.
to endogenous causes, e.g. acne, eczema, psoriasis. to exogenous cause, e.g. infections or contact dermatitis.
Localised Fig. 1.08 Nappy/diaper rash Generalised Fig. 1.09 Erythrodermic psoriasis Sun exposed Fig. 1.10 Fig. 1.11
Restricted to one area of skin. Covering most of the body’s surface. Involving the face, ‘V’ and back of the neck, dorsum of hands and forearms.
Note: behind ears and under chin and/or eyebrows will be spared (see p. 85).
4. ARRANGEMENT
Discrete Fig. 1.12 Psoriasis Coalescing Fig. 1.13 Eczema Disseminated Fig. 1.14 Psoriasis
Individual lesions separated from one another by normal Similar lesions merging together. Widespread discrete lesions.
skin.
Annular Fig. 1.15 Eczema Linear Fig. 1.16 Epidermal naevus Grouped Fig. 1.17 Insect bites
Arranged in ring (see p. 209). Arranged in line (see p. 212). Multiple similar lesions grouped together in one area.
PALPATION / 7
FEEL THE LESIONS

5. SURFACE PALPATION
Feel the surface with your
fingertips.
Smooth: feels like normal skin.
Uneven: found with fine
scaling or some warty lesions.
Rough: feels like sandpaper,
and is characteristic of solar
keratosis, cutaneous horn or
crust. Smooth Fig. 1.18 Urticaria Uneven Fig. 1.19 Compound naevus Rough Fig. 1.20 Solar keratosis
6. DEEP PALPATION
Compress the lesion between
thumb and index finger.
Normal: feels the same as the
normal surrounding skin.
Soft: easily compressible – feels
like the lips.
Firm: only slightly
compressible – feels like the tip
of the nose.
Hard: not compressible – feels Soft Fig. 1.21 Skin tags Firm Fig. 1.22 Keloid scar Hard Fig. 1.23 Osteoma on jaw
like bone.
7. TYPE OF LESION
Assess whether the lesions are flat or raised, solid or fluid filled, or have a broken surface. Flat lesions Any area of colour or surface
change which cannot be felt on palpation.
a. Flat lesions Raised solid lesions
Papule Any solid lesion (≤ 1 cm size) that

is raised above the surface or can be felt on
palpation.
Nodule Any elevated lesions (> 1 cm
diameter) which is palpable between finger
and thumb, i.e. there is substance to the
lesion. Often due to dermal pathology but
there may or may not be surface change.
Plaque Any lesion (size > 1 cm) where the
diameter is >> than the thickness, i.e. the
Macule ≤ 1 cm diameter Fig. 1.24 Lentigines Patch > 1 cm diameter Fig. 1.25 Port wine stain lesion can be felt only with finger tips.
Usually due to epidermal pathology with
b. Raised solid lesions surface scale, crust or keratin.
Papule ≤ 1 cm diameter Nodule > 1 cm diameter (= thickness) Plaque > 1 cm diameter (>> thickness)
Fig. 1.26 Compound naevus Fig. 1.27 Strawberry naevus Fig. 1.28 Discoid eczema
TYPE OF LESIONS / 9
c. Fluid-filled lesions Blisters (vesicles and bullae)

contain clear fluid (serum)
and last for a few days only.
The presence of fluid can be
confirmed by pricking with a
needle. The site of the blister can
be within the epidermis or at
the dermo-epidermal junction.
Intra-epidermal blisters break
easily to form erosions, while
sub-epidermal ones can persist
for several days and may contain
blood.
Vesicle ≤1 cm diameter Fig. 1.29 Bulla > 1 cm diameter Fig. 1.30 Pustule ≤1 cm diameter Fig. 1.31
Pustules (≤1 cm) contain opaque
Herpes simplex Bullous pemphigoid
fluid (pus). Prick the lesion and
pus comes out.
Loss of some or all of the

d. Lesions due to a broken surface
epidermis results in an erosion,
which will heal without scarring.
Erosions can be due to:
● a blister that has burst
● trauma.
Loss of dermis (from any cause)

will result in an ulcer, which will
heal with scar tissue formation.
There will be surface exudate,
crust or slough.
Splitting of the skin (fissure) is
due to abnormal keratin (usually
Erosion Fig. 1.32 Ulcer Fig. 1.33 Neuropathic ulcer Fissure Fig. 1.34 Psoriasis on palm secondary to eczema or psoriasis).
Loss of epidermis only Loss of epidermis and dermis Linear split in skin
e. Other terms used
Weal Fig. 1.35 Urticaria Cyst Fig. 1.36 Scrotal epidermoid cysts Scar Fig. 1.37 Surgical scar
Transient swelling (i.e. papule or plaque) due to dermal A fluctuant papule or nodule lined by epithelium A healed dermal lesion (macule, papule, plaque, nodule)
oedema – should last for less than 24 hours; usually containing fluid, pus or keratin. secondary to trauma, surgery, infection or loss of blood
synonymous with urticaria. supply.
Comedone Fig. 1.38 Solar elastosis Burrow Fig. 1.39 Scabies Abscess Fig. 1.40 Boil on angle of jaw
Papule due to a plugged sebaceous follicle containing Linear S-shaped papule 3–5 mm long found on the hands A large collection of pus.
altered sebum and keratin. and fingers of a patient with scabies.
SURFACE / 11
8. SURFACE FEATURES AND TEXTURE b. Abnormal keratinisation
a. Normal Fig. 1.41 Granuloma annulare Hyperkeratotic Fig. 1.42 Foot psoriasis Keratin horn Fig. 1.43 Keratoacanthoma
Surface not different from surrounding skin and feels Rough, uneven surface due to increased formation of Accumulation of compact keratin on the surface. Feels
smooth. Change in elevation and/or colour only. keratin. Seen usually on palms and soles. rough and is adherent so difficult to pick off.
Scale Fig. 1.44 Erythrodermic psoriasis Scratch test – before Fig. 1.45 Psoriasis Scratch test – after Fig. 1.46 Psoriasis
Dry/flaky surface due to abnormal stratum corneum with If surface is scaly, scratch surface of scale vigorously with Profuse silver scale indicates that the diagnosis is psoriasis.
increased shedding of keratinocytes. fingernail.
c. Broken surface
Exudate Fig. 1.47 Acute eczema Friable Fig. 1.48 Pyogenic granuloma Slough Fig. 1.49 Foot ulcer
Serum, blood or pus that has accumulated on the surface. Surface bleeds easily after minor trauma. A combination of exudate and necrotic tissue.
Crust Fig. 1.50 Impetigo Fig. 1.51 Basal cell carcinoma Fig. 1.52 Excoriation Fig. 1.53 Atopic eczema
Dried exudate. There should be a history of weeping, pus To find the cause of a crust, pick it off to see what is Localised damage to the skin due to scratching – linear
or bleeding. underneath. There will be either an ulcer or an erosion. erosions and crusts.
Under the crust in Fig. 1.51 there is an ulcer due to a basal
cell carcinoma (Fig. 1.52).
SURFACE / 13
d. Change in thickness
Lichenification Fig. 1.54 Lichen simplex Dermal atrophy Fig. 1.55 Due to topical steroids Epidermal atrophy Fig. 1.56 Lichen sclerosus
Thickening of the epidermis with increased skin markings Depression of the surface due to thinning of the dermis. Fine surface wrinkling like ‘cigarette paper’.
due to persistent scratching (found in atopic eczema or Blood vessels are easily seen under the skin.
lichen simplex).
Papillomatous Fig. 1.57 Congential naevus Warty Fig. 1.58 Filiform wart Umbilicated Fig. 1.59 Molluscum contagiosum
Surface consisting of minute, finger-like or round Surface consisting of rough, finger-like projections. Papule with central depression. Characteristically seen in
projections. molluscum contagiosum.
9. COLOUR OF LESION
a. Red, pink or purple b. Brown
Erythema Fig. 1.60 Psoriasis Fig. 1.61 Chilblains Hyperpigmentation Fig. 1.65 Lichen planus Fig. 1.66 Atopic eczema
Redness due to dilated blood vessels that blanche (become white) on pressure. It is the Increase in melanin pigmentation. It usually follows inflammation in the epidermis. In
result of inflammation and is seen most easily in white-skinned individuals. pigmented skin it can be the first sign of inflammation.
Telangiectasia Fig. 1.62 Purpura Fig. 1.63 Fig. 1.64 Haemosiderin pigment Fig. 1.67
Redness due to individually visible dilated Red, purple or orange colour due to blood that has leaked out of blood vessels. Purpura Orange-brown due to breakdown of
blood vessels. does not blanche on pressure and remains the same colour. haemoglobin following purpura.
COLOUR / 15
c. Blue-black d. White
Melanin Fig. 1.68 Blue naevus Depigmentation Fig. 1.69 Vitiligo Hypopigmentation Fig. 1.70 Eczema Reduced blood supply
Melanin pigment situated deep within Complete loss of melanin due to loss of Partial loss of melanin secondary to Fig. 1.71 Naevus anaemicus
dermis, seen in malignant melanoma and melanocytes in the epidermis. inflammation in the epidermis. White colour due to reduced blood supply.
blue naevus.
e. Black-purple f. Yellow g. Blue-grey
Stagnant blood Fig. 1.72 Angioma Lipid deposition Fig. 1.73 Xanthelasma Minocycline pigmentation Fig. 1.74 Gold pigment Fig. 1.75 Chrysiasis
Black-purple colour from dilated blood Yellow colour seen in xanthelasma on inner Grey-blue colour on eyebrow due to Grey-blue colour seen in patients on gold
vessels within the skin. eyelids. deposition of iron. therapy.
10. BORDER OF LESION OR RASH

a. Well defined or circumscribed b. Poorly defined c. Accentuated edge
Able to draw a line around the lesion with Lesions have a border that merges into Border of lesion shows increased scaling
confidence normal skin with relative clearing in the centre
Psoriasis: well-defined plaques Fig. 1.76 Eczema: poorly defined plaques Fig. 1.77 Tinea corporis with accentuated border Fig. 1.78
Superficial basal cell carcinoma: single Solar keratoses: poorly defined papules Fig. 1.80 Basal cell carcinoma with raised rolled edge
well-defined plaque Fig. 1.79 Fig. 1.81
SHAPE / 17
11. SHAPE OF LESION

a. From above
Round or oval Fig. 1.82 Benign moles Irregular Fig. 1.83 Malignant melanoma Square or rectangular Serpiginous Fig. 1.85 ‘S’ shaped – larva
Fig. 1.84 Straight sides – dermatitis artefacta migrans
b. In profile
Dome shaped Fig. 1.86 Benign Spherical Fig. 1.87 Epidermoid cysts/ Pedunculated Fig. 1.88 Fibroepithelial Flat topped Fig. 1.89 Plane warts
intradermal naevus milia polyp – skin tag
SPECIAL INVESTIGATIONS
WOOD’S LIGHT
This is a source of ultraviolet light where visible light is excluded by
a nickel oxide filter. It is useful in identifying scalp ringworm due
to Microsporum species, which fluoresce green (see Fig. 3.12, p. 77),
and erythrasma, which fluoresces bright pink (see Fig. 10.27, p. 348).
Porphyrins in urine and faeces also fluoresce a bright-pink colour.
In pigmentary disorders, the Wood’s light will help distinguish
Fig.1.90 Dermatoscope Fig. 1.91 Angioma: dilated vascular
complete loss of pigment in vitiligo (the skin is completely spaces with red-black colour
white) from hypopigmentation in pityriasis versicolor or post-
inflammatory hypopigmentation (the skin is paler than normal).
DERMOSCOPY
Applying oil to the surface of a skin lesion and looking through the
magnifying lens of a dermatoscope (see Fig. 1.90) is a useful tool for
the diagnosis of pigmented lesions and distinguishing them from
vascular lesions. The dermatoscope is useful also for identifying
scabetic burrows (see p. 249), and distinguishing between scale and
crust.
Vascular lesions are easily distinguished from melanocytic lesions Fig. 1.92 Hereditary haemorrhagic Fig. 1.93 Basal cell carcinoma: blood
because they are red not brown, and you may see individual dilated telangiectasia vessels over the edge
blood vessels.
Seborrhoeic keratoses have white or black keratin cysts on the
surface, and a regular edge.
Pigmented lesions. The main thing you want help with from a
dermatoscope is deciding whether a lesion is benign or malignant.
The majority of pigmented lesions seen in general practice will be
benign. The pigment in a benign naevus may appear as a reticular
network, as dots/globules or be amorphous. Two shades of brown
is acceptable providing there is overall symmetry and the absence of
malignant features. Fig. 1.94 Lentigo Fig. 1.95 Seborrhoeic keratosis
SPECIAL INVESTIGATIONS / 19
The things that would make you ● multiple patterns (reticular network, ● a blue-grey veil, where one or more
suspicious of a malignant melanoma are: streaks, globules of varying size, parts of the lesion is bluish/grey/white.
● asymmetry distribution and colour, blue-grey
For further images see the International
● multiple colours within the lesion (dark veil, amorphous)
Dermoscopy Society website (dermoscopy-
brown, light brown, black, red, grey, ● an irregular edge (i.e. streaks)
ids.org).
blue, white)
Fig. 1.96 Junctional naevus: two Fig. 1.97 Junctional naevus with Fig. 1.100 Abnormal network top Fig. 1.101 Early melanoma:
colours of light brown, symmetrical central amorphous area and regular left of image, and normal network at asymmetry, multiple colours and
reticular pattern peripheral dots bottom right in superficial spreading patterns
melanoma
Fig. 1.98 Junctional naevus with Fig. 1.99 Compound naevus with Fig. 1.102 Superficial spreading Fig. 1.103 Nodular malignant
multifocal hypopigmentation, minor symmetrical shape, globules and malignant melanoma: irregular melanoma: blue-grey veil and linear
colour variation and normal network regular border globules of varying size, no pigment streaks, multiple patterns and colours
pattern network visible
BACTERIOLOGY
Swabs can be taken from vesicles, pustules, erosions or ulcers to identify the causative
bacteria by Gram stain and culture. Viruses can be identified by electron microscopy or
culture. If you suspect herpes simplex or zoster you can do a Papanicolaou (PAP) stain on
blister fluid and see multinucleate giant cells.
MYCOLOGY
Superficial fungal infections caused by dermatophytes (ringworm/tinea) and yeasts
(candidiasis and pityriasis versicolor) all live on keratin and can be identified in scales
taken from the edge of a scaly lesion. Use a blunt scalpel blade (e.g. banana-shaped –
Fig. 1.104 Taking skin scraping using a Swann
Swann Major shape ‘U’, obtainable from Swann-Morton.com). If the scales are too dry major U blade
and do not stick to the blade, moistening the skin with surgical spirit helps. The scales can
be mixed with 20% KOH (potassium hydroxide) solution; to dissolve the keratin, gently
heat the mixture on a glass slide until the solution bubbles. You can examine immediately
under the microscope to see the fungal hyphae or yeast spores (see Fig. 10.03, p. 337, and
Fig. 10.15, p. 342).
Alternatively the skin scales may be sent to the mycology laboratory in special envelopes
(Dermapak.com, PO Box 841, Bedford, MK45 4WG; Mycotrans.com, PO Box 1172, Biggar,
ML12 6NN, Scotland) where direct microscopy and culture can be performed.
SKIN BIOPSY
If the diagnosis is in doubt, an ellipse of skin can be taken through the edge of the lesion,
so that both normal and abnormal skin is included in the specimen. It should include Fig. 1.105 Putting scales into a Dermapak envelope
epidermis, dermis and fat. (black paper so scales show up), which can be sent
to the mycology laboratory through the post
Immune complexes can be identified by immunofluorescence. The sample needs to be
sent to the laboratory in Michel’s medium. In some instances a ‘punch biopsy’ can be
used, which takes a 3–6 mm core of tissue, but this technique produces only a limited
sample, which may be inadequate for proper histological examination.
If a skin tumour is present, the whole lesion should be excised as an ellipse so that the
wound can be sewn up in a straight line.
SPECIAL INVESTIGATIONS / 21
PRICK TESTING PATCH TESTING

This identifies an immediate hypersensitivity reaction in asthma, This is used to identify a type IV hypersensitivity reaction in the
hay fever or allergic urticaria (contact urticaria to fragrances is skin, i.e. allergic contact dermatitis. The allergens are suspended in
done by short contact patch testing). It is not of any use in the white soft paraffin or aqueous solution and placed on aluminium
diagnosis of atopic eczema or idiopathic urticaria. It is useful in discs – 10 mounted on Scanpor tape (Finn Chambers). These are
identifying natural rubber latex allergy. A drop of latex protein applied to the back and left in place for 48 hours. The tapes are
is placed on the forearm and the surface of the skin is broken by removed and a small circular plaque of eczema at the site of the
pricking. A weal indicates a positive reaction. A saline (negative) aluminium disc at 48 and 96 hours indicates an allergic response
and histamine (positive) control should also be used. The risk of to a specific allergen. The relevance of the positive allergen(s)
anaphylaxis is low but resuscitation drugs and equipment should (see Table 1.02) is then determined, and if relevant the patient is
be available. If latex prick testing and a RAST test are negative, advised on avoidance.
then a ‘use test’ wearing a finger of a latex glove on wet skin for
15 minutes, with a finger of a vinyl glove as control, will confirm Table 1.02 Standard battery of allergens and their source
the diagnosis. Allergen Source of allergen
Prescription creams
Budesonide A marker of steroid allergy and suggests the need for further
assessment of possible reactions to other steroids
Caine mix Local anaesthetic ointments
Ethylenediamine Found in Tri-Adcortyl cream, topical antihistamines
Fucidic acid Antibiotic cream – Fucidin and Fucidin H
Neomycin Antibiotic ointment
Quinoline mix Antiseptic agent in steroid creams with letter C or word vioform
Tixocortol pivalate All hydrocortisone creams and ointments
Wool alcohols (lanolin) Oily cream, E45 cream, other ointments with lanolin as the base
Cosmetic products
Propolis Resin found in beehives, used in cosmetics, herbal remedies
Balsam of Peru Fragrances, citrus fruit peel
Fig. 1.106 Prick test: a positive Fig. 1.107 Patch test: 48-hour reading – Fragrance mix Cosmetics with fragrances
result shows a weal around the the patches have just been removed and Cetyl/stearyl alcohol Moisturiser and lubricant, prescribed creams and soap
needle prick after a few minutes a single test (top left) is positive (erythema substitutes, sunblocks
and vesicles = eczema)
Allergen Source of allergen Allergen Source of allergen

Benzalkonium chloride Antiseptic found in creams Rubber chemicals
Paraphenylenediamine (PPD) Permanent hair dyes, temporary tattoos, black rubber Black rubber IPPD Industrial black rubbers, car tyres, boots, hoses, face masks,
(isopropyl-phenyl-PPD) squash balls, black rubber clothing
Disperse Blue mix Dark blue dyes in synthetic materials
Thiuram mix Rubber gloves but also condoms, elasticated bandages,
Preservatives in creams
stockings, elastic in underwear
Formaldehyde Fabrics that are treated with formaldehyde resins to make them
Mercapto mix Rubber shoe soles and insoles, rubber in bandages, clothing,
crease resistant
swimwear, condoms
Preservative in household and industrial products, e.g. cosmetics, Mercaptobenzothiazole
shampoos, cleaners, disinfectants
Carba mix Rubber especially gloves, insoles of shoes, some bandages,
Parabens Preservative in creams and paste bandages condoms
Quaternium–15 Cosmetics: foundation, eye make up, blushers, moisturisers, Glues
shampoos and floor waxes and polishes
Colophony (rosin) Elastoplast, glues and adhesives, chewing gum, paper products,
Kathon CG Isothiazolinone Preservative in hair products, wet wipes, detergents, washing rosin used on violin bows
powders and liquids
PTBPF resin Glues used to stick two layers of leather together in watch
Methylisothiazolinone (MI) Preservative in cosmetics, shampoos and baby wipes (Para-tertiary butyl phenol straps, shoes, handbags and belts
formaldehyde) DIY glues, wood, rubber items
Chlorocresol (PCMC) Preservative in creams, ointments, moisturisers, (not cosmetics
and shampoos) Epoxy resin Glues and adhesives (Araldite), particularly used in boat building,
some dental bonding agents
2-Bromo-2-nitropropane-1-3 Preservative in shampoos, cosmetics, washing detergents and
diol fabric softeners Plants
Imidazolidinyl urea Preservative in cosmetics and hair gels Primin Indoor Primula obconica plant
(Germal 115)
Sesquiterpene Lactone mix Plants of the Compositae family: yarrow, tansy, arnica,
Diazolidinyl urea (Germal II) Preservative in cosmetics, shampoos, sunscreens, deodorants chrysanthemum, chamomile, feverfew, etc.
Compositae Mix II
Methyldibromoglutaronitrile Preservative in cosmetics, shampoos, baby wipes, sunscreens;
Metals
now banned in the European Union
Nickel Most non-rusting metals except silver and gold, especially watch
Chloroxylenol (PCMX) Mainly in Dettol; preservative in steroid creams, soaps,
and belt buckles and cheap jewellery
deodorants, cosmetics, topical antiseptics and industrial liquids Cobalt
Sodium metabisulphate Antioxidant and preservative in creams and ointments, and some Potassium dichromate Cement, leather gloves, leather shoes
foods, beer and wine
23
Introduction to dermatological
treatment
2
General principles of treatment 24
Topical treatment
The base 25
Emollients 26
Active ingredients
Topical steroids 31
Topical immune modulators, Tar 34
Dithranol/anthralin 35
Vitamin D3 analogues 36
Retinoids 36
Keratolytic agents 36
Antibiotics, Antiseptics, Antiviral agents, Antifungal agents 37
Local anaesthetics 38
Sunscreens, Skin camouflage agents 39
Topical agents for wound care 40
Debriding agents 43
Reducing bacterial counts and odour 44
Absorption of exudate 45
Wound and ulcer dressings 46
Systemic treatment
Antibiotics, Antifungal agents 47
Antiviral agents 48
Antihistamines, Retinoids 49
Systemic steroids 51
Immunosuppressive agents 52
Biologic agents 56
Physical treatments
Cryotherapy with liquid nitrogen 58
Iontophoresis 59
Ultraviolet light 60
Photodynamic therapy 63
Lasers 64
24 / INTRODUCTION TO TREATMENT
GENERAL PRINCIPLES OF TREATMENT The patient should be made aware of which of these categories
Make a diagnosis before embarking on treatment. Never think their skin disease fits in, so that they have a better idea of response
of treating a patient without first making a diagnosis or putting to treatment and prognosis.
in hand the necessary investigations so that a diagnosis can be Look at the whole person and not just at his or her rash. Often
reached. the problem that presents itself is quite straightforward but at the
Be realistic about what is possible. Because skin disease is same time there may be deeper needs shouting for attention. Body
visible, the patient will often assume that it must be easy to cure. language speaks louder than words.
Generally speaking, skin disease can be put into three groups with Patients with widespread skin disease often feel dirty, ashamed
regard to this. or guilty, thinking that somehow it is their own fault that they are
1. Those diseases that have a specific cause and hence a specific ill. They may be afraid that their skin disease is contagious, or that
treatment. Once this has been given correctly, this should be they have cancer or a sexually transmitted infection; women with
the end of the problem. Such conditions include: hirsutism may fear that they are turning into men; teenagers with
● allergic contact dermatitis acne lose their self-confidence.
● fungal and bacterial infections
● infestations such as scabies and lice Patients may also be embarrassed about having a rash because:
● skin tumours. ● It is on a part of the body that shows, such as the face or the
2. Those diseases where no cure is possible, but spontaneous hands. They will notice people looking at it and assume that
remissions and exacerbations occur. These may be helped people will think it is contagious, or that they have cancer or
considerably by treatment, but a cure is not possible and a sexually transmitted infection. They will often wear clothes
should not be sought. Examples include: that will hide it and limit their activities so that others will not
● atopic eczema see it (e.g. not going swimming or to the beach on holiday).
● pemphigus and pemphigoid ● The treatment makes a mess. Grease on the clothes and
● psoriasis bedding, and the smell and mess of tar preparations are not
● rosacea. popular with patients or their families.
3. Those diseases that persist for a limited period of time and then ● The shedding of scales makes a mess, particularly in psoriasis.
disappear on their own. This group may require symptomatic ● It smells, especially in patients with ulcerated legs.
treatment, but not always, and the patient should be reassured ● It is present on the genital area. It may interfere with sexual
of their benign nature. Examples of these are: activity because of embarrassment and the patient may be
● alopecia areata ● erythema multiforme afraid that his or her partner will think that it is catching.
● lichen planus ● pityriasis rosea It is important that you understand how the patient feels about
● guttate psoriasis. having a skin problem as well as what to do about it.
TOPICAL TREATMENT / 25
Listen to what the patient has to say. Very often the patient will TOPICAL TREATMENT
tell you what is wrong if you give him or her the opportunity. Any applied agent contains two components:
Understand that not everyone wants to get well. Some patients 1. the vehicle or base
get a lot of attention because of their illness and do not want to 2. the active constituent.
give it up by getting well. For others it is somehow respectable to Both are equally important, but often the right type of vehicle is
have a rash (which will not go away) but not to own up to guilt not taken into consideration when prescribing a treatment. The
about some person or event, a poor self-image or conflict in the function of the base is to transport the active constituent into
family. Using one ointment or pill after another will not resolve the skin so that it is delivered to where it is needed. Generally
any of these and it is better to face up to reality sooner rather than speaking the base is determined by the hydration of the skin at the
later. particular site, while the active constituent is determined by the
Treatment of acute rashes. Resting the skin is important in any pathological process.
acute or extensive skin disease. Going to bed is a helpful treatment
in its own right. It is the basis for most inpatient treatments THE BASE
but can often be done just as well at home (by this we mean All bases are made up from one or more of the following:
actually going to bed and not just lying down on the sofa, as the ● powders, e.g. zinc oxide, starch, calamine (zinc carbonate and
latter will not stop the patient from pottering about). Sedating ferric oxide)
antihistamines (promethazine or alimemazine) may be needed to ● liquids, e.g. water, alcohol, propylene glycol
keep the patient resting in bed. ● oils and greases (ointments), e.g. liquid paraffin, yellow and
white soft paraffinUK/petrolatumUSA, lanolin (wool alcohols),
Localised acute rashes should also be rested. If the patient has an polyethylene glycols (synthetic waxes).
acute blistering rash on the feet, it will not get better unless he or
she stops walking around. A patient with an acute hand eczema is These may be used singly or mixed together to produce shake
unlikely to get better while continuing to do the washing up. lotions, creams and pastes.
The more acute the rash, the more bland the treatment needs to be.
If in doubt, white soft paraffin is unlikely to do any harm and will
keep the patient comfortable.
Explain to the patient what is going on. It is important to explain
to the patient what is wrong with him or her, what the treatment
is and how to use it. Time spent at the first consultation explaining
the nature of the problem and the correct use of the treatment will
be time well spent.
Table 2.01a Emollient products: how and when to use

Type Class Oil (%) Examples (this list is not exhaustive) Definition Usage Patient groups
Leave-on Ointment (no water) 100 White soft paraffin (Vaseline), 100% paraffin base (no Very dry skin Severe atopic eczema
emollients 50/50 white soft/liquid paraffin, preservative required) Use twice a day Ichthyosis
Use as routine Diprobase ointment, Useful at night-time Sprays useful in the elderly
moisturiser Epaderm/Hydromol/Emulsifying oints, Greasy – may put off some and in hard-to-reach areas
anywhere patients
Aerosol spray Dermamist, Emollin spray
Occlusive cream 30–70 Oily cream/hydrous ointment (lanolin), Water-in-oil emulsion (oily/ Dry skin Moderate atopic eczema or
QV intensive, Unguentum M, cold creams) and 100% lipid Trunk and limbs psoriasis
Lipobase (used as a diluent in Lipocream). ointments 2–3 times a day
Emollient gel 30 Doublebase gel, Water and oil emulsion with Very dry skin Very dry skin
containing glycerol Doublebase Dayleve gel humectant Use 3–4× a day, or 2× a day Psoriasis,
Water held in stratum corneum for Dayleve Ichthyosis
by humectant (glycerol or urea)
Emollient cream 5–10% Aquadrate, Balneum cream, Calmurid, Dry skin Useful in older patients and in
containing urea urea E45 Itch Relief, Eucerin intensive, Use twice a day psoriasis
Hydromol intensive, Nutraplus.
Emollient cream 11–30 Aquamax, Aquamol, Oil-in-water emulsion (vanishing Normal to dry skin conditions Mild/moderate atopic eczema
(others without urea) Aveeno cream (colloidal oatmeal), cream) Face and flexures Other dry skin conditions such
Cetraben, Diprobase cream, (Note: tubs can become Good patient compliance as psoriasis and endogenous
Epaderm cream, E45 cream (lanolin), contaminated – prescribe 3–4x a day eczema
pumps)
Hydromol cream, Oilatum cream
QV cream (contains glycerol), Ultrabase
Zerocream, Zerobase cream, Zeroguent
with antimicrobial Dermol cream, Eczmol cream Product contains benzalkonium Useful in preventing flares of Infected/colonised atopic
chloride, and/or chlorhexidine atopic eczema eczema
Emollient lotion 5–14 Dermol lotion
Use lotions as a soap Healthcare workers
with antimicrobial
substitute Folliculitis
Easy to apply 4x day
without antimicrobial Aveeno lotion (colloidal oatmeal), Oil-in-water emulsion with low Poor compliers (teenagers,
oil content Hairy areas (e.g. trunk, scalp) men)
E45 lotion (lanolin),
Lighter than creams Summertime use
QV lotion
Antipruritic emollient Balneum Plus cream, Product contains antipruritic Pruritus, especially if due to First-line therapy for itching
E45 Itch Relief cream agents (lauromacrogols) dry skin (especially in the elderly)
Adapted from Moncrieff G, Cork M, Lawton S, et al. Use of emollients in dry-skin conditions: consensus statement. Clin Exp Dermatol. 2013; 38: 231–8.
Topical treatment / 27
Table 2.01b Wash and bath emollient products: how and when to use
Type Class Oil (%) Examples Definition When to use Patient groups
Wash Emollient wash 15–30 Aquamax cream wash, Products contain emulsifiers Instead of soap, which is an irritant Atopic eczema
products products Doublebase shower gel, Should NOT contain harsh and therefore should be avoided in Hand dermatitis and psoriasis
Use only for E45 wash cream, detergents such as sodium lauryl any dry skin conditions
washing, do Hydromol bath and shower emollient, sulphate (e.g. aqueous cream)
not leave on
QV gentle wash,
the skin
Oilatum shower emollient.
Antimicrobial wash 2–30 Dermol shower/wash/lotion, Emollient wash product containing Useful in managing and preventing Recurrent infections or
products Eczmol cream. topically active antimicrobial agents flares of atopic eczema relapses in atopic eczema and
(such as benzalkonium chloride and/ hand dermatitis
or chlorhexidine)
Bath Bath oil: 50–91 Aveeno (colloidal oatmeal), Deposits a layer of oil on the surface All patient with moderate-very dry Use as part of complete
emollients Semi-dispersible oil Balneum, Cetraben, Dermalo, of the water that leaves a slick skin (atopic eczema, ichthyosis) emollient therapy in all dry
Add to bath or Diprobath, around the bath; non-foaming and Bathing in water alone is drying; skin conditions (see p. xx)
water, can be fragrance free bath oils should not be rinsed off
dispersible Doublebase bath additive.
used to wash emulsion Oil disperses evenly through the
E45 bath oil,
with bath water
LPL 63.4, Oilatum,
QV bath oil, Zerolatum, Zeroneum
Antimicrobiol 50–55 Dermol bath, Bath oil containing topical Prevention of infection. Atopic eczema with recurrent
bath oil Emulsiderm, antiseptic agent infections
Oilatum Plus, Zerolatum Plus
Antipruritic bath 85 Balneum Plus bath oil (soya oil) Bath oil containing topical Protection of the skin barrier during Should be used in conjunction
oil antipruritic agent bathing if pruritus is a problem with an antipruritic emollient
Ointments Organic hydrocarbons are subdivided by their melting points:

Ointments contain little or no water and consist of organic ●● liquid paraffinUK/liquid petrolatumUSA is liquid at room
hydrocarbons, alcohols and acids. These are greasy and temperature and is used in bath oils
form an impermeable layer over the skin, which prevents ●● white soft paraffinUK/petrolatumUSA is semi-solid at room
evaporation of water. Examples include: temperature, but melts at body temperature, so rubs in easily; a
●● white soft paraffinUK/petrolatumUSA (Vaseline) mixture comprising equal parts of liquid paraffin and white soft
●● emulsifying ointmentUK paraffin is useful for covering large areas of the body with grease
●● lanolin (wool fat purified from sheep wool 6%, paraffins ●● waxes have high melting points and are useful for stiffening up an
94%). ointment base.
Some ointments may be water-soluble and consist of polyethylene such as parahydroxybenzoic acid esters (parabens), chlorocresol,
glycols such as fatty acid propylene glycol (used as the base for propylene glycol or ethylenediamine to prevent the cream from
Metosyn cream). These compounds are semi-solids similar to white becoming contaminated by bacteria. All these preservatives can
soft paraffin, so they spread well on the skin and wash off with act as sensitisers and cause an allergic contact dermatitis in some
water. patients.
2. A water-in-oil emulsion (like butter). These are the cold
Creams creams. They behave like oils in that they do not mix with any
Creams are a mixture (emulsion) of an ointment with water. In exudate from the skin. They are easier to apply than ointments,
order to prevent the two elements separating from one another, and more cosmetically acceptable, although they are greasier
stabilisers and emulsifiers have to be added. Sodium lauryl than the vanishing creams. Many of them contain lanolin as
sulphate (SLS) was first produced in 1958 as one of the first the oil, which can cause an allergic contact dermatitis in some
emulsifiers, but now should not be used in eczema, as it has been patients. Examples include:
shown to damage the natural moisturising factor found in the ● oily cream/hydrous ointmentUK (lanolin 50%, water 50%)
stratum corneum. There are two types of cream: ● Pond’s Dry Skin creamUSA.
1. An oil-in-water emulsion (like milk and cream). These are
the vanishing creams. They rub into the skin easily and mix Humectants (substances that retain water, such as glycerol,
readily with water so they are more cosmetically acceptable propylene glycol and urea) can be added to creams to reduce the
than oily creams or ointments. They contain a high proportion amount of oil in the base without losing the moisturising effect.
of water and the oil component is kept in solution by using an
emulsifying agent such as glycerol or sodium lauryl sulphate. Lotions
Examples of oil-in-water creams are: A lotion is any liquid such as normal saline or potassium
● aqueous creamUK – not to be used as a leave-on emollient permanganate solution. A shake lotion is a suspension of an
because it contains SLS insoluble powder in a liquid, such as calamine lotion (15%
● cetomacrogol A is used as a diluent for many steroid creams calamine, 5% zinc oxide, 5% glycerine, 75% water). This has a
● hydrophilic ointmentUSA. cooling effect because the liquid evaporates leaving the inert
powder on the skin. In practice these are hardly ever used except
One of the main disadvantages of creams is that they tend to to cool sunburn.
make dry skin even drier because the water in them evaporates.
Emollient lotions contain a low concentration of oil (5%) in water.
If the skin is dry (e.g. in atopic eczema) a vanishing cream may
They spread easily and are useful as moisturisers for hairy areas
make the condition worse; a cold cream or ointment will be better
such as the chest and back of men (see Table 2.01a).
A further disadvantage is that they must contain preservatives,
Pastes When to use which kind of vehicle

Pastes are a mixture of a powder in an ointment. They stay where Ointments and creams are used most of the time. Which you use
you put them and they do not spread away from that site like depends mainly on the patient’s preference and the hydration
creams and ointments do as the skin warms up. Examples include: of the skin. Start with a cream on normal or moist skin and an
● Lassar’s pasteUK – this contains 2% salicylic acid, 24% zinc ointment on dry skin.
oxide, 24% starch and 50% white soft paraffin
Creams are much more cosmetically acceptable, particularly on
● zinc oxide pasteUSA is the one most commonly used – it contains
the face (patients do not like walking around with a shiny face),
25% starch, 25% zinc oxide and 50% white soft paraffin.
in the flexures and when the medicament has to be applied all
Cooling pastes are preparations that contain a powder (zinc over (so that the clothes are not covered with grease), but may
oxide), water (lime water) and an oil (arachis oil). They are called be too drying if the skin is itself dry (e.g. in patients with atopic
creams rather than pastes in the United Kingdom. For example: eczema and ichthyosis). In general, ointments are more effective
● zinc cream BP (zinc oxide 32 g, oleic acid 0.5 mL, arachis oil than creams, as they are occlusive and do not contain potential
32 mL, wool fat 8 g, calcium hydroxide 45 mg, water to 100 g). allergens. You may have to try both to see which suits the patient
best. Because creams contain water, they must also contain
Gels preservatives to prevent contamination by bacteria and fungi;
Traditionally, gels are two-component semi-solid systems of these preservatives can cause an allergic contact dermatitis. In
natural or synthetic polymers (e.g. methylcellulose, agar, carbomer patients with an acute eczema or contact allergic dermatitis where
or gelatine) in a liquid (e.g. water). These polymers build a three- you do not know the cause, always use an ointment (and one
dimensional matrix throughout a hydrophilic liquid, from which that does not contain lanolin) rather than a cream until you have
the active ingredients diffuse relatively freely. They have the discovered the cause.
property of being semi-solid in the cold and becoming liquid on
Gels are used as alternatives to ointments on the body and lotions
warming up (e.g. when rubbed into the skin).
on hairy parts of the body. For instance, since all topical steroid
Emollient gels (Doublebase) are a water and oil emulsion with lotions are in an alcoholic base they are not suitable for applying
a jelly feel. Salts in the skin induce separation of the water and to excoriated eczematous skin, because they will sting. A steroid
oil. The water is held in the stratum corneum by a humectant gel (which does not contain alcohol) can be rubbed into the scalp
(glycerol), which is sealed in by a lipid layer. without causing stinging. It becomes liquid when it is rubbed in
and is therefore cosmetically acceptable (like a lotion).
Due to the lightweight feel and the absence of an oily phase, gels
are also popular as a moisturiser (Doublebase), or for delivering
the active ingredients in the treatment of acne vulgaris, and
psoriasis (Dovobet gel).
Lotions are used on wet surfaces and on hairy areas, for example:
● in the mouth as a mouthwash
● on the scalp so that it does not make a mess
● on wet rashes (e.g. weeping eczema).
For wet rashes, use an astringent that will coagulate protein

and dry up the exudate. The two that are commonly used are as
follows.
1. Potassium permanganate (KMnO4): this is dispensed as
crystals, as a tablet (PermitabsUK – see Fig. 2.01) or a made-up
solution. The affected area can be bathed in this solution to dry
up exudate. If the solution used is too strong (i.e. purple), the
skin and nails will be stained brown (see Fig. 2.02).
Fig. 2.01 Permitabs: place two tablets of potassium permanganate (above left)
2. Aluminium acetate (Burow’s solution): it is made by mixing in a universal container, add water and shake to produce a dark-purple solution
five parts of a 13% solution of aluminium acetate in 100 parts (left tube above right); add a few drops of this solution to a bowl of water to
of sterile water, or by dissolving a packet or tablet of Domeboro produce a light-pink colour, which is how it should be used (right tube)
or Bluboro in 1 pint of water. This is used as a soak. The neat
13% solution may be used as ear drops to treat exudative otitis
externa.
Pastes are used where you want to apply a noxious chemical to a
particular part of the skin without getting it onto the surrounding
normal skin, e.g. dithranolUK (anthralinUSA) in psoriasis. They are
rarely used except in hospital because they are unsightly. They Fig. 2.02 Staining of
have to be applied with a gloved hand or a spatula and they have toenails and feet from
to be cleaned off with oil (e.g. arachis oil) rather than soap and soaking in potassium
permanganate solution
water. that is too strong (purple
colour); if the pink colour
is used, this will not occur
ACTIVE INGREDIENTS Absorption of topical steroids

Topical steroids The potency of the steroid molecule can be enhanced by the base
Topical steroids are extremely useful in inflammatory conditions used, e.g. an ointment base makes the steroid more potent than a
of the skin, particularly in eczema, but they are not the treatment cream or lotion. Occlusion over the site of application increases the
for everything (they are contraindicated in acne, rosacea, all steroid potency 50-fold. Occlusion causes over-hydration of the
infections [bacterial, viral and fungal] and infestations). stratum corneum, reducing the skin’s natural barrier. It induces a
reservoir effect so that the steroid can persist in the skin for several
Topical steroids are divided into four groups in the United days. The site and degree of inflammation also affects absorption.
Kingdom and seven groups in the United States according to their The relative ability to be absorbed at various sites is:
potency (see Table 2.02).
back < forearm < scalp < forehead < cheeks < axilla < scrotum
There are a very large number to choose from and it is best to normal skin < inflamed skin < erythrodermic skin.
become familiar with a few (perhaps one or two from each group)
rather than all of them. Relative potencies of the different groups Application of topical steroids
compared with the potency of 1% hydrocortisone are important in Although topical steroids are traditionally applied twice a day,
deciding on which topical steroid to use. As a general rule, use the there is no evidence that this is the best way to use them. Since the
weakest possible steroid that is effective. steroid molecule persists in the stratum corneum and is slowly
We would recommend that you only use 1% hydrocortisone or absorbed, it may be that a single application at night would work
equivalent (weakUK/group 6–7USA) topical steroid on the face. just as well. Using a moisturiser frequently in the daytime might
For eczema on the trunk and limbs you can use a moderately be more effective than increasing the number of applications of a
potentUK/group 4–5USA steroid. The potentUK/group 2–3USA is topical steroid.
useful for localised persistent eczema. Remember that in the Repeated application of potent topical steroids can result in a
flexures absorption of the steroid will be increased because of diminished effect (tachyphylaxis). Recovery of response returns
occlusion. within a week of stopping. To prevent this happening, use potent
steroids for 3–5 days at a time followed by a moisturiser for the
There is little place for very potentUK/group 1USA steroids in
next 3 days.
general practice, and where you might be considering their
use, systemic steroids might be safer. As little as 50 g of 0.05% One 15 g tube of ointment or cream is enough to cover the adult
clobetasol propionate (DermovateUK/TemovateUSA) per week will body surface once; daily application for a week will require
suppress the patient’s adrenal glands. Hydrocortisone is 50 times over 100 g. If a patient has widespread eczema, adequate amounts
weaker so is obviously a lot safer; in theory a patient could use up of topical steroid should be prescribed or he or she is likely to
to 2.5 kg/week before getting the same side effects. relapse. A useful guide is the fingertip unit, which is the amount
that is squeezed onto the index finger from tip to the distal
interphalangeal joint.
Table 2.02 Classification of topical steroids by potency Table 2.03 Fingertip units as a guide to quantities
Group UK brands USA brands Clinical indication needed to cover body surfaces
WeakUK Hydrocortisone 0.5%, 1.0%, 2.5% Hydrocortisone 0.5%, 1.0%, 2.5% Eczema on the face No units Quantity g Area of skin to cover
Group 6–7USA (Dioderm, Mildison) (numerous products) Eczema at any site in 1 0.5 Both palms
Potency = 1% Fluocinolone 0.0025% Alclometasone 0.05% (Aclovate) infants
hydrocortisone (Synalar 1:10) cream Desonide 0.05% (Desowen/Tridesilon) 2.5 1.25 Face and neck
Medium potentUK Betamethasone valerate 0.025% Clocortolone pivalate 0.1% Eczema (atopic) on 3 1.5 Arm
Group 4–5USA (Betnovate RD) Desoximetasone 0.05% (Topicort LP) the trunk and limbs, or 6 3 Leg
Potency = 2.5 Clobetasone butyrate 0.05% Fluocinolone 0.025%* flexures (both adult or
7 3.5 Trunk front or back
(×1% (Eumovate) children)
Fluticasone 0.005% (Cutivate)
hydrocortisone) Fluocinolone .00625% (Synalar 1:4) Seborrhoeic eczema on Infants <1 year = ¼ of above; 1–3 years = ½ of above
Flurandrenolide 0.05%
Fluocortolone 0.25% (Ultralanum trunk
Hydrocortisone butyrate 0.1% (Locoid)
plain) Flexural psoriasis
Hydrocortisone valerate 0.2%*
Fludroxycortide 0.0125% (Haelan)
Hydrocortisone probutate 0.1%
Hydrocortisone 17-butyrate 0.1%
Prednicarbate 0.1%
(Locoid)
Triamcinolone 0.025%* (Kenalog)
PotentUK Betamethasone dipropionate 0.05% Amcinonide 0.1% (Cyclocort) Lichenified atopic eczema
Group 2–3USA (Diprosone) Betamethasone dipropionate 0.05% Discoid eczema
Potency = 10 Betamethasone valerate 0.1% (Diprolene) Varicose eczema
(×1% (Betnovate) Betamethasone valerate 0.1% (Beta-Val) Scalp eczema
hydrocortisone) Diflucortolone valerate 0.1% Desoximetasone 0.05% (Topicort) Hand and foot eczema or
(Nerisone) Diflorasone diacetate 0.05% (Apexicon) psoriasis Fig. 2.03 Fingertip unit
Fluocinolone acetonide 0.025% Fluocinonide 0.05% (Lidex) Lichen planus
(Synalar)
Halcinonide 0.1% (Halog)
Fluocinonide 0.05% (Metosyn)
Mometasone furoate 0.1%* (Elocon)
Fluticasone propionate 0.05%
Triamcinolone 0.5%, 0.1%*
(Cutivate)
Mometasone furoate 0.1% (Elocon)
Very potentUK Clobetasol propionate 0.05% Clobetasol propionate 0.05% Lichen simplex
Group 1USA (Dermovate) (Temovate) Resistant discoid eczema
Potency = 50 Diflucortolone valerate 0.3 (Nerisone Fluocinonide 0.1% (Vanos) Discoid lupus
(×1% forte) Halbetasol propionate 0.05% (Ultravate) erythematosus
hydrocortisone) Lichen sclerosus et
atrophicus
Note: *cream in a lower potency group; the ointment and cream base may result in differing groups for same molecule.
Side effects of topical steroids

● Skin atrophy (Fig. 2.04) and striae (p. 212) from loss of collagen
● Tearing of the skin leading to odd-shaped scars (stellate scars)
due to loss of dermal collagen (Fig. 2.05)
● Easy bruising due to loss of collagen support of the blood
vessels in the dermis (Fig. 2.05)
● Perioral dermatitis (see p. 115) when steroids stronger than 1%
hydrocortisone are applied to the face of young adults
● Telangiectasia on the face when steroids stronger than 1%
hydrocortisone are applied to the face in middle and old age
(see Fig. 5.21, p. 122)
● Rebound phenomenon causing worsening of the skin condition
when the steroid is stopped
● Susceptibility to infection (bacterial, viral and fungal)
● Tachyphylaxis: repeated use results in loss of effect Fig. 2.04 Skin atrophy in a patient with atopic eczema from long-term
● Allergic contact dermatitis: about 2% of patients being treated application of topical steroids – note patch of eczema on right
with topical steroids become allergic to the steroid itself (rather
than the base)
● Cushing’s syndrome when large amounts of potent or very
potentUK/groups 1–3USA steroids are used; this includes a moon
face and buffalo hump and all the systemic effects that you get
with oral steroids (see p. 51)
Fig. 2.05 Stellate scars and bruising due to loss of dermal collagen following
long-term use of topical steroids
Topical immune modulators other cytokines by activation of the TLR7 (Toll-like receptor) on
Calcineurin inhibitors monocytes, macrophages and dendritic cells. It has both anti-viral
and anti-tumour activity.
These are macrolide lactones isolated from Streptomyces
tsukubaensis. They block the activity of calcineurin and inhibit The following treatment regimens are used:
T-cell activation. Their action is very similar to that of ciclosporin, ● genital warts: three times a week for up to 16 weeks
but because of their lower molecular weight they are absorbed ● solar keratoses: three times a week for 4 weeks
through the skin. ● Bowen’s disease: five times a week for 6 weeks*
● superficial basal cell carcinomas: five times a week for 6 weeks*
Two agents are currently available: ● lentigo maligna five times a week for 12 weeks*
1. 0.03% and 0.1% tacrolimus (Protopic) ointment
2. 1% pimecrolimus (Elidel) cream. (*Stop and reduce to three times a week if a severe reaction
occurs.)
Their main use is in atopic eczema. Tacrolimus is as effective as a It produces a marked inflammatory reaction (see Fig. 9.72b, p. 291)
moderately potentUK/group 4–5USA steroid, while pimecrolimus that although dramatic is non-scarring. Assess the efficacy when
is more equivalent to 1% hydrocortisone in potency. Because the inflammatory response has subsided.
they have no effect on collagen synthesis, there is no thinning or
bruising of the skin from long-term use. The only important side Tar
effect is itching and burning of the skin in up to 50% of patients Tar is not used very much these days because it is brown and
when they are first applied. This lasts for 15–20 minutes but stops smelly and patients do not like it. It is still used occasionally in
after the first few days. both eczema and psoriasis. There are basically three types of tar
The standard regimen for their use is twice a day for 2 weeks, then available.
once a day for a month or so. They are useful as a prophylactic 1. Wood tars, which are produced by the destructive distillation
in eczema – applied twice weekly to at-risk sites. There are of beech, birch, pine or juniper. Oil of Cade can be used to treat
theoretical concerns about their use since they reduce the psoriasis of the scalp.
skin’s ability to repair sun damage. Sun protection should be 2. Bituminous tars were originally obtained from the distillation
recommended. Stop using it prior to sunny holidays or if light of shale deposits containing fossilised fish, hence the name
therapy is to be used. There is no firm evidence that they can lead ichthyol. They are mainly used today in paste bandages
to cutaneous lymphoma. (e.g. ichthammol bandages, IchthopasteUK) to soothe chronic
eczema.
Toll-like receptor 7 activators 3. Coal tars are a mixture of about 10 000 different compounds,
Imiquimod (Aldara) cream is the first of a new group of mainly aromatic hydrocarbons such as benzol, naphthalene
compounds that stimulate the production of interferon and and anthracene. Crude coal tar is what remains when coal
is heated without air, originally to Coal tar solution is less messy but also less effective. The messier the tar preparation
produce coal gas. Which compounds in the more effective it is, but less cosmetically acceptable for the patient. Coal tar solution
tar actually work is not known. They can be dispensed as an ointment (2%–10% coal tar solution in white soft paraffin) or as
reduce DNA synthesis and therefore numerous proprietary creams, lotions, scalp applications or bath oils.
epidermal proliferation and they are
useful for stopping itching. Crude coal Side effects of tar and problems with using it
tar can be refined by boiling and then ● It is brown, smelly, and it will stain the clothes and bedding.
alcoholic extraction to produce coal tar ● It can cause an irritant reaction on the skin.
solution (liquor picis carbonisUK/liquor ● Occasionally it will cause an allergic contact dermatitis.
carbonis detergensUSA). ● It may cause a photosensitivity reaction.
● It can cause a folliculitis on hairy areas and is best avoided in hairy patients.
Crude coal tar is now only used for
treating psoriasis and eczema as an DithranolUK/anthralinUSA
inpatient or in a treatment centre. It is
This is a synthetic anthracene derivative
usually prescribed as coal tar and salicylic
which can be very effective in the treatment
acid ointment BPUK (2% crude coal tar and
of stable plaque psoriasis. It is a yellow
2% salicylic acid), White’s tar ointmentUSA
powder that can be made up into a cream,
(5%), or various strengths (2%–10%) in
ointment, stick or paste. The major problems
white soft paraffin or Lassar’s paste.
with dithranol are:
● irritation and burning of normal skin
● brown discoloration of the skin and a
mauve/purple staining of the patient’s
clothes that will not wash out.
For these reasons it is rarely prescribed,

as patients find it difficult to use at home.
It is best applied in Lassar’s paste at a
dermatology department by trained nurses.
Fig. 2.06 Coal tar solution in WSP (left) and crude Fig. 2.07 Dithranol stain over treated psoriatic
coal tar ointment (right) plaques
Vitamin D3 analogues Keratolytic agents

Calcitriol (Silkis), calcipotriol (Dovonex), and tacalcitol These are used to remove hyperkeratosis in a whole variety of
(Curatoderm) are vitamin D3 analogues that are the first-line skin conditions including warts, hyperkeratotic eczema on the
treatment for psoriasis (see p. 228). They decrease epidermal palms and soles, psoriasis and palmoplantar keratoderma. The
proliferation and are effective in flattening the psoriatic plaques ones most commonly used include the following.
and removing the scale but not so good at getting rid of the 1. α-hydroxy acids
redness. Only calcitriol and tacalcitol can be used on the face and ● Salicylic acid ointment applied twice a day is useful for
flexures. Calcipotriol can cause redness and irritation at these sites treating hyperkeratosis of the palms and soles or plane
and occasionally elsewhere. They do not cause hypercalcaemia warts. The 2% ointment BP is readily available, but
and hypercalcuria, since less than 1% applied to the skin is higher strengths (5%, 10%, 20%) need to be made up by
absorbed. a pharmacy (and can be expensive). It can be mixed with
coal tar (coal tar and salicylic acid ointment BP) for treating
They can be used in conjunction with a potentUK/group 2–3USA
psoriasis, or with a topical steroid ointment (Diprosalic) for
topical steroid for a limited time only (not more than 1 month).
treating hyperkeratotic eczema.
● Lactic acid is a useful moisturiser, either in over-the-
Retinoids
counter products or combined with urea (AquadrateUK,
Topical retinoids act by increasing epidermal turnover and
CalmuridUK). It is also combined with salicylic acid in
differentiation of corneocytes. Clinically they are useful for
proprietary wart paints (see p. 434).
treatment of comedones in acne (see p. 119). They can occasionally
● Benzoic acid is combined with salicylic acid (in Whitfield’s
be useful in psoriasis (see p. 228). Retinoic acid also has an effect
ointment) for treating superficial fungal infections (see
on the dermis whereby solar damage and solar elastosis may be
p. 37).
reversed. The irritant effects of retinoic acid – inflammation and
2. Propylene glycol is included in over-the-counter products and
skin peeling – limit its usefulness.
acts as a humectant (absorbs and retains water) and keratolytic
The topical retinoids available for acne are: agent. For hyperkeratotic eczema of the hands and feet 50%
● 0.1% adapalene (Differin) cream and gel – a synthetic retinoid propylene glycol in water can be used under polythene
that avoids the irritancy of the retinoic acids occlusion at night to reduce the excess keratin.
● 0.05% isotretinoin (13-cis-retinoic acid) as Isotrex gel. 3. Urea, like propylene glycol, is both a humectant and a
keratolytic agent. 10% urea cream (multiple brands) can
The topical retinoid used for psoriasis is:
be used for keratosis pilaris (see p. 324) or mixed with 1%
● tazarotene 0.05% gel (Zorac). This can cause irritation if applied
hydrocortisone cream (AlphadermUK, Calmurid HCUK, Carmol
to the normal skin around the psoriasis.
HCUSA) to treat atopic eczema. It can be combined with lactic
acid as a moisturiser (AquadrateUK, CalmuridUK, UreacinUSA).
Antibiotics Antiseptics
As a general rule, topical antibiotics should not be used on the Chlorhexidine and benzalkonium chloride are combined with
skin because most of them are potent skin sensitisers and will moisturisers as soap substitutes (DermolUK, EczmolUK). Aqueous
cause an allergic contact dermatitis. You do not want to sensitise cream contains 1% phenoxyethanol. These can all be irritant,
someone to a drug that may at some future date be life-saving. It is especially in patients with atopic eczema.
much easier to become allergic to an antibiotic applied to the skin
Nasal and flexural carriage of S. aureus can result in recurrent skin
than to one taken by mouth or given parenterally.
infections. A 4% chlorhexidine wash to the body once daily for
Virtually everyone will become sensitised to penicillin so this 5 days can reduce infected episodes. Octenilin is an alternative to
should never be used topically. Tetracyclines rarely cause the irritant chlorhexidine-containing body washes in patients with
problems and would be safe to use, but in practice they are not atopic eczema.
much use because the common skin pathogens, Staphylococcus
aureus and Streptococcus pyogenes are not sensitive to tetracycline. Antiviral agents
Mupirocin (Bactroban), fusidic acid (Fucidin) and retapamulin The only topical antiviral agents currently available are 5%
(Altargo) are the ones most commonly used. aciclovir (Zovirax) cream and 1% penciclovir (VectavirUK/
DenavirUSA) cream. They are used for the treatment of herpes
Topical antibiotics should only be used in very superficial
simplex (see p. 108). They inhibit phosphorylation of viral
infections that will clear up in a matter of days, i.e. impetigo. They
thymidine kinase, which prevents viral DNA synthesis and virus
should not be used in infected eczema, as skin bacterial carriage
replication. There must be active viral replication to be effective so
is never cleared and antibacterial resistant strains are promoted.
they need to be used immediately the first symptoms are noticed
Also, the patient may well become sensitised after using it
(usually tingling or paraesthesia). They are applied five times a
several times. The same is true for chronically infected leg ulcers
day for 2–3 days until crusting has occurred.
(almost all patients with chronic venous ulceration are allergic to
a number of antibiotics on patch testing because they have been Antifungal agents
used inappropriately in the past).
Those active against dermatophyte fungi (tinea).
Do not be tempted to use steroid–antibiotic mixtures (e.g. Fucibet), ● Keratolytic agents act differently to all other antifungal agents.
because if the patient becomes allergic to the antibiotic in the They remove the keratin on which the fungus lives rather
mixture, the topical steroid will damp down the local reaction than killing the fungus itself. The one most commonly used is
and you will only realise what has happened when the patient Whitfield’s ointment, a mixture of 6% benzoic and 3% salicylic
develops a widespread eczema. Most bacterial infections of the acid in emulsifying ointment.
skin are more appropriately treated with systemic antibiotics.
The others all interfere with the synthesis of ergosterol in the ● Polyenes: nystatin (named after the New York State
fungal cell membrane. Department of Health) is only effective against Candida –
● Undecanoate as the acid zinc salt in MycotaUK, or DesenexUSA it is cheaper than the imidazoles but has the disadvantage
powder: these proprietary powders can be bought over the that it stains everything it comes into contact with yellow;
counter. amphotericin B is a broad-spectrum polyene antifungal agent
● Tolnaftate (MycilUK, TinactinUK, TinadermUK) is fungistatic. It is used as lozenges for treating Candida infections in the mouth.
sold over the counter as a powder or cream. ● Clioquinol is effective against Candida and various bacteria
● Amorolfine (Loceryl) is fungistatic. It is available as a nail but not against dermatophytes. It is usually combined with a
lacquer or cream. The nail lacquer needs to be applied topical steroid (e.g. Ala-QuinUSA, Betnovate CUK, Locoid CUK,
weekly after filing the surface of the nail. In the nails it also Vioform HCUK). It stains the skin and clothing yellow.
works against saprophytic moulds (such as Hendersonula or ● Rosaniline dyes: gentian violet is effective against yeasts and
Scopulariopsis). Gram-positive organisms. It is used as a 0.5% aqueous solution
● Imidazoles: there are a large number of drugs in this group but stains everything it comes into contact with purple. It is
available as creams (clotrimazole, econazole, ketoconazole, useful in wet areas, e.g. toe webs and flexures.
miconazole, oxiconazoleUSA, sulconazole). Tioconazole
(TrosylUK) is another used as a nail lacquer. They are all LOCAL ANAESTHETICS
fungistatic rather than fungicidal and of more or less equal Topical local anaesthetics are useful in children when applied
efficacy. A number of imidazole–hydrocortisone mixtures before giving an injection of local anaesthetic, or for providing
are also made; these generally are not a good idea, because it anaesthesia to large areas of skin, e.g. before cautery of comedones
encourages treatment without first making a diagnosis on the or laser treatment.
mistaken belief that they will work for both fungal infections
The one most commonly used is EMLA cream (a eutectic mixture
and eczema.
of local anaesthetics), which contains 2.5% lignocaine and 2.5%
● Allylamines: terbinafine (Lamisil) and naftifineUSA are
prilocaine in an oil-in-water cream base. This combination allows
fungicidal and more effective than any of the other topical
penetration of local anaesthetic through the stratum corneum.
antifungal agents.
It is applied under occlusion (i.e. a film dressing) and left on for
90 minutes for maximum effect. Both are amides so do not cause
Those active against yeasts such as Candida and Pityrosporum
contact sensitisation.
species.
● Imidazoles are broad-spectrum antifungal agents that work for Tetracaine (amethocaine, Ametop) gel is an alternative and needs
yeasts as well as dermatophytes (see previous list). to be applied for only 45 minutes. Occlusion is not necessary but it
can cause some local vasodilation and irritation.
SUNSCREENS particles that will scatter as well as absorb ultraviolet light

Sunscreens work either by absorbing or reflecting ultraviolet light. (not available in the United States)
● bemotrizinol (bis-ethylhexyloxyphenol
Absorbent sunscreens contain chemicals that absorb ultraviolet methoxyphenyltriazine) is highly photostable and helps
light. prevent the photodegradation of other compounds,
1. Those that protect the skin from UVB (290–320 nm). They are especially avobenzone (not available in the United States).
useful in protecting against sunburn, preventing solar urticaria
or polymorphic light eruption (see p. 100). Examples include: Reflectant sunscreens contain inert mineral pigments, either
● PABA (para-aminobenzoic acid) esters, e.g. Padimate O titanium dioxide or zinc oxide, which put an opaque barrier
(octyldimethyl PABA) – only gives partial protection against between the sun and the skin. They protect against both UVB
UVB, but penetrates into the stratum corneum after ½ to and UVA but are unsightly for the patient because they are white.
2 hours, so not easily removed by water Newer, microsized particles of titanium dioxide to some extent
● cinnamates – these have tended to replace PABA esters overcome this problem, but most high-factor sunscreens contain a
but are a less effective screen, e.g. octinoxate (octyl mixture of organic filters and an inorganic reflectant (TiO2).
methoxycinnamate), octocrylene, amiloxate (isoamyl The efficacy of sunscreens in protecting against UVB is measured
p-methoxycinnamate) by the sun protection factor (SPF). The higher the number, the
● salicylates are less effective but are water-resistant and safe
greater the protection. An SPF of 10, for example, allows a person
at higher concentrations, e.g. octisalate (octyl salicylate) to remain in the sun 10 times longer than he or she normally
● ensulizole (phenylbenzimidazole sulphonic acid) is water-
would before burning. Anything above SPF 30 is probably
soluble so used in lighter, less oily cosmetics for routine adequate. A sunscreen should be applied quite thickly and
cosmetic use. reapplied every 2 hours. This is probably more important than
2. Those that protect primarily against UVA (320–400 nm). These the actual SPF value. If UVA protection is required, make sure the
are needed for patients with porphyria, photosensitive eczema sunscreen contains either avobenzone or titanium dioxide.
or photosensitivity due to drugs:
● avobenzone (butyl methoxydibenzoylmethane) has SKIN CAMOUFLAGE AGENTS
excellent protection in the whole of the UVA range, but it These are used to cover up birthmarks, scars and pigmentary
needs to be carefully combined with other sunscreens. disorders. They are ointments with a high pigment content set
3. Those that protect against UVB and UVA up to 350 nm: with a finishing powder that makes them waterproof. They are
● oxybenzone (benzophenone-3)
smudge proof but not rub proof; they need to be touched up or
● anthranilates, e.g. meradimate (methyl anthranilate)
removed (on the face) after 8–16 hours. To get the right skin match
● bisoctrizole (methylene bis-benzotriazolyl
they need to be applied initially by a skilled professional. In the
tetramethylbutylphenol) is produced as microfine organic United Kingdom the Red Cross run private clinics. Patients with
hyperpigmentation may need an ‘undercoat’ before the skin match
is applied. Topical treatments and sunscreens can be applied done by using a debriding agent or surgically with a pair of
before the camouflage. Make-up should be applied afterwards. scissors or a scalpel by a competent practitioner.
Multiple products are available on prescription. ● Reduction of bacterial counts and treatment of clinical
infection (see Table 2.06). All wounds left open will become
TOPICAL AGENTS FOR WOUND CARE colonised by bacteria. Taking swabs is not usually helpful.
Wound healing occurs in three stages: Clinical signs of infection are cellulitis of the surrounding
1. an influx of inflammatory cells to aid reabsorption of necrotic skin, a foul odour, or increasing levels of pain, exudate or
cells and prevent infection – this causes erythema and exudate capillary bleeding with pitted/spongy granulation tissue.
2. the formation of granulation tissue and revascularisation – at The organisms that matter are:
this stage there is a reduction in exudate (i) a group A β-haemolytic streptococcus that causes
3. migration of epidermal cells to cover the wound and growth of cellulitis (see p. 373) – this should be treated with high
new connective tissue underneath. dose flucloxacillin, clindamycin or clarithromycin (see
p. 374).
Wound healing takes place most rapidly when:
(ii) Pseudomonas, which causes a green discoloration and
● there is a moist environment (not too wet, not too dry) and any
has a distinctive foul smell – this can be treated with
excess fluid is able to evaporate
0.75% metronidazole (Anabact) gel applied directly to
● the wound is warm – a drop in temperature of 2°C significantly
the wound, acetic acid (apply as household vinegar
reduces healing
diluted 50:50 in water, soaked onto a swab and left on
● there is good blood perfusion; dressings do not affect this, but
for 5 minutes) or silver dressings (see Table 2.06).
topical negative pressure (suction pump) may.
Do not use antibiotic impregnated tulle dressings because
Management of chronic wounds patients frequently become allergic to them.
Successful treatment of leg ulcers and other chronic wounds
Wounds being treated for infection should be reviewed
therefore depends on the following.
within 14 days; by that time treatment will have worked, if
1. Dealing with the underlying cause: e.g. compression
it is going to.
bandages for venous hypertension, taking the weight off
● Reduction of excessive exudate (see Table 2.07). Venous
pressure sores etc.
ulcers produce serous exudate because of the high
2. Attention to nutrition and correction of any deficiencies.
hydrostatic pressure. Exudate is a problem because it
3. Management of the wound itself (see Tables 2.04a & b):
soaks through bandages and makes a mess of clothing
● Removal of dead and necrotic tissue (see Table 2.05).
and bedding. Drawing the exudate away from the wound
Wound cleansing for its own sake is not a good thing. The
surface will allow better healing.
wound bed is disturbed and any new epithelium ripped
● Covering the wound (see Table 2.08). This helps to maintain
off. Any necrotic material should be removed – this can be
the temperature and prevent drying out of the wound.
TOPICAL AGENTS FOR WOUND CARE / 41
Table 2.04a Summary of types of wound and what dressings to use

Wound type Dry adherent slough Dirty superficial yellow Necrotic slough – moderate/ Local infection – low exudate Local infection – high
slough – low exudate high exudate exudate
Primary objective Debride Debride Absorb exudate and debride Reduce bacterial counts and Reduce bacterial counts
debride
Primary/wound Hydrogel/ Hydrogel Hydrocolloid/Hydrofiber Honey/Iodine/Silver Alginate + silver
contact Hydrocolloid/ (Aquacel) Flamazine, PHMB Hydrofiber + silver
Viscopaste PB7 Capillary action (polyhexamethylene biguanide) Cadexomer iodine
Secondary/surface Light foam or gauze Hydrocolloid or Bordered foam Super-absorbent dressing Light foam/ Super-absorbent dressing
Low adherent
Alternative Surgical debridement Maggots Maggots Maggots/ Potassium permanganate soaks
Surgical debridement
Table 2.04b Summary of types of wound and what dressings to use

Wound type Smelly fungating wound Granulating – low exudate Granulating – high exudate Epithelialising – low exudate Epithelialising – high exudate
Primary objective Reduce smell and bacterial Protect wound Reduce exudate Protect wound Reduce exudate
counts
Primary/wound Activated charcoal Bordered Foam/ Hydrofiber/Alginate Low adherent/Film Hydrofiber
contact Metronidazole Hydrocolloid
(Anabact) gel Low adherent dressing
Secondary/surface Super-absorbent dressing Gauze Super absorbent Gauze Super absorbent
Alternative Surgical debridement Film White soft paraffin Potassium permanganate soak
Table 2.05 Debriding agents

Type Brand names Available Used on How to use Comments and contraindications
Hydrogel ActivHeal hydrogel, Gel Dry Squeeze gel onto wound and cover with a Do not use on wet wounds
A three-dimensional Aquaform, Askina, Cutimed, Sloughy or necrotic secondary dressing Provides a moist environment for autolytic
polymer that absorbs Flexigran, GranuGel, wounds debridement
water Intrasite, Nu-Gel, Purilon
Actiform cool, Aquaflo, Gel Sheets Apply sheet and cover with secondary dressing
FX, Geliperm, Hydrosorb,
Intrasite conformable,
Novogel, Vacunet
Hydrocolloid ActivHeal hydrocolloid, Sheets Low to moderate Apply with a 2 cm overlap to hold in the exudate The hydrocolloid interacts with the ulcer exudate
Comprising Alione, Askina, Comfeel exudate that is produced; the dressing is changed as to form a soft moist gel that provides an acid
carboxymethyl plus, Duoderm, Flexigran, Clean, granulating soon as it begins to leak (approximately once environment allowing autolytic digestion of any
cellulose backed Granuflex, Hydrocoll, or sloughy wounds or twice a week); there is a tendency for the necrotic material
with waterproof NuDerm, Tegaderm exudate, as it accumulates, to force its way Aerobic and anaerobic bacteria will flourish in
polyurethane foam or hydrocolloid, Ultec Pro out of the dressing and run down the patient’s this environment producing an unpleasant smell
vapour-permeable film leg, particularly when walking about; emollient
ointment (see Table 2.01a) can be used to
protect the skin
Maggots LarvE Sterile maggots Very sloughy Add saline to the maggots and tip them onto Maggots are extremely efficient debriding
from BioMonde, Bridgend, in small container wounds with the fine mesh net provided; place this with agents, feeding on necrotic tissue without
CF31 3BG Wales or bag mild to moderate the maggots in contact with the ulcer inside a affecting normal skin
exudate hydrocolloid sheet cut to the size of the ulcer; Do not use if blood clotting is inhibited – either
cover the outside of the net with moistened naturally or by drugs
swabs, a non-adherent dressing and Sleek
adhesive tape; the maggots should be left in
place for 48–72 hours and then washed out
with saline or potassium permanganate
Table 2.06 Reducing bacterial counts and odour

PHMB (polyhexamethylene biguanide) Gauze dressing Low exudate As wound contact Can be used as a prophylactic dressing
Kendall AMD, Suprasorb, Telfa AMD Foam, Pad
DACC (dialkyl carbamoyl chloride) Swab Low-moderate As wound contact Novel anti-microbiological agent
Cutimed Pad exudate
Silver Flamazine Cream Infected wounds Apply direct onto wound or Silver is effective against pseudomonas but needs moisture to
(silver sulphadiazine) with low exudate mix with a hydrogel activate it
Multiple products Sheet only High exudate Direct to wound. Compound Silver products are expensive and some question their efficacy; silver
(see BNF) + alginate dressings available to aid ion Ag+ is the active agent – some question the availability of the ion
+ foam absorption of increased and its efficacy
exudate
+ hydrofibre
+ hydrocolloid
Manuka honey Activon, Algivon, Paste/ointment Infected sloughy Need covering with film Works by osmotic action, and by altering the pH to make the wound
Manuka pli, + alginate wounds dressing inhospitable for bacteria; it reduces inflammation (and pain) and
Medihoney, Melladerm + hydroactive gel as provides a good environment for debridement and granulation
Plus, Mesitran dressing
Iodine Inodine Fabric dressing Low exudate Apply direct to wound May cause allergic contact dermatitis; wide spectrum, quickly
Cadexomer Iodoflex, Iodosorb Paste, ointment High exudate deactivated by exudate
iodine
Iodozyme, Oxyzyme Hydrogel sheet Low-moderate Apply direct to wound Two component dressing where glucose oxidase and iodine ions
exudate release free iodine
Metronidazole Anabact 0.75% Gel Smelly wounds Apply direct to wound Needs secondary dressing
Activated Askina Carbosorb, Non-absorbent cloth Smelly wounds Needs absorbent pad + Charcoal absorbs odour but has no antibacterial activity; not effective
charcoal Carbopad VC, CliniSorb secondary dressing if wet
CarboFlex, Absorbent sheet Smelly wounds with Apply direct and change when 5 layers including alginate and hydrocolloid
Lyofoam C high exudate necessary Activated charcoal cloth with outer layer of polyurethane foam
Sorbsan Plus Carbon Alginate fibre pad with absorbent backing
Table 2.07 Absorption of exudate

Alginate ActivHeal, Sheet or ribbon Moderately Cut to the exact size and shape of the On contact with exudate, calcium ions in the alginate are
(naturally occurring Algisite M, exuding wounds ulcer; they expand laterally when wet so exchanged for sodium, which turns the fibres into a gel,
polysaccharides Algosteril, can cause maceration of the surrounding consisting of mannuronic or guluronic acid residues; the
found only in skin; leave in place for several days or up ratio of these determines whether a soft flexible gel forms
Kaltostat,
brown seaweeds to a week at a time; removed by irrigation (e.g. Sorbsan), which can be removed by irrigation, or a
Melgisorb, or by lifting off with a pair of forceps firm gel, which keeps its shape but needs to be removed
[Phaeophyceae])
Seasorb soft, A secondary dressing is required with forceps (e.g. Kaltostat)
Sorbalgon,
Sorbsan,
Suprasorb A,
Tegaderm,
UrgoSorb
Hydrofibre Aquacel Extra Sheet Heavily exuding Change according to the amount of The fibres absorb fluid and the material is drawn down
Aquacel Foam (foam wounds exudate being produced (daily to weekly) into the ulcer to form a gel. The advantage over alginates
backing) The solid gel needs to be removed before is that it will lock in moisture, as well as absorbing five
a new sheet is applied times the amount of exudate that alginates do
Capillary action Advadraw, Sheet or sachets Exuding and Apply to surface, or cut to shape in deep A polyester and cotton sheet with its fibres arranged in
Cerdak Basic, sloughy wounds wounds such a way that fluid is drawn away from the wound
Sumar, Avoid in bleeding wounds
Vacutex
Polyurethane matrix Cutinova hydro Sheet Moderately Place over the wound or cut into strips Highly absorbent dressings made from a polyurethane
exuding wounds to pack a deep wound; cover with matrix that absorbs water but leaves other molecules
a secondary dressing. Change every within the wound
2–3 days initially; leave on longer as
exudate diminishes
Super absorbent Cutisorb Ultra, DryMax Sheet Heavily exuding Available either as a pad or sheet to These contain super-absorbent polymers and cellulose
Extra, KerraMax, Pad wounds absorb excess fluid with a polyethylene wound contact layer
Sorbion,
Zetuvit Plus
Table 2.08 Wound and ulcer dressings

Type Brand names Available as Used on Comments and contraindications
Low-adherent Atrauman, Urgotul, Woven acrylic mesh Clean open wounds, low Will need retention bandage or skin adhesive to hold dressing in place
primary dressings N-A dressing and others dressing exudate
Jelonet and multiple other brands Paraffin gauze Clean open wounds, low Large mesh allows epidermis to grow through resulting in trauma on removal;
exudate needs a secondary dressing
NICE no longer recommends these
Mepitel, N-A Ultra and multiple Woven silicon mesh Clean open wounds, low These are more expensive but less adherent, so are less likely to damage the
other brands dressing exudate wound surface
Mepilex (+ foam backing) Will need a secondary dressing
Island dressings Mepore and multiple other brands Adhesive woven cloth For protection of dry surgical Absorbs moisture but vapour permeable
with central pad wounds
Film dressings Opsite, Tegaderm and multiple Transparent film Clean wounds with low exudate Waterproof and adhesive but lets vapour/air through; have no insulating
other brands (see BNF) ± absorbent pad properties so wounds become cooled and heal more slowly
Cavilon, SuperSkin Silicon liquid or spray Protects normal skin around Useful for skin in contact with faeces or urine
stomas
Cream/ointment Cavilon Cream Protects normal skin around Useful for skin in contact with faeces or urine and skin around leg ulcers
Vaseline (see Table 2.01a) Ointment and gel stomas etc.
Foam dressings Allevyn, Aquacel foam, Biatain and Sheet (various As a secondary dressing Polyurethane hydrophilic layer which absorbs limited amounts of exudate,
multiple other brands thicknesses) with or As a pressure pad and a thicker spongy outer hydrophobic breathable foamy layer, which
Mepilix (+Silicon weave contact) without adhesive For insulation keeps wound moist, warm and protected from trauma, while allowing some
border evaporation
For over granulation
Collagen & Promogran Sheet Clean, low exudate, no infection Derived from pig small intestine mucosa and containing collagen and
cellulose dressing or bleeding regenerated cellulose
SYSTEMIC TREATMENT / 47
SYSTEMIC TREATMENT the skin with conventional courses of flucloxacillin or

ANTIBIOTICS erythromycin. Its prevalence is increasing and PVL-positive
Systemic antibiotics are used for the following. S. aureus is associated with higher morbidity and mortality,
1. Staphylococcal infections and is more transmissible, when compared with PVL-
a. Staphylococcal infections in the skin, e.g. boils, carbuncles, negative S. aureus. Send microbiology samples specifically
ecthyma, staphylococcal scalded skin syndrome, sycosis requesting PVL gene detection, as well as microscopy,
barbae, and infected eczema and scabies. Flucloxacillin culture and sensitivity. The UK Health Protection Agency
500 mg every 6 hours (double this for severe infections will advises treating PVL-positive MRSA isolates with
also cover streptococcal infection) is the drug of choice. rifampicin and one other agent (clindamycin, doxycycline,
For patients who are allergic to penicillin, erythromycin sodium fusidate, or trimethoprim). All patients plus their
500 mg every 6 hours is an alternative. With this dose, close contacts should be treated with topical decolonisation
gastro-intestinal upsets occur in about 20% of patients. The (see 1a on left).
cephalosporins are not as good as flucloxacillin against 2. Streptococcal infections in the skin, e.g. erysipelas and
S. aureus so should not be used as the first line of treatment. cellulitis. Streptococci are always sensitive to penicillin, so
Nasal and flexural carriage of S. aureus can result in intravenous benzyl penicillin 1200 mg every 6 hours is the
recurrent skin infections. Take swabs from the nose, groin treatment of choice. Alternatively use high dose flucloxacillin
and open wounds. If positive, decolonise the skin with 4% 1 g every 6 hours. Erythromycin or clarithromycin 500 mg
chlorhexidine body wash daily for 5 days and mupirocin every 6 hours orally is useful in patients who are allergic to
ointment applied three times daily to the anterior nares. penicillin. Streptococcal ecthyma, or eczema and scabies that
Octenilin is an alternative to the irritant chlorhexidine- are secondarily infected with Streptococcus pyogenes, can be
containing washes in patients with eczema. treated with phenoxymethyl penicillin 500 mg every 6 hours.
b. MRSA (methicillin-resistant S. aureus) infected 3. Acne, perioral dermatitis and rosacea: these are not due to
wounds may need treatment with oral doxycycline or infection with bacteria but nevertheless respond well to low
intravenous vancomycin. It is best to liaise with your local doses of broad-spectrum antibiotics (see pp. 119, 116, 124). How
microbiologist or infection control team to check current they work is not fully understood.
sensitivities. Again chronic carriage as for S. aureus may
ANTIFUNGAL AGENTS
warrant decolonisation as outlined in previous point.
c. Panton–Valentine leukocidin (PVL) toxin-positive Normally superficial fungal infections of the skin are treated with
S. aureus skin infections can be acquired in the community topical antifungal agents. The exceptions are when the hair and
and lead to recurrent and potentially serious infections nails are involved when it is not possible to get the antifungal
of the skin (as per staphylococcal infections above) and agent to the site where it is needed. Four groups of antifungal
necrotising pneumonia. It is not easily eradicated from agents are available for systemic use.
1. Antibiotics – griseofulvin: this is the cheapest of the options Side effects of itraconazole include nausea, abdominal pain,
and works well for tinea capitis; it is not very effective for nail dyspepsia and headache. Do not use in patients with ventricular
infections. It is long-acting so only has to be given once a day dysfunction or risk of heart failure. Check liver function if given
but it has to be taken with food because it is absorbed with fat. for more than 1 month. As it is a potent inhibitor of cytochrome
Side effects are unusual – headache, irritability and nausea are P450 enzymes it may elevate the blood levels of other drugs
the most common. Occasionally it can cause photosensitivity being taken concurrently such as statins, midazolam, ciclosporin,
or a drug-induced lupus erythematosus. If the patient is warfarin and oral hypoglycaemics (check BNF before prescribing).
on warfarin, the INR will need to be checked because the Fluconazole rarely causes hepatotoxicity.
anticoagulant effect will be diminished. Do not use in patients
Nystatin is not absorbed when given by mouth so the only reason
with acute intermittent or variegate porphyria because it can
for using it is if you want to clear the gut of C. albicans, e.g. when a
induce acute attacks.
patient is getting recurrent perianal infection.
2. Allylamines – terbinafine: this is a fungicidal drug that is
much more effective than griseofulvin and also much more ANTIVIRAL AGENTS
expensive. It works well for any kind of dermatophyte
Aciclovir, famciclovir and valaciclovir are the systemic antiviral
infection (but not candida), but is particularly useful for
agents in current use for both herpes simplex and herpes zoster
tinea of the nails. It is taken once a day for 3 months for
infections. They all inhibit phosphorylation of viral thymidine
nail infections or for 2 weeks for infections on the skin. It
kinase, which prevents viral DNA synthesis and virus replication.
occasionally causes mild gastro-intestinal upsets – anorexia,
They are only effective while there is active viral replication and
nausea, diarrhoea, abdominal fullness and a morbilliform rash.
must therefore be given within 48 hours of the onset of vesicles.
Check liver function if given for more than 2 months. Do not
They can be used for treating:
use during pregnancy and lactation.
● herpes simplex if the patient has disseminated disease,
3. Imidazoles – ketoconazole: this is very effective for treating
frequent recurrences, eczema herpeticum or recurrent
pityriasis versicolor, where it is given as a single 400 mg dose. It
erythema multiforme (see pp. 108, 109, 175)
should not be used for longer periods of time because there is a
● herpes zoster – this is much less sensitive to these drugs than
small risk of liver toxicity. It is a potent inhibitor of cytochrome
herpes simplex, so bigger doses need to be given (see p. 180).
P450 (see side effects of triazoles).
4. Triazoles – itraconazole and fluconazole: they are used
Ganciclovir is active against herpes simplex but also
for infections with Candida albicans, cryptococcosis or
cytomegalovirus and human herpes-like viruses that are thought
histoplasmosis in patients who are immunosuppressed (those
to play a role in late deteriorating drug hypersensitivity eruptions
with malignant disease, HIV or those on cytotoxic drugs), and
such as DRESS (drug reaction with eosinophilia and systemic
in patients with myeloma.
symptoms, p. 168). It is given by intravenous infusion and needs
close monitoring.
ANTIHISTAMINES not been effective. Cimetidine (Tagamet) can also be given

Antihistamines act as competitive blockers of histamine receptors. to reduce haemolysis and methaemoglobinaemia in patients
They have a close structural resemblance to histamine. As there taking dapsone (see p. 246).
are two types of histamine receptor, H1 and H2, there are two types
of antihistamines. Cutaneous blood vessels have both H1 and RETINOIDS
H2 receptors, but for skin disease H1 antihistamines are the most Retinoids are derivatives of vitamin A. Their exact mode of action
effective. is unknown but they have many effects, including:
● Non-sedative antihistamines are the most useful drugs ● induction of differentiation of epidermal cells – this may be
in urticaria and angioedema. Cetirizine, levocetirizine, how they work in psoriasis, solar keratoses and Bowen’s
fexofenadine, loratadine, desloratadine, mizolastine and disease; in patients who have had organ transplants they may
rupatadine are the ones most commonly used. They are not suppress the development of epithelial tumours (e.g. basal cell
useful in eczema, as histamine is not the cause of the itching in carcinomas and squamous cell carcinomas), but they do not
this condition. High doses (off-licence) are often required in make established tumours go away
urticaria and four times the standard hay fever dose is accepted ● shrinking of sebaceous glands causing decreased production of
practice, e.g. cetirizine 20 mg bid. sebum
● Sedative antihistamines are useful for sedating children ● anti-inflammatory effects by reducing prostaglandins and
with atopic eczema to ensure that they and their parents get leukotrienes
a good night’s sleep. It is essential to give a big enough dose ● modulation of the immune response by enhancing T helper
(administered 2 hours before bedtime) to ensure the child cells and stimulating interleukin 1.
sleeps through the night. They are also useful for adults There are four retinoids in current use.
with very widespread rashes who need to rest the skin, e.g. 1. Isotretinoin, the 13-cis isomer of retinoic acid (RoaccutaneUK/
patients with erythrodermic eczema or psoriasis, and patients AccutaneUSA), is used for the treatment of severe acne (see
with acute blistering conditions on the feet who would p. 120) at a dose of 0.5–1.0 mg/kg/day for 4–6 months to
otherwise find it difficult to rest in bed. Hydroxyzine (Atarax), achieve a total dose of 120 mg/kg body weight. Lower total
promethazine (Phenergan) and alimemazine are the most dose regimens are associated with an increased recurrence rate
useful. Chlorphenamine (Piriton) is no good for treating any in both the long and short term.
of the above because it is short acting (4 hours). It can be used 2. Acitretin (Neotigason) is used to treat psoriasis and disorders
in acute urticaria and in patients with photosensitive eczema of keratinisation [Darier’s disease (see p. 247), pityriasis rubra
who may be allergic to the others. Warn the patients about the pilaris (see p. 244), severe types of ichthyosis (see p. 323)]. It
sedating and hangover effect (driving, operating machinery can also be used in conjunction with PUVA (RePUVA) in a
etc.). patient with psoriasis to decrease the amount of ultraviolet
● H2 antihistamines. Ranitidine (Zantac) can be worth trying
light that the patient is exposed to (see p. 61). Acitretin may
in patients with urticaria where H1 antihistamines alone have
help prevent the development of epithelial tumours (basal a patient is taking the drug from this sign. Vaseline or a lip salve
cell carcinomas and squamous cell carcinomas) in patients applied frequently will be necessary.
who are immunosuppressed, especially those who have ● Dryness of the nasal mucosa, which can lead to nose bleeds.
had renal transplants. It is given at a dose of 10–50 mg/day. ● Musculoskeletal aches and pains especially after exercise:
Female patients must not become pregnant while taking it or those on long-term acitretin therapy can develop ossification of
for 2 years after stopping because some of it is converted to ligaments. Monitor by yearly X-ray of the lumbar spine.
etretinate (an ester of acitretin), which has a long half life of ● Conjunctivitis and dry eyes are usually not a problem unless
2 years. the patient wears contact lenses. Hypromellose eye drops may
3. Alitretinoin (Toctino), the 9-cis-retinoic acid, is used for help.
treating severe chronic hand eczema. Due to the cost of the ● Itching of the skin with or without an eczematous rash may
drug it should only be used by dermatologists for patients who need treatment with a moisturiser or 1% hydrocortisone
have not responded to standard treatments (such as potent ointment.
topical corticosteroids) and when their eczema is severe and ● Rise in serum triglycerides due to decreased extra-hepatic
affecting their quality of life. Alitretinoin treatment should breakdown and increased secretion by the liver.
be stopped as soon as the eczema has clearly improved or if ● Increase in liver enzymes which will resolve on stopping
unresponsive to 12 weeks of treatment. The standard dose treatment.
is 30 mg/day unless it is not tolerated or there is a medical
Specific side effects of isotretinoin:
history of hyperlipidaemia, diabetes or significant risk factors
● Suicide risk and depression. Research indicates that acne itself
for ischaemic heart disease when 10 mg/day is used.
confers an increased risk of suicide, and any association with
4. Bexarotene (Targretin) is a retinoid specifically selective for
isotretinoin may be related to the fact that the severest cases
retinoid X receptors. It is an oral antineoplastic agent indicated
receive this treatment. There seems to be no way of predicting
for the treatment of cutaneous manifestations of cutaneous
this and in practice it is very uncommon (1:8000). Many
T-cell lymphoma in people who are refractory to at least one
patients who are already depressed benefit from the drug as
prior systemic therapy. Its side effects are similar to the other
this improves their acne, and it does not result in worsening of
retinoids but it has a greater tendency to produce a rise in
their depression. Any preceding affective disorder should be
triglycerides and can cause hypothyroidism.
treated and stabilised before considering systemic retinoids.
Side effects of retinoids If there are any concerns a psychiatrist should be involved
● Teratogenic (no effect on sperm). They must not be given to in the patient’s care. Regular assessment of mood should be
women of childbearing age unless on adequate contraception documented and any concerns (your own, the patient’s or that
(two concurrent forms ideal including either the oral of family/friends) should be acted on.
contraceptive pill or an implantable device). ● Irregularity or cessation of periods in women.
● Dryness of the lips: this always occurs and you can tell whether ● Possible association with inflammatory bowel disease.
Specific side effects of acitretin: not show the typical steroid facies until the disease comes under
● Peeling of palms and soles occurs at the beginning of control. For example, a patient can be on prednisolone 60 mg for
treatment; they may also feel sticky or clammy. several weeks without any evidence of a moon face, but as soon as
● Increased sweating does not usually cause problems. the disease comes under control the face fattens up.
● Poor wound healing. The skin easily bruises and cuts take
longer to heal.
● Hair loss bad enough to be noticeable only occurs in a few EQUIVALENT DOSES OF DIFFERENT SYSTEMIC STEROIDS
patients and is reversible on stopping treatment. Cortisone 100 mg
Hydrocortisone 80 mg
● Paronychia. Painful swelling around finger- and toenails occurs
Prednisone or prednisolone 20 mg
in a minority of patients.
Dexamethasone 2–4 mg
● Nausea, vomiting and abdominal pain are unusual complaints.
Long-term treatment requires monitoring of blood for liver Side effects of systemic steroids:
function and lipids, and X-ray of the spine for ossification of ● increased fat deposition on the face, shoulders and abdomen
ligaments. causing a moon face, buffalo hump and enlarged abdomen
● acne and hirsutism
SYSTEMIC STEROIDS ● easy bruising and tearing of the skin
Systemic steroids have a very limited use in the treatment of skin ● striae (see Fig. 8.38, p. 212)
disease and are best restricted to use by a dermatologist. They ● delayed tissue healing
should not be used in eczema or urticaria because, although the ● increased susceptibility to infections (bacterial, fungal and
response may initially be dramatic, the disease is likely to flare viral)
badly when the tablets are stopped and it is then very difficult to ● salt and water retention leading to oedema, hypertension and
get the patient off them. It is better to refer such a patient for an congestive cardiac failure
urgent dermatological opinion than to start him on prednisone. ● diabetes
● peptic ulceration leading to bleeding and perforation
Systemic steroids are essential and may be life-saving in:
● proximal muscle weakness
● pemphigus (see p. 259)
● osteoporosis leading to fractures particularly of the vertebrae
● pemphigoid (see p. 256)
and ribs
● systemic lupus erythematosus (see p. 131)
● aseptic necrosis of the femoral head
● dermatomyositis (see p. 132).
● cataracts and glaucoma
● depression or euphoria (steroid psychosis)
High doses are needed in all of these conditions and the risk of
● growth retardation in young children; this is not usually a
side effects is considerable. Interestingly such patients often do
problem unless steroids are given for more than 6 months
● suppression of the pituitary-adrenal axis leading to adrenal IMMUNOSUPPRESSIVE AGENTS

insufficiency on withdrawal or if the patient has some A number of different immunosuppressive agents are used for
intercurrent illness or needs surgery. severe skin disease, either in their own right or as steroid-sparing
agents. They are all potentially dangerous and should only be
To prevent complications initiated by a dermatologist.
1. Patients will need regular checking of:
● weight – to pick up fluid gain (monthly) Methotrexate
● blood pressure – looking for hypertension (monthly) Methotrexate is used for psoriasis, eczema, the autoimmune
● urinalysis – looking for glycosuria (monthly) bullous disorders, Hailey–Hailey disease (chronic benign familial
● DEXA scan (yearly) if patient is on steroids for more pemphigus, see p. 340) and dermatomyositis (see p. 132). It inhibits
than 3 months), though pragmatically all female patients dihydrofolate reductase and therefore cell division. It is probably
should be started on preventive treatment regardless if the most effective of the systemic agents in use for the treatment of
postmenopausal psoriasis and it works very quickly (within 48 hours).
● chest X-ray – looking for reactivation of tuberculosis
(yearly). Following routine blood tests (see under bone marrow suppression
2. Patients should carry a steroid card or medical alert tag with on p. 53), a 5 mg test dose is given and provided no adverse
them all the time. If they have an accident or have some other reaction has occurred it is given as a single dose of 10–25 mg
illness extra steroids can be given to prevent an Addisonian orally, subcutaneously or intramuscularly once a week. It is excreted
crisis. unchanged principally through the kidneys, so the dose needs
3. To prevent stomach ulceration either use enteric coated to be reduced if renal function is impaired or the patient elderly.
prednisolone (expensive), or prescribe a proton pump inhibitor It can be continued long term at the lowest dose that keeps the
(e.g. omeprazole 10 mg day) in addition to the steroid. psoriasis under control.
4. To prevent osteoporosis give lifestyle advice – regular exercise, Methotrexate is available in 2.5 mg and 10 mg tablets that look
stop smoking, reduce alcohol intake. Start the patient on identical. Most reports of acute toxicity have been related to
Calcichew D3 forte, two tablets a day. Patients over the age inadvertent switching between tablet size and mistaken daily
of 45 (or postmenopausal women) or at risk of osteoporosis instead of weekly dosing. It is therefore advised that only 2.5 mg
should also be on a bisphosphonate to reduce bone turnover tablets ever be supplied (with close liaison with local prescribing
e.g. alendronate (Fosamax) 70 mg/week. If intolerant to this (or chemists to facilitate this) and that all patients receive and carry a
there are contraindications to this drug) alternatives should be patient booklet where all doses, side effects and monitoring results
discussed with a rheumatologist. are recorded.
Serious side effects: (headache, lethargy, irritability and depression) for about
● Teratogenic so must not be used in women who might become 24 hours after a dose of methotrexate
pregnant. In men it causes reversible oligospermia. ● extensive ulceration of the skin – this usually occurs at the
● Bone marrow suppression: check full blood count before same time as a profound fall in the white blood cell count
starting, then weekly for 1 month and then every 2–3 months. ● hair loss – theoretically this is possible but is extremely rare
If the mean corpuscular volume becomes elevated (over 100), ● lung problems such as acute pneumonitis or diffuse interstitial
reduce the dose. fibrosis can occur when methotrexate is used for treating
● Fibrosis of the liver can occur after several years of treatment, neoplastic disease; with the lower doses used for treating
so do not give to a patient with pre-existing liver disease psoriasis, these changes do not seem to happen.
or anyone who has a history of alcohol abuse. Patients on
methotrexate should not drink any alcohol. Measuring blood Most side effects can be prevented by giving 5 mg folic acid once
levels of type III procollagen (P3NP) every 6 months can a week (3–4 days after the methotrexate) without stopping the
monitor the development of liver fibrosis. This is a non-specific therapeutic effect.
marker of fibrosis and can be raised by other causes of fibrosis
Patients on methotrexate must not take aspirin, diuretics,
rendering it less useful, e.g. in patients with psoriatic arthritis.
hypoglycaemics, non-steroidal anti-inflammatory drugs,
In the psoriatic population other causes of liver fibrosis are
phenytoin, probenecid, sulphonamides or trimethoprim. These all
also commoner such as alcoholic and non-alcoholic fatty liver
increase the risk of pancytopenia.
disease.
Ciclosporin
P3NP LEVELS Ciclosporin is an immunosuppressive drug that is useful in the
<4.2 mg/L normal treatment of severe atopic eczema and psoriasis. The starting dose
>8.0 mg/L consider liver biopsy is 3–5 mg/kg/day. Its effect is rapid (within 2 weeks). Once the
>10.0 mg/L stop methotrexate disease is under control the dose can be reduced and replaced by
a safer agent long term, as its continuous use beyond 1 to 2 years
is associated with oncogenesis. It is not teratogenic so it can be
Less serious side effects: useful in severe skin disease in pregnancy.
● nausea, vomiting, diarrhoea and abdominal discomfort –
The bioavailability and pharmacodynamics of different ciclosporin
these effects can often be avoided by changing from oral to
formulations varies significantly and it is advised to stick to a
intramuscular methotrexate
single available agent from a single manufacturer in a prescribing
● stomatitis and ulceration of the mouth
region, as loss of efficacy as well as toxicity has been described on
● general malaise – patients frequently feel generally unwell
inadvertent brand switching.
Side effects: Azathioprine

● nephrotoxicity (this is most important side effect) – ciclosporin Azathioprine is used for atopic and photosensitive eczema,
reduces renal blood flow and causes a rise in urea and and as a steroid-sparing drug in pemphigus, pemphigoid,
creatinine; keeping the maximum dose below 5 mg/kg/day dermatomyositis and systemic lupus erythematosus. It is given at
reduces toxicity; if the blood creatinine levels increase by 30% a dose of 1–3 mg/kg/day, usually 50–100 mg bid. Before starting,
over baseline, the dose should be reduced check the thiopurine methyltransferase (TPMT) level (normal
● hypertension secondary to reduced kidney blood flow; if 25–50, carrier 10–25, deficiency <10 pmole/L/mg Hb), since if
blood pressure increases above 160/95 use a calcium channel it is low, there is an increased risk of myelosuppression. It takes
blocker, e.g. amlodipine (5–10 mg od) to reduce it 6–8 weeks before there is any effect so it is no good as a first line
● increased liver enzymes, serum uric acid and cholesterol treatment in patients with pemphigus and pemphigoid. The
● nausea and vomiting patient is often started on azathioprine as well as the steroids;
● gingival hyperplasia in patients with poor dental hygiene after 6–8 weeks, when the azathioprine will have begun to work,
● tiredness, headaches, parasthesiae, tremor and convulsions are the dose of steroid is gradually reduced.
rare and reversible on reduction of the dose
● hypertrichosis (particularly a problem in women; may not be Side effects:
noticed in men) ● nausea, vomiting and diarrhoea, particularly in the elderly – if
● increased risk of lymphoma and non-melanoma skin cancer. this is going to occur it usually does so in the first week; it may
be so severe that the drug must be stopped
To prevent complications ● bone marrow depression – a full blood count should be
Ideally measure the GFR (glomerular filtration rate) before measured regularly (once a week for the first month and then
starting treatment. Always check blood pressure, potassium, blood every 2–3 months)
creatinine, liver function and lipids before treatment. Monitor ● teratogenicity – do not give to pregnant women; safe in men
these fortnightly for 6 weeks, monthly for 3 months and then ● mild cholestasis – not usually a problem, unlike methotrexate
every 2–3 months. Repeat GFR if creatinine levels increase more ● long term (> 10 years) there an increased risk of lymphoma and
than 30% above baseline. non melanoma skin cancer especially squamous cell carcinoma.
Mycophenolate mofetil measured regularly (once a week for the first month and then
Mycophenolate mofetil is a drug normally used to prevent every 2 months).
rejection of organ transplants. It is used for treating recalcitrant
eczema and autoimmune bullous conditions in conjunction with Fumaric acid esters
prednisolone, as well as for pyoderma gangrenosum. It takes The fumaric acid esters are used to treat psoriasis, and have been
about 8 weeks to work. The usual dose is 1.0 g bid (maximum 1.5 g used and marketed for over 30 years in Germany. They have to be
bid). imported and used on a named patient basis, which makes them
expensive. Fumarates are thought to work by shifting a Th1-type
Side effects are gastro-intestinal upsets (nausea, vomiting, cytokine response to a Th2-type pattern (see p. 225). They comes in
diarrhoea), bone marrow suppression (check full blood count two strengths: initial (30 mg) and high strength (120 mg).
weekly for 1 month and then monthly) and an increased risk of
infection, particularly in the elderly. Side effects:
● gastro-intestinal complaints including diarrhoea, stomach
Cyclophosphamide cramps and tenesmus occur in up to 60% of patients
Cyclophosphamide is used in mucous membrane pemphigoid ● flushing with headaches in 30% of patients; both are greatest at
where it is the drug of first choice (see p. 146). It takes 6–8 weeks to the onset of therapy and decrease with time
work, given at a dose of 1–3 mg/kg/day (50–100 mg bid). ● lymphopenia seen in 75% of patients which is usually mild;
transient eosinophilia is occasionally observed; liver enzymes
Side effects: are frequently raised (25% of patients); check full blood count
● pancytopenia – the patient should have a full blood count and liver function monthly.
measured regularly (weekly for a month and then 2 monthly)
● hair loss In about 7% of patients these side effects lead to drug withdrawal.
● haemorrhagic cystitis – drink plenty of fluids to prevent this. This can be minimised by using a slow incremental dose regimen,
which will delay the response to around 8–12 weeks.
Hydroxycarbamide (hydroxyurea)
There are no reports of severe long-term toxicity, development
This is an antimetabolite which inhibits DNA synthesis without of cancers or a higher susceptibility to bacterial infections. This
affecting RNA or protein synthesis. It is used for psoriasis in makes fumaric acid esters a safe regimen, compared to other
patients who have not responded to methotrexate but it takes agents. Dosing starts at 30 mg daily, increasing weekly to a
8–12 weeks to work. It is given at a dose of 500 mg bid. maximum of 240 mg three times a day.
Side effects are mainly on the bone marrow. It causes a macrocytic
anaemia or pancytopenia. Patients should have a full blood count
BIOLOGIC AGENTS is given subcutaneously (45 mg) at 0, 4 and 12 weeks and then
Toxic epidermal necrolysis every 12 weeks.
Human immunoglobulin from purified plasma of multiple They are very useful in severe cases of psoriasis unresponsive to
donors has been available since the 1980s, and is given by slow immunosuppressives and seem to have a good side effect profile,
intravenous infusion usually at 1 g/kg body weight for 3–4 days in not affecting either the liver or kidneys. Etanercept or adalimumab
severe cases of toxic epidermal necrosis, although its effectiveness should be used first for stable plaque psoriasis; patients requiring
is vigorously debated. It may cause hypersensitivity reactions, rapid disease control may benefit from infliximab. In patients who
acute renal tubular necrosis and thromboembolic episodes (due fail to respond to one of these, another TNF-α antagonist should
to the volume infused and hydration status of the patient). The be tried next. As it is the newest antipsoriatic biologic with the
potential transmission of unknown infective agents is also of shortest long-term safety data, ustekinumab should only be used
concern. when anti TNF-α therapy has failed or is contraindicated.
Psoriasis All these drugs lose efficacy over time probably due to
Biologics are antibodies that target specific cells, mediators or the development of antibodies. Continuous treatment is
molecules. Their number and uses are expanding rapidly, and recommended as infusion reactions may occur on retreatment.
are revolutionising the care of many medical conditions. Five Efficacy can be enhanced by the addition of methotrexate, which
new agents – efalizumab, etanercept, infliximab, adalimumab may prevent the development of antibodies; this is an area
and ustekinumab – have been released in Europe and the of ongoing research. Additionally monoclonal antibodies to
United States for the treatment of severe psoriasis. However, the IL17 and small molecules (which have the benefit in being oral
first, efalizumab, which inhibits T-cell activation, has already formulations) which inhibit enzymes such as phosphodiesterase 4
been withdrawn due to JC virus reactivation and subsequent and the JAK/STAT pathway, are all approaching licensing for use
progressive multifocal leukoencephalopathy (incidence 1 in 500). in psoriasis.
Infliximab (Remicade), adalimumab (Humira) and etanercept Screening of patients with psoriasis before starting biologics
(Enbrel), inhibit the cytokine TNF-α (tumour necrosis factor-α). ● Patient meets NICE criteria for use:
Infliximab is a modified mouse monoclonal antibody and is — failure of topical and systemic therapy
given by intravenous infusion fortnightly (5 mg/kg) for 6 weeks — PASI > 10, DLQI > 10 or involved body surface area >10%
and then every 8 weeks. It seems to have the most rapid onset ● Tuberculosis screen – history, chest X-ray, Mantoux
of action. Adalimumab is a human monoclonal antibody and is ● Baseline bloods – full blood count, liver function tests, urea and
better tolerated than infliximab. It is given on alternate weeks electrolytes, lupus autoantibodies
subcutaneously (40 mg). Etanercept is a receptor blocker to TNF-α ● History of cardiac disease, malignancy, demyelination
and is also given subcutaneously (50 mg) weekly. Ustekinumab ● Screening for hepatitis B and C antibodies
(Stelara), is directed against interleukin 12 and 23 (IL-12/23), and
If there is no effect after 12–16 weeks, the drug should be stopped.
Complications Biologics in skin cancer

● Infection – especially reactivation of tuberculosis, but also other ● Vismodegib, an oral inhibitor of the ‘hedgehog signalling
bacterial, viral and fungal infections pathway’, has been licensed for inoperable basal cell
● Constitutional symptoms carcinomas, as well as basal cell carcinomas occurring in
● Injection site reaction Gorlin’s syndrome (where huge numbers of disfiguring basal
● Hepatitis (infliximab) cell carcinomas can occur). It offers response rates of 30%–60%.
● Rarer possible side effects: ● Vemurafenib and ipilimumab have recently both been
i. deterioration of psoriasis (with acral and pustular pattern approved by NICE for clinical use in inoperable malignant
seen) melanoma. They are the first really promising treatments
ii. malignancy (lymphoma, non-melanoma skin cancers) available for metastatic melanoma. They improve life
iii. drug-induced lupus (usually subacute cutaneous lupus expectancy and disease-free survival by months in many
type) with possible anti-histone antibodies patients and years in some, but they are extremely expensive
iv. aplastic anaemia, pancytopenia (£2000 a week).
v. demyelination ● Vemurafenib is an oral inhibitor of mutant BRAF, a cell
vi. cardiac – increase in ischaemic heart disease, arrhythmias, signalling defect found in around 50% of melanoma cases.
cardiomyopathy and heart failure. Blocking this pathway prevents melanoma cell proliferation.
Unfortunately escape pathways exist which accounts for
For all these drugs, registration with BADBIR (the British its loss of efficacy over time. Blocking this pathway also
Association of Dermatologists Biologic Interventions Register) is selectively induces an alternate MEK pathway, which induces
recommended for monitoring long-term safety and effectiveness. multiple keratoacanthomas and squamous cell carcinomas
in treated patients. Photosensitivity and other skin rashes
Biologics for other conditions occasionally require a reduction in the dose. Trials of
Omalizumab (Xolair) is a recombinant human monoclonal combination BRAF and MEK inhibitors are underway in an
antibody that binds to immunoglobulin E (IgE), so inhibiting IgE- attempt to improve efficacy and reduce the cutaneous side
FCRI receptors present on mast cells and basophils. It is licensed effects.
for severe asthma but can also be used for difficult cases of chronic ● Ipilimumab as an infusion is useful in melanomas that do
urticaria. not have the BRAF mutation. It is a monoclonal antibody to
CTLA-4, which dampens down the activity of cytotoxic T-cells.
Off licence the anti-CD20 (B-cell) molecule rituximab (MabThera)
Blocking this increases the body’s own immune response
is used in severe bullous disorders and the anti-TNFs in pyoderma
to melanoma. It is currently licensed for use after standard
gangrenosum and hidradenitis suppurativa. Sometimes they
chemotherapy has failed. Ten per cent of patients are unable to
work, sometimes they do not.
tolerate it due to side effects on the gastro-intestinal tract, skin,
eyes, liver and endocrine systems.
● Nivolumab blocks proteins in tumour cells that protect them be at least three times as long as the freezing time. Repeated
from the immune system, which can then recognise and freeze–thaw cycles are more effective than a single long freeze.
destroy such tumours (e.g. metastatic melanoma).
Table 2.09 Freeze times for various lesions treated with liquid nitrogen
Skin condition Approximate freeze time
PHYSICAL TREATMENTS
Viral warts
CRYOTHERAPY WITH LIQUID NITROGEN filiform 5 seconds
The indications for using cryotherapy are limited. It is not a common 10 seconds
treatment to be used on any skin lesion that you think is probably periungual 15–20 seconds
benign. Do not use it on dermal lesions (e.g. melanocytic naevi) genital 10–30 seconds (depends on size)
and malignant lesions (except Bowen’s disease). Molluscum contagiosum 5 seconds
It is essential to make an accurate diagnosis before treatment. If Seborrhoeic warts 5–10 seconds
there is any doubt, do a biopsy first, as once a lesions has been Solar keratoses 5–10 seconds
frozen the histology is much more difficult to interpret. We would Bowen’s disease 15 seconds × 2
recommend that in general practice it is only used for treating Lentigo maligna 15–30 seconds × 2
viral warts, seborrhoeic warts and solar keratoses.
Note: on lower legs cut the freeze time by half.
Freezing the skin produces changes similar to those caused by a
burn:
● erythema depending
● a blister at the dermo-epidermal junction
● necrosis of the skin
} on how long
you freeze for.
For most skin lesions for which freezing is an appropriate
treatment (viral and seborrhoeic warts, solar keratoses) you will
want to cause a blister at the dermo-epidermal junction so that the
abnormal tissue (in the epidermis) is lifted off in the blister roof.
For pre-malignant lesions, necrosis of the abnormal cells is
required. Cell death occurs at a skin temperature of −40°C. At
this temperature ice crystals form within the cells and disrupt the
cells as they are rewarmed. Maximum damage occurs if the skin is
frozen rapidly and allowed to thaw slowly. The thaw time should Fig. 2.08 Cryotherapy using a Cry-Ac Fig. 2.09 Blister after cryotherapy to a
spray gun solar keratosis
PHYSICAL TREATMENTS / 59
Freezing can most easily be done using a Cry-Ac or Cryo-Pro Pharmaceutical (Plough Lane, Hereford HR4 0EL, England, tel.
spray gun (see Fig. 2.08). This is a stainless steel insulated vacuum 01432 373555) or IontoCentre (Unit 19 Mahoney Green Ind Park,
flask with a side arm and a spray tip. Different tips are available Green Lane West, Rackheath NR13 6JY, England, tel. 0800 472
depending on the size of lesion to be frozen. Spray liquid nitrogen 5461) for treatment at home.
onto the middle of the lesion to be treated. A white ball of ice
The hand or foot to be treated is placed in a container with
will form and gradually expand. Keep freezing until it is 2 mm
only enough tap water to cover the palmar or plantar surface.
outside the margin of the lesion you are treating. At that stage,
A solution of an anticholinergic agent (0.05% glycopyrronium
stop freezing and give short, sharp squirts of liquid nitrogen to
bromide in distilled water) works better but is expensive to
hold the ice ball at a constant size for the period of time given in
make up. This is connected to the positive terminal of a DC unit
Table 2.09. After a time you will become experienced at estimating
producing up to 50 milliamps. The opposite foot or hand (not
the amount of freeze that is necessary for treating a particular type
of lesion. Do not freeze over-enthusiastically at first, and when
freezing the lower legs, halve the freeze time recommended in Table 2.09
(excessive freezing on the lower legs can lead to ulceration).
Cryotherapy with dimethyl ether/propane

Dimethyl ether/propane gas can be obtained in an aerosol can
(Histofreezer or Wartner). The gas is discharged through a cotton
bud or directly onto the skin and can freeze the skin to –50°C. This
is a useful method of freezing if you only wish to freeze warts
very occasionally. There are reports of patients self-treating what
has turned out to be squamous cell carcinomas or melanoma
(thought to be a viral wart or seborrhoeic keratosis).
IONTOPHORESIS
Iontophoresis involves passing a low electric current into the
skin. Skin resistance is lower through the sweat ducts than the
skin so the current passes preferentially down them. This is a
useful treatment for hyperhidrosis of the hands and feet and
with a new attachment for the axillae. It is available in most
dermatology or physiotherapy departments, where the first course
of treatment should be given. If this is beneficial, then mains
and battery-operated units are commercially available from STD Fig. 2.10 Iontophoresis
being treated) is placed in a deep bath of tap water connected to UVC radiation (200–290 nm), UVC from the sun is filtered out by
the negative terminal (see Fig. 2.10). A current of 10 milliamps is the ozone in the atmosphere. It is not used therapeutically.
given for 10 minutes three times (first week), two times (second
UVB radiation (290–320 nm) is responsible for tanning and
week) and then weekly until the sweating stops. The current and
sunburn. UVB is present in sunlight but is filtered out by window
time can be increased if the treatment is not effective, and pulsed
glass. For treating psoriasis UVB (especially at 311–313 nm) works
current machines can allow greater currents to be used if required.
much better than UVA. As a treatment UVB is given either by
The sweating will gradually return after weeks to months, when
tubes emitting the whole UVB spectrum (broadband UVB) or by
the treatment can be repeated. Treatment response tends to be
special TL01 tubes emitting at 311–313 nm (narrowband UVB).
variable; not all patients respond well.
Narrowband UVB is theoretically safer than broadband UVB
ULTRAVIOLET LIGHT because it is less carcinogenic and more effective for psoriasis.
Narrowband UVB is given three times a week and is the
ultraviolet light treatment of choice in psoriasis. Pregnant women
can have UVB but not PUVA. Medical UV light sources can be
purchased on-line. This is not recommended until the patient
has undergone supervised treatment through a dermatology
department. They are obtained from skinmattersbristol.com or
androv-medical.com.
Although tar has traditionally been used in conjunction with
UVB the reason for its apparent benefit is not clear. It has been
assumed that the phototoxic agents in tar potentiate the effect
Fig. 2.11 The electromagnetic spectrum of the radiation. In practice, if erythemogenic doses of UVB are
used, there is no evidence that the topical application of tar is any
Many skin diseases improve in the summer and particularly better than using a simple lubricant (e.g. white soft paraffin). If a
on sun exposure. For some of these, treatment with artificial suberythema dose of UVB is used, tar is helpful.
ultraviolet light can be beneficial. The light is produced by banks UVA radiation (320–400 nm) is ineffective on its own. Sunbeds
of fluorescent lamps in stand-up booths (see Fig. 2.12) or lie-down bought commercially produce mainly UVA, although a low dose
units. The lamps (whether UVB or UVA) must be of sufficient of UVB also is emitted, which probably produces the tan. Addition
intensity (watts = joules/sec) to deliver a therapeutic dose (joules/ of a psoralen followed by UVA (PUVA therapy) has been found to
cm2) within a short period of time and it must also be possible to be an effective treatment for several conditions (see Table 2.10).
measure accurately the dose given.
PUVA therapy (P = psoralen + UVA) the minimal erythematous dose (MED). The MED for UVB or
Psoralens are three-ringed compounds that can cross link DNA the minimal phototoxic dose (MPD) for PUVA are measured
(through thymidine or cytosine in one chain of the double helix by applying a template with a number of 1 cm2 cut-outs to the
and pyrimidine in the other) in the presence of UVA light. The patient’s skin (see Fig. 2.13) and irradiating them with increasing
cross linking of DNA chains prevents cell division which is how doses of ultraviolet light (the rest of the patient’s skin being
it works in psoriasis. There may also be an effect on the immune completely covered up). This is done in the same treatment booth
system and increased production of melanin. that will be used for the treatment. For PUVA it is done 2 hours
after the ingestion of 8-MOP. The tests are read at 72 hours and a
Either 8-methoxypsoralen (8-MOP) or 5-methoxypsoralen
barely perceptible erythema is the end point that you are looking
(5-MOP) can be used. Maximum photosensitivity occurs 2–3 hours
for. The dose of ultraviolet light (joules/cm2) needed to produce
after ingestion and exposure to the UVA is timed to coincide
this amount of erythema is the MED or MPD. The starting dose for
with this. UVA penetrates further into the dermis than UVB, and
treatment is 75% of the MED/MPD. Each dose is increased by 25%
combined with the psoralen is more effective. The psoralen is
of the previous dose given until the disease is clear. Alternatively,
taken 2 hours before irradiation at a dose dependent on weight
the starting dose can be assessed according to skin type (see p. 3).
(8-MOP tablets – 0.6 mg/kg body weight; 5-MOP tablets – 1.2 mg/
kg body weight). Alternatively the 8-MOP can be put in a bath It is recommended that the lifetime exposure to PUVA should be
and the patient soaks in the solution for 15 minutes immediately limited to 1000 joules/cm2 or 200 treatments to reduce the long-
before UVA exposure (bath PUVA), or applied directly to the skin term risk of skin cancer. No limit has been established as yet
as a gel (usually for hands and feet). Treatment is given twice for narrowband UVB, although every effort is made to keep the
weekly for 6–12 weeks until the skin is clear. amount of radiation to a minimum.
Determining the patient’s sensitivity to UVB or PUVA

In an ultraviolet light machine the patient must protect his eyes
against damage from ultraviolet light during and with PUVA for
The dose of UVA or UVB is worked out in terms of light energy
24 hours after the treatment by wearing glasses that filter out both
(joules/cm2), and depending on the output of the machine
UVB and UVA.
(measured by an internal ultraviolet light meter), the time of
exposure is calculated. The reaction on the patient’s skin induced RePUVA therapy
by PUVA or UVB is a phototoxic one, i.e. erythema, oedema and as
Some patients with psoriasis who do not respond to either PUVA
a maximum response, blistering. The erythema caused by PUVA
or oral retinoids (see p. 49) will respond when they are given
differs from that produced by UVB in that it appears later, lasts
together. The retinoid (acitretin 20–50 mg/day) is started 2 weeks
longer and is more intense. It does not peak until 48–72 hours (and
before the PUVA therapy. Then both are continued together (the
sometimes not until 96 hours). The aim of UVB or PUVA therapy
retinoid taken daily, the PUVA given twice a week) until the skin
is to deliver to the patient as much ultraviolet light as possible
is clear. The PUVA can then be stopped and the retinoid continued
without producing more than a barely perceptible erythema,
long term.
Table 2.10 Diseases that may respond to ultraviolet

light treatment
UVB PUVA
Psoriasis Psoriasis
Atopic eczema Severe atopic eczema
Chronic superficial scaly Mycosis fungoides
dermatosis
Acne Polymorphic light eruption
Pityriasis lichenoides Pityriasis lichenoides acuta
chronica
The itching of AIDS Urticaria pigmentosum
Vitiligo – in conjunction Vitiligo especially in dark-
with a topical steroid skinned individuals
The itching of chronic renal Alopecia areata
failure
Fig. 2.12 Ultraviolet machine Fig. 2.13 Determining the MED. The MED is where
the erythema just fills the square seen on the right
of the bottom line (arrowed)
Short-term side effects of PUVA with the 8-MOP. Rarely severe persistent itching makes the
● Nausea: this can be prevented by taking the 8-MOP tablets patient stop treatment. It can persist for several days or even
with food or a glass of milk. Occasionally an antiemetic weeks after treatment.
is required; we usually give 10 mg metoclopramide ● Erythema and tenderness: a few patients will get excessive
hydrochloride (Maxolon) at the same time as the 8-MOP. erythema, oedema and tenderness of the skin 48–72 hours after
● Dryness and itching of the skin: this is very common and may treatment. This is the main reason why treatment is only given
need an antihistamine such as chlorphenamine 4–8 mg given twice a week. If the patient gets burnt, the dose of irradiation
is reduced for the next treatment. All PHOTODYNAMIC THERAPY 8 minutes at 37 j/cm2). The patient feels a
patients are at risk of developing a Photodynamic therapy (PDT) is a burning sensation, which may last for a
phototoxic reaction after PUVA and treatment for pre-malignant lesions (solar few hours. The site is retreated a second
should avoid direct sunlight for 8 hours keratoses and Bowen’s disease) and non- time after 7 days.
after treatment by using a sunscreen melanoma skin cancers (superficial basal
that blocks out both UVB and UVA. The affected skin becomes inflamed,
cell carcinomas). Off-licence benefits have
PUVA pain: severe skin pain is unusual crusts after about a week, and heals
● also been reported in the acantholytic
but when it occurs treatment needs to within 4 weeks. Oedema, pain or redness
dermatoses, Hailey–Hailey disease and
be stopped. It can sometimes persist can occur. Itching, ulceration, infection
Darier’s disease: treatment during a mildly
for several weeks after treatment is or pigmentary changes are less likely.
inflammatory phase seems most beneficial.
stopped. In general PDT works very well on the
A photosensitising chemical, 5-amino- scalp and face, but less well on the limbs.
Long-term side effects of PUVA levulinic acid (ALA), is converted to Patients for PDT should be referred to a
● Cataracts: the eyes are protected during protoporphyrin-9 when irradiated with red dermatology department who have a lamp
treatment and for 24 hours afterwards light (630 nm). The porphyrin accumulates emitting the correct spectrum of light.
by wearing sunglasses to prevent in the abnormal cells and in the presence
cataract formation. of oxygen releases singlet oxygen,
● Skin cancer: there is an acceleration which causes cell death. Topical ALA
of the ageing process in the skin of is available as the methyl ester (methyl
patients who have been treated with aminolevulinate, Metvix cream) or the acid
PUVA and an increase in the incidence (LevulanUSA only). The methyl ester has the
of basal and squamous cell carcinomas advantage of being taken up preferentially
in the skin after 5–10 years. There have into neoplastic cells (due to their defective
also been some reports of malignant stratum corneum).
melanoma occurring. Lesions to be treated have any scale or
● Men must shield the genitalia during crust removed from the surface with saline,
treatment because there is an increased forceps or a curette. The Metvix cream
risk of squamous cell carcinoma of the is applied to the affected skin in a 1 mm
penis. thick layer, covered with a non-adherent
dressing and left in place for 3 hours.
After this it is removed and the area
irradiated with red light (Aktilite produces Fig. 2.14 Photodynamic therapy with red light to
a continuous spectrum 570–670 nm for lesion on face
High voltage power supply

LASERS
Laser is an acronym for Light Amplification by Stimulated
Emission of Radiation. It is a device that produces coherent,
collimated, monochromatic (single wavelength) light: an GAS
intense beam of pure monochromatic light that does not diverge Monochromatic beam
of light produced here
(collimated) and in which all the light waves are of the same Lasing tube
polarity and travel in step in the same direction (coherent). 100% reflective mirror 85% reflective mirror
How lasers work

Various gases, liquids and solids (laser medium) will emit light Fig. 2.15 How a gas laser works
when they are suitably stimulated or pumped (excitation source).
In a typical gas laser (CO2 or argon), the gas is contained in a
lasing tube that has a fully reflective mirror at one end and a
partially reflective mirror at the opposite end (see Fig. 2.15). The
laser medium is stimulated by means of a high voltage electric
current. A stimulated molecule of the gas emits a photon (a light
particle), which strikes another stimulated molecule causing it
to emit an identical photon (amplification). Emission of photons
occurs in all directions but the light waves become aligned by
resonance between the mirrors at either end of the laser tube,
and the coherent light exits through the partially reflective mirror
at one end. The type of gas, liquid or solid in the lasing tube
determines the wavelength of the coherent light that is produced.
The objective for any medical laser treatment is to restrict laser-
induced injury only to selected sites such as blood vessels or
pigment cells with minimal damage to the surrounding adjacent Fig. 2.16 Absorption spectrum of haemoglobin (solid line) and melanin (hatched
tissues. This effect is called selective photothermolysis. line)
It is achieved if the laser fulfils three requirements. adequate penetration. Pulse duration is selected depending
1. The laser light emission is at the same wavelength that the on the diameter of the vessel being treated. If it is too long
target absorbs, e.g. for haemoglobin at 542 or 577 nm (see scarring may result; if it is too short it causes purpura without
Fig. 2.16). destroying the vessel. The ‘V’-beam modification to the pulsed
2. The laser emits sufficient energy to damage the target tissue. dye laser results in a longer pulse with more energy into the
3. The duration of exposure of the tissue is short enough to limit blood vessels. This is meant to produce uniform damage to the
damage mainly to the target without excess heat diffusing vessels and less purpura.
outwards and damaging the surrounding tissues. This is ● Resurfacing or cutting lasers target the water in the skin using
determined by the thermal relaxation time of the surrounding infrared radiation. A short pulse duration and high energy
tissue, which is how long it takes for the target to dissipate results in vaporisation of tissue with minimal damage to
half its thermal energy. For a blood vessel in a port wine stain underlying structures (ablative lasers). Healing comes from
this is 1–10 milliseconds, while for tattoo pigment it is only re-epithelisation from hair follicles like a burn. Healing takes
1–10 nanoseconds (10–9). The pulse duration of the lasers about 2 weeks with considerable post-operative pain, redness
treating these targets must be of these magnitudes. and swelling. Possible problems include scarring, secondary
infection with herpes simplex or bacteria. Redness and
The penetration into the skin is determined by the wavelength tenderness can last several months. About 75% improvement
of the light (up to 2000 nm). Longer wavelengths penetrate can be expected with a CO2 laser. The systems used are the CO2
deeper but tend to have less energy. For hair removal, the laser laser and the Erbium-YAG lasers. The CO2 laser penetrates into
must penetrate to the root of the hair follicle. The Alexandrite the dermis. The Erbium is more superficial, penetrating only
laser with a longer wavelength (755 nm) will be able to reach the into the epidermis and resulting in less tissue damage, faster
dermal papilla at the depth of a follicle (1 mm) with more energy healing and fewer side effects; however, it is also less effective.
than the Ruby (694 nm). For port wine stains the highest peak ● Fractional resurfacing lasers punch very fine holes into
of haemoglobin absorption at 418 nm is no good, as light of this the epidermis and dermis but leave the intervening skin
wavelength will not penetrate very far. The light of the pulsed dye undamaged. This results in faster healing times with less
laser at 585 nm provides a compromise between penetration and tissue damage. The idea is to promote epidermal and
energy absorption by haemoglobin. collagen regeneration with less patient morbidity. Four to five
treatments are needed at monthly intervals. The improvement
There are several groups of skin lasers (see Table 2.11) depending
of wrinkles is not as good as with conventional resurfacing
on the target tissue.
lasers. The systems used are the CO2 and Erbium-YAG lasers.
● Vascular lasers target haemoglobin. Wavelengths selected are
Some systems use a combination of these lasers, while others
around the 577 nm absorption peak (see Fig. 2.16) to ensure
use only a CO2 laser.
Table 2.11 Types of dermatological laser

Type of laser λ nm Pulse time Function Comments
Vascular lasers
Pulsed dye (PDL) 585 (yellow) 0.45 msec Port wine stain (capillary Recommended – causes bruising that lasts 2 weeks; large spot size good for larger
malformation) lesions, multiple treatments required (see p. 127)
595 1.5 msec Telangiectasia Visible lesions on face; no good for erythema
Spider naevi
KTP 532 (green) 2–10 msec Telangiectasia Does not cause bruising, so good for cosmetic lesions; use if PDL not effective, since the
(Port wine stains) longer pulse duration is better for larger vessels
Copper bromide 578 (yellow) 10–50 msec Telangiectasia, Small spot size useful for small lesions, impractical for large lesions such as port wine
510 (green) Spider neavi stains
Lentigines and freckles
IPL (intense pulsed light) 560 filter Erythema and telangiectasia of Around 50% improvement after four treatments at 3-weekly intervals (Br J Dermatol.
rosacea 2008;159: 628–3)
Resurfacing or cutting lasers
Ablative Ablative = tissue vapourisation
Carbon dioxide (CO2 ) 10 600 10–20 msec Resurfacing actinic damage and Thermal damage up to 100 μm deep, which stimulates collagen and elastic tissue
(infrared) scarring (acne, trauma) regeneration
Erbium-YAG 2940 200–400 msec Resurfacing and removal of epidermal Thermal damage only 10 μm deep – no deep damage; quicker recovery time but less
(infrared) lesions effective for marked scarring
Fractional lasers Wrinkles and facial lines Punch micro-sized holes with normal skin intervening – quicker recovery, less damage
Erbium-YAG 2940 60 nsec but less effective than full ablative lasers; better on neck, chest, hands; CO2 penetrates
Carbon dioxide 10 600 deep, Erbium-YAG superficial
Non-ablative Non-ablative
Pulsed dye 1320 50 msec Correction of facial lines and wrinkles Dermal collagen targeted, epidermis undamaged; low risk with little post-operative
Nd:YAG 1064 effects. Less effective, multiple treatments required; needs skin cooling device to prevent
IPL (intense pulsed 550 epidermal damage and pain
light) IPL not good for pigmented skin, as light absorbed by melanin
Type of laser λ nm Pulse time Function Comments

Pigment lasers
Nd:YAG 532 6 nsec Lentigines and freckles Good response – short wavelength for surface lesions
1064 (Q-switched) Café au lait patches and Becker’s Variable to poor response
naevus
Naevus of Ota/Ito Variable response – longer wavelength for deeper lesions
Tattoo removal
Nd:YAG 1064 6 nsec Blue-black tattoos Useful laser as two options in one machine (1064 and 532 nm)
(Q-switched)
532 Red, orange, yellow tattoos Preferred option due to fast repetition rate (10 Hz = shots/sec)
Ruby 694 25–40 nsec Blue-black, green tattoos Slower repetition rate (1 Hz), mainly useful for green, more painful
Hair removal
Alexandrite 755 2–20 msec Hair needs to be dark but patient’s Preferred laser since penetrates deeper than Ruby
skin type I or II
Ruby 694 (red) 270 μsec Slow repetition rate (1 Hz) = long treatment times
Nd:YAG 1064 50 msec Skin types IV–VI Deeper penetration, very painful, better for darker skin types
IPL 700–750 Hair needs to be dark but patient’s Not true coherent laser light; filters used to produce narrow wavelength bands; less
skin type I or II effective than true laser
Phototherapy
Excimer (XeCl) 308 (UVA) 120 nsec Psoriasis, vitiligo Same wavelength as ultraviolet light for phototherapy
● Non-ablative lasers target the dermis leaving the epidermis ● Pigment lasers target melanin and tattoo pigment. Between
unaffected. They are meant to stimulate new collagen 650 and 1100 nm there is good penetration and preferred
formation. They are much safer and provide a rapid recovery absorption by melanin compared with haemoglobin. Tattoo
time, but are not as effective as the ablative lasers. The systems ink will also absorb laser light at a specified wavelength. Very
used are the Nd:YAG, pulsed dye lasers and intense pulsed short pulse widths, which are generated by ‘Q-switching’
light (IPL). produces a shock wave within the pigment which shatters the
pigment granule into sufficiently small particles that can be of non-coherent light, usually in the 500–1200 nm range. A
absorbed and removed by macrophages. Hair removal targets range of filters can be used to deliver more specific narrow
melanin also but longer pulse widths and longer wavelengths bands of wavelengths. Modern devices can be used safely and
are needed to reach and damage the follicle. effectively for the cosmetic treatment of many vascular lesions,
● IPL is a technology used by both the cosmetic industry and unwanted hair and pigmented lesions. Newer technologies
medical practitioners to perform various skin treatments may give results equal to those of laser treatments. IPL has
including hair removal and photo-rejuvenation. IPL devices been shown to be particularly useful for the treatment of
are non-laser high-intensity light sources that make use of a telangiectatic erythema of rosacea.
high-output flash lamp to produce a broad wavelength output
a b
Fig. 2.17 Tattoo: (a) before Q-switched Nd:YAG laser treatment; (b) after five Fig. 2.18 Bruising from the pulsed Fig. 2.19 Dermabrasion of the face
treatments: note ‘ghosting’ – some pigment still present dye laser on a capillary malformation using a carbon dioxide laser
(port wine stain)
69
Hair and hairy scalp

(For bald scalp see Chapters 5 and 9)
3
Hair physiology
What is hair? 70
Hair cycle 70
Excess hair 71
Hair loss
Discrete bald patches 73
without scarring 73
with scarring 79
Diffuse hair loss 83
Structural abnormalities of hair 86
Rashes and lesions in the hairy scalp
Itch, erythema, scaling 87
Pustules, crust, exudate 90
Non-erythematous papules, plaques and nodules 94
70 / HAIRY SCALP
HAIR PHYSIOLOGY HAIR CYCLE

WHAT IS HAIR? There are between 100 000 and 150 000 hairs on the scalp. The
Hair is a modified type of keratin produced by the hair matrix hair cycle (see Fig. 3.02) occurs randomly in each follicle over the
(equivalent to epidermis). On the scalp, apart from its social and scalp so that up to 100 hairs are being lost daily, but in normal
cosmetic function, hair protects the underlying skin from sun circumstances moulting does not occur.
damage. The three phases of the hair cycle are:
Three types of hair occur in humans. 1. anagen (80%–90% of hairs) – this is the growing phase and on
1. Lanugo hair is the soft, silky hair that covers the foetus in the scalp lasts 2–6 years
utero. It is usually shed before birth. 2. catagen – the hair matrix cells stop dividing and hair growth
2. Vellus hair is the short, fine, unpigmented hair that covers the stops; it lasts about 2 weeks
whole skin surface apart from palms and soles. 3. telogen (10%–20%) – this is the resting phase; the hair shaft
3. Terminal hair is longer, coarser and pigmented. Before puberty, moves up in the dermis; it lasts 3 months and at the end of that
terminal hair is restricted to the scalp, eyebrows and eyelashes. time the hair is shed.
After puberty, secondary terminal hair develops in response
to androgens in the axillae, pubic area and on the front of the
chest in men.
Anagen Telogen
Plucked hair has white Plucked hair has
sheath 2–3 mm long at end small white tip at
with a dark tip (papilla) the end
Fig. 3.01 How to tell the difference between plucked anagen and telogen hairs Fig. 3.02 The hair cycle
EXCESS HAIR / 71
EXCESS HAIR The amount of hair on the face, breasts and lower abdomen in
Hair in the wrong place or hair that is coarser or longer than women is under androgen control. Testosterone produced by the
is socially acceptable is regarded as excessive. There are two ovary is converted to dihydrotestosterone in the skin by the action
different patterns, hirsutism and hypertrichosis. of 5α-reductase and it is this that causes the increase in hair. If the
periods are abnormal in any way it is always worth checking the
HIRSUTISM serum testosterone level. If it is more than twice the upper limit
Coarse terminal hair in the moustache or beard area for women of normal, the patient should be referred to an endocrinologist
and on the chest or lower abdomen in the normal pattern for men for a full endocrine work-up to exclude a testosterone-secreting
is known as hirsutism. It is extremely common, the amount of tumour. Many such patients have polycystic ovary syndrome
hair being genetically determined. How much facial and body with infertility, irregular periods, acne (70%), as well as hirsutism
hair is cosmetically acceptable in an individual is dependent (90%). They are frequently obese with insulin resistance, raised
on many factors, but particularly the patient’s cultural and lipids and hypertension (metabolic syndrome). This does not
social background. What is considered normal in many parts of require any specific treatment unless associated with diabetes or
Southern Europe is deemed unacceptable in the United Kingdom ischaemic heart disease.
or the United States.
TREATMENT: HIRSUTISM
By the time the patient seeks help from the doctor she will usually have tried all the
simple things that do not require medical advice. If she has not, the following options
are available and may be helpful.
● Bleaching the hairs. There are a number of bleaching agents available commercially.
For patients with very dark hairs, bleaching will often disguise them enough to be
acceptable.
● Depilatory creams. The common active ingredients are calcium thioglycolate or
potasium thioglycolate, which break down the disulfide bonds in keratin and weaken
the hair so that it is easily scraped off where it emerges from the hair follicle. In some
patients these creams will make the skin sore by a direct irritant effect; they can also
cause a contact allergic dermatitis and folliculitis, which will limit their usefulness.
● Waxing and sugaring. These are basically methods of mass plucking of hairs. Hot
wax or a thick sugar solution is applied to the hairy area of skin; it is allowed to
cool and is then peeled off, pulling the hairs out at the same time. Both methods are
available from reputable beauticians. This method is suitable for removal of excess
hair from the legs and body as well as the face.
(cont.)
Fig. 3.03 Hirsutism
72 / HAIRY SCALP
HYPERTRICHOSIS TREATMENT: HYPERTRICHOSIS

● Threading is another effective method of hair removal also available from some Hypertrichosis is excessive
salons. hair all over the body. Either There is no good treatment for
● Plucking and shaving. A surprising number of women still remove unwanted hair by hypertrichosis. If it is due to a drug
the foetal lanugo hair is not
plucking and shaving. Most do not like doing it but have found that other methods and it is possible to stop the drug,
lost before birth or it regrows
make their skin too sore. This does not lead to increased hair growth or thickening of the hypertrichosis will be reversible,
at some later stage. When although it may take up to a year for
the hair shaft – the cut hair shaft just looks thicker.
● Electrolysis. If the amount of unwanted hair is not too extensive, electrolysis
confined to the lumbosacral the hairiness to disappear.
and epilation using a short-wave diathermy machine can provide a permanent area (fawn tail) it may be a
For other methods of hair removal see
answer. A fine sterile needle is placed into the hair follicle down to the level of the marker of an underlying spina
hirsutism.
papilla. A high-frequency alternating current is then passed through the needle bifida.
for a microsecond. This destroys the papilla permanently and the hair is lifted out
Some drugs cause
without pain. This process works well but is rather time-consuming and expensive.
Practitioners should be members of the British Institute and Association of
hypertrichosis in all patients to
Electrolysis. Side effects may include pain, scarring and pigmentary changes. a greater or lesser degree:
● Lasers are an effective method of removing hair. The light is absorbed by melanin ● ciclosporin
in the hair shaft and the heat generated damages the follicle. The treatment works ● diazoxide
best on dark hair in a fair-skinned individual. Dark-skinned patients are at risk of ● minoxidil.
developing hyperpigmentation after treatment. The best laser for hair removal is the
Alexandrite (at 755 nm). Tanning should be avoided while undergoing treatment.
The following drugs
Intense pulse light is also an effective means of hair removal and works in a similar occasionally cause
way to lasers. Shaving is the only method of hair removal permitted while undergoing hypertrichosis:
treatment. Several treatments are necessary, as only follicles in anagen (growth ● diphenylhydantoin
phase) respond. The hair loss is not permanent but a 60% reduction in hair density is ● minocycline
seen after about six treatments spread over a year. Twice-yearly ‘top-up’ treatments ● penicillamine
will maintain things. ● psoralens.
● Eflornithine (Vaniqa) cream is an ornithine decarboxylase inhibitor that reduces hair
growth over a 2- to 4-month period. It is useful alone or before laser treatment.
● Anti-androgens Yasmin or Dianette (co-cyprindiol – contains cyproterone acetate)
can be tried in general practice, but risks for thromboembolism need to be assessed.
Spironolactone can also be helpful in reducing excess hair.
Fig. 3.04 Hypertrichosis
HAIR LOSS / 73
HAIR LOSS
Hairy scalp
Discrete bald patches BALD PATCHES WITHOUT OBVIOUS SCARRING
Without scarring
Scalp normal Affected scalp scaly
One/several well- Complete hair loss Single area, hairs Afro-Caribbean Scalp margins ‘Moth eaten’ Short broken-off Thick scale present
defined areas of all short (<1 cm) with tightly only affected appearance hairs
complete hair plaited hair
loss
! mark hairs ? Hair loss Children/ Hair has been Anterior loss, Patient unwell, Mycology Itching ++
around edge ± elsewhere teenagers pulled back under Erythema around body rash,
eyebrows and tension hairs ± eyebrows lymphadenopathy
beard
biopsy Positive Negative
ALOPECIA ALOPECIA TRICHO- TRACTION FRONTAL SECONDARY SCALP LICHEN

AREATA TOTALIS/ TILLOMANIA ALOPECIA FIBROSING SYPHILIS RINGWORM SIMPLEX,
UNIVERSALIS ALOPECIA PSORIASIS,
PITYRIASIS
AMIANTACEA
p. 74 p. 74 p. 78 p. 78 see p. 81 see p. 353 p. 76 see p. 88

74 / HAIRY SCALP
ALOPECIA AREATA It will usually regrow white or blonde initially, but it goes back
Alopecia areata is the commonest cause of discrete hair loss in to its original colour after 6–8 weeks. Five per cent of individuals
both children and adults. The trigger is often a stressful event affected will have total scalp hair loss, alopecia totalis, and 1%
and alopecia areata itself is often very distressing, especially will have alopecia univeralis, total loss of both scalp and body
if it affects a large area. There is no redness or scaling of the hair.
underlying scalp. There may be one or several bald patches on Alopecia incognito (diffuse alopecia areata) causes rapid
the scalp or on any other hairy area (e.g. eyebrows, eyelashes, diffuse thinning of scalp hair and may be confused with telogen
beard). The hair loss is sudden. While the disease is active, effluvium (see p. 84). If there is any doubt as to the diagnosis, a
exclamation mark (!) hairs will be seen around the edge of the scalp biopsy is helpful to distinguish between the two.
bald patches. These are short, broken-off hairs. Only pigmented
hairs are affected, so normal white or grey hairs will remain in Alopecia areata is a common autoimmune disease and spans
the middle of a bald area. It can take months or years to grow all ages and ethnic groups. It is worth asking about a family
back and new patches may develop. history of autoimmune disease and checking blood sugar and
autoimmune profile including thyroid antibodies.
Fig. 3.05 Alopecia areata: discrete bald patches Fig. 3.06 Alopecia areata: regrowth of white hair – Fig. 3.07 Alopecia areata: ! hairs at edge of bald
with no evidence of erythema or scaling this will repigment in due course patch
HAIR LOSS / 75
TREATMENT: ALOPECIA AREATA
Discuss with the patient that hair may take many months to grow back and that there is 12–16 weeks and should be reserved for individuals who have had hair loss within
a risk it may not grow back at all. This is more likely if the hair loss is extensive or occurs the last year. Potential side effects should be discussed with patients before starting
in an ophiasis pattern (margin of scalp). Warn the patient that the hair may regrow treatment. Continued use of systemic steroids is not justified for alopecia areata
white or blonde until it is about 1.5 cm long, but that it will go back to its normal because of long-term complications (see p. 51).
colour. ● Azathioprine may be trialled in steroid-responsive patients (see p. 54). Future
treatments include abatacept, a drug available for the treatment of rheumatoid
A wig may be needed temporarily if the hair loss is extensive.
arthritis. It inhibits co-stimulation of T-cells. It is currently being trialled in the United
Treatment currently available is unsatisfactory but includes the following options. States for alopecia totalis and alopecia universalis.
● Topical steroid: 0.5% clobetasol proprionate (Dermovate) applied twice daily (not
to the face). Referral to a clinical psychologist can play an important role in helping patients come to
● Intralesional injection of triamcinolone (10 mg/mL): this is a suitable and often terms with their hair loss.
effective treatment for limited areas of hair loss. Side effects include skin atrophy,
which is usually temporary, and it may cause hypopigmentation in individuals with
darker skin types.
● Topical minoxidil (Regaine) lotion or foam. The 5% formulation is unlicensed in
women but is likely to be more effective than the 2% preparation. It is expensive but
cheaper generics may be found online. It is rubbed into the affected area twice a day.
Any hair growth induced will fall out if the treatment is discontinued. Oral minoxidil
2.5 mg is an alternative but there is a risk of downy facial hair growth in women.
● Topical prostaglandins: Latisse (0.3% bimatoprost) is available online and may be
used to improve eyelash and eyebrow growth.

● Application of potent skin sensitisers to the bald areas: Diphencyprone is the
drug most commonly used. It is most effective in those whose hair loss has been
present for less than 1 year. The scalp skin is sensitised by painting a 2% lotion to
the upper inner arm, which becomes eczematised over 2 weeks. The whole scalp is
then painted with a diluted solution of the lowest concentration (0.001%–0.1%),
which will produce mild erythema. If it works, it is painted on the bald areas once a
week until regrowth of hair is well established. Diphencyprone is degraded by light
so patients have to keep their heads covered for 24 hours after treatment. Any hair
growth may be lost if treatment is stopped, so maintenance is usually required.
● Oral steroids (e.g. prednisolone 30–40 mg/day) are effective in a proportion of
cases, but over half of those who respond will relapse when the dose is reduced or
stopped. There is no standard regimen but treatment should be for a minimum of
Fig. 3.08 Alopecia areata: bald patches in the beard area
76 / HAIRY SCALP
a b
Fig. 3.09 Scalp ringworm: discrete bald Fig. 3.10 Kerion in a 10-year-old child: (a) a red, boggy
patch with scaly surface swelling due to animal ringworm, (b) after treatment and
(c) with regrowth of hair
SCALP RINGWORM (TINEA CAPITIS)

Scalp ringworm only occurs in children; it is not a cause of hair
loss in adults except those with HIV/AIDS. It is often due to
Trichophyton tonsurans (caught from other children) or Microsporum
canis (caught from kittens or puppies). Discrete bald areas occur
out the short, broken hairs, and sending them for mycology. Scalp
with short, broken-off hairs in which the underlying skin is scaly
ringworm due to M. canis fluoresces green under the Wood’s light
and/or red. If the skin is red or if there is associated ringworm on
(see Fig. 3.12). T. tonsurans does not fluoresce.
the face or neck, it is more likely to be due to animal ringworm.
There will be a history of other children with similar hair loss (in Animal ringworm of the scalp (due to M. canis) can sometimes
human ringworm), or a new kitten or puppy whose fur is falling produce a red, boggy swelling discharging pus; this is called a
out (in animal ringworm). The diagnosis is confirmed by pulling kerion (see Fig. 3.10a).
HAIR LOSS / 77
Fig. 3.11 Animal ringworm: child with Fig. 3.12 Tinea capitis: green fluorescence Fig. 3.13 Diagram showing hair shaft invaded by fungal spores that are
lesions in scalp and on face and neck of Microsporum canis under a Wood’s inaccessible to topical treatment
(ultraviolet) light
TREATMENT: TINEA CAPITIS
Treatment is griseofulvin 15–20 mg/kg body weight/day given as a single dose with is most commonly grown), but is less effective for Microspsorum (M. canis or
food daily for 6 weeks. It can be given as tablets (125 mg each) or as a suspension M. audouinii). The dose depends on the child’s weight: 10–20 kg–62.5 mg/day;
(125 mg/5 mL). Alternatively, it can be given as a single large dose (5 g) in ice cream. 21–40 kg–125 mg/day; > 41 kg–250 mg/day, given for 4 weeks.
There is no need for topical treatment as well, as this is ineffective, since treatment
applied to the surface cannot get into the hair shaft (see Fig. 3.13). As human-acquired tinea capitis is contagious, and adults may act as carriers, all family
members and possibly classmates should be screened for evidence of infection.
If it is due to M. canis, the affected pet (kitten or puppy) must be treated with
griseofulvin too. The pet should be taken to the local vet to get the treatment. If the child has a kerion, the crusts should be softened with arachis oil and then
removed. It is worth taking a bacteriology swab from under the crust or from a pustule.
Terbinafine (Lamasil) works well for infections with Trichophyton species (T. tonsurans If Staphylococcus aureus is grown, treat with flucloxacillin as well as with the antifungal.
78 / HAIRY SCALP
TRICHOTILLOMANIA and the hair will not regrow. Minoxidil can be helpful in boosting
Trichotillomania is a well-defined area of apparent hair loss. growth where there are still active follicles to improve volume but
Close examination will reveal not a bald area, but an area where in many patients the hair loss is so advanced that a wig may be
all the hairs are short – longer hairs having been pulled out. The necessary.
remaining hair is just too short to twist around the fingers to pull
out. It usually occurs in children as a habit tic or in teenagers who
are unhappy.
The only thing likely to be confused with this is alopecia areata.
If the diagnosis is in doubt, a biopsy from the abnormal area will
show empty anagen follicles and melanin pigment casts.
TREATMENT: TRICHOTILLOMANIA
Most cases in young children are due to a habit tic, but there may be an obvious
emotional reason – one of the parents has left home or died, or some other major
stress has occurred. Often the parent(s) have not noticed the child twisting the hairs
around one of the fingers or pulling them out but will do so once you tell them what is
happening. It is best for them not to make a big thing of it, particularly not to punish Fig. 3.14 Trichotillomania: looks like a bald patch but in fact
the child for it, and to give the child as much love and security as they can during the short hairs are present
difficult time. Once the time of trauma is over, the child will nearly always stop pulling
the hair out and the hair will regrow normally. In teenagers who pull out their hair the
cause is often less obvious, but most will need psychiatric help to resolve the problem.
TRACTION ALOPECIA
This is a common condition in races with tight curly hair but much
less common in Europeans. It causes hair loss at the temples and
sometimes the crown and is due to the hair being tightly pulled
back, tied up, plaited, braided or straightened with hot combs. It is
important to ask about hair styling practices when Afro-Caribbean
or African patients, usually woman, present with hair loss. The
hair loss may be reversible if the hair pulling is stopped early.
Usually by the time patients present there is significant scarring Fig. 3.15 Traction alopecia: note loss of hair on the frontal hairline
HAIR LOSS / 79
Hairy scalp
Discrete bald patches SCARRING ALOPECIA
With scarring
(All are uncommon; the hair follicle is replaced by scar tissue, so the hair loss is permanent)
Single lesion Multiple lesions
Present since Occurs later

birth
Previous injury/ Linear, extends Gradually Gradually Diffuse Scattered papules/

infection from forehead expanding expanding irregular pustules → crusts
to scalp patches
Central scale/ Peripheral Red/scaly areas No surface/ Discrete round Keloids on nape
crust scale around colour change scars of neck
follicles +
pustules
APLASIA POST- LINEAR TUMOUR FOLLICULITIS LICHEN IDIOPATHIC SCALP ACNE KELOID
CUTIS/NAEVUS TRAUMATIC MORPHOEA (BCC, SCC, DECALVANS PLANUS/ SCARRING FOLLICULITIS NUCHAE
SEBACEOUS burn/herpes LYMPHOMA, DISCOID LUPUS ALOPECIA
zoster/ SARCOMA)
radiotherapy/
fungal kerion
pp. 80, 94 p. 82 p. 80 p. 93 p. 81 p. 81 p. 82 see p. 91 see p. 96

80 / HAIRY SCALP
APLASIA CUTIS MORPHOEA

Aplasia cutis presents at birth as an Linear morphoea on the forehead may extend into the scalp resulting in a linear scar (en
ulcerated, red area on the scalp. This heals coup de sabre). It often involves the underlying subcutaneous fat leaving a depression
to leave a permanent scar (see also naevus in the skin. It can sometimes be associated with hemifacial atrophy. Aggressive early
sebaceous, p. 94). It is not due to birth treatment is required to prevent permanent deformity. Pulsed methyl prednisolone
trauma. followed by methotrexate or mycophenolate mofetil are preferred. Surgery can improve
the appearance once the disease has burnt out.
Fig. 3.16 Linear morphoea on scalp and forehead, Fig. 3.17 Folliculitis decalvans: bald areas with Fig. 3.18 Lichen planus in scalp: note the mauve
known as ‘en coup de sabre’ pustules and crusts around hairs colour of the underlying skin
HAIR LOSS / 81
FOLLICULITIS DECALVANS
Folliculitis decalvans is a rare condition in which there is an abnormal host reaction to an
infection with S. aureus. There is a slow progressive scarring alopecia with pustules and
crusts around the affected hairs.
TREATMENT: FOLLICULITIS DECALVANS
Once scarring has occurred the hair will not regrow. It is important, therefore, to start treatment as soon as possible
to minimise the hair loss. Although due to S. aureus, treatment with flucloxacillin does not work. Lymecycline 408 mg
bid can be helpful in less severe cases or a combination of rifampicin 300 mg bid with clindamycin 300 mg bid given
for 10–12 weeks (up to 2 years if relapse occurs). Isotretinoin 1 mg/kg is an alternative. Patients should be counselled
regarding potential side effects of these drugs.
Fig. 3.19 Frontal fibrosing alopecia: progressive

LICHEN PLANUS AND DISCOID LUPUS ERYTHEMATOSUS scarring of anterior hairline
Lichen planopilaris (LPP, lichen planus of the scalp) and discoid lupus erythematosus
both cause scarring alopecia. In lupus the skin over the bald patches is usually red and
scaly and there may be follicular plugging.
Different patterns of LPP are recognised. It may present in an androgenic or female
pattern scarring hair loss or as ‘footprints in the snow’, where small, discrete, scarred
areas are seen. Perifollicular erythema and scale may be noted in a more diffuse pattern.
Frontal fibrosing alopecia is another variant of LPP. It results in a progressive scarring
alopecia of the fronto-temporo-parietal hairline. It is usually but not always seen in
postmenopausal women. Often the process has been going on for many years before
patients notice that their frontal hairline has moved back. Often these patients have
associated eyebrow loss and may have also lost hair elsewhere, e.g. axillae. Prominent
follicles with perifollicular erythema and scale may be seen along the frontal hairline.
Often these patients complain of a burning sensation on their scalp. The cause is not
known but it is thought that hormones may play a role, given that the majority of patients Fig. 3.20 Discoid lupus erythematosus: scarring and
affected are postmenopausal women loss of pigment on scalp
82 / HAIRY SCALP
Sometimes the diagnosis is obvious from TREATMENT: LICHEN PLANUS AND DISCOID LUPUS ERYTHEMATOSUS
the rash elsewhere. If in doubt, a biopsy
will confirm the diagnosis. Sometimes Very potent topical steroids (0.05% clobetasol proprionate) and oral hydroxychloroquine 200 mg bid may be effective if
nothing is seen histologically except the used early enough to prevent scarring in both conditions. Once scarring has occurred, no regrowth is possible. Doxycycline
replacement of hair follicles with scar 100 mg daily has been found to be partially effective in lichen planus. Anti-androgens such as finasteride 5 mg weekly
tissue. This is called idiopathic scarring and dutasteride 500 μg weekly may help in stabilising, and in some cases improving, frontal fibrosing alopecia. For
treatment of lichen planus see p. 198; for discoid lupus erythematosus see p. 137.
alopecia or pseudopelade of Brocq.
POST-TRAUMATIC ALOPECIA
Any injury or infection resulting in
scarring will result in hair loss. Usually
the history will make the cause obvious.
Before griseofulvin was introduced in 1958,
radiotherapy was the usual treatment for
scalp ringworm. It caused the anagen hairs
to fall out and resulted in cure. If too big a
dose was given, the resulting alopecia was
permanent. Many of these patients are now
developing basal cell and squamous cell
carcinomas on their bald scalps.
Hot combing, chemical straightening and
hot oil treatments used to straighten black
curly hair can all result in permanent hair
loss, particularly if aggravated by tight or
corn-rolling styling that applies additional
traction to hair roots.
Fig. 3.21 Discoid lupus erythematosus in scalp: note Fig. 3.22 Idiopathic scarring alopecia of the scalp
red scaly plaques in bald area (no cause found on biopsy)
HAIR LOSS / 83
Hairy scalp
Diffuse hair loss DIFFUSE HAIR LOSS
Recent extensive hair loss Gradual thinning of hair Hair breaks
easily
Hairs coming Hairs coming Restricted to top of scalp All over scalp
out are out are
telogen anagen
Occurs Patient on Frontal Normal Check Patient taking ! hairs Patient Elderly female Texture of hair
3 months cytotoxic recession frontal thyroid/ anticoagulant, present unwell, lymph abnormal
after drugs hairline ferritin levels antithyroid, or nodes
childbirth/ retinoids
fever/illness/
diet/major
surgery
TELOGEN ANAGEN MALE FEMALE THYROID/ DRUG CAUSE DIFFUSE SECONDARY LOSS DUE TO STRUCTURAL
EFFLUVIUM EFFLUVIUM BALDNESS PATTERN IRON ALOPECIA SYPHILIS OLD AGE ABNORMALITY
ALOPECIA DEFICIENCY AREATA OF HAIR
p. 84 p. 84 p. 85 p. 85 p. 84 p. 84 see p. 74 see p. 353 p. 84 p. 86

84 / HAIRY SCALP
TELOGEN EFFLUVIUM ANAGEN EFFLUVIUM

Telogen effluvium occurs when there is a shift in the normal hair Cytotoxic drugs affect any rapidly dividing cells and the hair
cycle resulting in temporary hair loss. A trigger such as hormonal matrix is affected, as well as the bone marrow and tumour cells.
changes (e.g. post pregnancy or stopping the oral contraceptive It is the anagen hairs that are shed, so 90% of all scalp hair will
pill), extreme dieting, severe illness, stress or certain medications be lost. Once the drug is discontinued, hair will usually regrow
(e.g. retinoids) usually precedes it. Patients may describe noticing normally, although permanent alopecia may sometimes occur,
increased hair in the shower, on their hairbrush or on the pillow. especially after docetaxel for breast cancer (1 in 30 risk).
The hair will often come out in handfuls when you pull gently
on the hair. A positive hair pull test is classified as six or more
hairs. A false negative result may occur if the patient has washed
his or her hair within 48 hours. Telogen hairs have a club-shaped
tip (see p. 70). Shedding of telogen hairs is followed by regrowth
of anagen hairs. Such hair loss peaks after a few months and
gradually reverts to normal over 6–9 months. Usually the hair
recovers fully but in some cases may be incomplete. Short fronds
of hair may be noted at the frontal hairline.
Some patients may notice continued intermittent shedding known
as chronic telogen effluvium. They should be reassured that this
will not result in baldness, although it may unmask an underlying
genetic predisposition to a patterned hair loss.
OTHER CAUSES OF DIFFUSE HAIR LOSS

The hair density gradually decreases with age and the hairs
become finer. In younger patients, consider:
● hypothyroidism
● iron deficiency
● diffuse alopecia areata – look for ! hairs
● secondary syphilis – the patient will be unwell with
widespread lymphadenopathy and a rash (see p. 207)
● systemic lupus erythematosus (see p. 131)
● drugs: anticoagulant, antithyroid or retinoids. Fig. 3.23 Telogen effluvium: a lot of hair pulls out easily
HAIR LOSS / 85
Fig. 3.24 Anagen effluvium in a child on Fig. 3.25 Male pattern baldness: frontal recession Fig. 3.26 Female pattern alopecia: note retention of
chemotherapy with loss on the crown – the sides and occiput are the frontal hairline with thinning over the vertex of
normal the scalp
MALE PATTERN BALDNESS FEMALE PATTERN ALOPECIA

This is hair loss occurring over the temples or on the crown due This is similar to male pattern baldness but usually without the
to androgens (dihydrotestosterone). The hair on the occiput and frontal recession (see Fig. 3.26). Decreased hair density from the
around the sides of the scalp is never lost (see Fig. 3.25). The effect crown forward with normal hair density at the back and sides
of dihydrotestosterone is a shortening of the anagen growth phase occurs. Minor degrees of this are extremely common.
and a corresponding increase in telogen hairs. Gradually the hair
An androgen-secreting tumour should be considered in women
follicles get smaller and terminal hairs are replaced by vellus
with male pattern alopecia if it is very extensive or if there is a
hairs. The amount of hair loss and the age of onset is genetically
change in the menstrual cycle.
determined (from mother or father).
86 / HAIRY SCALP
TREATMENT: MALE PATTERN BALDNESS TREATMENT: FEMALE PATTERN ALOPECIA
For most men, no treatment is needed or sought since this is a normal physiological For minor degrees of this, no treatment is needed, but if it is noticeable consider one of
process. For a few, who cannot come to terms with their baldness, the following are the following options.
available (not under the National Health Service). ● Anti-androgens: Dianette is an option, particularly if there is associated polycystic
● A 5% minoxidil solution or foam: 1 mL is rubbed into the bald scalp twice daily. ovarian syndrome.
This does not produce regrowth of normal terminal hair, but of long vellus hair in ● Spironolactone: start with 50 mg bid and increase to 100 mg bid depending on side
about a third of those who use it. If treatment is stopped, the longer hair will fall out, effects. It is worth trying this for 6 months. In younger women it may cause menstrual
so once started it will need to be continued indefinitely. A 2% solution is used for irregularities and postural hypotension. Premenopausal women should be counselled
maintenance treatment. against becoming pregnant on this treatment. It may be stopped during pregnancy
● Finasteride: 1 mg orally daily (or 5 mg weekly, which is cheaper!) inhibits type and restarted when breastfeeding has finished. Check renal function and electrolytes
II 5α-reductase, the enzyme that converts testosterone to the more active (potassium).
dihydrotestosterone in scalp follicles. One-third of men will have marked regrowth of ● Topical minoxidil, as for male pattern baldness.
hair, one-third will have moderate regrowth and one-third will have little regrowth. ● Finasteride 5 mg weekly is sometimes used in postmenopausal women.
Side effects (in about 5% of patients) should be discussed. They include impotence, ● Other treatments that have been found to be helpful include topical oestrogens,
ejaculatory dysfunction and loss of libido. Patients should be warned that there have topical prostaglandins (e.g. bimatoprost) and ketoconazole.
been cases of prolonged sexual side effects even after stopping treatment. Unfortunately, on stopping treatment with any of the drugs listed here, the hair loss
● Hair transplants: hairs are taken from the occipital area or sides of the scalp by will reoccur.
punch biopsy. Follicular units (containing one to four follicles) are transplanted into ● Hair transplants: although expensive, this is an effective treatment in selected
the bald areas. This is an effective treatment in selected cases. patients.

● A wig is another option and is available on the National Health Service.
STRUCTURAL ABNORMALITIES OF HAIR

Some patients notice that their hair breaks easily and will not More common is a phenomenon known as ‘weathering’ in which
grow to the desired length. There are numerous structural hair becomes more coarse and breaks easily secondary to long-
abnormalities of the hair shaft that cause hair to break off short. term use of hairstyling techniques such as colouring, perming
All are uncommon. In trichorrhexis nodosa (see Fig. 3.27) the hair or straightening of the hair. Various shampoos and conditioners
shaft looks like two paint brushes pushed together (see Fig. 3.28). on the market, e.g. Dove repair and Fibrology, claim to improve
In pili torti the hair shaft is flattened and twisted. In monilethrix appearance. Patients should refrain from continuing harsh
the hair shaft shows elliptical nodules. hairstyling techniques.
RASHES AND LESIONS IN THE HAIRY SCALP / 87
RASHES AND LESIONS IN THE HAIRY SCALP

Hairy scalp
Itch, erythema, scaling ITCH/ERYTHEMA/SCALING
No hair loss
Scaling present No scaling
Palpable scale Impalpable Erythema and itch Nits firmly attached

uniform scale to hair shaft
Well-defined Scale growing out Scaling sides Eczema elsewhere

plaques along hairs nose/ears
eyebrows/lashes
Fig. 3.27 Trichorrhexis nodosa: hair breaks off easily
and is difficult to comb or keep tidy
PSORIASIS PITYRIASIS SEBORRHOEIC ATOPIC ECZEMA HEAD LICE

AMIANTACEA ECZEMA
Fig. 3.28 Trichorrhexis
nodosa: microscopy
showing nodular
swelling at which point p. 88 p. 88 p. 88 p. 88 see p. 92
the hair breaks
88 / HAIRY SCALP
PSORIASIS ECZEMA
Psoriasis in the scalp is common, and it may start there. The Eczema is differentiated from psoriasis on the scalp because it
diagnosis is made by running your hands through the scalp usually covers all the hairy scalp and is more easily seen than
and feeling the thick, heaped-up scales, which are not shed felt. Wherever you look it is red and scaly. Seborrhoeic eczema
because the scale binds to the hair. When you look, the lesions are typically starts in the scalp, causing fine scaling (dandruff). This
identical to those found elsewhere, i.e. discrete, well-defined, red is associated with scaling behind and in front of the ears, in the
scaly plaques. Hair loss may occur in scalp psoriasis but rarely external auditory meatus and on the face (see p. 135)
becomes long-standing. The plaques may extend away from the
Atopic eczema also commonly affects the scalp but typical
hairline onto the forehead, neck or around the ears, causing social
changes will be seen elsewhere (see p. 236). When acute, eczema
embarrassment.
on the scalp may exude serum and become crusted.
PITYRIASIS AMIANTACEA
The term ‘pityriasis amiantacea’ is used to describe thick scales
growing out along the hair shaft. It can be due to either psoriasis
or eczema. It is seen more commonly in children than in adults.
Fig. 3.29 (left) Scalp

psoriasis: thick scale
extending from the
hairline onto the
forehead (compare with
seborrhoeic eczema
Fig. 3.32)
Fig. 3.30 (right) Scalp

psoriasis: thick scaling
with some hair loss due
to scratching
TREATMENT: SCALP PSORIASIS/PITYRIASIS

AMIANTACEA the patient goes to bed and washed off the following morning with a tar-based shampoo (again left for 5–10 minutes
and washed off). Because it makes a mess, the head should be covered overnight with a scarf or shower cap to keep the
For mild scalp psoriasis where the scales are not ointment off the pillow. The treatment is repeated each night and washed off each morning until the scalp is clear. This
very thick, shampooing the scalp twice weekly with a usually takes 7–10 days. Once it is clear, the treatment can be done once a week or once a fortnight to keep it clear.
tar-based shampoo such as CapasalUK, Polytar or T-Gel
Seborrheoic eczema is treated with ketoconazole (Nizoral) shampoo two to three times weekly. It should be left on for
may be all that is needed. It is useful to alternate with
5 minutes and then rinsed off. It should be used for 4 weeks, and then fortnightly to keep it clear. Any thick scaling can be
an anti-yeast shampoo, such as ketoconazole (Nizoral)
removed (see thick plaques of psoriasis).
shampoo. Both should be used two to three times a
week, left on for 5–10 minutes and then rinsed off.
Another alternative is Dermax shampoo.
If that is not enough, or if the scalp is very itchy, a
topical steroid lotion or gel can be applied every night
until it is clear. Calcipotriol lotion may be tried as an
alternative twice daily. Topical scalp lotions contain
alcohol, so warn the patient that it will sting if the skin
is broken. Steroid gels and mousses are water miscible
and will not sting. None of these will work if there is
thick scaling. Clobetasol shampoo (Etrivex) is a useful
alternative for short periods. Apply dry, massage into
the scalp and leave on for 10 minutes before rinsing
off backwards two to three times a week. Dovobet
(calcipotriol/betamethasone) gel can also be applied
at night for 4–8 weeks. It. repels water, so it must be
removed with dry shampoo before rinsing.
Thick plaques of psoriasis on the scalp or pityriasis
amiantacea require something to soften up the scale.
The most effective treatment is coconut oil compound
ointment (unguentum cocois compound [Sebco/
CocoisUK]) or Dermol lotion (which is less smelly). The
hair is parted and the ointment rubbed onto the scalp,
it is then parted again a little further along and more
ointment applied; this is continued until the whole
scalp has been treated. It is done every night before Fig. 3.31 Pityriasis amiantacea: thick plaque with Fig. 3.32 Seborrhoeic eczema: fine impalpable
scale growing out along hair scaling over the whole scalp
90 / HAIRY SCALP
Rash in hairy scalp ALLERGIC CONTACT DERMATITIS

Pustules, crust, exudate PUSTULES/CRUST/EXUDATE Allergic contact dermatitis on the scalp
Widespread Localised lesions Localised is not common and is usually due to
Over all scalp swelling hair dyes (paraphenylenediamine, PPD)
or perming solutions (thioglycolates).
It usually presents as an acute weeping
Affects neck, Scalp only Rash elsewhere Recurrent Fixed lesion* Hair pulls out eczema at the hair margins and on the
forehead, ears papules/ BIOPSY easily forehead, face and neck, rather than in the
as well pustules scalp itself. The diagnosis is confirmed
once the patient is better by patch testing.
Recent perm or Look for nits Poorly defined Crusting/ Lesions on nape Mycology + ve
hair dye plaques scarring of neck
ALLERGIC HEAD LICE ATOPIC SCALP SYCHOSIS/ TINEA CAPITIS

CONTACT ECZEMA FOLLICULITIS ACNE KELOID (KERION)
DERMATITIS
p. 90 p. 92 see p. 88 p. 91 p. 96 see p. 76
* Fixed lesions require a biopsy to exclude tumours, e.g. squamous cell carcinoma or basal cell carcinoma, see p. 93 Fig. 3.33 Allergic contact dermatitis to hair dye:
acute eczematous reaction affecting neck and back
TREATMENT: ALLERGIC CONTACT DERMATITIS
Stop using hair dyes/perming solutions. If it is very weepy, dry up any exudate by
soaking the scalp in a diluted potassium permanganate or aluminium acetate solution
(see p. 30). Then apply a potentUK/group 2–3USA steroid ointment. Once it is better, refer
to a dermatologist for patch testing to establish the cause.
SCALP FOLLICULITIS
Recurrent pustules on the scalp present a diagnostic and
therapeutic difficulty. Sometimes the cause is a staphylococcal
folliculitis, which can be confirmed by taking a swab. This is
particularly common in African children because of the practice
of rubbing petroleum jelly (Vaseline) into the scalp. This is often
associated with posterior cervical lymphadenopathy. In Europe
and the United States usually no bacteria are grown and it is
assumed that the condition is a variant of acne. Some lesions may Fig. 3.34 Allergic contact dermatitis to hair dye: lichenified hyperpigmented
heal to leave a scar. eczema on forehead
Fig. 3.35 Scalp folliculitis: crusted lesions that may heal to leave a scar Fig. 3.36 Scalp folliculitis: isolated pustules within the hairy scalp
92 / HAIRY SCALP
HEAD LICE (PEDICULOSIS CAPITIS) TREATMENT: SCALP FOLLICULITIS

Lice are wingless insects that pierce the skin to feed on human
blood. The head louse is about 3 mm long. The female lays Stop applying greasy ointments on the scalp. Take swabs. If S. aureus is grown, treat
7–10 eggs each day during a life span of 1 month. The eggs are with flucloxacillin or erythromycin 500 mg qid till clear. If swabs are negative, treat with
a tetracycline (e.g. lymecycline 408 mg once to twice daily). Alternatively, rifampicin/
firmly attached to the base of the hair, and they hatch in about a
clindamycin 300 mg bid may be tried. If these fail, isotretinoin 40 mg daily is usually
week. Head lice are spread by direct contact from head to head,
effective (see pp. 120–1) but relapse is common and low-dose maintenance (10 mg day)
mainly in children. It has nothing to do with poor hygiene. Lice may be necessary.
are not transmitted by combs, hats or hairbrushes. Infestation is
extremely common and usually asymptomatic. If there are large
numbers of lice, itching may be intolerable and result in secondary TREATMENT: HEAD LICE
bacterial infection (impetigo and pustules). Enlarged posterior
cervical glands should always make you think of head lice. The There are a number of insecticides available that kill both adult lice and eggs.
diagnosis is made by finding the nits (egg cases), which are white, Dimeticone may be used and acts on the surface of the lice. It should be rubbed into
opalescent oval capsules, firmly attached to hairs (see Fig. 3.38), the scalp, left overnight and rinsed off with shampoo in the morning. Two treatments
easily distinguished from the scale of seborrhoeic dermatitis should be given, 7 days apart. Malathion is an alternative but some lice are resistant
(dandruff), which comes off easily (see Fig. 3.39). to this. Permethrin can also be used. Lotions are better than shampoo formulations
because the latter have too short a contact time to be effective. The lotion is applied
all over the scalp, left on for 12 hours, and then washed off with a normal shampoo.
The permethrin cream rinse is used like a conditioner. It coats the lice and eggs with
a balsam containing the insecticide, so combining a long contact time with a short
treatment time. The egg cases can be removed by combing with a nit comb.
PROBLEMS WITH TREATING HEAD LICE

● Resistance to insecticides is common, and if one treatment fails to cure the
infestation, you should try another one. The Bug Buster Kit consists of a nit comb and
a conditioner. The wet hair should be combed for 10 minutes every night for about
2 weeks. This is useful if you want to avoid excessive use of insecticides.
● To prevent re-infection, the whole family and school friends or contacts should be
treated, whether or not they are itching. You may need to involve the health visitor,
practice nurse or school nurse.
(cont.)
Fig. 3.37 Head lice bites on back of neck

● People are often worried that some of the lice may be missed in children or adults
with very long hair. Since the eggs are laid onto the hairs where they leave the
scalp, all the viable eggs will be close to the scalp and will be killed, as long as
the insecticide has been applied to the scalp (not the hair). In the same way, the
adult lice and the immature walking stages have to go to the scalp to feed, so the
insecticide will kill them then.
● Only water-based insecticide lotions should be used in patients with eczema, because
the alcoholic-based ones will sting excoriated skin.
TUMOURS
Basal cell carcinomas may occur in the hairy scalp as a persistent
area of crusting or hair loss. The unusual site results in a
misdiagnosis of eczema or ‘infection’ so that the lesion may
become quite large before being recognised.
Fig. 3.38 Head lice: nits attached to hair shaft
Squamous cell carcinomas occur in the elderly who have
significant hair loss or thinning. They present as an ulcer with
an overlying crust that has become matted down with hair (see
Fig. 9.162, p. 333).
Fig. 3.40 Basal

cell carcinoma with
secondary hair loss: a
biopsy will be needed
Fig. 3.39 Dandruff: fine scale that is not attached to the hairs to confirm the diagnosis
94 / HAIRY SCALP
Hairy scalp
Non-erythematous lesions COMMON LESIONS
Papules, plaques and nodules
Present since Onset after puberty Onset after age 40
birth/early
childhood
Yellow plaque Subcutaneous Dome shaped/ Papules/ Brown plaque Hair loss and
nodule papillomatous nodules on crusting
occipital area
Warty surface Normal surface Warty/smooth Very firm Warty surface Biopsy
with hair loss
NAEVUS PILAR CYST INTRADERMAL ACNE KELOID SEBORRHOEIC BCC

SEBACEOUS NAEVUS KERATOSIS SCC
p. 94 p. 95 p. 96 p. 96 see p. 320 see p. 93

Fig. 3.41 Naevus sebaceous present since birth
NAEVUS SEBACEOUS
happens it is obvious, because there will be a lump within the
This is present from birth or early childhood. It differs from a
naevus or a discharge from it.
congenital melanocytic naevus in being yellowish with a flat,
warty surface and hair loss. A basal cell carcinoma or other No treatment is necessary. It can be excised to reduce the area of
adnexal tumour may develop within it in middle age. If this hair loss. If a tumour develops, this will need removing.
Fig. 3.42 Naevus sebaceous on cheek with basal cell Fig. 3.43 Multiple pilar cysts in scalp Fig. 3.44 Excision of overlying skin over a pilar cyst
carcinomas arising from it to reveal the right plane for removal
PILAR (TRICHILEMMAL) CYST TREATMENT: PILAR CYST

Pilar (or trichilemmal) cysts are derived from the external root
sheath of hair follicles and occur predominantly on the scalp. They First excise the overlying skin with a small ellipse. The top of the cyst will then be visible
are inherited as an autosomal dominant trait, they appear between (see Fig. 3.44). It will now shell out very easily, since these cysts have a connective
the ages of 15 and 30, and present to the doctor because the patient tissue sheath around them. If this is not the case, it is likely that it is an epidermoid cyst.
notices a lump when brushing or combing the hair. One or several An alternative method of removal is to cut straight into the cyst with a scalpel, squeeze
subcutaneous nodules are present. They do not have a punctum out the contents and then remove the cyst lining with a pair of artery forceps. It should
and do not usually become inflamed (compare with epidermoid come out intact and very easily.
cysts, see p. 273).
96 / HAIRY SCALP
INTRADERMAL NAEVUS ACNE KELOID NUCHALIS

Flat, pigmented naevi are not usually recognised on the hairy Acne keloid nuchalis is a chronic inflammatory condition of
scalp. Once they become raised they are likely to be caught the nape of the neck, most commonly seen in men of African
in combs. Most skin-coloured or light-brown papules on the or Afro-Caribbean origin. Itchy follicular pustules develop in
scalp will be intradermal naevi. They may have a smooth or the occipital area, which later become keloid scars. In the early
papillomatous surface (see p. 264). stages of the disease (pustules present), long-term, low-dose
antibiotics as for scalp folliculitis can be used (see p. 92). Once
TREATMENT: INTRADERMAL NAEVUS keloid papules, nodules or plaques are present treatment is
more difficult. Possibilities include intralesional triamcinolone
Reassure the patient that they are harmless. They can be easily removed by shave and once a month or wide excision of the affected area down to and
cautery if they become a problem. including the fat.
Fig. 3.45 Pedunculated intradermal naevus in scalp Fig. 3.46 Keloid scars at site of folliculitis on nape Fig. 3.47 Acne keloid nuchalis
of neck
97
Acute erythematous rash on the face

Normal surface
Widespread patches, papules, plaques, swelling 98
Localised lesions (papules and nodules) see p. 177
4
Crust or exudate on surface
Papules, plaques, blisters, erosions 104
Pustules see p. 183
98 / ACUTE RASH ON FACE
Face
Acute erythematous rash WIDESPREAD RASH – NO EXUDATE
Surface normal/smooth
Widespread patches, papules, plaques, swelling
Swelling No swelling
Only around eyes Whole face Not related to sun exposure Occurs after sun exposure
and/or lips/tongue
No erythema Exanthematous rash Itchy papules and Erythema on sun-exposed sites

plaques
± urticaria elsewhere Ill and fever++ Poorly defined Bright-red erythema ± similar rash on No excessive sun ± pinpoint vesicles/
Recent new drug, papules and plaques on cheeks other sun-exposed exposure crusts
2–6 weeks sites only Drug history?
ANGIO-OEDEMA DRESS SUBACUTE FIFTH DISEASE POLYMORPHIC LIGHT PHOTOTOXIC DRUG SUNBURN
ECZEMA ERUPTION RASH
p. 99 see p. 168 p. 103 p. 103 p. 100 p. 101 p. 106

WIDESPREAD RASH / 99
Fig. 4.01 Angio-oedema and urticaria: note oedema Fig. 4.02 Acute eczema: swelling of eyelids with Fig. 4.03 Erysipelas: swelling of eyelids and cheeks
around eyes and lips without redness, scaling or exudate and crusting with large blisters
exudate
ANGIO-OEDEMA Angio-oedema without weals is often idiopathic, but you should

Angio-oedema is oedema in the dermis due to increased vascular exclude a drug cause or possible C1 esterase deficiency (hereditary
permeability. There should be no associated redness. On the angio-oedema), especially if there is a family history or previous
face the swelling involves the eyelids and lips. Less commonly episodes of laryngeal oedema or abdominal pain.
the tongue and larynx can be involved, leading to difficulty
in swallowing and breathing. The onset is often dramatic. The TREATMENT: ANGIO-OEDEMA
patient may feel unwell and the eyelid swelling may cause
complete closure of the eyes. It should start going down quite Use a long-acting non-sedative antihistamine such as cetirizine or loratidine at a
quickly but can last up to 48 hours. If there is associated urticaria high dose, 10–20 mg every 12 hours (maximum of four times the standard hay fever
dose) until it settles. In a life-threatening situation in the context of anaphylaxis (not
(see p. 171) the diagnosis is easy. When it occurs alone it needs
hereditary angio-oedema) with swelling of the larynx or tongue, inject 0.5 mL of 1:1000
to be distinguished from an acute eczema or erysipelas. The fact
adrenaline solution intramuscularly (prescribable to appropriate at-risk patients, with
that the swelling is not red and there are no blisters or scaling appropriate training, in the form of an EpiPen) with strict directions to attend A&E for
should make the diagnosis easy. follow-up, as its benefits are short term and further treatment may well be required.
Fig. 4.04 Polymorphic light eruption. Itchy papules Fig. 4.05 Polymorphic light eruption. Itchy papules Fig. 4.06 Polymorphic light eruption. Distribution
and vesicles on face and neck sparing the area under on dorsum of hand over sun exposed sites
the chin
POLYMORPHIC LIGHT ERUPTION face, but not all sun-exposed sites need to be involved, and quite
often the face may be clear.
This is a common rash due to ultraviolet light. It occurs in early
adult life and affects twice as many females as males. The rash Most patients are aware of the connection with the sun. The rash
consists of itchy red papules, vesicles or plaques. The size of the typically occurs several hours after sun exposure and, if there is no
papules varies in different patients, from pinpoint up to 5 mm. further exposure, lasts for 2–5 days. It usually occurs in spring and
The plaques may be urticarial (i.e. non-scaly dermal oedema) or early summer and tends to improve as the summer progresses,
eczematous (scaly and poorly defined). Vesicles are less common. due to some form of tolerance. In some patients it only occurs
It occurs only on sun-exposed parts, especially the backs of the when they are away from home (on holiday) in more intense
hands, forearms, ‘V’ of neck and below the ears, as well as the sunlight.
TREATMENT: POLYMORPHIC LIGHT ERUPTION a
● Keep out of strong sunlight, wear protective clothing and use a high-factor sunblock
with both medium wave ultraviolet light (UVB) and long-wave ultraviolet light (UVA)
protection.
● Refer to dermatology department for TL01, UVB or PUVA desensitisation therapy. This
can be given in early summer to prevent the rash developing, or as a treatment to
induce tolerance. It is given twice a week for 6 weeks. Following treatment, regular
sun exposure is necessary to maintain tolerance.
● Systemic steroids (prednisolone 20 mg/day) may suppress the eruption for the
duration of a short 2-week holiday.
● Hydroxychloroquine 400 mg daily may provide partial protection.
PHOTOTOXIC RASHES
A phototoxic rash looks like sunburn but occurs in a patient
who has not been exposed to excessive sunlight. It is caused by
sunlight plus: b c
● chemicals applied to the skin, e.g. psoralens in sun creams,
photodynamic therapy photosensitizers – aminolevulinic acid
● accidental contamination of the skin by wood tars in creosote
● drugs taken by mouth, e.g.
— antiarrhythmics: amiodarone (30%–50% of patients on this
drug), quinidine
— antibiotics: tetracyclines (doxycycline and demeclocycline),
nalidixic acid, quinolones (e.g. ciprofloxacin)
— diuretics: thiazides and furosemide
— hypoglycaemics, sulphonylureas
— NSAIDs (e.g. naproxen)
— phenothiazines: chlorpromazine
— psoralens
— sulphonamides.
Fig. 4.07 Phototoxic rash showing sparing of shaded sites: a. under nose (top),
b. behind ear (above left) and c. upper eye lid (above right).
The diagnosis is suggested by the distribution of the rash with

shaded sites (upper eyelids, behind ears, under chin, see Fig. 4.07)
spared. It can be confused with a contact allergic dermatitis but
there should not be any scaling. The history of drug ingestion or
creams applied to the face should enable the cause to be identified.
TREATMENT: PHOTOTOXIC RASHES
Stop the drug responsible. If this is not possible, use an opaque total sunblock
containing titanium dioxide or zinc oxide to screen out all UVA (almost all drug
sensitivity rashes are due to UVA). Note that UVA penetrates glass, so protection is
needed even indoors or inside a car.
Fig. 4.09 Eczema involving upper eyelids: to be distinguished from

photosensitive rashes, which spare this site
Fig. 4.08 (left)

Eczema: ill-defined
papules and plaques
without exudate or
scaling Fig. 4.10 Atopic eczema involving both eyelids as well as cheeks
SUBACUTE ECZEMA FIFTH DISEASE (ERYTHEMA INFECTIOSUM)

Subacute eczema occurs without obvious vesicles and exudate. This is a viral infection due to parvovirus B19. It is characterised
There will be erythematous patches and plaques where the border by the appearance of red papules on the cheeks that coalesce
of the rash is ill defined, merging imperceptibly into normal within hours to form symmetrical, red, oedematous plaques,
skin. It can be due to an allergic contact dermatitis (to cosmetics, sparing the nasolabial fold and eyelids, the so-called ‘slapped
perfumes, medicaments), or to a new occurrence of an unclassified cheek’ appearance. Other symptoms are mild (sore throat, pruritis,
endogenous eczema or an exacerbation of existing eczema (atopic fever) or even absent. The rash on the face fades after 4 days, but
or seborrhoeic). within 48 hours of the onset of the facial erythema, a lace-like
pattern of erythema appears on the proximal limbs, extending
to the trunk and extremities. This fades within 6–14 days. No
treatment is needed, as it gets better on its own.
Fig. 4.11 Fifth

disease (erythema
infectiosum): typical
‘slapped cheek’
appearance Fig. 4.12 Fifth disease: lace-like pattern on the leg
Face
Acute erythematous rash CRUST, EXUDATE or BLISTERS
Crust or exudate on surface
Papules, plaques, blisters, erosions
Most of face affected Localised lesions
Patient ill with fever Patient not ill Crusts+++ Blisters initially → crusts later
No fever No blisters
Well- Isolated Sun- Coalescing Poorly Well-defined Multiple coalescing vesicles Unilateral Discrete
defined lesions exposed lesions defined rash scattered Dermatomal lesions
erythema sites only lesions
Large bullae Papules ± small Vesicles, ± Golden Golden Recurrent Previous First Grouped Separated by
→ pustules vesicles exudate crust crusts same site eczema episode vesicles normal skin
→ crusts and crusts Previous Usually child Painful++ Surrounding
eczema First episode oedema
ERYSIPELAS CHICKEN SUNBURN ACUTE INFECTED IMPETIGO RECURRENT ECZEMA PRIMARY HERPES INSECT
POX ECZEMA ECZEMA HERPES HERPETICUM HERPES ZOSTER BITES
SIMPLEX SIMPLEX
p. 105 see p. 184 p. 106 p. 106 p. 107 p. 107 p. 109 p. 109 p. 108 p. 110 see p. 198
CRUST OR EXUDATE / 105
Fig. 4.13 Erysipelas: blisters on well-defined Fig. 4.14 Acute contact dermatitis due to lanolin in Fig. 4.15 Acute sunburn in an African albino:
erythema (see also Fig. 4.03) moisturising cream: exudate and crusting painful redness and blistering on sun-exposed sites
ERYSIPELAS TREATMENT: ERYSIPELAS

This is an acute, rapidly spreading rash usually caused by a
group A β-haemolytic streptococcus. The patient is unwell with Ideally treat with intravenous benzyl penicillin 1200 mg 6 hourly. Alternatively, oral
fever, rigors and general malaise. The rash itself is bright red, flucloxacillin 1 g every 6 hours will cover Staph as well as Streptococci. If the patient is
allergic to penicillin, use oral clindamycin 300 mg or clarithromycin 500 mg 6 hourly. The
well demarcated and may or may not contain large blisters in the
patient should be dramatically better within 24 hours.
centre. There is no associated lymphangitis or lymphadenopathy.
It is not usually possible to culture the organism, and
measurement of the ASO titre is not helpful. Diagnosis is made on
TREATMENT: ACUTE SUNBURN
the characteristic clinical picture.
Topical calamine lotion will produce symptomatic relief. If severe, a single application of
a very potentUK/group 1USA topical steroid (0.05% clobetasol propionate) ointment will
reduce redness and bring instant relief.
ACUTE SUNBURN A photoallergic dermatitis is identical in appearance to an allergic

Acute sunburn presents as painful erythema with or without contact dermatitis but it needs a combination of UVA and a drug
blisters, between a few hours to 2 days after sun exposure. Usually to cause it. The commonest drugs are:
the cause will be obvious, as the patient will have been exposed ● chlorpromazine
to strong sunlight, although a delay in symptoms can lead to ● promethazine
misdiagnosis. Any exposed areas will be burnt. ● sulphonamides
● alimemazine.
ACUTE ECZEMA
Acute eczema on the face presents as tiny vesicles, weeping and
crusting, and is usually due to a contact allergic dermatitis or
atopic eczema. The onset of the rash is sudden with a well-defined
erythema followed by vesicles, profuse exudate and crusting. If
the eyelids are involved there may be marked oedema and the
patient may not be able to open the eyes (see Fig. 4.14). The rash
is usually symmetrical and uncomfortable and itchy rather than
painful as in herpes zoster. Angio-oedema causes swelling only,
with no weeping, and there is no associated fever as in erysipelas.
Acute allergic contact dermatitis of the face can be due to
medicaments applied to the face or airborne allergens such as
sawdust, cement dust, epoxyresins or phosphorus sesquisulphide
from the smoke of ‘strike anywhere’ matches. Common applied
allergens include lanolin (in ointment bases), formaldehyde and
parabens (preservatives in creams), topical antihistamines or
antibiotics, cosmetics and fragrances within perfumes. The exact
pattern of the rash depends on the allergen responsible. Airborne
allergens cause a symmetrical eczema especially affecting the
upper eyelids and cheeks, while allergens in medicaments and
cosmetics only involve areas where these have been applied.
Linear streaking can be due to nail varnish. A rash around the hair
margins and ears can be due to hair dyes or perming solutions (see Fig. 4.16 Baby with acute onset of atopic eczema: weeping and crusting on the
p. 90). cheeks
TREATMENT: ALLERGIC CONTACT DERMATITIS
Remove the patient from all possible allergens. Dry up any exudate with wet dressings of
potassium permanganate (1:10 000) or aluminium acetate (see p. 30) twice a day. Dry the
skin and then apply 1% hydrocortisone or 0.05% clobetasone ointment bid. Always use
a steroid ointment rather than a cream, which may contain potential allergens. Once the
rash is better, refer the patient to a dermatologist for patch testing (see p. 21).
IMPETIGINISED ECZEMA
Any itchy rash may become secondarily infected with
Staphylococcus aureus once scratching has broken the skin.
Weeping occurs and a golden-yellow crust forms on the surface.
The diagnosis is made by a history of a preceding rash (usually
atopic eczema or scabies). Individual lesions may be difficult to
Fig. 4.17 Impetiginised eczema: exudate and golden crusts in a child with distinguish from impetigo.
atopic eczema
TREATMENT: IMPETIGINISED ECZEMA
It is best to give a systemic antibiotic, either flucloxacillin or erythromycin four times a day
(125 mg dose for children, 250 mg for adults). At the same time, treat the atopic eczema
(see p. 236) or scabies (see p. 248) or the infection will reoccur.
IMPETIGO
This is a very superficial infection of the epidermis (see Fig. 7.31,
p. 187) due to S. aureus, a group A β-haemlytic streptococcus or a
mixture of both. Children are mainly affected, since the organisms
gain entrance through broken skin (cuts and grazes). It is very
contagious. Typically it starts as vesicles, which rapidly break down
to form honey-coloured crusts; less commonly there may be just a
glazed erythema. On the trunk occasionally flaccid cloudy bullae
(Fig. 7.32, p. 187) are seen, which burst and form the typical golden
Fig. 4.18 Impetigo: typical honey-coloured crusts on chin crusts.
TREATMENT: IMPETIGO PRIMARY HERPES SIMPLEX

Infection with the Herpesvirus hominis type 1 most commonly
Because the infection is very superficial, topical antibiotics are more effective than affects the buccal mucosa (see p. 143) and occurs in the first
systemic (if present without underlying chronic eczema). If thick crust is present, remove 5 years of life. It is usually asymptomatic but may cause an
it by applying arachis oil (or olive/sunflower oil) for 15–20 minutes. This will soften
acute gingivostomatitis. A primary infection on the skin causes
it so that it can be wiped off. Once the crust has been removed, apply 2% mupirocin
painful blistering on an oedematous background (see Fig. 4.21 and
(Bactroban), 2% fusidic acid (Fucidin) or 0.3% neomycin ointment four times a day for
3 days. Apply the antibiotic ointment to the anterior nares at the same time.
Fig. 13.04, p. 406).
In parts of the world where impetigo is commonly due to a group A β-haemolytic TREATMENT: RECURRENT HERPES SIMPLEX
streptococcus, the child will need to be treated with oral penicillin V four times a day for
7 days to prevent acute glomerulonephritis from occurring. Most patients need no treatment. Topical aciclovir or penciclovir cream applied every
2 hours for 2 days, beginning as soon as the prodromal symptoms occur, will shorten
the attack but will not prevent further episodes. If recurrent episodes occur frequently or
result in erythema multiforme, these can be suppressed by giving oral aciclovir 400 mg
bid or famciclovir 250 mg daily for at least 6 months.
Fig. 4.19 Impetigo: golden-coloured crusts and Fig. 4.20 Impetigo: glazed erythema and erosions Fig. 4.21 Primary herpes simplex: grouped vesicles
erosions on nose associated with marked surrounding oedema
RECURRENT HERPES SIMPLEX ECZEMA HERPETICUM

If the primary infection of herpes simplex was in the mouth, recurrent episodes affect Atopic eczema may become secondarily
the lips or the skin around the lips. Primary infections elsewhere on the skin produce infected by herpes simplex. The
recurrences at the same site (e.g. finger, buttock). Most patients know that a recurrence characteristic feature is small umbilicated
is beginning because of the prodromal sensation of itching, burning or tingling. A few vesicles that are painful rather than itchy,
hours later, small grouped vesicles appear (see Fig. 1.29, p. 9), burst, crust and then heal often with sudden onset and deterioration
in 7–10 days. These episodes can be precipitated by fever (hence the name ‘cold sores’), of previous eczema. The patient will be
sunlight, menstruation and stress, and can continue throughout life. Herpes simplex is ill and more miserable than might be
differentiated from impetigo by the history of recurrent episodes, prodromal pain and expected from normal eczema. Swabs
initial vesicles containing clear fluid, and in adults it is the more likely diagnosis. If in from the vesicles will confirm the presence
doubt, a Tzanck smear from the base of a blister will show multinucleate giant cells in of the herpes simplex virus. Pemphigus,
herpes simplex. pemphigoid and Darier’s disease may
all become similarly infected with herpes
simplex virus. Treat the same as herpes
zoster (see p. 180).
Fig. 4.22 Herpes simplex, recurrent lesions with Fig. 4.23 Eczema herpeticum: painful umbilicated Fig. 4.24 Close up of umbilicated vesicles
localised crusts on the lower lip vesicles on cheek
HERPES ZOSTER
Herpes zoster on the face is the result of involvement of the rash extends from the upper eyelid to the vertex of the skull, but
trigeminal nerve. It presents as groups of small vesicles on a if vesicles occur on the side of the nose (nasocillary branch), the
red background, followed by weeping and crusting. The rash is eye is likely to be involved. These patients should be referred to an
unilateral. Healing takes 3–4 weeks. With ophthalmic zoster the ophthalmologist. See also p. 179.
Fig. 4.25 Ophthalmic zoster: vesicles on the side of Fig. 4.26 Maxillary zoster affecting the maxillary Fig. 4.27 Mandibular zoster: involvement of the
the nose mean the eye will be involved branch: the eye is not affected mandibular branch of the fifth cranial nerve affects
the chin and half of the tongue (see Fig. 6.04, p. 143)
111
Chronic erythematous
rash on the face
5
Normal surface
Macules 112
Papules and pustules
Single/few see p. 262
Multiple 114
Patches, plaques and nodules
Well defined 126
Poorly defined 130
Nodules 126
Scaly surface
Papules and plaques 133
Nodules see p. 325
Crust, exudate or excoriated surface
Papules, plaques, erosions, ulcers 138
Nodules see p. 329
112 / CHRONIC RASH ON FACE
Face
Chronic erythematous MACULES
lesions
Surface normal
Macules
Erythema Dilated blood vessels
Lesion fixed Lesion Central pressure lesion

Patient over 50 variable in disappears
site over
time
Surface Well Poorly Yes No

rough defined defined
Fig. 5.01 Multiple solar keratoses on forehead: often misdiagnosed as eczema
SOLAR BOWEN’S ECZEMA SPIDER TELANGI-

KERATOSIS BCC NAEVUS ECTASIA
p. 112 see p. 220 see p. 134 p. 113 p. 113
SOLAR KERATOSIS
Solar keratoses may present as an area of fixed erythema on the
face of a middle-aged or elderly fair-skinned individual who has
had a lot of sun exposure in the past. They are often misdiagnosed
(as eczema), but the key to the diagnosis is to feel the surface,
which is rough. The individual lesions remain fixed over a period Fig. 5.02 Eczema on
the face: the erythema
of time. may be variable in
extent and time
MACULES / 113
SPIDER NAEVUS (SPIDER ANGIOMA)

A red papule with a central arteriole and peripheral
radiating arms is a common normal finding
especially in children. Pressure (use the end
of a paper clip) on the central vessel results in
obliteration of the lesion. Large numbers occur in
pregnancy and in association with chronic liver
disease.
TREATMENT: SPIDER NAEVUS
The central feeding vessel can be cauterised with a ‘cold point’ or

fine looped wire cautery or a Hyfrecator. This takes about 1 second
so local anaesthetic is not necessary, unless the lesion is very large.
The pulse dye laser is also effective – a single shot is all that is
Fig. 5.03 Spider naevus Fig. 5.04 Spider naevus: central arteriole
necessary, and if available it may be preferable in children.
compressed (insert before compression)
TELANGIECTASIA
Small areas of visibly dilated blood vessels
where there is no central vessel feeding are called
telangiectasia. They are very common on the face due
to weathering and may be associated with rosacea,
scleroderma and the use of potent topical steroids.
TREATMENT: TELANGIECTASIA
Any vascular laser such as the pulsed dye or KTP laser will
remove visible telangiectasia on the face (see p. 66). The KTP
laser does not cause bruising, so patients can continue to work.
Several treatments may be needed at 6-weekly intervals. The
patient should not have a suntan otherwise post-inflammatory
hyperpigmentation can occur. Fig. 5.05 Telangiectasia
on the cheek
Face
Chronic erythematous rash MULTIPLE PAPULES AND PUSTULES
Surface normal
(Single/few lesions, see p. 262)
Look at the size of lesions and the site
Micropapules (size <2 mm) Papules (size 2–10 mm)
Cheeks (also upper Around mouth/eyes Face, chest and back Cheeks, chin, Beard area only
arms and thighs) forehead, nose
Lesions rough to Lesions smooth Associated comedones, Papules and pustules No ingrowing hairs Tight, curly ingrowing
the touch pustules, nodules and scars on erythematous hairs
background
Usually children Usually young Teenagers/young Infants (age <2) Associated Bacteriology Bacteriology negative
adults adults telangiectasia Staphylococcus
aureus +++
KERATOSIS PERIORAL ACNE INFANTILE ACNE ROSACEA SYCOSIS BARBAE PSEUDO-SYCOSIS

PILARIS DERMATITIS VULGARIS BARBAE
p. 115 p. 115 p. 116 p. 122 p. 123 p. 125 p. 124

PAPULES AND PUSTULES / 115
Fig. 5.06 Keratosis pilaris: redness associated with Fig. 5.07 Atrophoderma vermiculata Fig. 5.08 Perioral dermatitis
pinhead follicular plugs
KERATOSIS PILARIS PERIORAL DERMATITIS

Keratosis pilaris may affect the cheeks and eyebrows in children. Perioral dermatitis is a condition of young adults who have been
Redness associated with pinhead follicular plugs is seen, applying moderately potent or potent topical corticosteroids to
and as the plugs are shed, atrophy can occur (atrophoderma the face. Minute red papules and pustules appear around the
vermiculata). On the (outer) eyebrows this is associated with mouth, typically sparing the skin immediately adjacent to the lips.
loss of hair follicles. In some cases the forehead may be involved. Occasionally it occurs around the eyes (periocular dermatitis). In
These changes are usually accompanied by typical keratosis pilaris some cases there is no history of topical steroid use.
on the upper arms and thighs (see Fig. 9.144, p. 324).
TREATMENT: PERIORAL DERMATITIS
Stop any topical steroid use. This may lead to worsening of the rash initially; warn the
patient about this and tell him or her on no account to use the topical steroid again.
Oxytetracycline 250 mg bid (on an empty stomach) or lymecycline 408 mg daily taken
for 6 weeks usually speeds up its resolution.
ACNE VULGARIS
Acne is a disease of the pilosebaceous unit. The hallmark of the
disease is the comedo, a single blocked follicle. Everyone gets
some acne. In girls it may appear before menstruation commences,
sometimes as early as 9 years of age. In both sexes the peak
incidence is 13–16 years, although it may continue into the 20s,
30s and occasionally later. Acne occurs on the face, chest and back,
depending on the distribution of the sebaceous follicles in that
individual.
Fig. 5.09 Aetiology of acne Fig. 5.10 Diagram to show the evolution of acne lesions
Fig. 5.11 Open and closed comedones with some Fig. 5.12 Typical acne with papules, pustules and Fig. 5.13 Ice pick scarring following acne that has
inflammatory lesions few comedones resolved
The factors involved in the aetiology are shown in Fig. 5.09. The cysts and scars on the face or trunk of a young person are unique
evolution of acne lesions from a blocked sebaceous follicle is to acne, but occasionally folliculitis or even a papular form of
shown in Fig. 5.10. Genetic factors are important in determining eczema can mimic acne. Multiple epidermoid cysts may be
the severity, duration and clinical pattern. Recent evidence confused with severe nodulocystic acne. Rosacea looks similar on
suggests that diet can influence acne, with high glycaemic loads the face but affects an older population. There are no comedones,
and excess dairy consumption aggravating severity. The black and the papules and pustules remain the same size and occur
colour of open comedones is due to melanin, not dirt. over a general erythematous background (see Fig. 5.23). In perioral
dermatitis there are no comedones, and tiny papules and pustules
The diagnosis of acne is usually easy, but comedones should be
occur around the mouth (see Fig. 5.08).
present before it is made. Comedones, papules, pustules, nodules,
SUMMARY OF TREATMENT OF ACNE VULGARIS

COMEDONAL ACNE INFLAMMATORY ACNE
Mild Moderate Severe
Lesions Comedones only Comedones, papules and pustules Papules and pustules Nodules and cysts
First Choice Topical retinoid e.g. adapalene, Topical retinoid plus oral tetracycline Any oral tetracycline for 6 months e.g. Oral isotretinoin (urgent referral to
isotretinoin, tretinoin (not available e.g. oxytetracycline, lymecycline, oxytetracycline, lymecycline, doxycycline dermatologist)
in UK) doxycycline
Alternatives Azelaic acid Benzoyl peroxide plus topical antibiotic Oral isotretinoin if acne persistent over High-dose oral antibiotic plus topical
Benzoyl peroxide 6 months retinoid/benzoyl peroxide
Female alternative As above As above Oral anti-androgen plus topical retinoid Oral isotretinoin plus oral contraceptive
Maintenance Topical retinoid or benzoyl peroxide
TREATMENT: ACNE VULGARIS

1. Topical therapy
Topical therapies are slow to work and will not induce complete eradication. They are — 1% clindamycin (DuacUK)
designed to prevent acne, so should be used daily at night-time regardless of how the — 0.5% potassium hydroxyquinoline sulphate (Quinoderm)
skin looks, as opposed to applying to spots that are already present in the hope of note that benzoyl peroxide can bleach bed linen and clothing
clearing them quicker. ● 0.1% adapalene cream or gel (Differin)
● 15%–20% azelaic acid cream (AzelexUSA, FinaceaUK, SkinorenUK).
Squeezing with the fingers should be avoided, since this can convert a comedo into an
inflammatory papule. Female patients can use make-up to cover their spots during the
Topical antibiotics
daytime, but they must wash it off at night so that the follicles do not become blocked.
● Erythromycin (StiemycinUK, ZinerytUK)
● Clindamycin (Dalacin TUK, ZindaclinUK)

COMEDONES
Keratolytic agents remove the surface keratin and unplug the follicular openings. These work nearly as well as systemic antibiotics but have the disadvantage of causing
Retinoids are the most effective, for example: resistant bacteria. Using a combination such as Duac (clindamycin and benzoyl
● adapalene 0.1% cream or gel (Differin) peroxide) can reduce this. They are useful in pregnancy, as there is negligible systemic
● isotretinoin 0.05% gel (IsotrexUK) absorption. There is no evidence that combining topical and systemic antibiotics is
beneficial.
Instruction for the use of keratolytic agents
Before going to bed the patient should wash the skin with soap and water (medicated
washes are not any better) and then apply the weakest strength of retinoid cream or 2. Systemic antibiotics
benzoyl peroxide. Build up slowly by applying to a small area initially or by short contact
and rinsing off after a few minutes’ application. Emphasise the need to induce tolerance A single daily dose of lymecycline 408 mg or doxycycline 100 mg is preferred by
to side effects and that there is a slow onset in benefit. Online advice and application teenagers over oxytetracycline 500 mg bid because the latter has to be taken
videos are available from various pharmaceutical companies. 30 minutes before or 2 hours after food. The cost benefit of oxytetracycline is likely to be
If the skin becomes too sore, stop the treatment for a few days and then restart on outweighed by probable lack of compliance. Maintenance treatment must be continued
alternate nights. In the morning, if the skin becomes dry apply a non-greasy moisturiser. until the acne gets better spontaneously, however long that is.
Increase the strength of the keratolytic if side effects are tolerated. Do not use tetracyclines in those under the age of 12, in females who are pregnant
Ultraviolet light has a similar effect and a suntan tends to hide acne spots. or breastfeeding (it causes staining of teeth in the foetus and in children) or if renal
function is impaired. Side effects are few – diarrhoea and vaginal candidiasis. At this
INFLAMMATORY LESIONS dose they do not interfere with the absorption of the contraceptive pill, although extra
If inflammatory lesions are present as well as the comedones, use: precautions are needed for the first month of treatment as the gut flora changes.
● benzoyl peroxide (2.5%, 5%, 10%) as a cream, lotion or gel Erythromycin 500 mg bid or trimethoprim 200–300 mg bid are useful alternatives.
● benzoyl peroxide combined (5%) with Treatment with antibiotics should be given for at least 6 months.
Fig. 5.15 Severe acne before treatment with Fig. 5.16 Same patient as Fig. 5.15 after 4 months’
Fig. 5.14 Acne cyst: this can be injected with 10 mg/ isotretinoin treatment with isotretinoin
mL triamcinolone, which will reduce the size
3. Anti-androgens 4. Isotretinoin
Anti-androgens are useful in female patients if antibiotics have not worked and they are INDICATIONS FOR ORAL ISOTRETINOIN
already on a contraceptive pill. They should be avoided in patients with a family history ● Severe acne that will lead to permanent scarring
of thromboembolic disease or personal history of hemiplegic migraine. Co-cyprindiol ● Acne that has not responded to 6 months or more of oral antibiotics or anti-
(Dianette) contains 2 mg of cyproterone acetate plus 35 μg of oestrogen. It will act as a androgens
contraceptive pill as well as an anti-acne agent. The maximum effect does not occur for ● Patients who are depressed by the state of their skin (even though isotretinoin has
2–3 months and treatment needs to be continued long term. been associated with depressive episodes, if the acne is the cause of the depression,
then its use is likely to be beneficial; close psychiatric follow-up is advised)
(cont)
DRUG- AND CHEMICAL-INDUCED ACNE

● Persistent low-grade acne in patients over the age of 30 A rash that looks like acne occurring in the wrong site or in the
● Patients with acne excoriée wrong age group may be due to drugs, chemicals or systemic
hormonal imbalance. Anabolic steroids (which can be purchased
Isotretinoin is given as a single daily dose (0.5–1 mg/kg body weight/day) with food
on the internet for bodybuilding), corticosteroids (including
for 4–6 months (120 mg/kg total course dose). Early use can prevent scarring. A single
pituitary tumour and adrenal causes) or isoniazid may worsen
course of treatment gives long-term remission (permanent in over 70% of individuals).
Recurrence is more likely with lower doses or incomplete courses. For the side effects of
or precipitate acne. Chlorinated aromatic hydrocarbons used in
isotretinoin, see p. 50. Female patients (of childbearing age) should be on established insecticides, fungicides and wood preservatives cause severe acne,
contraception during the course and for 1 month after stopping. Pregnancy testing which may continue after exposure has ceased. Insoluble cutting
before (and during) treatment is recommended. oils, coal tars, corticosteroids and cosmetics may induce acne
when applied topically to the skin (see Fig. 5.19).
Isolated acne cysts can be injected with 10 mg/mL triamcinolone.
Fig. 5.17 Dry lips and skin during isotretinoin Fig. 5.18 Pyogenic granuloma-like lesions on chest Fig. 5.19 Oil acne on thigh
treatment during treatment with isotretinoin
INFANTILE ACNE
Acne is occasionally seen in boys in the first 2 years of life. It
is confined to the face, with comedones, papules, pustules and
nodules. It gets better spontaneously and is presumably due to
maternal androgens. It is not seen in girls.
TREATMENT: INFANTILE ACNE
A trial of topical antibiotics is worthwhile but systemic antibiotics for 4–6 months
are usually needed. All forms of tetracycline are contraindicated because they stain
developing teeth. Co-trimoxazole paediatric suspension 240 mg bid or erythromycin
125 mg bid can be used, although the latter needs replacing weekly. If there are only
comedones present a keratolytic agent can be used.
STEROID ROSACEA Fig. 5.20 Infantile acne

Application of potent topical fluorinated steroids to the face can
result in a rosacea-like rash. Telangiectasia is the most obvious
feature, although small papules and pustules may also be present.
TREATMENT: STEROID ROSACEA
The topical steroids must be stopped or the rash will not get better. Usually when the
steroids are stopped the rash gets very much worse. You will need to warn the patient
about this and it is a good idea to see him or her 3 days later for reassurance or he or
she may be tempted to restart the topical steroid.
The resolution of the rash can be speeded up by taking oxytetracycline 250 mg bid or
lymecycline 408 mg daily for 6 weeks. If the patient wants to use a topical preparation
for dry skin or itching, prescribe a moisturiser that can be used as often as he or she
likes.
Fig. 5.21 Steroid rosacea

ROSACEA Rosacea needs to be distinguished from acne, seborrhoeic eczema

Rosacea is a rash that looks like acne but on a red background. and perioral dermatitis. Acne occurs at a younger age and there
Red patches (erythema and telangiectasia) occur on the cheeks, should be comedones present as well as papules and pustules.
chin, forehead and tip of nose. On top of this there are papules Seborrhoeic eczema may be confused with rosacea. Seborrhoeic
and pustules, but no comedones. If the patient is undressed, eczema is scaly, there are no pustules and the nasolabial folds
papules and pustules may be seen on the upper trunk as well. rather than cheeks are affected; scaling will also be present in the
Rosacea affects women more commonly than men, and the main scalp and possibly elsewhere (see p. 135). Perioral dermatitis (see
incidence is over the age of 40 (although it can occur at any age). p. 115) occurs around the mouth in young adults. Systemic lupus
Complications, such as sore, red eyes (blepharitis, conjunctivitis erythematous (see p. 131) causes redness of the face but there are
and keratitis), chronic lymphoedema of the face (see Fig. 5.24) and no papules or pustules and the patient is usually unwell.
rhinophyma (see Fig. 5.25) occur more commonly in men.
Fig. 5.22 Erythematous rosacea showing Fig. 5.23 Papulopustular rosacea on cheek: papules Fig. 5.24 Lymphoedematous rosacea on cheeks and
distribution: flushing and redness are the main and pustules on background erythema nose with overgrowth of sebaceous tissue
features
124 / Chronic rash on face
Treatment: rosacea
The papular form of rosacea responds well to broad-spectrum antibiotics, but how they work is not understood.
Oxytetracycline or lymecycline for 2 months are the best options. One course clears up a third of patients; another third
respond to a second course; while a third may need more long-term therapy. There is no harm in giving a tetracycline
indefinitely if necessary.
Other options include erythromycin 250 mg bid, or metronidazole 200 mg tid. If you do not want to use a systemic
antibiotic, 0.75% metronidazole cream (RosexUK) or gel applied twice a day is effective in some instances. Minocycline
should not be used, as long-term use can lead to blue-grey pigmentation on the face (see Fig. 1.74, p. 15).
Telangiectasia alone does not respond to oral antibiotics but can be treated with a vascular laser (see p. 65). Redness is more
difficult to treat but intense pulsed light therapy (see p. 68) can be very effective. It is not available on the National Health Service.
If flushing is a problem, the patient should reduce the things that induce it, such as hot drinks, spicy foods, and so
forth. Brimonidine 0.33% (Mirvaso) gel is an α-andrenogenic agonist which reduces redness for several hours only.
Occasionally it may cause reflex redness. Clonidine 25–50 mg bid may be helpful.
Fig. 5.25 Rhinophyma in a 68-year-old man before
shaving off the excess tissue
Rhinophyma
Enlargement of the skin of the nose due to hyperplasia of the sebaceous glands can occur
in individuals with rosacea. Contrary to popular belief it is not associated with excessive
alcohol intake.
Treatment: rhinophyma
First treat any active rosacea. The excess sebaceous tissue can then be shaved off under a local or general anaesthetic
using a suitable electrocautery machine or a carbon dioxide laser. Provided the shave is no deeper than the base of the
sebaceous glands, complete healing without scarring occurs in 4 weeks.
Pseudo-sycosis barbae
Pseudo-sycosis barbae is a condition caused by ingrowing hairs in the beard area. It
occurs in men with tight, curly hair. The inflammatory papules and pustules are due to a
foreign body reaction to the ingrowing hair.
Fig. 5.26 After 4 weeks when skin healed
TREATMENT: PSEUDO-SYCOSIS BARBAE SYCOSIS BARBAE TREATMENT: SYCOSIS BARBAE

This is folliculitis of the beard area caused
This is not an infection, so antibiotics are not needed. by infection with S. aureus. Shaving results Take swabs for bacteriology culture from a pustule
If the patient will grow a beard or put up with a short in spread and inoculation of the bacteria and from the anterior nares before starting treatment.
stubble by shaving less closely, the hairs will uncurl Start with flucloxacillin 500 mg qid orally for 7 days. If
over the beard area. The organism is often
as they get longer and the problem will be solved. staphylococci are grown from the nose, apply topical
cultured from the nose as well as the
The only other alternative is to persuade a partner to mupirocin (Bactroban) qid for 2 weeks. Recurrent
uncurl the ingrowing hairs with a needle each day,
infected follicles. It occurs only in men infection may require long-term antibiotics for 6
which is both time-consuming and tedious. who shave, and it presents with follicular months or more with erythromycin 500 mg bid or co-
papules and pustules in the beard area. trimoxazole 480–960 mg bid.
Fig. 5.27 Pseudo-sycosis barbae Fig. 5.28 Pseudo-sycosis barbae: close-up of Fig. 5.29 Sycosis barbae
ingrowing hairs
Face
Chronic erythematous rash PATCHES, PLAQUES AND NODULES
Normal surface WELL-DEFINED BORDER
Well-defined patches, plaques, nodules
Present at birth Occurs later in life
Patch Patch Indurated plaque Nodule
Pale pink Dark red/ Orange colour Pink/red colour Mauve/ Orange Red, rapidly Sinus Red and tender
purple Long history purple Slow growth growing discharging
side of jaw
May clear Permanent Biopsy Biopsy Biopsy Biopsy Biopsy Check teeth Fluctuant
SALMON PORT WINE LUPUS DISCOID LUPUS JESSNER’S LUPUS GRANULOMA LYMPHOMA/ DENTAL ACNE/
PATCH STAIN VULGARIS ERYTHEMATOSUS LYMPHOCYTIC PERNIO FACIALE AMELANOTIC SINUS INFECTED
INFILTRATE (Sarcoidosis) MELANOMA EPIDERMOID
CYST
p. 127 p. 127 p. 128 see p. 137 p. 128 p. 129 p. 129 see p. 216 p. 129 see pp. 116,
178, 273
PATCHES AND PLAQUES / 127
SALMON PATCH (NAEVUS FLAMMEUS) PORT WINE STAIN (CAPILLARY MALFORMATION)

This is a pale pink patch that has been present since birth and is A permanent, more obvious and cosmetically disfiguring
situated on the nape of the neck, forehead or eyelid. Pressure over birthmark, being darker in colour than a salmon patch. It is
the area will cause blanching, showing that it is due to dilated present at birth and is usually unilateral. It increases in size only
blood vessels. Those on the face usually disappear during the in proportion with growth. Port wine stains are very variable in
first year of life; those on the nape of the neck do not, usually size and colour. They tend to darken with age and may develop
persisting throughout life. Often the occipital patch is not noticed papules within them. If involving trigeminal (V1) area, the port
unless there has been hair loss at this site. No treatment is needed wine stain may rarely be associated with ocular and intracranial
because it is usually covered by hair. angiomas, sometimes resulting in blindness, focal epilepsy,
hemiplegia or mental retardation (Sturge–Weber syndrome).
Palpable segmental capillary malformations have increased
association with internal abnormalities and should be referred for
imaging and specialist investigation.
Fig. 5.30 Naevus flammeus on occiput Fig. 5.31 Port wine stain, before laser treatment Fig. 5.32 Port wine stain after 15 treatments with
the pulsed dye laser: improved but not cleared
TREATMENT: PORT WINE STAIN TREATMENT: LUPUS VULGARIS
The pulsed dye laser is the treatment of choice, Triple therapy as for pulmonary tuberculosis: isoniazid
although results are variable. Only 10% of patients get 300 mg/day single dose, rifampicin 600 mg/day single
complete clearance. The majority respond but do not dose and pyrazinamide 20 mg/kg body weight three
totally clear (see Figs 5.31 and 5.32). Recurrence can to four times day or ethambutol 15 mg/kg weight as
occur later. Treatment is painful, so children will need a single dose. After 2 months two drugs can be used for
general anaesthetic. If laser treatment is not successful the next 4 months, usually isoniazid and rifampicin. This
or possible, then cosmetic camouflage can be used to treatment is usually instigated via respiratory teams
hide the mark. with monitoring schemes in place.
LUPUS VULGARIS
Lupus vulgaris is a chronic tuberculous
infection of the skin. A slowly enlarging
orange-pink plaque is typical. Nowadays it Fig. 5.34 Jessner’s lymphocytic infiltrate
is exceedingly rare but it is a diagnosis that
still needs to be considered. Confirm the
diagnosis by biopsy.
JESSNER’S LYMPHOCYTIC INFILTRATE

Fixed, red, indurated plaque(s) with a
smooth, non-scaly surface are scattered over
the face or trunk. Individual lesions are
round, oval or serpiginous in outline. The
diagnosis can be confirmed by taking a skin
biopsy, which shows a dense perivascular
lymphocytic infiltrate in the dermis. A
biopsy will distinguish this condition
from discoid lupus erythematosus and a
lymphoma. It tends to be unresponsive
to treatment but antimalarials (see discoid Fig. 5.33 Lupus vulgaris: this orange patch had Fig. 5.35 Lupus pernio in black skin
lupus erythematosus, p. 137) can be tried. been present for 40 years and was assumed to be a
birthmark
SARCOIDOSIS – LUPUS PERNIO TREATMENT: SARCOIDOSIS GRANULOMA FACIALE

Around a quarter of patients with sarcoid Granuloma faciale is characterised by a
have skin involvement. Sarcoid of the Refer the patient to a dermatologist and respiratory chronic nodule or indurated plaque with
skin can present with macules, papules, physician to confirm the diagnosis and to look for an orange colour and prominent follicular
sarcoid elsewhere. For multi-system disease the
patches and plaques. They can be red, openings. Histologically both a granuloma
patient will need systemic steroids; this will also
orange or purple in colour. On the face the and a vasculitis are present.
improve the skin lesions. Steroid-sparing regimens
commonest appearance is of a mauve/ include methotrexate (10–25 mg/week), azathioprine
purple plaque (lupus pernio) on the nose (100–150 mg/day), hydroxychloroquine (200 mg bid)
DENTAL SINUS
or cheek. Sarcoid seems to be commoner or acitretin (25 mg/day). If there is only lupus pernio, This is due to a tooth abscess that
in black skin. Diagnosis is made by skin inject triamcinalone (5 mg/mL) intradermally every discharges through to the skin on the
biopsy, and if positive, look for evidence of 4–6 weeks. Err on the side of caution because steroid- cheek, chin or under the jaw. The diagnosis
sarcoid elsewhere. induced atrophy of the skin may be unsightly and can be confirmed by looking in the mouth,
permanent. where a rotten tooth is usually seen. The
offending tooth needs to be removed.
Fig. 5.36 Lupus pernio Fig. 5.37 Granuloma faciale Fig. 5.38 Dental sinus from rotten pre-molar tooth
Face
Chronic erythematous rash PATCHES AND PLAQUES
Normal/smooth surface POORLY DEFINED BORDER
Poorly defined patches/plaques
Patient well Patient ill, with fever, arthralgia
or muscle weakness
Child Adult Fever, arthralgia Proximal muscle

weakness
Follicular erythema Any site Erythema of Erythema around Erythema on cheeks/ Erythema across Violaceous rash/
on cheeks nasolabial folds mouth/eyelids chin/forehead nose and on cheeks swelling around eyes
Rough papules on Itchy ++ Scaling in scalp Micropapules and Papules/pustules Check auto- Check CPK
outer arms eyebrows/eyelashes pustules (swelling) antibodies (ANF, Muscle biopsy
DNA, Ro, La, etc.)
KERATOSIS ECZEMA SEBORRHOEIC PERIORAL ROSACEA SYSTEMIC LUPUS DERMATOMYOSITIS

PILARIS ECZEMA DERMATITIS (RHINOPHYMA) ERYTHEMATOSUS
see p. 115 see p. 134 see p. 135 see p. 115 see p. 123 p. 131 p. 132
Fig. 5.39 Systemic lupus erythematosus: butterfly Fig. 5.40 Systemic lupus erythematosus showing Fig. 5.41 Subacute cutaneous LE on forearm
erythema on face photo-accentuated distribution
SYSTEMIC LUPUS ERYTHEMATOSUS TREATMENT: SYSTEMIC LUPUS ERYTHEMATOSUS

An erythema on the face associated with fever and arthralgia in a female
patient is suggestive of systemic lupus erythematosus (SLE). The rash Referral to a specialist (rheumatologist, physician or dermatologist) with an
characteristically occurs in a ‘butterfly’ distribution (cheeks and bridge interest in this condition is necessary. Treatment depends on which organs
are involved. Severe disease involving the kidneys, pleura, pericardium, central
of nose), but does not always do so. There is also nail-fold telangiectasia
nervous system or blood requires high doses of systemic steroids, starting
with ragged cuticles. Although the site may be similar to rosacea, there
with prednisolone 1.0 mg/kg/day. Steroid-sparing agents such as azathioprine,
are no papules or pustules. The patient may have renal involvement, methotrexate or mycophenolate mofetil are used long term as well as newer
psychiatric or neurological symptoms, pericarditis, pleurisy or biologics such as anti-TNFs and anti-IL6 (see p. 56).
abdominal pain. Chilblains and Raynaud’s phenomenon are likely. A
The skin should be protected from the sun by using a high-factor sunscreen
positive anti-nuclear factor will confirm the diagnosis. Drugs such as
(SPF 30 or above).
procainamide, hydralazine, minocycline and the anti-TNF monoclonal
biologic therapies can cause an illness identical to SLE. Subacute If the joints are the main problem, non-steroidal anti-inflammatory drugs
cutaneous lupus erythematosus looks like SLE or consists of non-scaly will be the treatment of choice. If it is only the skin and joints involved,
plaques on the face. There may be positive auto-antibodies, but systemic hydroxychloroquine 200 mg bid or mepacrine 100 mg bid can be used.
symptoms are absent.
DERMATOMYOSITIS TREATMENT: DERMATOMYOSITIS

Weakness and tenderness of proximal muscles associated with
a mauve or pink rash on the face, ‘V’ of the neck, upper eyelids Refer urgently to a dermatologist for diagnosis and treatment. A search for an internal
or in lines along the backs of the fingers and over the metacarpal malignancy is essential (especially carcinoma of the lung, stomach, ovary or breast); if
found and treated successfully, the dermatomyositis will disappear. If the cancer is not
bones (see Fig. 5.43) is typical. There may be considerable oedema
curable it may be very difficult to control the dermatomyositis.
on the face and arms (see Fig. 5.42) and dilatation of the nail-fold
capillaries (see Fig. 5.44). The diagnosis can be confirmed by Initial treatment is with prednisolone 1.0 mg/kg/day. This is gradually reduced as the
measuring muscle enzymes (creatine phosphokinase), muscle disease comes under control. Steroid-sparing agents such as azathioprine, methotrexate
biopsy or electromyography. In patients over the age of 40 there or mycophenolate mofetil may also be needed. Patients not responding to these may
require high dose intravenous immunoglobulin as well.
may be an associated internal malignancy.
Muscle enzyme levels can be used to monitor disease activity. In the acute phase rest is
important; later, passive muscle exercises and physiotherapy will be needed.
Fig. 5.42 Dermatomyositis: oedema of upper and Fig. 5.43 Linear erythema along back of the fingers Fig. 5.44 Nail-fold telangiectasia seen in systemic
lower eyelids lupus erythematosus and dermatomyositis
SCALY SURFACE / 133
Face SOLAR KERATOSES

Chronic erythematous rash SCALY SURFACE Widespread solar keratoses may be
Scaly surface confused with eczema on the face but
Papules and plaques will feel rough to the touch. The patient
will probably be over 50, have fair skin
Scratch rash with nail and feel surface with your fingertips
(burn rather than tan on sun exposure)
and blue eyes. Often there will be a
Poorly defined border to lesions Well-defined border
history of working out of doors or living
abroad (20+ years ago). Solar elastosis (see
p. 287) will be present – this is a yellowish
Sandpaper rough Not rough and no increase Profuse silver Adherent scale discolouration of the skin with increased
in scale on scratching scale on skin markings and follicular openings on
scratching the face, neck and back of the neck. These
‘wrinkles’ are not due to ageing per se but
to long term sun damage.
Age 50+ Fair skin Nasolabial Any part of face Improves in Worse in sunlight
fold, eyebrows, sunlight
eyelashes
Symmetrical Asymmetrical Symmetrical Biopsy

Mycology -ve Mycology +ve
SOLAR SEBORRHOEIC ECZEMA TINEA PSORIASIS DISCOID LUPUS

KERATOSIS ECZEMA FACIALE ERYTHEMATOSUS
p. 133 p. 135 p. 134 p. 136 see p. 225 p. 137 Fig. 5.45 Solar keratoses on face of elderly patient
with sun-damaged type I fair skin
ECZEMA ON THE FACE

The most likely cause of poorly defined, red, scaly plaques on the
face is chronic eczema. The distribution and age of the patient
determine the type of eczema.
Atopic eczema. Eczema on the face in infants and children is
likely to be due to atopic eczema. In infants it often starts on the
cheeks and scalp before affecting the rest of the body, especially
the anticubital and popliteal fossae (see p. 236). Atopic eczema
persisting into adult life is often lichenified (see Fig. 5.48).
Allergic contact dermatitis may be due to cosmetics, nail
varnish (from the fingernails touching the face), creams applied
to the face and from airborne allergens such as cement dust or
sawdust. Plastic and metal frames from glasses can result in a
patch of eczema on the sides of the nose and behind the ears. All Fig. 5.46 Eczema around the eyes: a common pattern
unexplained instances of facial eczema should be referred to a
dermatologist for patch testing.
Seborrhoeic eczema on the face involves the nasolabial folds and
hairy areas such as eyebrows, eyelids, scalp and beard.
Fig. 5.47 Allergic contact dermatitis on side of nose from spectacle frames
SCALY SURFACE / 135
Fig. 5.48 Lichenified atopic eczema Fig. 5.49 Atopic eczema on face of a Fig. 5.50 Seborrhoeic eczema Fig. 5.51 Psoriasis of the face
9-year-old boy
TREATMENT: ECZEMA ON THE FACE SEBORRHOEIC ECZEMA

In adults this common type of eczema is due to an overgrowth
On the face use only a weakUK/group 7USA topical steroid such as 1% hydrocortisone. of the yeast Pityrosporum ovale. It is diagnosed by its distribution
Use an ointment if the skin is particularly dry or an allergic contact dermatitis is on the skin (see Fig. 5.53) – scalp, eyebrows, eyelashes, nasolabial
suspected (creams can contain preservatives that are potential sensitisers). Instead
folds, external ear, centre of chest and centre of back (see also
of soap use a wash product such as Dermol lotion, and moisturise with a leave-on
p. 201, 205). On the face you will see greasy scaling spreading
emollient such as Cetroben, Dermol or Diprobase creams.
out from the nasolabial folds onto the cheeks. The hairy areas are
Tacrolimus 0.1% ointment and pimecrolimus cream are alternatives in atopic eczema usually involved – eyebrows, eyelashes, hairy scalp and beard.
(see p. 34), and can be used prophylactically twice a week. Scaling can also be seen around the external auditory meatus and
behind the ear (see Fig. 6.46, p. 163).
TREATMENT: SEBORRHOEIC ECZEMA
Only treat seborrhoeic eczema when it is present.

Start with 2% ketoconazole (Nizoral) cream twice a
day until it is clear. This will reduce the pityrosporum
yeasts.
If it does not work use 1% hydrocortisone cream
twice a day or 2% miconazole plus 1% hydrocortisone
cream (Daktacort). Treat the scalp with ketoconazole
shampoo (see p. 89).
TINEA ON THE FACE

Fig. 5.52 Seborrhoeic eczema: erythema and scale Fig. 5.53 Distribution of seborrhoeic eczema on the
in the nasolabial fold face Ringworm is uncommon on the face. It
should be suspected if a red scaly rash
is unilateral or very much more on one
side than the other. It will have a well-
demarcated edge, with relatively normal
skin in the centre. It is often itchy and
slowly gets bigger. The border needs to be
scraped and the scale sent off for mycology
(see p. 20).
TREATMENT: TINEA ON THE FACE
Apply either terbinafine (Lamasil) cream once daily for

7–10 days or an imidazole cream twice a day for 2
weeks. All the imidazoles work equally well. Systemic
antifungals are not needed.
Fig. 5.54 Tinea around mouth caught from a Fig. 5.55 Tinea on nose of black child
puppy: always think of this diagnosis with an
asymmetrical rash
SCALY SURFACE / 137
DISCOID LUPUS ERYTHEMATOSUS

Discoid lupus erythematosus is a benign form of lupus erythematosus where the skin
is involved usually without any systemic involvement (although 5% of patients have
autoantibodies). Females are more commonly affected than males and it usually starts
between the ages of 25 and 40 years. Well-defined, red, scaly plaques occur on the
face and scalp. The scale is quite different from that occurring in psoriasis or eczema.
Scratching with the fingernail does not produce silver scaling as in psoriasis and the
scale is rougher and more adherent than that of eczema. Follicular plugging, atrophy
and a change in pigment (both hypo- and hyperpigmentation) may also be present. It is
exacerbated by sunlight, so it often starts or worsens in the summer. The diagnosis should
only be considered when more common causes of scaling on the face are excluded.
On occasions indurated non-scaly plaques are seen and the diagnosis will need to be
confirmed by skin biopsy.
Fig. 5.56 Discoid lupus erythematosus: scaly
TREATMENT: DISCOID LUPUS ERYTHEMATOSUS plaques on face
Discoid lupus erythematosus is the only condition where a very potentUK/group 1USA topical steroid can be used on the
face. 0.05% clobetasol propionate (DermovateUK, TemovateUSA) ointment should be applied carefully to the plaques twice
daily until they disappear. Only use while there are active lesions present (the plaques are red and scaly). It will not help
atrophy or pigment change.
Discoid lupus erythematosus is also made worse by sunlight, so use a sunscreen (SPF 30+) in the summer. Topical 0.1%
tacrolimus (Protopic) and pimecrolimus (Elidel) can be useful steroid-sparing agents in preventing flares but are rarely
effective for acute flares.
If topical steroids do not help or if there are extensive lesions, use an antimalarial by mouth instead. Try
hydroxychloroquine 200 mg bid or mepacrine 100 mg bid for at least 3 months.
Hydroxychloroquine can affect the retina, so check the visual acuity and fields yearly. It may also stain the nails a greyish-
blue colour. Mepacrine makes the patient’s skin and urine yellow and can also cause vomiting or diarrhoea. The patient
should be warned about these side effects.
Fig. 5.57 Discoid lupus erythematosus in black skin

with hypo- and hyperpigmentation
CRUST, EXUDATE OR EXCORIATED SURFACE

Face
Chronic erythematous rash SURFACE CRUST, EROSION, EXCORIATION
Crust, excoriated or eroded surface
Papules, plaques, erosions, ulcers
Poorly defined Discrete lesions (separated by normal skin)
papules/plaques
Papules Erosions Excoriated Boggy Ulcer

swelling
Eczema Pustules and Grouped Superficial Round shape Linear/odd Confluent Recent travel: Slow growth Rapid growth
elsewhere comedones Central crust White scars shape pustules Middle East,
± crust punctum Southern Europe,
Central America
ECZEMA ACNE INSECT IMPETIGO ACNE DERMATITIS TINEA LEISHMANIASIS BASAL CELL SQUAMOUS
VULGARIS BITES EXCORIÉE ARTEFACTA BARBAE CARCINOMA CELL
CARCINOMA
see p. 134 see p. 116 see p. 198 see p. 107 p. 139 see p. 260 p. 139 p. 140 see p. 330 see p. 332
CRUST, EXUDATE OR EXCORIATED SURFACE / 139
ACNE EXCORIÉE TINEA BARBAE

This variety of acne occurs predominantly in women over the age of 30. The acne is Tine barbae is an uncommon infection due
usually mild but most of the lesions are excoriated. Round or oval, white scars are the to animal ringworm (usually Trichophyton
most obvious finding confirming that the condition is largely self-induced. verrucosum from calves). It usually
occurs in farm workers. A confluent
TREATMENT: ACNE EXCORIÉE boggy swelling is studded with multiple
pustules. The hairs come out easily and
It usually responds well to low-dose isotretinoin (20 mg/day) on a long-term basis (see pp. 49 and 121). Adequate can be examined for fungi. Secondary
contraception is essential if this is going to be used. infection with staphylococci can produce a
misleading positive bacterial culture.
Fig. 5.58 Acne excoriée Fig. 5.59 Tinea barbae: kerion in beard area Fig. 5.60 Tinea barbae: crusting in beard area
TREATMENT: TINEA BARBAE
Oral griseofulvin 500 mg daily with food for 4–6 weeks works better for animal ringworm than
terbinafine.
LEISHMANIASIS
Leishmaniasis results from the bite of an infected sandfly. It is a common
disease around the southern Mediterranean, in the Middle East, North
Africa, India, Pakistan and Central and South America. A few weeks
after the sandfly bite, a boil-like nodule appears at the site of the bite. It
gradually flattens off to form a plaque, which may or may not ulcerate.
One or more lesions appear on exposed sites – face, arms and legs.
They are painless and heal spontaneously after about 1 year to leave a
cribriform scar. Some patients with leishmaniasis develop a chronic form Fig. 5.61 Cutaneous leishmaniasis: ulcerated nodules on cheek
of the disease in which new granulomatous papules or plaques occur
around the edge of the scar (lupoid leishmaniasis, see Fig. 5.62). This
condition may continue for many years.
In Central and South America, a much more destructive picture is seen
(New World leishmaniasis) with ulcerated nodules, and later systemic
spread to mucous membranes (mucocutaneous leishmaniasis). Refer to a
specialist for diagnosis and treatment.
TREATMENT: LEISHMANIASIS
● Leave alone to heal spontaneously

● Weekly intralesional injection with sodium stibogluconate (Pentostam) or N-methylglucamine
antimonate (Glucantime) until healed
● Intraveneous (through a peripherally inserted central catheter line) of sodium stibogluconate at
a daily dose of 20 mg/kg body weight for 20 days; this is particularly recommended for
New World leishmaniasis Fig. 5.62 Lupoid leishmaniasis on cheek, note the previous scarring on
the nose
141
Mouth, tongue, lips and ears

Mouth 142
Ulcers and erosions
Acute 142
6
Chronic 145
White, yellow and brown lesions 148
Tongue 150
Lips 152
Normal surface 152
Scale/rough surface 153
Vesicles/erosions/ulcers
Acute see p. 142
Chronic 153
Ears 159
Patches and plaques 159
Papules and nodules 160
142 / MOUTH, TONGUE, LIPS, EARS
MOUTH TREATMENT: APHTHOUS ULCERS
Mouth, tongue, lip

This is a self-limiting condition that often needs no
Acute lesions ACUTE ULCERS AND EROSIONS treatment. Most patients will use things like Bonjela
(<2 weeks’ duration) (choline salicylate and cetalkonium chloride) for
symptomatic relief. For more troublesome ulcers
Single/few lesions Multiple grouped lesions
consider one of the following:
● 2% sodium cromoglicate nasal spray (Rynacrom)
sprayed directly onto the ulcers three times a day –

about 50% of patients find this extremely helpful; it
Painful Painless Painful Paraesthesia Patient unwell
is not known how it works
● Tetracycline mouthwash, 250 mg/5 mL, held in the
mouth and swished around for about 5 minutes

four to five times a day; do not use in children
under 12, since it stains teeth
● 0.1% triamcinolone acetonide (Adcortyl) in Orabase
Round ulcer Round Single, Anterior ²⁄³ Around lips Erosions Buccal applied to the ulcers three times a day
with red erosions indurated tongue and Target lesions mucosa ● Beclometasone dipropionate inhaler, 50 g/puff, can
margin with red margin rash on chin Rash on hands swollen
margin be sprayed on the ulcers several times a day until
they heal
● 10% hydrocortisone in equal parts of glycerine
and water as a mouthwash three times a day;

APHTHOUS HAND, FOOT PRIMARY HERPES RECURRENT STEVENS– PRIMARY the patient must spit it out after use rather than
ULCERS AND MOUTH SYPHILIS ZOSTER HERPES JOHNSON HERPES swallow it, to make sure that not too much steroid
DISEASE SIMPLEX SYNDROME SIMPLEX is absorbed
● 2.5% hydrocortisone sodium succinate (Corlan)
pellet, held against the ulcer(s) until the pellet

p. 142 p. 143 see p. 353 p. 143 see p. 109 p. 144 p. 143 dissolves, twice daily.
APHTHOUS ULCERS
Aphthous ulcers are the commonest cause of recurrent mouth ulcers. The single
or multiple small, round ulcers with a red margin last 7–10 days before healing
spontaneously. They begin in the teens and may continue throughout life. Aphthous
ulcers may be rarely associated with Crohn’s disease, ulcerative colitis or coeliac disease.
MOUTH / 143
HAND, FOOT AND MOUTH DISEASE

This mild infection is due to Coxsackie
virus A16. Round erosions with a red
margin are seen in the mouth. They
look like small aphthous ulcers but are
associated with small, grey blisters with
a red halo on the fingers and toes (see
Fig. 13.03, p. 405). The condition gets better
spontaneously in a few days.
PRIMARY HERPES SIMPLEX

Most primary infections with the herpes
simplex virus occur in early childhood
and are asymptomatic, with only a few
vesicles/erosions on the hard palate or
buccal mucosa. Occasionally it may cause
an acute gingivostomatitis associated with
fever and general malaise.
HERPES ZOSTER
Herpes zoster involving the mandibular
branch of the fifth cranial nerve is
uncommon, but it presents with unilateral
Fig. 6.01 (top left) Aphthous ulcers on the tongue vesicles and ulceration on the anterior
two-thirds of the tongue, as well as the
Fig. 6.02 (middle left) Hand, foot and mouth
disease: blisters and erosions on lower lip characteristic vesicles on the same side of
the chin.
Fig. 6.03 (bottom left) Primary herpes simplex,
blisters and erosions on tongue
Fig. 6.04 (above) Herpes zoster affecting the

mandibular branch of the fifith cranial nerve: blisters
and ulceration on anterior two-thirds of tongue and
a rash on the side of the chin
STEVENS–JOHNSON SYNDROME TREATMENT: STEVENS–JOHNSON SYNDROME

Erythema multiforme involving the mouth presents with multiple
irregular erosions on the buccal mucosa. Extensive involvement Many of these patients will need to be admitted to hospital because they are unable to
of the mouth, lips, conjunctiva and genitalia is called Stevens– eat or drink. Frequent mouth washes with glycerine and thymol (made up by dissolving
a glycerine and thymol tablet in a tumbler of water) should be swished around the
Johnson syndrome. The causes of this are the same as for erythema
mouth for several minutes every hour, or applied on a cotton wool swab by a nurse if
multiforme (see p. 174) but usually drugs (often co-trimoxazole)
the patient cannot manage a mouthwash by him- or herself. This will keep the buccal
rather than infections are the cause. Toxic epidermal necrolysis (see mucosa relatively comfortable. If this is not done, the lips can stick together, which
p. 192), Stevens–Johnson syndrome and erythema multiforme are initially will make eating and drinking even more difficult, and will at some stage
a clinical continuum of decreasing severity. necessitate surgical separation. Benzydamine hydrochloride (Difflam) or chlorhexidine
gluconate (Corsodyl) are alternative mouthwashes.
For the eyes, frequent bathing with normal saline and insertion of hypromellose eye
drops (artificial tears) will be needed to keep them comfortable. If there are extensive
skin lesions as well as extensive mucosal involvement, the patient may need nursing in
a burns unit where there are facilities to prevent ulceration of the skin.
There is no evidence that systemic steroids are helpful.
Fig. 6.06 Stevens–Johnson syndrome Fig. 6.05 Stevens–Johnson syndrome Fig. 6.07 Erythema multiforme affecting the tongue
MOUTH / 145
Mouth
Ulcers and erosions CHRONIC MOUTH ULCERS
Chronic lesions (>2 weeks’ duration)
Patient does not feel ill Patient feels unwell
Associated skin lesions No associated skin lesions
Indurated base Widespread Scaly red Tense blisters Erosions and Conjunctiva Genital ulcers ? on drugs Lymph-
mauve papules plaques on face/ on body flaccid blisters and genitals also adenopathy
scalp on body involved Trunk rash
Biopsy Biopsy Biopsy lesion if rash absent or not diagnostic ± iritis, arthritis Check full Positive VDRL
blood count test
SQUAMOUS LICHEN DISCOID LUPUS BULLOUS PEMPHIGUS MUCOUS BEHÇET’S NEUTROPENIA SECONDARY
CELL PLANUS ERYTHEMATOSUS PEMPHIGOID VULGARIS MEMBRANE DISEASE SYPHILIS
CARCINOMA PEMPHIGOID
see p. 158 see p. 197 see p. 137 see p. 256 p. 146 p. 146 p. 147 p. 146 see pp. 207, 353
PEMPHIGUS VULGARIS TREATMENT: MUCOUS MEMBRANE PEMPHIGOID

Blisters and erosions in the mouth are usually the first sign of
pemphigus vulgaris; the rash often comes later (see p. 257). Unlike bullous pemphigoid, mucous membrane pemphigoid does not respond well to
systemic steroids. There is no single treatment that always works and it is a question of
MUCOUS MEMBRANE PEMPHIGOID finding the right drug for any individual patient. Start with dapsone 50 mg tid, as this
is the safest choice. It can cause haemolytic anaemia and/or methaemoglobinaemia,
This is a rare autoimmune disease in which there are antibodies
so check the full blood count after 1 week and every 2–3 months. To prevent this, also
against the epidermal basement membrane. Mucous membranes give the patient cimetidine 400 mg tid. If this fails to work cyclophosphamide 50 mg
(mouth, eyes and genitalia) are predominantly involved with bid is more effective but you will need to check the full blood count regularly (monthly).
blisters, erosions and scarring. Blisters can also occur on the skin A third alternative is azathioprine 50 mg tid. If there is scarring of the conjunctivae, it
adjacent to orifices. The diagnosis is usually made by looking may sometimes be necessary to inject steroids intralesionally to inactivate the disease.
in the eyes. Scarring and adhesions between the palpebral All patients with this rare disorder should be under the care of a dermatologist or
conjuctivae are characteristic, and can lead to blindness if not ophthalmologist.
treated. Bullous pemphigoid less commonly involves the mucous
membranes. The diagnosis is made from the characteristic skin
rash (see p. 256). BLOOD DYSCRASIA
Agranulocytosis and neutropenia can cause mouth ulcers. They
may be the first manifestation of leukaemia, or they may be a side
effect of cytotoxic drugs such as methotrexate.
Fig. 6.08 Pemphigus: erosions on palate Fig. 6.09 Mucous membrane pemphigoid with Fig. 6.10 Mucous membrane pemphigoid: ulcers on
conjunctival adhesions in corner of the eye hard palate
MOUTH / 147
BEHÇET’S SYNDROME
Behçet’s syndrome is a rare condition
mainly affecting young men. You should
think of it in any patient with recurrent
oral and genital ulceration. The ulcers
tend to be larger, deeper and last longer
than aphthous ulcers. There will also
be one or more of the following: iritis,
arthritis, thrombophlebitis, sterile pustules
on the skin, erythema nodosum and
meningoencephalitis. Such patients should
be referred to hospital for treatment.
TREATMENT: BEHÇET’S SYNDROME

Fig. 6.11 Behçet’s syndrome: eye conjunctivitis Fig. 6.12 Behçet’s syndrome: erosions on tongue
Since the cause is unknown, treatment is empirical and lips
and often unsatisfactory. The drugs used are:
● colchicine 500 μg bid
● azathioprine 2 mg/kg body weight/day (average =
50 mg tid)
● thalidomide 100 mg nocte given ‘on a named
patient basis’.
For the mouth ulcers it is worth the patient trying:

● 10% hydrocortisone in equal parts of glycerine
and water, used as a mouthwash after each meal

– the patient should be warned that it has a very
bitter taste; it should be spat out so that the steroid
is not absorbed
● Steroid inhaler: beclometasone dipropionate,
50 g/puff, is usually used for asthma, but instead of
inhaling it, the patient sprays it on the ulcers several Fig. 6.13 (left) Behçet’s syndrome: pustules on lower leg
times a day until the ulcers heal.
Fig. 6.14 (above) Behçet’s syndrome: vasculitic pustules on
lower leg
Mouth lesions PIGMENTATION IN THE MOUTH

Macules, patches, papules and plaques WHITE/YELLOW/BROWN Melanin pigmentation in the mouth and on
White papules/plaques White/ Brown macules the tongue is a normal finding in patients
yellow with black skin. If present from childhood,
1 mm multiple small, brown macules may be due
macules/ to Peutz–Jeghers syndrome (see p. 155). In
papules
later life pigmented macules are likely to
be lentigines (see p. 288).
TREATMENT: ORAL LICHEN PLANUS

Removed Adherent Small, 1–3 mm Larger, >3 mm
easily with
spatula Most oral lichen planus is asymptomatic and needs
no treatment. Treatment of erosive lichen planus is
unsatisfactory. The following can be tried:
Red base Lacy Thickened Along Inside Present Adult/ Black skin ● ordinary mouthwashes as used for aphthous ulcers
exposed pattern plaque teeth cheeks and since elderly (see p. 142); if these fail to work, some kind of
Mycology Biopsy line lips childhood systemic therapy is necessary
+ve
● prednisone 15–30 mg/day may occasionally be
needed for the most severe forms of ulceration; the

CANDIDA LICHEN LEUKOPLAKIA CHEEK FORDYCE PEUTZ– LENTIGO RACIAL dose is reduced to a maintenance dose of 5–10 mg/
(THRUSH) PLANUS BITING SPOTS JEGHERS PIGMENTATION
day as soon as the ulceration is healed – you want
to get the patient off steroids as soon as possible,
because otherwise he or she will end up taking
p. 149 p. 148 see p. 158 p. 148 see p. 155 see see p. 148 them for years
p. 155 p. 288 ● rarely one of the oral retinoids may be needed as an
alternative to systemic steroids (acitretin, 0.5–1 mg/

LICHEN PLANUS kg body weight/day, see p. 49).
Lichen planus in the mouth is usually asymptomatic. The diagnosis is made from the
typical skin rash (see p. 197). In the mouth there is a white lacy pattern on the buccal
mucosa. Rarely there may be erosions and ulceration and the patient will have a sore
mouth and find eating painful. The edge of the ulcer is usually white. At the start there
may have been the characteristic rash of lichen planus, but ulceration can go on for years,
and can continue long after the rash is gone. It needs to be distinguished from cheek
biting, where a fold of mucous membrane is seen heaped up along the teeth line.
MOUTH / 149
ORAL CANDIDIASIS TREATMENT: ORAL CANDIDIASIS

Thrush occurs in the very young,
the very old and patients who are ● In infancy, miconazole gel applied directly to the
immunosuppressed or who are taking plaques by an adult’s finger four times daily
antibiotics or cytotoxic drugs. Small, white ● In adults, nystatin oral suspension (1 mL) swirled
papules scrape off easily with a spatula around the mouth several times before swallowing,
four times a day; continue for 48 hours after clinical
to leave a red surface. If these are mixed
cure
with potassium hydroxide, the spores ● Alternatives are nystatin pastilles or amphotericin B
and hyphae are easily seen on direct lozenges sucked until they dissolve, four times a day
microscopy (see Fig. 10.15, p. 342) or can be ● Oral itraconazole (100 mg/day for 2 weeks) or
cultured on Sabouraud’s medium. fluconazole (50 mg/day for 7–14 days); if the
patient is on antibiotics, treatment will need to be
continued until they are finished; if the patient has
cancer or is immunosuppressed, treatment may
Fig. 6.15 Candida of the tongue and hard palate need to be prolonged
(may extend down the oesophagus)
Fig. 6.16 Racial pigmentation Fig. 6.17 Oral candida of the tongue: Fig. 6.18 Bite line along buccal Fig. 6.19 Lichen planus of buccal
involving the palate and tongue easily scraped off with a spatula mucosa mucosa: white lacy pattern
ABNORMALITIES OF THE TONGUE

ORAL HAIRY LEUKOPLAKIA
A white plaque consisting of multiple papules (looking like hairs) is found along the
side of the tongue. It is due to the Epstein–Barr virus and is found in patients with HIV
infection. It is usually asymptomatic.
Fig. 6.21 Smooth tongue due to pernicious

anaemia
Fig. 6.20 Oral hairy leukoplakia in patient with HIV
LARGE TONGUE (MACROGLOSSIA)

The tongue may be large from birth or from early childhood in individuals with Down’s
syndrome or with a lymphangioma, haemangioma or neurofibroma of the tongue.
Intermittent enlargement of the tongue (lasting <24 hours) is due to angio-oedema (see
p. 99) and is usually associated with urticaria. After middle age, enlargement of the
tongue should make you think of systemic amyloid. Fig. 6.22 Fissured tongue
TONGUE / 151
SMOOTH TONGUE GEOGRAPHIC TONGUE FURRED AND BLACK HAIRY TONGUE

A smooth tongue may be associated Geographic tongue is a very common These common conditions are due to
with iron deficiency, malabsorption or benign condition where smooth red hypertrophy of the filiform papillae
pernicious anaemia. A dry tongue is patches appear on the dorsum of the and are completely harmless. They are
associated with Sjögren’s syndrome. tongue, giving a map-like appearance. asymptomatic and not indicative of any
These move about from day to day. The internal disease.
FISSURED TONGUE condition is generally asymptomatic
Apply 0.05% isotretinoin (Isotrex) gel
Deep grooves in the tongue may be a although its appearance can cause alarm.
and brush it off with a soft toothbrush 5
congenital abnormality or seen together
Any soreness can be treated with glycerine minutes later. This is repeated daily until it
with facial nerve palsy and swelling of the
and thymol mouthwash. Tell the patient to clears (about 2 weeks).
lips in Melkersson–Rosenthal syndrome
avoid acidic foods such as citrus fruits or
(see p. 155).
vinegar.
Fig. 6.23 Dry tongue due to Sjögren’s syndrome Fig. 6.24 Geographic tongue Fig. 6.25 Black hairy tongue
LIPS
Lips
Lesions LIPS: NORMAL SURFACE
Normal surface
Single lesions Multiple small macules/papules Diffuse swelling
Brown macule Blue/purple Red Red Yellow/white Brown Intermittent, Constant

papule papule lasts <48 hours
Uniform Compress Bleeds easily Disappears on ± on buccal Around/on lips Associated with Onset as adult From birth or
colour empties pressure mucosa urticaria and infancy
swollen eyes
LENTIGO VENOUS PYOGENIC HEREDITARY FORDYCE PEUTZ– ANGIO- GRANULOMATOUS HAEMANGIOMA

LAKE GRANULOMA HAEMORRHAGIC SPOTS JEGHERS OEDEMA CHEILITIS/ LYMPHANGIOMA
TELANGIECTASIA SYNDROME CROHN’S DISEASE NEUROFIBROMA
see p. 288 p. 154 see p. 334 p. 154 p. 155 p. 155 see p. 155 p. 155 see pp. 312, 315,
266
LIPS / 153
Lips
Scale, fissures, hyperkeratotic, crust, warty, surface LIPS: ABNORMAL SURFACE
Chronic papules, plaques, ulcers
(Acute ulcers and erosions, see p. 142)
Scale Fissures Rough keratin Ulcer Crust Warty
Chronic Acute
Similar rash on Skin Lips only Angle of Lower lip Upper lip First Recurrent Round
cheeks/scalp around lips mouth episode same site papules
only Adult
Child +ve Surface Surface Indurated Ulcer Erosions Prodromal

Candida rough only thickened nodule/ulcer Rolled edge Child paraesthesia
albicans and white
Biopsy Biopsy Biopsy Biopsy Positive Positive

Staph. virology
DISCOID LUPUS LIP CHEILITIS ANGULAR SOLAR LEUKOPLAKIA SQUAMOUS BASAL CELL IMPETIGO HERPES VIRAL
ERYTHEMATOSUS LICKING/ (Eczema) CHEILITIS KERATOSIS CELL CARCINOMA SIMPLEX WARTS
SUCKING DRUGS CARCINOMA
see p. 137 p. 156 p. 156 p. 157 p. 157 p. 158 p. 158 p. 158 see p. 107 p. 158 see
p. 318
VENOUS LAKE
A solitary soft, purple papule on the upper or lower lip is common
in the middle-aged or elderly.
TREATMENT: VENOUS LAKE
Most patients do not seem to mind having these lesions on their lips. If they want them
removed there are various ways of doing it.
● Surgical excision under a local anaesthetic: the lip will heal well if the excision line is
sited perpendicularly across the lip.

● The pulsed dye laser can be used without any anaesthetic and gives excellent
cosmetic results. This is the treatment of choice if there is one in use near where the
patient lives.
HEREDITARY HAEMORRHAGIC TELANGIECTASIA

Fig. 6.26 Venous lake
Small red macules and papules occur on the lips, tongue and
fingers associated with nosebleeds and gastro-intestinal bleeding.
It is inherited as an autosomal dominant trait.
TREATMENT: HEREDITARY HAEMORRHAGIC TELANGIECTASIA
The skin lesions do not need any treatment, although the pulsed dye laser is very
effective at removing them. Nosebleeds may need cauterising if they will not stop with
ordinary pressure. Anaemia due to recurrent bleeding from the nose or gastro-intestinal
tract will need treating with oral iron. The familial nature of the disorder should be
explained to the patient and his or her family.
Fig. 6.27 Hereditary haemorrhagic telangiectasia

LIPS / 155
FORDYCE SPOTS
These are small, discrete, white or yellow papules on the lips or
buccal mucosa due to sebaceous gland hyperplasia. They are very
common and completely harmless.
PEUTZ–JEGHERS SYNDROME
A rare genetically determined condition, transmitted as an
autosomal dominant trait. Brown macules on the lips, the skin
around the mouth and on the fingers and toes occur in early
childhood. They may be associated with small bowel polyps that
can cause intussusception.
ANGIO-OEDEMA
Intermittent swelling of the lips lasting less than 24 hours before
starting to go down is usually associated with urticaria and
Fig. 6.28 Fordyce spots on inside of the upper lip swelling around the eyes (see p. 99).
GRANULOMATOUS CHEILITIS
In granulomatous cheilitis the whole lip (upper or lower) (see
Fig. 6.31) is swollen. Initially this may fluctuate quite a lot,
but eventually the swelling becomes permanent. The cause is
unknown, although it can sometimes be due to an allergic contact
dermatitis to toothpaste. If the buccal mucosa is also thickened
consider Crohn’s disease. Ask about abdominal symptoms
and look inside the mouth for the characteristic cobblestone
appearance of the buccal mucosa. If necessary, do a barium
follow-through and a biopsy. If there is an associated facial nerve
palsy and/or a fissured tongue (see p. 151) consider Melkersson–
Rosenthal syndrome. Injection of triamcinolone 5 mg/mL into the
swollen lip is often helpful.
Fig. 6.29 Peutz–Jeghers syndrome

ECZEMA ON THE LIPS (CHEILITIS)

Allergic contact eczema can occur on the lips from lipstick, lip salves, toothpaste or
mouthwashes. The diagnosis is confirmed by patch testing (see p. 21). Atopic eczema may
affect the lips as well as the rest of the skin of the face (see p. 236). Many children suck or
lick their lips, causing a red scaly rash around the mouth that only extends as far as the
tongue can reach (see Fig. 6.33).
Oral retinoids cause dryness and scaling of the lips and the skin around the mouth (see
Fig. 5.17, p. 121).
TREATMENT: LIP ECZEMA
It is important to use white soft paraffinUK/petrolatumUSA as a regular moisturiser. A weakUK/group 7USA topical steroid such
as 1% hydrocortisone ointment will be effective if applied twice a day.
Lip licking/sucking in children can usually be stopped once the parents realise what is happening. Applying a thick paste
(e.g. Lassar’s paste) will discourage the habit.
Fig. 6.30 Cheilitis: eczema on the lower lip
Fig. 6.31 Granulomatous cheilitis on lower lip Fig. 6.32 Cheilitis (contact allergic dermatitis) to Fig. 6.33 Lip licking
toothpaste
LIPS / 157
ANGULAR CHEILITIS ACTINIC CHEILITIS & SOLAR KERATOSES

Cheilitis means inflammation of the lips, and in angular cheilitis Chronic sun exposure to the lower lip in older fair skinned
only the corners of the lips are involved. It occurs in individuals (Type I) individuals leads to atrophy, loss of the normal creases
who wear dentures, and it is usually due to infection with Candida and vermilion border. Histologically epithelial dysplasia is seen
albicans from under the top denture. Poorly fitting dentures may which may progress to in-situ or invasive SCC.
also lead to overlap of the lower by the upper lip resulting in
Rough keratin on the lower lip in older patients who have had
angular cheilitis.
a lot of sun exposure on the lip are solar keratoses. This change
TREATMENT: ANGULAR CHEILITIS
is not seen on the upper lip. If there is any induration under the
keratosis, then a biopsy is necessary to exclude a squamous cell
First scrape the underside of the denture and examine for the spores and hyphae of carcinoma
C. albicans or send for culture. Tell the patient to clean his or her dentures after every
meal with a hard toothbrush and soap. Specific anti-candida treatment is not usually TREATMENT ACTINIC CHEILITIS & SOLAR KERATOSES
necessary.
Cryotherapy is the treatment of choice for solar keratoses. Extensive involvement of the
lower lip can be treated with 5-fluorouracil cream, imiquimod or photodynamic therapy,
or the whole lower lip can be excised, and by pulling forward the buccal mucous
membrane can be sutured back onto the vermilion border.
Fig. 6.34 Angular cheilitis Fig. 6.35 Actinic cheilitis in African albino Fig. 6.36 Solar keratoses on lower lip
LEUKOPLAKIA SQUAMOUS AND BASAL CELL CARCINOMAS

This is a persistent white, hyperkeratotic plaque in the mouth Squamous cell carcinomas occur on the lower lip as ulcers or
or on the tongue or lips due to epithelial dysplasia or carcinoma indurated nodules and will need urgent referral for removal.
in situ. Squamous cell carcinomas on mucous membranes are more likely
to spread than those on exposed skin (see p. 332).
TREATMENT: LEUKOPLAKIA
An ulcer or nodule on the upper lip, often involving the vermilion
Since leukoplakia is usually caused by smoking, the first thing for the patient to do is to border, is more likely to be a basal cell carcinoma (see p. 330).
stop smoking. This may result in the lesion(s) disappearing. If it does not, consider one
of the following. RECURRENT HERPES SIMPLEX
● If the area involved is small, excise it. Recurrent herpes simplex is usually preceded by prodromal
● If it is too large for excision, it can be frozen with liquid nitrogen (two freeze–thaw itching, burning or tingling on the lips. Small grouped vesicles
cycles, see p. 58). appear, burst, crust and then heal in 7–10 days (see also p. 109).
● Widespread involvement can be treated by removing the lip epidermis with the
carbon dioxide laser and allowing the epidermis to regenerate.
Such patients are probably best cared for by an oral surgeon.
Fig. 6.37 Leukoplakia on lower lip Fig. 6.38 Squamous cell carcinoma on underside of Fig. 6.39 Squamous cell carcinoma on lower lip
the tongue
EARS / 159
EARS
Ears
Patches and plaques RASH ON EARS
Helix Scaly surface Crust/exudate
Antihelix
Well defined Poorly defined Widespread Localised to one site
External auditory
meatus
Tragus Anywhere Meatus, antihelix All over ear Meatus and Earlobes Anywhere on ear
on ear and behind ear antihelix
Earlobe
Bright red Pink-red colour Pink scale Pink Patch test Patch test Biopsy
White scale Adherent scale Crust/scale
-ve +ve +ve
Thick scalp scaling Biopsy Also scalp scaling Eczema on Recent use of Pierced ears Fixed rolled edge
face/flexures ear drops
PSORIASIS DISCOID LUPUS SEBORRHOEIC ATOPIC MEDICAMENT NICKEL BASAL CELL

ERYTHEMATOSUS DERMATITIS ECZEMA ALLERGIC ALLERGIC CARCINOMA
DERMATITIS DERMATITIS
see p. 225 see p. 137 p. 163 see p. 236 p. 163 p. 163 see p. 330
Ears
Papules and nodules LESIONS ON EARS
Acute Chronic papule(s) Chronic nodule
Tender Itchy Rough/keratin Smooth surface Crust/ulcerated Smooth

Purple papules
Helix/lobe Helix only Anterior Superior Helix or Behind ear Slow growth Rapid Lobe
of helix or surface of antihelix where glasses growth
antihelix helix rest
After After sun Tender on Not tender Pink/skin White Pink, red Not Indurated Red White
exposure to exposure compression coloured indurated
cold
Young boys Crust or Elderly Annular Uric acid Tender Bleeds or Tender Previous Spherical
erosion papules high exudes ear-piercing subcutaneous
CHILBLAINS JUVENILE CHONDRO- SOLAR GRANULOMA GOUTY GRANULOMA BASAL CELL SQUAMOUS KELOID EPIDERMOID
SPRING DERMATITIS KERATOSIS ANNULARE/ TOPHI FISSURATUM CARCINOMA CELL SCAR CYST
ERUPTION RHEUMATOID CARCINOMA
NODULE
p. 161 p. 164 p. 161 p. 164 see p. 210 p. 162 p. 164 see p. 330 see p. 332 p. 162 p. 273
EARS / 161
CHILBLAINS history of pain in bed at night when the

Tender, itchy, mauve papules and nodules patient lies on that side differentiates it
on the earlobes and helix occur in cold from solar keratoses and skin tumours,
weather and last up to 2 weeks. Similar which, if painful, hurt all the time.
lesions can occur on other exposed sites,
e.g. fingers, toes and nose. They occur TREATMENT: CHONDRODERMATITIS
in individuals who get very cold and
warm up too quickly. The lesions are due Excision biopsy of the painful papule together with the
underlying cartilage is usually curative. Removing the
to an abnormal reaction to cold where
cartilage is more important than removing the skin.
constriction of arterioles is followed by
It is usually necessary to take the adjoining cartilage
exudation of fluid into the tissues on away to prevent a new pressure point occurring and
rewarming. the problem returning.
TREATMENT: CHILBLAINS
Fig. 6.41 Chondrodermatitis at pressure point at

Prevention is better than cure, i.e. do not allow
top of helix
the skin to get too cold. Those at risk, particularly
individuals who work out of doors and the elderly who
live in unheated accommodation, should wear warm
gloves, boots and hats in the winter. When they come
in from the cold they should warm up slowly.
Nifedipine retard 20 mg tid can reduce the pain,
soreness and irritation of chilblains. For patients who
get severe recurrent chilblains, it is worth considering
continuing the drug for several weeks if the weather is
particularly cold.
CHONDRODERMATITIS
Chondrodermatitis nodularis helicis
chronica is a painful skin-coloured or pink
papule on the helix or antihelix. There may
be a central area of scaling or crusting. A
Fig. 6.40 Chilblains on the helix Fig. 6.42 Chondrodermatitis on the antihelix
GOUTY TOPHI TREATMENT: GOUTY TOPHI KELOID SCAR

These are hard white or cream-coloured A round pink or purple papule or nodule
papules or plaques due to deposition Allopurinol competitively inhibits the enzyme xanthine may develop on the earlobe following ear-
of sodium urate crystals in the dermis. oxidase, which oxidises xanthine to uric acid. It causes piercing. It may gradually increase in size
a rapid fall in serum uric acid. Start with 100 mg
Classically they occur on the helix or and become unsightly. It is differentiated
daily as a single oral dose, and gradually increase to
antihelix of the ear, but occasionally they from an inclusion epidermoid cyst (due to
300–400 mg a day, which will need to be continued
are found on the dorsum of the hands and indefinitely. By gradually increasing the dose you will
epidermis being implanted into the dermis
feet (see Fig. 13.12, p. 411). Patients with hope to avoid precipitating acute attacks of gout at at the time of ear-piercing) by its colour,
tophi are likely to suffer from gout. the beginning of treatment. With this treatment the an epidermoid cyst being white or skin
tophi gradually become smaller and disappear. coloured.
Fig. 6.43 Gouty tophi on antihelix Fig. 6.44 Epidermoid cyst on earlobe Fig. 6.45 Keloid scar on earlobe following ear-piercing
EARS / 163
ECZEMA ON THE EAR will be typical plaques elsewhere, with or without thick scaly
Allergic contact dermatitis on the ears presents with an acute plaques in the scalp (see p. 88). Discoid lupus erythematosus (see
eczema (vesicles, exudate and crusting, see Fig. 6.47). On the p. 137) usually involves the antihelix but not the external auditory
earlobes this is usually due to nickel in cheap earrings. In the canal. A biopsy will be needed to confirm this diagnosis.
external auditory meatus and on the rest of the ear it is usually Because of the narrow ear canal, eczema here can cause problems:
due to antibiotic or antihistamine ear drops, creams or ointments. ● scale tends to accumulate, blocking the ear and causing pain
Chronic eczema on the ear usually occurs in association with ● secondary infection (with Staphylococcus aureus, Gram-negative
eczema elsewhere. Otitis externa, i.e. eczema of the external organisms, C. albicans and Aspergillus) is common, especially in
auditory canal and meatus, is usually due to seborrhoeic eczema wet conditions (e.g. after swimming)
(see Fig. 6.46), and there will be other evidence of this, e.g. scaling ● the itching encourages the patient to poke things down the ear
in the scalp (see p. 88). Psoriasis is red rather than pink and there canal.
Fig. 6.46 Seborrhoeic eczema with Fig. 6.47 Acute contact allergic Fig. 6.48 Contact allergic dermatitis Fig. 6.49 Psoriasis in external auditory
associated scaling in scalp dermatitis from neomycin ear drops to nickel from earrings meatus
TREATMENT: OTITIS EXTERNA (see Fig. 6.51) 2–12 hours after sun exposure in spring, and can
last about 2 weeks. It is a form of polymorphic light eruption (see
If the eczema is dry and scaly, the treatment is the same as for seborrhoeic eczema p. 100) called juvenile spring eruption.
elsewhere, i.e. 1% hydrocortisone cream or 2% ketoconazole cream used twice a day
until it is better. Chronic sun exposure, especially in skin types I and II, leads
to solar keratoses developing on the superior aspect of the
If there is a lot of scale and/or pain, the patient should see an ear, nose and throat
helix, usually in men. These are rough papules that can be felt
surgeon. A perforated eardrum and a co-existant otitis media must be excluded. Aural
better than seen (see p. 326). Squamous cell carcinoma and
toilet, with removal of the excess scale can be done in the ear, nose and throat clinic,
which will help the pain. keratoacanthomas (see pp. 328), also due to chronic sun exposure,
present as rapidly growing nodules on the helix with an ulcerating
If there is an acute weeping eczema, do not be tempted to use one of the topical or keratotic surface. Basal cell carcinomas (see p. 330) tend to grow
steroid/antibiotic/antifunga ear drops or sprays. You will only make things worse by
slowly, and can occur anywhere on the ear. They usually present
exposing the patient to the risk of developing a further acute allergic contact dermatitis
with bleeding or exudate that the patient notices on the pillow.
on top of what he or she already has. Take a swab for bacteriology and mycology
culture. If there is a bacterial infection present, use a systemic antibiotic depending on
the sensitivities (probably flucloxacillin or erythromycin 250 mg qid for 7 days). If there
is a fungal infection, ketoconazole will be required rather than a topical steroid. First dry
up the exudate with an astringent such as 13% aluminium acetate ear drops. When it is
dry, use 1% hydrocortisone ointment twice a day until it is better. Send the patient for
patch testing when the rash has settled to exclude an allergic contact dermatitis.
An ichthammol wick inserted into the ear canal is useful in patients with recurrent otitis
externa.
GRANULOMA FISSURATUM
Granuloma fissuratum occurs from the pressure of spectacles and
occurs at the side of the bridge of the nose or behind the ear (see
Fig. 6.50). It looks like a basal cell carcinoma and is distinguished
by skin biopsy. Changing from heavy- to light-framed glasses
usually resolves the problem.
EAR CONDITIONS INDUCED BY SUN EXPOSURE

The ears, especially in males, are exposed to the sun. In young Fig. 6.50 Granuloma fissuratum: a Fig. 6.51 Juvenile spring eruption:
tender nodule behind the ear where itchy papules on sun-exposed site
boys and men with short hair, itchy papules can occur on the helix
glasses rest
165
Acute erythematous rash

on the trunk and limbs
7
Surface normal: no blisters or exudate
Progressive macular rashes 166
Widespread or multiple papules, patches, plaques 170
Transient lesions (urticaria) 171
Single, few papules, nodules 177
Crusting on surface
Vesicles or bullae 179
Pustules 183
Erosions or ulcers 186
Generalised rash (>50% body surface) 190
166 / ACUTE RASH ON TRUNK AND LIMBS
Trunk and limbs

Acute progressive erythematous rash ACUTE MACULO-PAPULAR RASH
Surface normal
Macules and papules
(Erythematous maculopapular rashes consist of small, red macules and papules that coalesce to become confluent)
No/mild fever High fever initially (>40°C)
Occipital nodes Axillary and No lymph Recent new drug Conjunctivitis/cough, Sore throat Rash occurs
inguinal nodes nodes 2–6 weeks ago runny nose abdominal pain after fever
Rash, oedema settled
Rubella Papules Papules Recent new Lymph node Small lymph Large lymph Face flushed Rash neck and
antibodies buttocks and abdomen → drug, gastro- enlarged nodes nodes Circumoral trunk
thighs → arms thighs intestinal pallor
upset/URTI
Child 6 mth to Patient Eosinophils ↑↑ Koplik’s spots Stomatitis, red

12 yrs pregnant Arthralgia palms and soles
(3rd trimester)
RUBELLA GIANOTTI– POLYMORPHIC TOXIC DRESS (Drug MEASLES KAWASAKI’S SCARLET FEVER ROSEOLA
(German CROSTI ERUPTION OF ERYTHEMA hypersensitivity) DISEASE (Sixth disease)
Measles) SYNDROME PREGNANCY (Drugs/viruses)
p. 167 see p. 177 see p. 206 p. 167 p. 168 p. 167 p. 169 p. 169 p. 168
MACULO-PAPULAR RASHES / 167
TOXIC ERYTHEMA MEASLES behind the ears and spreads onto the face,
This is a rash in which pink/red macules Measles is caused by a paramyxovirus. trunk and limbs. The macules may become
and papules appear and then coalesce to After an incubation period of about papules, which join together to become
become a widespread erythema. The rash 10 days, the child becomes miserable with confluent. It lasts up to 10 days, leaving
may look like measles (morbilliform), a high fever, runny nose, conjunctivitis, brown staining and some scaling.
rubella (rubelliform) or roseola photophobia, brassy cough, and inflamed
(roseoliform). There are no prodromal tonsils. Koplik’s spots on the buccal RUBELLA (GERMAN MEASLES)
symptoms. It is usually due to an mucosa are diagnostic at this stage (look Rubella is a common viral illness of
enterovirus (ECHO or Coxsackie) or a drug like grains of salt on a red base). On day 4 children due to a rubivirus. It is spread by
(see p. 176). of the illness a red macular rash appears inhalation of infected droplets. After an
incubation period of 14–21 days, a macular
rash begins on the face and neck. It spreads
down the body over 24–48 hours and then
clears from the face downwards over the
next 2–3 days. It is often associated with
enlarged occipital and posterior cervical
lymph nodes, and sometimes arthritis. The
child is infectious from 5 days before to 3
days after the rash appears.
If the diagnosis is suspected rubella
antibody titres should be measured
immediately and after 10 days so that the
diagnosis can be confirmed. Many other
viral infections look like rubella but do not
carry the same risk to pregnant mothers
(foetal cataracts, nerve deafness and
cardiac abnormalities) if infection occurs in
the first trimester.
Fig. 7.01 Toxic erythema on arm Fig. 7.02 Rubella

ROSEOLA INFANTUM (SIXTH DISEASE) Drugs implicated include:

This is the commonest rash of this kind in children under the age ● anticonvulsants (phenobarbitone, carbamazepine, phenytoin)
of 2, and is due to the human herpes virus-6. The rash is preceded ● sulphonamides
by a high fever but the child remains well. After 3–5 days the fever ● minocycline
goes and the rash, which looks like rubella, appears on the trunk. ● allopurinol
It lasts only 1–2 days and then disappears. ● dapsone
● gold salts
TREATMENT: MEASLES AND OTHER VIRAL EXANTHEMS ● HIV drugs.
Treatment is symptomatic since they get better spontaneously. Bed rest is necessary if
the child is sick, and the pyrexia can be treated with cool sponging and paracetamol
elixir.
Measles and rubella can be prevented by immunisation, but with reduced uptake of
vaccines, these diseases are becoming more common.
DRESS
DRESS (drug reaction with eosinophilia and systemic symptoms)
starts 2–6 weeks after first taking a drug, initially as a morbilliform
rash, which later becomes more oedematous. Vesicles and bullae
may occur, and there is often oedema of the face. Lymph nodes
are enlarged and systemic symptoms include severe arthralgia.
The diagnosis is made by the combination of a severe drug rash, a
high eosinophil count and abnormalities in liver function tests and
renal function.
Fig. 7.03 DRESS: oedema and morbilliform rash on face

MACULO-PAPULAR RASHES / 169
TREATMENT: DRESS widespread punctate erythema, which rapidly becomes confluent.

The face is flushed except for circumoral pallor. After about
It is essential that the offending drug is identified and stopped immediately. Systemic a week the rash fades followed by skin peeling. Streptococcus
corticosteroids are usually effective (prednisolone 40 mg daily). They should be pyogenes can be grown from the throat and the antistreptolysin O
continued till the systemic symptoms have resolved, and then slowly tapered off to titre is raised.
prevent relapse.
TREATMENT: SCARLET FEVER
KAWASAKI’S DISEASE (MUCOCUTANEOUS LYMPH NODE Give oral phenoxymethylpenicillin (Penicillin V) 62.5–125 mg every 6 hours for 10 days
SYNDROME) depending on the child’s age. Gargling with paracetamol suspension (120 mg/5 mL)
This disease may be confused with measles, but it must be every 4 hours and then swallowing it may help the sore throat.
recognised because of the potentially serious association with
myocarditis. It occurs in young children under the age of 5 (50%
under 2 years age). The onset is acute with fever, red eyes, dry lips
and prominent papillae on the tongue. The most characteristic
signs are the large glands in the neck, the rash on the trunk and
limbs, and the red palms and soles that later peel.
TREATMENT: KAWASAKI’S DISEASE
If given immediately, a high dose of intravenous γ-globulin (2 g/kg body weight) as a

single infusion over 10 hours will reduce the overall morbidity.
SCARLET FEVER
Scarlet fever is due to an infection with a group A β-haemolytic
streptococcus that produces an erythrogenic toxin. The condition
seems to be less common than it used to be. After an incubation
period of 2–5 days there is a sudden fever with anorexia and
sore throat. The tonsils are swollen with a white exudate and
there is painful lymphadenopathy in the neck. The tongue is
furred initially, but later it becomes red with prominent papillae
(strawberry tongue). The rash appears on the second day as a
Fig. 7.04 Scarlet fever: erythematous rash with secondary peeling on arm
Trunk and limbs

Acute erythematous rash ACUTE ERYTHEMATOUS RASHES
Surface normal
Widespread multiple papules, patches, plaques
Lesions come Lesions expand in rings over a Rash becoming more extensive Slow extension over 1–2 weeks Lesions occur
and go or move few days over a few days several hours
around over 24- after sun exposure
hour period
Patch/plaque Circular Small macules Child 1–12 Purpuric lesions: Patches/plaques Sun exposed sites
with scale ‘target’ lesions and papules years do not blanch Lesions blanch only
inside ring 1 cm or less in becoming Papules on on pressure on pressure
diameter confluent buttocks and
thighs→arms
Pink-red Dull, red Purple-orange Mauve-red Pink colour

colour Well defined Poorly defined
URTICARIA ANNULAR ERYTHEMA TOXIC GIANOTTI– PURPURIC RASH LICHENOID SUBACUTE POLYMORPHIC
ERYTHEMA MULTIFORME ERYTHEMA CROSTI (Idiopathic/ (Drug) RASH ECZEMA LIGHT
Drugs/virus drugs) ERUPTION
p. 171 see p. 210 p. 174 pp. 175, 176 p. 177 see p. 400 p. 176 see p. 248 see p. 100
URTICARIA / 171
Trunk and limbs

Acute erythematous rash URTICARIA
Transient (<24 hours) patches, papules, plaques
Obvious No obvious cause After exercise/ After scratching After pressure/
precipitating factor hot bath cold/sunlight
Weals occur within Weals come and Small 1–2 mm Linear weals Weal at site of
minutes and last go at various sites papules with flare precipitating factor
<1 hour daily around
ACUTE CHRONIC CHOLINERGIC DERMOGRAPHISM PHYSICAL

URTICARIA URTICARIA URTICARIA URTICARIA
p. 171 p. 172 p. 173 p. 173 p. 174

Fig. 7.05 Acute urticaria: large weals
ACUTE URTICARIA
Acute urticaria is defined as urticaria that has been present for long the weals last, draw around one, and ask to see the patient
less than 6 weeks. Individual lesions last for less than 24 hours the following day. Lesions that last for longer than 24 hours
(‘here today and gone tomorrow’). A central itchy white papule should be classified as urticarial dermatoses and require a biopsy
or plaque due to dermal oedema (weal) is surrounded by an for diagnosis. The weal is the result of degranulation of mast
erythematous flare. The lesions are variable in size and shape, cells releasing histamine and other mediators of inflammation;
and may be associated with swelling of the soft tissues of the degranulation can be stimulated by allergic (IgE) and non-allergic
eyelids, lips and tongue (angio-oedema, see p. 99). To identify how stimuli.
Acute urticaria may be caused by: These can occur at any time of the day or night. This is not a type I
1. A type 1 allergic response that occurs within a few minutes allergic response.
of contact with an allergen either on the skin (e.g. nettle
Possible causes of chronic urticaria can be identified by a good
rash, latex allergy, see p. 405) or ingested (e.g. strawberries or
history, so extensive investigation, unless supported by this, is not
penicillin). The rash disappears spontaneously within an hour.
indicated.
Contact with the same allergen again will result in a further
episode. Most cases will be idiopathic. No cause can be found, but exclude:
2. Direct release of histamine from mast cells by aspirin, ● psychological factors – ongoing stress; very hectic lifestyle
codeine or opiates. IgE is not involved. This is the commonest ● regular ingestion of drugs such as aspirin, codeine and opiates
cause of infrequent acute episodes of urticaria, occurring when ● food additives such as tartrazines, benzoates, and so forth,
a patient takes aspirin for a cold or headache. which are chemically similar to aspirin
3. Drugs that cause serum sickness (an immune complex ● chronic infections and infestations – bacterial (sinus, dental,
reaction): urticaria, arthralgia, fever and lymphadenopathy are chest, gall bladder), fungal (candidiasis), intestinal worms
the hallmarks of this. It may be caused by the following drugs: ● general medical conditions, e.g. hyperthyroidism, chronic
● penicillin active hepatitis, systemic lupus erythematosus.
● nitrofurantoin
● phenothiazines
● thiazide diuretics
● thiouracils.
TREATMENT: ACUTE URTICARIA
Use a non-sedative, long-acting antihistamine such as cetirizine or loratadine at high

doses (10–20 mg bid), or, if in extremis, intravenous chlorpheniramine 10 mg. If life-
threatening swelling of the larynx or tongue occurs, inject 0.5 mL of 1:1000 adrenaline/
epinephrine solution intramuscularly via an EpiPen. Do not give systemic steroids except
in serum sickness.
CHRONIC URTICARIA
Urticaria is classified as chronic if the weals come and go over a
period of more than 6 weeks. Individual lesions always last less
than 24 hours, but new lesions appear daily or every few days.
Fig. 7.06 Cholinergic urticaria
URTICARIA / 173
Around 40% of patients show a positive autologous skin test CHOLINERGIC URTICARIA
(used as a research tool). The patient’s own serum is injected Small red papules (1–3 mm diameter) surrounded by an area of
intradermally into the forearm and produces a weal. This indicates vasoconstriction occur after exercise or hot baths, mainly in young
that IgE is present in the serum, which will degranulate mast cells adults. The diagnosis can be confirmed by making the patient
in the skin. exercise vigorously for a few minutes.
TREATMENT: CHRONIC URTICARIA DERMOGRAPHISM

Weals occur only after scratching or rubbing the skin. Obviously
Ask the patient to avoid aspirin (and proprietary cold and flu remedies), codeine, and the more the skin is scratched in response to itch, the worse the
foods containing azo dyes (tartrazine – orange yellow) and benzoic acid (used as a
lesions can become. Dermographism is not usually associated
preservative in peas and bananas).
with urticaria.
Long-acting, non-sedative antihistamines need to be given regularly and in sufficient
dosage to prevent the urticaria. Try one of the following:
● cetirizine 10–40 g daily (ZirtekUK/ZyrtecUSA) or levocetirizine 5–20 mg daily (Xyzal)
● fexofenadine 180 mg daily (TelfastUK/AllegraUSA)
● loratadine 10 mg or desloratadine 5 mg (Neoclarityn)
If standard (hay fever) doses do not control it, increase up to four time this. Although
this is not licensed, it is recommended in UK guidelines. Do not mix antihistamines.
Once the patient has been free of the rash for 4 weeks, the antihistamine can be
stopped. If it reoccurs then further long-term treatment is needed, and in some cases
this can last for months.
If non-sedative antihistamines do not work try:
● a sedative antihistamine such as hydroxyzine (Atarax) 10–50 mg 2 hours before
bedtime (the dose depending on effect and degree of sedation produced)

● an H blocker such as ranitidine 150 mg bid as well.
2
Then refer to a dermatologist for consideration of:

● oral ciclosporin (useful in patients with a positive autologous skin test not responding
to antihistamines)
● omalizumab (a monoclonal antibody that targets IgE) has been shown to be effective
in severe recalcitrant cases.

Do not use systemic steroids in urticaria. They do work but generally the problem
reoccurs on stopping and there is a risk of long-term dependence.
Fig. 7.07 Dermographism
PHYSICAL URTICARIA TREATMENT: CHOLINERGIC AND PHYSICAL URTICARIA

Cold, pressure, water and sunlight can all induce an immediate
urticarial reaction. Delayed pressure urticaria occurs after a The options are to take a long-acting antihistamine on a regular basis to prevent the
delay of 30 minutes to 12 hours and occurs at sites of prolonged attacks, or take a short-acting one (such as chlorphenamine 4–8 mg) before exercise or
the precipitating cause.
pressure. Weals or deeper oedema occur, which are itchy and
painful, and persist for several days. It can occur on the feet from Avoidance of exercise or the physical cause should be an obvious priority.
tight shoes, on soles after climbing a ladder, around the waist, on
palms from gripping, and so forth. Diagnosis requires specific
questioning. ERYTHEMA MULTIFORME
Multiple small (<1 cm diameter), round blisters made up of rings
of different colours (‘target’ or ‘iris’ lesions) occur on the palms,
dorsum of hands and forearms, knees and dorsum of the feet. It
may be very itchy.
The rash occurs 10–14 days after some precipitating cause:
● viral infections, especially herpes simplex– this is the
commonest cause of recurrent episodes of erythema
multiforme (90%)
● immunisations
● bacterial infections, especially streptococcal sore throats
● mycoplasma pneumoniae infection
● drugs – sulphonamides, phenylbutazone and other non-
steroidal anti-inflammatory drugs (NSAIDs).
Occasionally the skin lesions may be widespread and associated
with blisters or erosions in the mouth. Stevens–Johnson
syndrome is erythema multiforme with extensive mucous
membrane involvement (see p. 144).
Fig. 7.09 (above)

Close-up of ‘target
lesions’
Fig. 7.08 (left) Erythema

multiforme on the palm
DRUG RASHES / 175
TREATMENT: ERYTHEMA MULTIFORME
Erythema multiforme gets better on its own after 2 weeks and does not require treatment. Even in severe episodes the
case for systemic steroids is controversial. Treatment is symptomatic. Causes of erythema multiforme should be sought
and treated if necessary.
● make sure you know what is in a tablet

DRUG RASHES
or injection when you prescribe it;
Some drug rashes are life-threatening and it is essential that the offending drug is always use proper names
stopped. Although immediate life-threatening IgE-mediated anaphylactic reactions can ● do not give ampicillin/amoxicillin for
occur, delayed (type IV) reactions are more common but tend to be idiosyncratic and sore throats.
unpredictable. Mostly they are asymptomatic and get better whether or not the drug is
stopped. Unfortunately there is no simple test to identify the cause of a drug rash, and if List of drug rashes covered elsewhere
patients are taking numerous drugs it is often not possible to be sure of the exact cause or Acne, see p. 121
even whether a drug is responsible (a viral exanthem may look identical). This leaves the Bullous, see p. 183
doctor with a problem, not only during the current episode but also in the future, because Exanthematous (morbiliform), see p. 176
he or she needs to know whether it is safe to prescribe the drug again. Erythema multiforme, see p. 174
If you think the patient has a drug rash you need to find out the following. Erythema nodosum, see p. 378
● A complete list of all drugs the patient is taking (prescribed, over-the-counter or Erythrodermic, see p. 194
borrowed). Drug reaction with eosinophia, see p. 168
● The exact date each one was started and stopped. It is more likely that a rash is from Lichenoid, see p. 176
a recently started drug than one that has been taken for years. A drug rash is unlikely Fixed drug eruption, see p. 181
to have developed in less than 4 days if the drug has not been taken before. Most Hair loss, see p. 84
drug rashes take 7–10 days to occur, but they sometimes do not appear for 28 days Hyperpigmentation, see p. 298
(especially if concomitant immunomodulating drugs are being taken). Look for the Hypertrichosis, see p. 72
drug that was started 7–14 days before the rash began. Lupus erythematosus, see p. 131
● Has the suspected drug or any chemically related drug been taken before? Photoallergic, see p. 106
● Has there ever been an adverse reaction to a drug before and to which one? Phototoxic, see p. 101
Purpuric/vasculitic, see p. 401
Avoid drug rashes by remembering the following: Serum sickness, see p. 172
● only prescribe drugs that are necessary Toxic epidermal necrolysis, see p. 192
● always ask the patient if he or she has had any previous drug allergies
Urticarial drug rashes, see p. 172
EXANTHEMATOUS DRUG RASH LICHENOID DRUG REACTION

This is the most common kind of drug rash. In the United Rarely, a rash that looks like lichen planus (although usually
Kingdom, antibiotics, sleeping tablets and tranquillisers are the atypical) can be due to a drug. The rash has the typical mauve
most frequent causative agents. The rash mimics the common hue of lichen planus but the lesions are larger and more confluent.
viral exanthems and is made up of symmetrical red or pink Histology shows lichenoid features. Drugs that can cause it
macules or papules mainly on the trunk; on the legs it may be include:
purpuric. Almost any drug can cause this kind of reaction but the ● β-blockers ● chloroquine
commonest are: ● chlorpropamide ● ethambutol
● ampicillin (amoxicillin) ● other penicillins ● gold ● mepacrine
● benzodiazepines ● captopril ● methyldopa ● penicillamine
● carbamazepine ● NSAIDs ● quinine ● thiazide diuretics.
● phenothiazines ● sulphonamides
● thiazide diuretics ● thiouracils.
Fig. 7.10 Exanthematous rash due to sulphonamide Fig. 7.11 Lichenoid drug rash
PAPULES AND NODULES / 177
GIANOTTI–CROSTI SYNDROME Face, trunk and limbs

Gianotti–Crosti syndrome is a papular eruption occurring in Acute erythematous lesion PAPULES and NODULES
children between the ages of 6 months and 12 years and is usually Surface normal/crust
a response to a viral infection especially hepatitis B. A profuse Single/few (2–5) isolated
papular rash starts on the buttocks and thighs, and quickly
Nodule within dermis Papule(s) on surface
spreads over 3–4 days to the arms and face. The lesions may be
a dull-red colour. There is often an associated lymphadenopathy
of inguinal and axillary glands. The rash fades after 2–8 weeks.
Always check the liver function tests. Painful Not painful Very itchy Rapid growth
No previous cyst Previous cyst Comedones Punctum in Bleeds easily

present centre
BOIL INFECTED ACNE INSECT BITE PYOGENIC

CARBUNCLE EPIDERMOID NODULE/ GRANULOMA
CYST CYST
p. 177 p. 178 p. 178 see p. 198 see p. 334
BOIL/FURUNCLE
A boil is an abscess of a single hair follicle (see Fig. 7.31) caused by
Staphylococcus aureus, which may also be isolated from the nose
or perineum. Single or multiple tender, red nodules with a central
punctum can occur anywhere on the body except the palms or
Fig. 7.12 Gianotti–Crosti soles. Without treatment the abscess will eventually point on the
syndrome on leg of infant surface, discharge and heal leaving a scar.
Acne cysts are not due to an infection but to a sudden severe TREATMENT: BOILS, CARBUNCLES AND INFECTED CYSTS
inflammatory reaction in an acne nodule. They usually respond
quite rapidly to an injection of intralesional steroid (triamcinolone Check the patient’s blood to exclude diabetes (fasting blood sugar or HbA1c). If the
10 mg/mL). boil is already pointing, it can be lanced to let the pus out. Otherwise, treat with oral
flucloxacillin (or erythromycin) 500 mg qid for 7 days. Take swabs for bacteriology
Epidermoid cysts have a microscopic opening and through this, from the boil, the nose, perianal skin and any rash. The infection usually comes from
staphylococci can enter. Sudden painful enlargement of a previous the patient him- or herself, so carriage sites should be treated with topical mupirocin,
cyst is indicative of secondary infection or rupture of the cyst and fucidic acid or neomycin ointment twice daily for 2 weeks. If recurrent boils occur even if
a subsequent foreign body reaction (see also p. 273). carriage sites have been treated, take swabs from other members of the family and treat
them if infected. Long-term low-dose antibiotics (flucloxacillin or erythromycin 250 mg
CARBUNCLE bid) may be necessary if the boils reoccur or persist. For cysts, excise after the infection
An abscess of several adjacent hair follicles is called a carbuncle. has settled down, not at the time the cyst is red and painful.
It looks just like a boil but is larger and has several openings to the
surface.
Fig. 7.13 Boil on back of hand Fig. 7.14 Acne cyst on right cheek Fig. 7.15 Carbuncle on back with multiple openings
VESICLES AND BULLAE / 179
Trunk and limbs

Acute erythematous rash/lesions VESICLES AND BULLAE
Vesicles and bullae
Multiple vesicles Bullae
Widespread, coalescing Localised, Limbs, Sun exposed/ Unilateral Single/ Recent new drug started Pus-filled
grouped symmetrical linear streaks Dermatomal grouped Flaccid
Itchy Sudden Prodromal ‘Target’ Itchy Prodromal Very itchy Single lesion, Multiple, Multiple,
worsening of tingling lesions pain Tense recurrent at clear serum golden crusts
eczema same site
ACUTE ECZEMA HERPES ERYTHEMA PHYTOPHOTO HERPES INSECT FIXED DRUG BULLOUS BULLOUS
ECZEMA HERPETICUM SIMPLEX MULTIFORME or ALLERGIC ZOSTER BITE REACTION DRUG RASH IMPETIGO
DERMATITIS
see p. 189 see p. 109 see p. 109 see p. 174 p. 182 p. 179 see p. 198 p. 181 p. 183 p. 187
HERPES ZOSTER (SHINGLES) sensation in the skin. Then comes the rash – groups of small
Herpes zoster occurs in people who have previously had vesicles on a red background, followed by weeping and crusting.
chickenpox. The virus, varicella zoster, lies dormant in the dorsal Healing takes 3–4 weeks. The rash is unilateral and confined to
root ganglion following chickenpox and later travels down the one or two adjacent dermatomes with a sharp cut-off at or near
cutaneous nerves to infect the epidermal cells. Destruction of the midline. This feature and the associated pain makes any other
these cells results in the formation of intraepidermal vesicles. For diagnosis unlikely. The pain may continue until healing occurs,
several days before the rash appears there is pain or an abnormal but in the elderly may go on for months or even years.
TREATMENT: HERPES ZOSTER a
If the patient is seen during the prodromal phase of pain or paraesthesia, or within 48 hours of the development of
blisters, treat with a 7-day course of an oral antiviral agent such as:
● aciclovir 800 mg 5 times a day
● famciclovir 250 mg tid
● valaciclovir 1 g tid.
These drugs are competitive inhibitors of guanosine and because they are converted to the triphosphate by viral
thymidine kinase, they are effective only in the presence of actively replicating virus. They are all very expensive so should
only be given in the early phase of the disease.
Give regular analgesics for the pain, e.g. paracetamol 1 g every 4 hours, two co-dydramol tablets 4-hourly, or
dihydrocodeine prolonged-release tablets 60 mg 12-hourly. In the elderly, prophylactic amitriptyline10–25 mg taken at
night, gradually increasing to 75 mg, may help to prevent post-herpetic neuralgia if given as soon as the rash appears.
b c d
Fig. 7.16 Herpes zoster T1,2 at: (a) 7 days – vesicular stage; (b) 14 days – erosions; (c) 21 days – crusting; (d) 28 days – healing with some residual crusts and erythema
CRUSTING ON SURFACE / 181
FIXED DRUG ERUPTION

This is a curious reaction, whereby each time a drug is given,
a well-demarcated, round or oval, red plaque with/without
blistering occurs at the same site, usually within 2 hours, and
certainly within 24 hours. The only differential diagnosis is a
recurrent herpes simplex infection. Any drug can cause it. In the
United Kingdom and the United States the common ones are:
● barbiturates ● benzodiazepines
● sulphonamides ● tetracycline
● phenophthalein (in over-the-counter laxatives)
● NSAIDs
● quinine (tablets and in tonic water or bitter lemon drinks).
The redness and swelling disappears after about 10 days to leave

a dark-brown patch that remains for several months (see p. 297).
Fig. 7.17 Herpes zoster: right T11,12 Stopping the drug will resolve the problem. You can confirm
which drug is the cause, as giving it again will produce the same
reaction at the same site within 2 hours.
Fig. 7.18 Herpes zoster: left T3 Fig. 7.19 Fixed drug reaction after taking Septrin: erythema and blisters on arm
Fig. 7.20 Phytophotodermatitis (strimmer rash): sun- Fig. 7.21 Allergic contact dermatitis to Primula Fig. 7.22 Bullous drug rash on the ankle: this occurs
exposed skin below the trouser where plant juices obconica plant: streaks where plant juices have within days of starting the drug (nitrofurantoin)
containing psoralens have triggered a phototoxic touched forearm; no sun is necessary for this
reaction reaction; poison Ivy will produce a similar reaction
PHYTOPHOTODERMATITIS PLANT CONTACT DERMATITIS

Phytophotodermatitis is due to plant juices containing Several plants (Primula obconica, Rhus – poison ivy) can cause an allergic
photoactive chemicals (usually psoralens) being contact dermatitis. Linear blisters (see Fig. 7.21) are seen where the
accidentally brushed onto the skin. In the presence of leaves have brushed against the skin, affecting hands, forearms and
sunlight this causes an irritant or phototoxic dermatitis. face). Sometimes the distribution affects the exposed or light-aggravated
Giant hogweed, rue, mustard and St John’s wort are sites of face, neck, hands and arms with a chronic lichenified dermatitis
common causes. The patient gives a history of having (chrysanthemums and other compositae). Tulip bulbs and garlic can
been in the garden clearing weeds, often using a strimmer, affect the fingertips (see p. 415).
or walking in the countryside on a sunny day. The rash
Compositae dermatitis occurs in florists and gardeners, and if suspected
is characteristically linear, made up of blisters where the
it should be patch tested for. Poison ivy, oak or sumac dermatitis is very
plants have touched the skin, usually on the lower legs or
common in North America and the Far East. The rash generally takes
arms.
around 24 hours to develop and lasts up to 2 weeks.
PUSTULAR RASHES / 183
TREATMENT: PHYTOPHOTO AND PLANT CONTACT Face, trunk and limbs

DERMATITIS Acute erythematous rash PUSTULAR RASHES
Pustules present
Ideally the plant involved should be identified, so that it can
be avoided in the future, but this is often not possible. If the Isolated lesions Lesion on erythematous base
rash is due to strimming, the patient should wear trousers Intervening skin normal
tucked inside his or her socks or boots in future. If the rash is
very acute with blistering and weeping, dry it with potassium
permanganateUK or aluminium acetateUSA soaks (see p. 30).
Previous/present eczema Previous/present
Once dry, apply a potentUK/group 2–3USA topical steroid
psoriasis
ointment until better.
BULLOUS DRUG REACTIONS

Bullae at the site of pressure can occur in
unconscious patients due to the following drugs: Lesion evolve: Follicular lesions Pustules on top Umbilicated Shallow pustules
Papules→vesicles only of eczema vesicles → on erythematous
● barbiturates
→pustules→crusts pustules base
● imipramine
● methadone
● meprobamate
● nitrazepam.
Usually children Staphylococcus Staphylococcus Herpes virus Bacteriology
Bullous pemphigoid can on occasions be +++ +++ +ve -ve
induced by:
● clonidine
● diclofenac
● furosemide
● ibuprofen.
CHICKENPOX FOLLICULITIS ECZEMA with ECZEMA GENERALISED
A pemphigus type of drug reaction is seen with: FOLLICULITIS HERPETICUM PUSTULAR
● captopril
PSORIASIS
● penicillamine
● rifampicin.
p. 184 p. 185 p. 185 see p. 109 see p. 193
CHICKENPOX (VARICELLA)
Chickenpox (varicella zoster) is a highly infectious
illness spread by droplet infection from the upper
respiratory tract. In urban communities most children
under the age of 10 have been infected. The incubation
period is usually 14–15 days. The prodromal illness
is usually mild so that the rash is the first evidence of
illness. The lesions start off as pink macules, which
develop quickly into papules (see Fig. 7.23), tense
vesicles (see Fig. 7.24), pustules (see Fig. 7.25) and then
crusts (see Fig. 7.26). Crops of lesions occur over a few
days so that there are always lesions at different stages
of development present. The spots are very itchy and
secondary infection may lead to pock-like scarring
(see Fig. 7.27). Typically it occurs on the face and trunk Fig. 7.25 Chickenpox pustules on adult face Fig. 7.26 Chickenpox resolving lesions on
rather than the limbs. back of adult
Fig. 7.23 Chickenpox: early lesions showing papules Fig. 7.24 Chickenpox: vesicles on baby’s face Fig. 7.27 Resolving scars from chickenpox
and vesicles
PUSTULAR RASHES / 185
FOLLICULITIS TREATMENT: CHICKENPOX

Superficial infection of hair follicles is
very common. A small bead of pus sits In most instances chickenpox requires no treatment. In adults and immunocompromised patients, treatment with
around a protruding hair and there may be famciclovir or valaciclovir will reduce the severity of the disease (see p. 180 for doses).
slight erythema at the base. One or several
follicles may be involved, but there is no
TREATMENT: FOLLICULITIS
tenderness or involvement of the deep part
of the follicle. It is usually due to S. aureus,
Take swabs from a pustule and any possible carriage sites (anterior nares, perineum and any other skin rash). Stop
which may be carried in the patient’s applying greasy ointments to the site. If this is the cause then nothing else is necessary. If folliculitis occurs in a patient
nose or perineum. It can be caused by, or with atopic eczema, change the patient’s steroid ointment to a cream for a few weeks.
made worse by, the application of greasy
ointments to the skin, tar preparations Oral flucloxacillin or erythromycin 500 mg qid for a week will clear most cases. Treat any infected carriage sites with
topical mupiricin, fucidin or neomycin cream bid for 2 weeks. Persistent folliculitis may require long-term suppressive
or plasters. The wearing of oily overalls
treatment with low-dose oral antibiotics (250 mg bid for up to 6 months).
may precipitate folliculitis of the thighs
(oil acne).
Fig. 7.28 Folliculitis on thigh: Staphylococcus aureus Fig. 7.29 Folliculitis: bead of pus at opening of a Fig. 7.30 Folliculitis on leg from applying greasy
grown from pustules hair follicle ointments
Trunk and limbs

Acute erythematous lesions CRUST AND EXUDATE
Surface crust/exudate
Erosions and ulcers
If crust present, remove it Exudate +++ (may form crusts)
Ulcer underneath Erosion underneath
First episode Recurrent at same Previous/present eczema

site
Single/multiple Usually child Usually adult Sudden worsening of previous eczema Poorly defined Well defined discs,
isolated lesions itchy++
Bacteriology +ve Bacteriology +ve +ve Herpes simplex Very painful +ve Bacteriology +ve Bacteriology -ve
Staph. Staph. H. simplex Staph.
ECTHYMA IMPETIGO HERPES ECZEMA IMPETIGINISED ACUTE DISCOID

SIMPLEX HERPETICUM ECZEMA ECZEMA ECZEMA
p. 187 see p. 107 see p. 109 see p. 109 see p. 107 p. 189 p. 189
CRUSTING AND EXUDATE / 187
STAPHYLOCOCCAL SKIN INFECTIONS

Pathogenic S. aureus can cause a variety of skin infections
depending on the depth of inoculation (see Fig. 7.31). An infection
just under the stratum corneum causes impetigo (see Fig. 4.18,
p. 107) where the superficial blisters rapidly break to form
erosions with golden crusts on the surface. In the newborn you
may see intact blisters with pus in them (bullous impetigo, see
Fig. 7.32). Ecthyma is an infection of the full thickness of the
epidermis (see below). Folliculitis is a superficial infection of the
hair follicle with a pustule at the opening of the follicle (see p. 185).
Deeper infection results in either a boil, if the whole follicle is
involved, or a carbuncle, if multiple adjacent follicles are involved
(see pp. 177, 178).
A new strain of S. aureus producing Panton–Valentine leukocidin
(PVL) has been identified recently. PVL is a cytotoxin that can
Fig. 7.31 Sites of involvement of staphylococcal infection of the skin
destroy white blood cells and cause extensive tissue necrosis. PVL-
positive S. aureus is usually methicillin resistant but is acquired
in the community, unlike methicillin-resistant S. aureus. It causes
recurrent skin abscesses and cellulitis, which do not respond to
routine doses of flucloxacillin or erythromycin. Infection with
PVL-positive S. aureus should be suspected in anyone with
recurrent or antibiotic-resistant furunculosis (boils), abscesses or
necrotising fasciitis. Swabs should be sent to the laboratory with a
request to screen for PVL.
ECTHYMA
Ecthyma can be caused by either S. aureus or Steptococcus pyogenes
and is always secondary to a break in the skin (following an
injury, insect bite or scabies). It presents as a round, punched-out
ulcer with a thick crust on top. It is usually seen in children but
may occur in adults, especially in hot humid climates, and those
infected with PVL-positive S. aureus. The lesions will heal with
scarring. Fig. 7.32 Bullous impetigo: pus-filled bullae on trunk of newborn
TREATMENT: ECTHYMA
Take swabs and give oral flucloxacillin or erythromycin by mouth, 125–500 mg qid for
7–10 days depending on age. Do not treat with topical antibiotics, as the infection
is deep and they will not work. The ulcer itself will take at least 4 weeks to heal, but
antibiotics do not need to be continued for this long. Extensive tissue necrosis should
raise the possibility of PVL-positive S. aureus.
TREATMENT: PVL-POSITIVE S. AUREUS
Cases not responding to flucloxallin 500 mg qid acquired in the community should be
treated with:
● clindamycin 450 mg qid
● rifampicin 300 mg bid plus doxycycline 100 mg bid (not for children <12 years); the
doxycycline can be replace by fucidic acid 500 mg tid or trimethoprim 200 mg bid.
Treat carriage sites, the nose with mupirocin (Bactroban) ointment and the skin by
washing with 1% chlorhexidine wash for 5 days.
Fig. 7.34 Ecthyma: punched-out ulcers following insect bites
a b
Fig. 7.33 Ecthyma: (a) with crust on surface; (b) with crust removed to reveal pus Fig. 7.35 Multiple lesions of ecthyma on legs in a patient with PVL +ve S. aureus
CRUSTING AND EXUDATE / 189
ACUTE ECZEMA
Acute eczema clinically presents with tiny vesicles that burst to
produce erosions, exudate and crusts. It may be due to an acute
flare of chronic atopic eczema (see p. 236), or an allergic contact
dermatitis. It may be difficult to distinguish from impetiginised
eczema (see p. 107). A common mistake is to assume that weeping
eczema is infected and treat it with antibiotics rather than topical
steroids.
Fig. 7.37 Acute eczema: broken Fig. 7.38 Acute eczema with erosions
vesicles and exudate
TREATMENT: ACUTE ECZEMA
It is no good trying to apply creams or ointments to an exuding rash, because they

Fig. 7.36 Histology of acute eczema showing vesicles within the epidermis are not able to penetrate the skin. First, dry up the exudate with an astringent such
as Burow’s solution (aluminium acetate) or diluted potassium permanganate solution
(1:10 000), see p. 30. The latter should be a light-pink colour (see Fig. 2.01, p. 30).
DISCOID ECZEMA (WET TYPE) Either put the solution in a bath or bowl and soak the affected area or soak a towel or
flannel in the solution and apply it to the affected area for 10 minutes four times a day.
Discoid eczema presents as well-defined, coin-shaped (nummular)
After soaking, dry the skin with a towel and then apply a potentUK/group 2–3USA steroid
plaques. The wet type is made up of coalescing erosions with
ointment. If a contact allergy is suspected, refer the patient for patch testing once the
exudate on the surface. The exudate dries to form crusts. There rash has settled.
may be one or a number of lesions (see also p. 243).
Face, Trunk and Limbs

Acute erythematous rash GENERALISED RASH (>50% body surface)
Generalised rash (>50% body surface)
Normal surface Skin shears off → Tender erosions Pustules on erythema Scaling on surface
Discrete macules coalescing Infant Adult Patient unwell, fever Patient feels cold but skin hot
? sibling with impetigo ? previous drugs
TOXIC ERYTHEMA STAPHYLOCOCCAL SCALDED TOXIC EPIDERMAL NECROLYSIS GENERALISED PUSTULAR ERYTHRODERMA
(Drugs, viral, idiopathic) SKIN SYNDROME (Drugs) PSORIASIS (Eczema, psoriasis, drugs,
lymphoma, carcinoma)
see pp. 167, 176 p. 191 p. 192 p. 193 p. 194

GENERALISED RASH / 191
STAPHYLOCOCCAL SCALDED SKIN SYNDROME

This is an infection due to phage type 71 S. aureus, which produces
a toxin that causes a split in the upper part of the epidermis. It
occurs almost entirely in infants and young children. The skin
becomes red and very tender (like a scald) and then peels off. It
often begins in the flexures but usually spreads to involve the
whole body. The child will be screaming with pain. The source of
infection is often an older sibling with impetigo, infected eczema
or scabies.
TREATMENT: STAPHYLOCOCCAL
SCALDED SKIN SYNDROME Fig. 7.40 Staphylococcal scalded skin syndrome in a young child
Treatment is flucloxacillin elixir

62.5 mg (children under age 2) or
125 mg (age over 2 years) every
6 hours for 7 days. The pain will stop
almost immediately but the skin
peeling takes longer to stop due
to persistence of the toxin. Other
children in the family may require
treatment for impetigo or infected
eczema at the same time.
Fig. 7.39 Staphylococcal scalded skin Fig. 7.41 Toxic erythema: the skin is just red, with no evidence of skin peeling or
syndrome systemic upset
TOXIC EPIDERMAL NECROLYSIS

This is an uncommon but serious skin disease in which the whole of
the epidermis dies and shears off. It is most commonly due to drugs:
● allopurinol ● barbiturates
● carbamazepine ● NSAIDs
● phenytoin ● sulphonamides
● thiacetazone.
However, it can also occur in patients with a lymphoma or HIV

infection. In some cases no cause is found.
The prognosis of toxic epidermal necrolysis can be very poor,
especially if large amounts of skin are lost. The following scoring
system will help determine the prognosis. Score one point for each of
the following features:
● age >40 ● heart rate >120
Fig. 7.42 Toxic epidermal necrolysis: the whole epidermis is shearing off
● cancer or HIV ● blood sugar >14 mM/L
● loss of >30% skin ● bicarbonate <20 mM/L
● urea >10 mM/L.
Mortality: score 0–1 = 3%; score 3 = 35%; score >5 = 90%
TREATMENT: TOXIC EPIDERMAL NECROLYSIS
Stop the suspected drug. The extensive skin loss will need to be treated just like a burn
and admission to a burns unit or intensive care unit is essential. Surgical debridement is
not necessary, as only the epidermis is shed. Survival depends on good management with
replacement of fluids and electrolytes lost through the skin, prevention of infection and
septicaemia, and careful handling of the patient’s skin, which tends to tear off easily.
Early treatment with large doses of intravenous immunoglobulin (2 g/kg body weight given
daily for 3–4 days) may be life saving. The immunoglobulins inhibit Fas-mediated epidermal
cell death and allow the epidermis to recover. Systemic steroids do not help and may be
harmful.
Fig. 7.43 Toxic epidermal necrolysis

GENERALISED RASH / 193
GENERALISED PUSTULAR PSORIASIS

This acute, serious and unstable form of psoriasis is often
precipitated by withdrawal of systemic or very potent topical
steroids. Sheets of erythema studded with tiny sterile pustules
come in waves associated with fever (see Figs. 7.44, 45, 46) and
general malaise. This is the main reason why psoriasis should not
be treated with either topical or systemic steroids.
Fig. 7.45 Generalised pustular psoriasis
Fig. 7.44 Temperature chart for patient with generalised pustular psoriasis
TREATMENT: GENERALISED PUSTULAR PSORIASIS
This is a dermatological emergency and carries a significant mortality. The patient

should be admitted to hospital for bed rest and sedation. Initially the skin will be
treated with emollients (e.g. equal parts white soft paraffin and liquid paraffinUK/
petrolatumUSA). The patient should be nursed under a ‘space blanket’ to prevent
hypothermia. The associated fever is not due to infection, so there is no need for
antibiotics. Both topical and systemic steroids are contraindicated. If the patient fails
to improve on the aforementioned measures, systemic treatment will be needed with
methotrexate or ciclosporin.
Fig. 7.46 Generalised pustular psoriasis: sheets of shallow pustules on an
erythematous background
ERYTHRODERMA (EXFOLIATIVE DERMATITIS)

Erythroderma is the term used when >90% of the body’s surface is
red and scaly. It can be caused by:
● eczema
● psoriasis
● a drug reaction, e.g. due to:
— allopurinol — cimetidine
— barbiturates — gold
— captopril — isoniazid
— carbamazepine — nalidixic acid
— chlorpromazine — phenytoin
— chloroquine — sulphonamides
● Sézary syndrome (cutaneous T-cell lymphoma, see p. 231)
● an underlying carcinoma.
Fig. 7.48 Erythroderma due to Fig. 7.49 Erythroderma in black skin

carcinoma of the pancreas
TREATMENT: ERYTHRODERMA
These patients should be managed in hospital, both to find the cause and to prevent
hypothermia, congestive cardiac failure or renal failure. Initially the skin should be
treated with emollients such as white soft paraffinUK/petrolatumUSA. Specific causes
should be treated, e.g. psoriasis can be treated with methotrexate, or eczema with
topical steroids. Stop any drugs and look for an underlying carcinoma or lymphoma.
Fig. 7.47 Sézary syndrome
195
Chronic erythematous lesions

on trunk and limbs
8
Normal surface
Macules 202
Papules: single or few
Small (<5 mm) see p. 262
Large (>5 mm) 213
Papules: multiple
Small (<5 mm) 196
Large (>5 mm) 202
Pustules 201
Patches and plaques
Small (<2 cm) 202
Large (>2 cm) 208
Annular lesions 209
Linear lesions 212
Nodules (>1 cm) 213
Scaly surface
Papules (<10 mm) 222
Patches and plaques (>10 mm)
Single or few (two to five) lesions 218
Multiple 224
Chronic eczema 234
Nodules see p. 325
Generalised rash 244
Crust, exudate, excoriated surface
No blisters present
Single or few plaques and erosions see p. 218
Multiple papules, plaques and small erosions 245
Generalised itching/pruritus 252
Nodules and ulcers see p. 329
Vesicles, bullae and large erosions 255
196 / CHRONIC RASHES ON TRUNK AND LIMBS
Trunk and limbs

Chronic erythematous rash MULTIPLE SMALL PAPULES (<5 mm)
Normal surface (For single papules see p. 213)
No pustules (pustules present, see p. 201)
Multiple papules >5 mm Papules 2–5 mm, not follicular Papules <2 mm, follicular Papules <2 mm,
see p. 202 not follicular
Symmetrical Asymmetrical Comedones Symmetrical Chest and back Outer arms, Chest, abdomen
Flat-topped present Itch++ thighs, buttocks arms, genitalia
Shiny surface Dull surface Grouped Teenagers and ± Associated Most follicles Some follicles All follicles All lesions same
Mauve colour Pink/brown Itch ++ young adults poorly defined involved involved involved densely packed
plaques
Biopsy = Biopsy = Central Biopsy = Itch+ Swab for Not itchy Biopsy =
lichenoid viral wart punctum spongiosis Naso-labial bacteria +ve Children lichenoid
scaling?/ (+ adults)
dandruff?
LICHEN PLANE INSECT ACNE PAPULAR SEBORRHOEIC FOLLICULITIS KERATOSIS LICHEN

PLANUS WARTS BITES ECZEMA ECZEMA PILARIS NITIDUS
p. 197 see p. 268 p. 198 see p. 116 p. 199 p. 201 p. 200 p. 200 p. 198
PAPULES AND PUSTULES (<5 mm) / 197
LICHEN PLANUS from mauve to brown (see Fig. 1.65, p. 14). It is uncommon in
The lesions in lichen planus are small mauve, flat-topped, shiny children. The buccal mucosa may be involved, with a white,
papules, which sometimes have white streaky areas on the lace-like, streaky pattern (see Fig. 6.19, p. 149). The rash tends
surface (Wickham’s striae). The most characteristic place to look to last 9–18 months before disappearing. There may be some
for the rash is on the flexor aspect of the wrist, but it is usually residual post-inflammatory hyperpigmentation for a time. In
widespread on the trunk and limbs, and may occur at sites of pigmented skin the rash tends to become hyperpigmented with
trauma (Köebner phenomenon). Some lesions may become a characteristic bluish-black colour (see Fig. 8.06). Lichen nitidus
plaques. Although it is very itchy, scratch marks are not usually is a variant where the papules are less than 2 mm in diameter (see
seen. As the rash gets better the colour of the papules change Fig. 8.04).
Fig. 8.01 Lichen planus: flat-topped shiny papules Fig. 8.02 Lichen planus: Wickham’s striae Fig. 8.03 Lichen planus: Köebner phenomenon
on flexor aspect of wrist
TREATMENT: LICHEN PLANUS INSECT BITES (PAPULAR URTICARIA)

Insect bites present as itchy papules with a
Topical treatment will not make the rash go away central punctum. If there are groups or rows of
any quicker, but the application of a potentUK/ three or four bites, think of flea bites. Single very
group 2–3USA topical steroid will control the
large lesions on the face or hands are suggestive
itching.
of bedbugs, particularly where new lesions are
Patients with extensive blistering (bullous) or found each morning. Numerous other insects
severe erosive mucous membrane lichen planus can also bite humans. Usually the patient is not
may require treatment with systemic steroids and able to identify the insect involved. Sometimes
should be referred urgently to a dermatologist
large blisters follow insect bites.
Fig. 8.04 Lichen nitidus TREATMENT: INSECT BITES
Most patients will have acquired flea bites from an infestation

in the home. Cats and dogs catch fleas from other pets and
bring them into the home, mostly during the summer but
at other times of the year during spells of warm weather.
Humans can be bitten by fleas, which live on cats and dogs
throughout the adult stage of their life cycle. Fleas lay eggs
on their cat or dog host, which will drop to the ground and
undergo several life cycle stages before reaching adulthood,
when they can return to the host and feed. If no animal host
is available they may remain on furniture, bedding or carpets
for months.
To get rid of animal fleas, use both a drug that kills adult
fleas, such as Frontline (fipronil) or Advocate (imidacloprid),
as a monthly topical treatment on the pet and an insect
development inhibitor, such as Program (lufenuron), for the
larval stages. These are available from veterinary surgeons.
It may also be necessary to spray areas of the house such as
carpets, sofas and pet bedding, where eggs will have fallen,
with a suitable product such as Indorex, which contains
Fig. 8.05 Lichen planus: the rash may become Fig. 8.06 Lichen planus in pigmented skin permethrin, piperonyl butoxide and pyriproxyfen.
hyperpigmented as it gets better
Insect repellents PAPULAR ECZEMA

Eczema may sometimes present as papules
Mosquitos can be discouraged from biting by using an insect repellent. DEET (N,N-diethyl-m-toluamide) is the most that remain discrete rather than coalescing
effective insect repellent available at the moment, but it can cause irritation on the skin and should not be used around into poorly defined plaques. It can be
the eyes. It is available as a lotion, stick or spray. Lotions are generally cheaper than sticks or sprays. All are equally
difficult to diagnose. A biopsy may be
effective if they are applied often enough. Aerosols and sprays last 1–2 hours; liquids, lotions, creams and pump sprays
necessary to distinguish it from folliculitis.
last 2–3 hours. Gels and sticks last 4 hours. In children the insect repellent is applied to clothing near to the exposed skin,
rather than on the skin itself so there will be no local irritation and no risk of the child getting it in his or her eyes.
Fig. 8.07 Flea bites: grouped papules with Fig. 8.08 Large blisters on the lower leg from flea Fig. 8.09 Papular eczema
intervening skin normal bites
KERATOSIS PILARIS FOLLICULITIS the patient also has eczema. Folliculitis

Erythematous follicular papules develop Inflammation of hair follicles is very can be caused by, or made worse by,
on the upper arms and thighs. It is common. One (see Fig. 7.29, p. 185) or the application of greasy ointments, tar
distinguished from folliculitis, as it is several follicles may be involved. Pustules preparations or plasters on the skin. The
rough to the touch. Also, all follicles are are often present. It is usually due to wearing of oily overalls may precipitate
involved and there are no pustules (see Staphylococcus aureus, particularly if folliculitis of the thighs (oil acne).
p. 324).
Fig. 8.10 Keratosis pilaris on thigh: erythematous Fig. 8.11 Folliculitis infection of hair follicles on Fig. 8.12 Folliculitis in black skin caused by the
follicular papules that are rough to the touch lower leg in a patient with atopic eczema application of greasy ointments
Trunk and limbs TINEA CORPORIS

Chronic erythematous rash PUSTULES PRESENT Tinea uncommonly presents with pustules
Surface normal (or crust) on a background of erythema. Think
Papules and plaques of it when the lesions are unilateral or
asymmetrical. The diagnosis is made
Pustules situated on hair follicles Comedones Pustules on background erythema
present by taking swabs for bacteriology (to
exclude secondarily infected eczema), and
mycology scrapings that will confirm a
dermatophyte fungus (see p. 233).
Buttocks, legs Upper back, chest Upper trunk Well defined with Poorly defined
central clearing lesions
FOLLICULITIS SEBORRHOEIC ACNE TINEA ECZEMA with

ECZEMA VULGARIS CORPORIS FOLLICULITIS
p. 200 p. 201 see p. 116 see p. 233 p. 200
SEBORRHOEIC ECZEMA (PITYROSPORUM FOLLICULITIS)

On the trunk, seborrhoeic eczema may present as extensive follicular papules
and pustules that are caused by overgrowth of pityrosporum yeast in the follicles
(pityrosporum folliculitis, see Fig. 8.13). This rash tends to come and go. The diagnosis is
made by the association with typical seborrhoeic eczema on the face (see p. 135) and scalp
(see p. 89). For treatment see p. 136.
Fig. 8.13 Pityrosporum folliculitis: papules and
pustules on the back or chest; look for seborrhoeic
dermatitis at other sites
Face, trunk and limbs

Chronic erythematous rash MULTIPLE LESIONS (all >5 mm and <2 cm)
Macules, small patches and plaques (Multiple large plaques >2 cm, see p. 208)
Normal surface (or slight scale) (Single/few large papules and nodules, see p. 213)
If scaly, scratch surface – if scales become detached see p. 222
Well-defined Poorly defined

border to lesions border to lesions
Orange-brown Mauve, shiny, Pink/red Longer history Papules coalescing Discrete, rough
Oval/round macules/patches flat-topped Recent onset Itch ++ Itch++ on palpation
(<6 weeks)
Coalescing: scales Isolated: weals Look in mouth for Young adult, ± Follicular Fingers wrists and Third trimester of Elderly
on scratching on rubbing white streaks scale within papules genitalia involved pregnancy, starts Skin type I
lesion on lower abdomen Sun-exposed sites
Mycology positive Biopsy Biopsy No Yes Biopsy
PITYRIASIS URTICARIA LICHEN PITYRIASIS SEBORRHOEIC SCABIES POLYMORPHIC SOLAR

VERSICOLOR PIGMENTOSA PLANUS ROSEA* ECZEMA* ERUPTION OF KERATOSES
PREGNANCY
p. 203 p. 204 see p. 197 p. 205 see p. 205 see p. 248 p. 206 see p. 326
*If patient unwell, has lymphadenopathy and lesions on palms and soles, think of secondary syphilis, see p. 207.
MACULES, SMALL PATCHES AND PLAQUES / 203
PITYRIASIS VERSICOLOR predominantly on the upper trunk. It is due to an infection with a

The word pityriasis means ‘bran-like’ and here means a scaly yeast, Pityrosporum orbiculare, which we all have on our skin as a
rash; versicolor means different colours. Pityriasis versicolor is harmless commensal. Under certain conditions, the yeast produces
a scaly rash of different colours. In different individuals it may hyphae and becomes pathogenic. It is then known as Malassezia
be white, orange brown or dark brown. The lesions are small, globosa. The depigmentation is due to inhibition of tyrosinase by
less than 1 cm in diameter, usually round and always scaly dicarboxylic acids produced by the pityrosporum yeast leading to
when scratched. Some may join together to form larger lesions suppression of melanin production.
or confluent plaques. It is a disease of young adults and occurs
Fig. 8.14 Pityriasis versicolor, white variety Fig. 8.15 Pityriasis versicolor, orange-brown variety Fig. 8.16 Pityriasis versicolor in black skin, dark-
brown variety
Most people with the rash have picked up the pathogenic form URTICARIA PIGMENTOSA
of the organism from someone else with it when on holiday in a This rare condition is due to increased mast cells in the skin.
warm climate; it is possible to transform your own commensal Orange-brown pigmented macules and small patches appear
organisms if you are on steroids or other immunosuppressive in children and young adults. The lesions may coalesce to
therapy. form larger patches. The surface is not scaly but on rubbing a
The orange-brown variety can be confused with pityriasis weal appears (Darier’s sign), due to release of histamine from
rosea, but the diagnosis can be easily confirmed by scraping off the mast cells. Most patients are asymptomatic but do not like
the scales, mixing them with a mixture of equal parts of 20% the appearance of the rash; some patients may itch. Systemic
potassium hydroxide solution and Parker blue-black ink. The symptoms of histamine release (flushing, headaches, dyspnoea,
organism takes up the blue colour of the ink and shows both wheeze, diarrhoea or syncope) are extremely rare.
spores and hyphae (‘spaghetti and meatballs’, see Fig. 8.17). Avoid any mast cell degranulating agents (aspirin, alcohol,
morphine, codeine). Antihistamines (both H1- and H2-antagonists)
TREATMENT: PITYRIASIS VERSICOLOR can be tried. If the patient is itching, PUVA therapy (see p. 61) is
helpful and the tan it produces will mask the rash.
If the rash is localised, use an imidazole cream such as clotrimazole twice a day for
2 weeks. If it is extensive then a single dose of oral ketaconazole 400 mg works well. An
alternative is itraconazole 100 mg/day for 5 days. Griseofulvin and terbinafine do not
work.
It is important to tell the patient that any hypopigmented areas will look the same after
treatment. It usually takes 3 months for the pigment to return to normal. Patients with
the orange-brown or dark-brown variety will look normal immediately after treatment.
Fig. 8.17 Direct microscopy

of scale in pityriasis versicolor
(‘spaghetti and meatballs’) Fig. 8.18 Urticaria pigmentosa
PITYRIASIS ROSEA TREATMENT: PITYRIASIS ROSEA

This condition is a viral infection due to the human herpesvirus-7.
It occurs in otherwise fit and healthy children or young adults, It is usually asymptomatic and needs no treatment other than reassurance that it is
and lasts about 6 weeks. First a single oval, scaly plaque 2–3 cm harmless and will get better on its own in about 6 weeks. If it is particularly itchy you
can use a simple moisturiser or 1% hydrocortisone cream twice a day.
in diameter appears on the trunk or on a limb. This is the ‘herald
patch’, which can sometimes be misdiagnosed as ringworm.
A few days later, the rest of the rash appears. It consists of two
SEBORRHOEIC ECZEMA
different kinds of lesions: first, petaloid lesions, which are similar
to the herald patch but smaller in size and consisting of oval pink On the trunk, seborrhoeic dermatitis may present as petaloid
scaly macules or plaques where the scale is just inside the edge plaques over the sternum (Fig. 8.22) and central back, extensive
of the lesion; second, small, pink follicular papules. If the herald follicular papules and pustules (pityrosporum folliculitis, see
patch is on the trunk, the rest of the rash is confined to the vest p. 201) or a pityriasis rosea-like rash. The clue to the diagnosis
and pants area, and the individual lesions follow Langer’s lines, is that it has been present for more than 6 weeks and there is
giving a ‘Christmas tree’ pattern. Look at the hands for evidence other evidence of seborrhoeic eczema such as scaling around
of scabetic burrows, especially if the rash is particularly itchy at the nasolabial folds (see p. 135) and on the scalp (see p. 89). For
night (see p. 248). treatment see p. 136.
Fig. 8.19 Pityriasis rosea: herald patch Fig. 8.20 Pityriasis rosea showing Fig. 8.21 Pityriasis rosea showing Fig. 8.22 Seborrhoeic eczema,
with numerous petaloid and papular ‘Christmas tree’ distribution, petaloid scale within a petaloid lesion petaloid lesions in the centre of the
lesions and follicular lesions back
POLYMORPHIC ERUPTION OF PREGNANCY (PRURITIC

URTICARIAL PAPULES AND PLAQUES OF PREGNANCY)
This is a common rash (about 1:150 pregnancies) that usually
occurs in the third trimester of the first pregnancy. It is a very
itchy condition, which starts on the abdomen. It is made up of
urticated papules, plaques and sometimes vesicles. It clears up
within 2–3 weeks of delivery and does not reoccur in subsequent
pregnancies. The baby is not affected. It needs to be distinguished
from prurigo of pregnancy (see p. 252) and the more serious
pemphigoid gestationis.
Table 8.01 Features of polymorphic eruption of pregnancy and pemphigoid

gestationis
Polymorphic eruption Pemphigoid gestationis (see p. 256)
Common Very rare Fig. 8.23 Polymorphic rash of pregnancy over abdomen
Urticated papules, vesicles, plaques Tense vesicles and bullae
Cause unknown Antibodies to basement membrane
Very itchy Very itchy
Usually primigravida Reoccurs in each pregnancy
Occurs third trimester Second and third trimester
Clears 2–3 weeks after delivery May take weeks to months to clear
Baby not affected Baby may be born with same rash
TREATMENT: POLYMORPHIC ERUPTION OF PREGNANCY
Apply a moderately potentUK/group 4–5USA topical steroid cream twice a day to

relieve the itching. Occasionally an oral antihistamine will also be needed, such as
chlorphenamine (Piriton) 4–8 mg every 4 hours (maximum of 24 mg in 24 hours). If
these measures fail to work, oral prednisolone 20–30 mg/day for 5 days, and tapered
off over 2 weeks, is safe and effective carried out in liaison with an obstetrician.
Fig. 8.24 Pemphigoid gestationis: plaques and blisters on abdomen; the rash
may look like erythema multiforme
SECONDARY SYPHILIS
Secondary syphilis occurs about 6 weeks after a primary infection with
Treponema pallidum. The skin lesions are preceded by a flu-like illness and
painless lymphadenopathy. The rash is very variable and may consist of
macules, papules, pustules and plaques ranging in colour from pink to mauve,
orange to brown. There are often lesions on the palms and soles (see Figs 8.28
and 8.29), patchy alopecia and flat warty lesions on the genitalia (see Fig. 11.02,
p. 353) and perianal skin. The diagnosis can be confirmed by demonstrating
T. pallidum on dark ground microscopy (see Fig. 11.04, p. 353), and a positive
VDRL test, which distinguishes it from all the other non-itchy rashes on
the skin.
For treatment see p. 354.
Fig. 8.27 Secondary syphilis: lesions around the mouth
Fig. 8.25 Secondary syphilis: papular Fig. 8.26 Secondary syphilis: pityriasis Fig. 8.28 Secondary syphilis lesions Fig. 8.29 Secondary syphilis lesions
rash on black skin rosea-like rash on trunk on palm on soles
Trunk and limbs

Chronic erythematous rash/multiple lesions LARGE LESIONS (>2 cm): NORMAL SURFACE
Normal surface
Large patches and plaques (>2 cm)
Lesions come Ring shape/annular Round or irregular shape Linear lesions
and go (see also p. 205) (see also p. 212)
Lesions Lesion Lesions expand Lesions fixed Well defined, Poorly defined Stretch Previous
expand over expanding over weeks over site and fixed lesions lesions marks injury/
hours over few time surgery
days
Peripheral red Central Central Accentuated Ring of Red/purple Lesion empties 3rd trimester Teenager
flare/white clearing punctum border/ papules plaque on compression of pregnancy Pregnancy
weal Fine scale ? Previous central Obesity
inside ring tick bite clearing
+ve Lyme Mycology Biopsy Starts on

serology +ve abdomen
URTICARIA ANNULAR LYME TINEA GRANULOMA SARCOID/ CAPILLARY ECZEMA POLYMORPHIC STRIAE SCAR
ERYTHEMA DISEASE INCOGNITO ANNULARE JESSNER’S/ MALFORMATION ERUPTION OF
LYMPHOMA PREGNANCY
see p. 171 p. 210 p. 209 p. 211 p. 210 pp. 213, see p. 312 see see p. 206 p. 212 p. 212
128, 216 p. 235
LARGE PAPULES AND PLAQUES / 209
Causes of annular lesions

With normal surface:
● annular erythema (see p. 210)
● erythema chronicum migrans (Lyme disease)
● erythema multiforme (see p. 174)
● granuloma annulare (see p. 210)
● Jessner’s lymphocytic infiltrate (see p. 128)
● urticaria (see p. 171).
With crust or scale:

● annular psoriasis (see p. 225)
● discoid eczema (see p. 243)
● porokeratosis (see p. 326)
● pityriasis rosea (see p. 205)
Fig. 8.30 Erythema chronicum migrans (Lyme
● tinea corporis (see p. 233)
disease)
LYME DISEASE
A single lesion of gradually expanding erythema (erythema chronicum migrans) with
or without a central punctum is likely to be Lyme disease, especially if the patient has
been walking in an area where ticks are common. It is due to a tick bite, which transmits
a spirochaete (Borrelia burgdorferi) into the skin. Outbreaks of Lyme disease tend to occur
in late May and early June, when the ticks leave the ground vegetation to feed on their
animal hosts (deer and sheep). They may wander onto humans walking through the
countryside.
If treatment is delayed, patients can go on to develop arthritis (initially intermittent
swelling of large joints and later a chronic erosive arthritis), meningoencephalitis, facial
nerve palsy and heart problems (conduction defects, myocarditis and pericarditis) weeks
or months later. If suspected the diagnosis can be confirmed by finding antibodies to
the spirochaete in the patient’s serum. There should be a fourfold rise in antibody titre
over 2–3 weeks. The antibody (ELISA, enzyme-linked immunosorbent assay) test can be
performed at your local hospital. Fig. 8.31 Tick before (left) and after (right) feeding
TREATMENT: LYME DISEASE ANNULAR ERYTHEMA GRANULOMA ANNULARE

This describes areas of erythema that are Granuloma annulare can present in one of
Doxycycline 100 mg bid, amoxicillin 500 mg tid or annular or figurate in shape. Over a period three ways.
cefuroxime 250 mg bid for 14 days is the treatment of days the areas of erythema gradually 1. Small pink papules that join together to
of choice. In children under the age of 12, give
expand or change. The lesions are often form rings. There is never any scale on
phenoxymethylpenicillin (Penicillin V) 50 mg/kg body
scaly just inside the spreading edge. In the surface, so it should not be confused
weight per day in divided doses instead. If children are
allergic to penicillin, they can be given erythromycin
most instances no cause can be found, with tinea. It is usually seen on the
50 mg/kg body weight per day in divided doses for but very rarely some patients may have dorsum of hands, elbows and knees,
10–14 days. an underlying neoplasm (lymphoma or but it can occur anywhere.
leukaemia). No treatment is available 2. A flat pink or mauve patch often seen
unless there is an underlying cause. on the thighs, upper arms, trunk or
dorsum of the foot (see Fig. 8.36).
3. A generalised asymptomatic macular
rash with no surface change (a biopsy is
usually needed for diagnosis).
Localised granuloma annulare is not
associated with diabetes mellitus; three-
quarters of cases of generalised granuloma
annulare are.
Fig. 8.32 Widespread annular erythema Fig. 8.33 Annular erythema showing scale within Fig. 8.34 Granuloma annulare: annular ring on
ring dorsum of hand
LARGE PAPULES AND PLAQUES / 211
Fig. 8.36 Granuloma annulare: patch of erythema on back of thigh; note this
is never scaly so should not be confused with tinea (see Figs. 8.37, 8.51, 8.74
and 8.75)
Fig. 8.35 Granuloma annulare on back of the hand
TREATMENT: GRANULOMA ANNULARE
If it is asymptomatic, which it usually is, the patient can be reassured that it is harmless
and will eventually go away on its own. It may take quite a long time – months or
even years rather than weeks. If it is painful, injection of triamcinolone 5–10 mg/mL
intralesionally will stop the pain and may make it go away.
TINEA INCOGNITO
Tinea incognito develops when tinea corporis (ringworm) is
inadvertently treated with topical steroids. This alters the clinical
appearance so that the lesions have no appreciable scale, and may
be distributed symmetrically. Nevertheless, scraping the edge
will reveal fungus. Stop applying the steroid and for treatment see Fig. 8.37 Tinea incognito: symmetrical and non-scaly plaques due to treatment
p. 233. of tinea with steroids – mycology will be positive
LINEAR LESIONS — allergic contact dermatitis due to plant sap (see p. 182)
Linear lesions occur in the following. — Berloque dematititis due to sunlight and psoralen (from
cosmetics) in contact with skin.
With a normal surface ● Dermatomal – herpes zoster (see p. 179).
● Striae or stretch marks (see Fig. 8.38). ● Dermatitis artefacta – self-inflicted (see p. 260).
● Surgical scars:
— normal, keloid or hypertrophic (see p. 214) STRIAE
— sarcoid can occur in old scars (see p. 213). Linear red/purple plaques occur commonly on the thighs and
● Köebner phenomenon – when due to a scratch will be linear, lumbosacral regions in teenagers. With time they flatten off and
e.g. in psoriasis, lichen planus, plane warts (see Fig. 8.03, p. 197). become atrophic. Similar lesions occur on the abdomen and
● Along the line of blood vessels or lymphatics: breasts in pregnancy, and in the flexures in patients on systemic
— thrombophlebitis: inflammation of superficial veins steroids or using potent topical steroids. No treatment will get rid
— lymphangitis: inflammation of lymphatics associated with of them.
cellulitis (see p. 373)
— sporotrichosis: deep fungal infection in which nodules
occur along the course of a lymphatic vessel (see p. 410).
● Larva migrans – larvae leave a serpiginous track (see p. 428).
● Linear morphoea (see p. 80).
● Dermatomyositis – erythema over metacarpals and along
fingers (see p. 132).
With a scale or warty surface

● Köebner phenomenon – psoriasis and plane warts.
● Present from birth or early childhood down the length of a
limb or around the side of the trunk:
— epidermal naevus (see p. 317)
— inflammatory linear verrucous epidermal naevus
— lichen striatus.
With blistering, exudate or erosions

● Linear contact dermatitis from external agents: Fig. 8.38 Striae: linear stretch marks Fig. 8.39 Striae in patient with
— phytophotodermatitis due to sunlight and plant sap on the back of a teenager psoriasis who has used excessive
brushed onto the skin (see p. 182) topical steroids
LARGE PAPULES AND NODULES (>5 mm) / 213
Trunk and limbs

Chronic erythematous lesions NODULES AND LARGE PAPULES
Normal surface (All lesions >5 mm – normal surface)
Nodules
Fixed in size Gradually enlarging Rapidly enlarging
Firm-hard Previous acne Empties on Purple/orange Pink/red Red/mauve Bleeds easily Onset age
on palpation scar/injury compression colour colour colour after trauma 1–4 weeks
Biopsy Biopsy Biopsy Biopsy Biopsy
DERMATO- KELOID/ HAEMANGIOMA SARCOID/ BASAL CELL LYMPHOMA AMELANOTIC PYOGENIC INFANTILE
FIBROMA HYPERTROPHIC GRANULOMA CARCINOMA 2º CARCINOMA MALIGNANT GRANULOMA HAEMANGIOMA
SCAR MELANOMA (Strawberry
naevus)
see p. 301 p. 214 see p. 312 pp. 213, 215 see p. 330 p. 216 see p. 305 see p. 334 p. 216
SARCOID
Multiple mauve/purple papules or plaques on the trunk and change needs to be biopsied to establish the histological diagnosis.
limbs may be due to sarcoid, especially if old scars are affected. Skin histology is usually diagnostic but you will also need to
Sarcoid can present with very different features – papules, plaques X-ray the chest, check the eyes and do a serum calcium to confirm
or even hypopigmented patches. The clinical appearance can be the diagnosis. If there is evidence of sarcoid elsewhere, referral to
very varied. For this reason, any rash where there is no surface a chest physician is advised.
TREATMENT: SARCOIDOSIS KELOID AND HYPERTROPHIC SCARS

Hypertrophic scars are an overgrowth of scar tissue confined to
Whether or not you treat the skin lesions will depend on whether there is sarcoid the site of injury, while keloid scars grow out beyond the original
elsewhere. Topical steroids are not of any help. Systemic steroids work well but cannot site of injury. The commonest sites for keloid scarring are on the
be justified for skin lesions alone (the side effects [see p. 51] may outweigh the
front of chest, around the shoulders, on the earlobes (see p. 162)
benefits). If the lesions are not visible and do not itch, the patient may be prepared to
and at the back of the scalp (see p. 96).
put up with it. Methotrexate 10–25 mg (see p. 52) once a week may be used as an
alternative to systemic steroids.
Fig. 8.40 Plaque of sarcoidosis on the back and Fig. 8.41 Close-up of sarcoid papule and plaques Fig. 8.42 Hypertrophic scars on chest in black skin
arm; the colour gives a clue to diagnosis but a secondary to acne
biopsy needs to be done to confirm this
TREATMENT: KELOID SCARS
Injection of triamcinolone 10 mg/mL directly into the scar will flatten it off and reduce
the red colour. Use a 25-gauge needle rather than a smaller one, because considerable
pressure is needed to get the triamcinolone into the scar. Repeat every 4–6 weeks until
the scar is flat. The resulting scar will be atrophic with obvious telangiectasia. You will
need to warn the patient about this. An alternative is Haelan (fludroxycortide) tape
applied daily to the scar for up to 6 months.
Silicone gel has been shown to be effective, especially in preventing keloids developing
after surgery at high-risk sites. Various formulations from gels to sheets are available
over the counter.
The pulse dye laser will improve the pruritus and erythema of scars but will not reduce
the thickness. Re-excision of the scar is contraindicated but sometimes this may work
if, following surgery, you inject triamcinolone around the wound or irradiate it within
24 hours with superficial X-rays (1–3 fractions of 7 Gy).
Fig. 8.43 Keloid scars secondary to acne
GRANULOMATOUS INFILTRATES IN THE SKIN

A granuloma is strictly a histological term referring to a collection
of monocytes, macrophages, epithelioid and giant cells in the
dermis. It occurs in response to a persistent irritant such as a
foreign body (lipid, oil, glass fibre, talc, silica, metals) or infection
(tuberculosis, leprosy, atypical mycobacterium, fungi). Quite often
no obvious cause for a granuloma is found. Clinically, granulomas
are indurated nodules, orange to purple in colour with a normal
surface. They tend to grow very slowly. Diagnosis is made by skin
biopsy for histology and culture looking for atypical mycobacteria
(incubate at <30°C), tuberculosis or fungi. A foreign body can be
identified on histology by using polarised light. Treat any infection
(atypical mycobacteria, see p. 410; tuberculosis, see p. 128; leprosy,
see p. 283; fungus, see p. 47) and surgically excise foreign bodies.
Fig. 8.44 Granulomas secondary to insulin injections in the thigh; a lymphoma
would look the same – a biopsy is necessary to confirm the diagnosis
Fig. 8.45 B-cell lymphoma on calf Fig. 8.46 Metastatic breast carcinoma Fig. 8.47 Amelanotic melanoma on
on the neck cheek with enlarged lymph gland in
neck (indicated with arrow)
LYMPHOMA, CARCINOMA, SARCOMA, AMELANOTIC MELANOMA INFANTILE HAEMANGIOMA

A cutaneous B-cell lymphoma usually presents as a rapidly growing red/purple (STRAWBERRY NAEVUS)
indurated nodule with no surface changes. There may be one or several lesions, and in An accurate history of when it occurred
many instances is not associated with an internal lymphoma; a full systemic workup is is vital in making the correct diagnosis
necessary, however. Cutaneous B-cell lymphoma nodules on the leg have a particularly for vascular lesions in childhood. A
poor prognosis and need early histological identification. Cutaneous T-cell lymphoma can lesion present at birth is a vascular
mimic eczema or psoriasis (see p. 231). malformation, and these will never
resolve. The commonest is the capillary
Lymphoma, granuloma, metastatic carcinoma in the skin, a soft tissue sarcoma or
malformation (port wine stain, see p. 127).
an amelanotic malignant melanoma can all look the same, presenting as nodules or
indurated plaques with no surface change (because the epidermis is usually unaffected). Haemangiomas occur after birth and
Diagnosis can only be made by skin biopsy. the commonest is the strawberry naevus
(infantile haemangioma). These red
nodules are quite unmistakable. They
a b c
Fig. 8.48 (a) Infantile haemangioma at age of 14 months; (b) same patient at age of 5 years; (c) same patient at age of 13 years
are not present at birth but appear during the first 4 weeks of Treatment: Infantile haemangioma
life. They grow quite quickly up to the age of 12–24 months,
and then they gradually and spontaneously involute. During Most lesions will resolve spontaneously so they should be left alone to do so. Treatment
this phase the colour becomes blue/purple, and as the nodule is only needed if very large or when there are complications such as bleeding,
shrinks the overlying skin becomes slightly flaccid. Most lesions thrombosis or interference with function (e.g. eyesight, eating, airway obstruction,
resolve completely by the age of 10 years (70% by 7 years, 90% by defecation). Treatment with propranolol 1–2 mg/kg/day with feeds for up to 12
months will rapidly resolve the lesion. This is initially administered as an inpatient
9 years), but may leave some residual flaccidity of the skin. The
by a dermatologist or paediatrician. Side effects include bradycardia, heart failure,
main problem is a cosmetic one, but if traumatised, haemorrhage hypotension, cardiac conduction disorders, bronchospasm, weakness and fatigue,
and ulceration can occur. Very rarely platelet consumption can disturbed sleep, and hypoglycaemia. Blood pressure and heart rate are monitored
occur causing thrombocytopenia (Kasabach–Merritt syndrome). weekly in the community. Topical β-blockers such as 0.1% timoptol gel applied five
If the child has multiple strawberry naevi or an odd segmental times daily for 6 months can also be used in cases of poor response to oral propranolol.
presentation (e.g. craniofacial/sacral), refer for investigation to
exclude systemic haemangiomatosis.
Trunk and limbs

Chronic erythematous rash SINGLE OR FEW SCALY PLAQUES
Scaly surface
Plaques: single or few
Itch++ No/slight itch
Poorly defined Well defined Variable in extent Long history >6 months
border border over time Slow increase in size
Lichenified Edge accentuated/ No increased Profuse scale on Edge not raised Raised rolled Unilateral, around
central clearing scale on scratching edge nipple
scratching
ECZEMA LICHEN TINEA DISCOID PSORIASIS BOWEN’S SUPERFICIAL PAGET’S

SIMPLEX CORPORIS ECZEMA DISEASE BASAL CELL DISEASE
(Dry type) CARCINOMA
see p. 235 p. 219 p. 219 see p. 243 see p. 225 p. 220 p. 220 p. 221
SCALY LESIONS / 219
LICHEN SIMPLEX TREATMENT: LICHEN SIMPLEX TINEA CORPORIS

Lichen simplex is a well- (RINGWORM)
defined itchy plaque with If the patient stops scratching it will get better, but this is often easier said than done. Ringworm of the body is due
increased skin markings on The patient may need to look at the circumstances in his or her life that are causing him to dermatophyte fungi, which
or her to scratch and deal with or come to terms with them.
the surface (lichenification) live on keratin, so the clinical
due to persistent scratching. Apply a very potentUK/group 1USA topical steroid such as 0.05% clobetasol propionate picture is of one or more pink,
The commonest sites are the (DermovateUK/TemovateUSA) bid, or Haelan tape daily. This will reduce the itching. Once scaly plaques, which gradually
occiput, ankles, elbows and this has happened, reduce the strength of the steroid to a moderately potentUK/group extend outwards and heal from
genitalia. Single or multiple 4–5USA one. If topical steroids do not work, try an occlusive bandage Zipzoc (left in place the centre, forming a ring (see
for a week at a time).
sites may be involved. p. 233).
Fig. 8.49 Lichen simplex on sacrum Fig. 8.50 Lichen simplex on elbow Fig. 8.51 Tinea corporis on dorsum of hand
SUPERFICIAL BASAL CELL CARCINOMA

On the trunk, basal cell carcinomas often spread superficially and
slowly over several years, presenting as a flat, scaly plaque (see
Fig. 8.52). The edge of the lesion is just like a basal cell carcinoma
elsewhere with a slightly raised, rolled edge; this can be seen
more easily if the skin is put on the stretch (see Fig. 1.81, p. 16).
The centre of the lesion may be scaly and can be confused with
Bowen’s disease, or even eczema. A biopsy will distinguish
between them.
TREATMENT: SUPERFICIAL BASAL CELL CARCINOMA
If the lesion is small, excision is the best option. Lesions bigger than 2 cm or where
excision is difficult can be treated with the following:
● imiquimod 5% (Aldara) cream five times a week for 6 weeks; if the inflammatory Fig. 8.52 Superficial basal cell Fig. 8.53 Bowen’s disease: plaque on
reaction is very severe, stop treatment to allow it to settle down, and recommence carcinoma with ‘rolled’ edge lower leg looking like psoriasis
at three times a week, to complete a total of 6 weeks’ treatment (see also Fig. 9.72,
p. 291)
● photodynamic therapy using methyl aminolevulinate (Metvix) cream and a red light
source (see p. 63).
Both produce an inflammatory reaction leading to resolution of the lesion.
BOWEN’S DISEASE
Bowen’s disease is an intraepidermal squamous cell carcinoma
(in situ). It presents as a fixed red, scaly plaque that looks like
psoriasis or eczema. It does not respond to treatment with topical
steroids but gradually expands in size over many months. It can
occur on any sun-exposed site but characteristically occurs on the
lower legs. Multiple lesions are common. Change to an invasive
a b
squamous cell carcinoma is uncommon and only occurs after
many years. Fig. 8.54 (a) Bowen’s disease on finger; (b) after 4 weeks’ treatment with
5-fluorouracil cream
SCALY LESIONS / 221
TREATMENT: BOWEN’S DISEASE
The options for treatment include:

● cryotherapy
● 5-fluorouracil (EfudixUK/EffudexUSA) cream bid for 4 weeks
● imiquimod (Aldara) cream three times a week for 12 weeks (see pp. 34, 291)
● photodynamic therapy (see p. 63)
● curettage and cautery
● excision.
Which you choose will depend on the size and site of the lesion, what facilities are
available and the convenience of the patient. Only curettage and excision will give you
histology unless a biopsy is taken first. Care should be taken on the lower legs because
all these options can lead to leg ulceration.
Fig. 8.55 Paget’s disease of the nipple

PAGET’S DISEASE OF THE NIPPLE
This is due to invasion of the skin around the nipple by malignant
cells derived from an intraductal carcinoma. There is a unilateral
red, scaly plaque surrounding the nipple with or without crusting.
It gradually increases in size and is often mistaken for eczema. The
fact that it is unilateral and does not respond to topical steroids
should alert you to the diagnosis, which can be confirmed by a
skin biopsy. Patients should be referred to a breast surgeon.
ECZEMA OF THE NIPPLE AND AREOLA

Eczema of the areola and nipple is much more common than
Paget’s disease and may or may not be associated with atopic
eczema. A red, scaly, itchy rash confined to the nipple and areola
of one or both breasts is quite common in teenagers and young
women particularly in Africans. Treatment is the same as for
eczema elsewhere (see p. 239).
Fig. 8.56 Eczema on and around nipple


Chronic erythematous rash MULTIPLE SCALY PAPULES
Scaly surface
Multiple papules (<1 cm)
Profuse/detached scale Fine scale Rough scale
Scale removed Profuse silver Scattered papules on trunk Young, outer Elderly, type I
in one piece scale arms, thighs skin, sun-
exposed sites
Discrete papules Well-defined red Nasolabial Burrows on Follicular Poorly defined

lesions scale/dandruff fingers lesions feels rough
PITYRIASIS* GUTTATE SEBORRHOEIC SCABIES KERATOSIS SOLAR

LICHENOIDES PSORIASIS* ECZEMA* PILARIS KERATOSES
p. 223 p. 222 see p. 205 see p. 248 see p. 324 see p. 326
*If the patient is unwell, has lesions on palms and soles, lymphadenopathy, consider
secondary syphilis (see pp. 207, 353). Fig. 8.57 Guttate psoriasis
GUTTATE PSORIASIS
This is an acute form of psoriasis that appears suddenly It may be the first manifestation of psoriasis or it may occur in
10–14 days after a streptococcal sore throat. The individual lesions someone who has had psoriasis for years. It differs from small
are typical of psoriasis, being bright red and well demarcated with plaque psoriasis because there is no variation in size of the lesions.
silvery scaling, but all the lesions are uniformly small (0.5–1 cm Since it is usually not itchy, it can be confused with pityriasis rosea
in diameter). The rash may be very widespread, appearing more and secondary syphilis (see pp. 205 and 207). For treatment see
or less overnight. It gets better spontaneously after 2–3 months. p. 230.
SCALY RASHES / 223
PITYRIASIS LICHENOIDES TREATMENT: PITYRIASIS LICHENOIDES

This rash is rarely recognised by non-
dermatologists. The chronic form consists This responds well to ultraviolet light. In the summer
of widespread small, red-brown, scaly the patient can get out into the sunshine and
expose the affected skin for half an hour each day.
papules, from which the scale can be
Alternatively, narrowband ultraviolet light (UVB) three
‘picked off’ in one piece (the ‘mica scale’).
times a week for 6–8 weeks clears it up. Rarely PUVA
It occurs mainly in children and young treatment needs to be given (see p. 61). Tetracycline
adults and lasts for several months. It often 500 mg qid or lymecycline 408 mg daily for 3 weeks
improves in the sun. may work well in adults.
The acute form presents as necrotic Fig. 8.59 Pityriasis lichenoides chronica: close-up of
papules, erosions or ulcers, and it may heal mica scale
with scarring. The more typical chronic
scaly lesions may also be present. The
diagnosis of pityriasis lichenoides is made
by histology, which shows a cutaneous
vasculitis.
Fig. 8.58 Pityriasis lichenoides acuta: small necrotic Fig. 8.60 Pityriasis lichenoides chronica: scaly papules
papules

Chronic erythematous rash MULTIPLE SCALY PLAQUES (>1 cm)
Scaly surface
Multiple plaques
Scratch lesions vigorously with nail, note colour
Profuse scale Greasy Scale more No/little scaling

Red colour scale obvious Pink/orange colour
Orange-brown
colour
Discrete well Papules Small lesions Discrete well Coalescing

defined lesions coalescing coalescing defined border papules defined
Normal skin Trunk and Upper trunk Expanding Scale only Crusts present
between lesions axillae ring as well as scale
Check elbows, +ve family Scale within Individual Finger-like lesions Accentuated Uniformly Irregular shape
knees, scalp, nails history ring lesions are on trunk/limbs edge > centre involved in
different colours centre
Biopsy: Mycology Biopsy: Biopsy: Mycology Biopsy;

acantholysis +ve microscopy clonal T-cells non-specific +ve -ve spongiosis
PLAQUE DARIER’S PITYRIASIS ANNULAR CUTANEOUS CHRONIC TINEA DISCOID ECZEMA

PSORIASIS DISEASE VERSICOLOR ERYTHEMA T-CELL SUPERFICIAL CORPORIS ECZEMA
LYMPHOMA SCALY DERMATITIS
p. 225 see p. 247 see p. 203 see p. 210 p. 231 p. 231 p. 233 p. 243 p. 235
SCALY RASHES / 225
CHRONIC PLAQUE PSORIASIS (psoriatic arthropathy). The severity of the psoriatic arthropathy is
Psoriasis is a common chronic, inflammatory skin disease that often unrelated to the extent of the skin involvement.
affects about 2% of the population worldwide. The inheritance
of psoriasis is probably controlled by several genes, so that the Sharp cut-off between normal
occurrence within families is variable. It is characterised by rapid and abnormal skin = well-defined border.
turnover of epidermal cells so that the keratin is immature and Immature keratin (parakeratosis)
therefore scaly. This is a result of abnormalities in both innate and = silvery scale when scratched.
adaptive immunity. Psoriasis was thought to be a Th1-mediated
disease, because of a predominance of Th1 pathway cytokines, Dilated capillaries = red colour.
such as tumour necrosis factor-α (TNF-α), interferon gamma If scratching continued these are reached
(IFN-γ), interleukin–2 (IL-2) and IL-12 in psoriatic plaques. = small bleeding points.
However, in the last few years, a far more complex interplay
has been demonstrated, where IL-23 secreted by dendritic cells
activates Th17 T-cells to produce IL-17A and IL-17F, which drive Rapid proliferation of epidermal cells = immature keratin
at surface and prolonged rete pegs.
the keratinocyte proliferation seen in psoriasis. Increased levels
of vascular endothelial growth factor from activated lymphocytes Fig. 8.61 Correlation of pathology of psoriasis with physical signs
causes vascular dilation and hyperplasia, while mast cells secrete
large amounts of TNF-α, IFN-γ and IL-8, recruiting the large
numbers of neutrophils seen in plaques. Neutrophils then further
recruit and activate T lymphocytes and the cycle continues, which
the new biologic therapies aim to block.
Psoriasis can occur at any age but most often begins between the
ages of 15 and 25 years. The clinical features can be explained by
the pathology (see Fig. 8.61). The lesions are bright red in colour,
have clearly defined borders (edges) and a silvery scale. The scale
becomes more obviously silvery when scratched (see Figs 1.45 and
1.46, p. 11), comes off easily and may make a mess on the floor.
Characteristically the lesions are symmetrical, commonly affecting
the elbows, knees, sacral area and lower legs, but any part of the
skin can be involved, including the scalp and nails. Most patients
only have a few plaques but psoriasis can become very extensive.
A small proportion will have involvement of their joints as well Fig. 8.62 Plaque psoriasis on elbows
TREATMENT: PLAQUE PSORIASIS
Assess the following. TREATMENT OPTIONS

a. The extent of body coverage, and the number and size of lesions as this will ● Emollients and salicylic acid ointment BP are useful for softening scale.
determine the type of treatment required (see Table, p. 227). ● Vitamin D3 analogues are more effective than emollients and useful if used frequently
b. The disease severity using these simple descriptive terms: clear, nearly clear, mild, and regularly.
moderate, severe, very severe. ● Tar and dithranol are messy and are rarely used these days.
c. Quality of life issues: the physical, social and psychological impact (i.e. any arthritis, ● Topical steroids are very effective, but strong ones need to be used for short periods
depression or work issues). You might want to use a quality of life questionnaire to only; unfortunately, relapse or even rebound (psoriasis worsens afterwards) is
assess this and progress after treatment. generally the rule. Combination with a vitamin D3 analogue may reduce steroid side
d. Any co-morbidities such as cardiovascular risk (if psoriasis severe). effects.
● 0.1% Protopic ointment or a topical retinoid (0.05% tazarotene) can be tried.
Adopt a stepladder approach: try the first option and move down the list if the initial ● Sun exposure and holidays will help if possible.
option is not effective. ● Extensive psoriasis will need the help of a dermatologist at a specialist centre.
Fig. 8.63 Psoriasis in black skin: the clinical features Fig. 8.64 Psoriasis showing post-inflammatory Fig. 8.65 Widespread psoriasis that requires
are exactly the same as in white skin hyperpigmentation and some erythema on the ultraviolet light treatment or systemic therapy
active areas
SCALY RASHES / 227
Summary of treatment of psoriasis

Few localised plaques Large plaques Guttate psoriasis or widespread small Widespread plaques
(<2% surface area) (2%–10% surface area) plaques (>10% surface area)
General practice 1. Emollients 1. Vitamin D3 analogue 1. Emollients Refer to specialist for:

choice 2. Keratolytics 2. Vitamin D3 analogue and steroid 2. Tar cream (e.g. Exorex lotion – not 1. narrowband UVB
3. Vitamin D3 analogue combination (e.g. Dovobet) alternating cream) 2. day treatment with tar or dithranol (if
4. Dithrocream, Miconal short contact with an emollient every 2 weeks 3. Recreational sun exposure available)
therapy 3. Protopic ointment especially for the face 3. PUVA
5. Potent topical steroid (max 4 weeks 4. systemic treatment, e.g. methotrexate
only) ± salicylic acid (Diprosalic or ciclosporin
ointment) 5. biologics, which should be given if the
above fail to control the disease
Specialist’s Retinoid (tazarotene) gel or cream Narrowband UVB therapy Narrowband UVB phototherapy
alternative Dithranol in Lassar’s paste or crude coal
tar ointment – either of these combined
with UVB as a day treatment
Keratolytics and moisturisers Coal tar
Many patients are content to reduce the scaling of psoriasis with emollients containing For very superficial or very numerous small plaques of psoriasis, tar is easier to use than
urea or lactic acid (Lacticare, Calmurid), or salicylic acid ointment BP (2%). dithranol because it can be rubbed all over the skin without taking any special care. For
superficial plaques use a proprietary cream containing coal tar solution (see p. 34). For
thicker plaques, crude coal tar can be used. This is very messy and is usually used in a
Vitamin D3 analogues day care unit or as an inpatient (see p. 230).
● Calcitriol (Silkis) ointment: apply once daily

● CalcipotriolUK/calcipotrieneUSA (Dovonex) ointment: apply twice a day Vitamin D3 analogue and topical steroid
● Tacalcitol (Curatoderm) ointment: apply once daily
A vitamin D3 analogue can be combined with a potentUK/group 2–3USA topical steroid,
These are the first-line treatment for most patients with psoriasis because they are not either each applied separately (vitamin D3 analogue in the morning and steroid in the
messy to use. The main problem is that they do not clear psoriasis, usually only reducing evening) or as Dovobet gel or ointment (calcipotriol + betamethasone). The combination
the scaling and thickness of the plaques. To be at all effective they must be applied is more effective than the vitamin D3 analogue alone, and using the combination
twice daily regularly. They can irritate the skin of the face and flexures (calcitriol less so probably diminishes steroid side effects. It should not be used for more than 4 weeks at
than the others). a time because of the long-term side effects of topical steroids (see p. 33). A steroid-free
interval of 2 weeks (using a moisturiser or vitamin D3 analogue) should be maintained
between treatments.
DithranolUK/anthralinUSA
DithranolUK/anthralinUSA is rarely used because it stains skin (see Fig. 8.69) and clothing
and can irritate normal skin. In selected individuals with a few plaques it can be applied
using the short contact method. In this method DithrocreamUK/DrithocremeUSA is applied
by rubbing it carefully on to the individual plaques. Leave it on for 30 minutes and then
wash off with soap and water. If no irritation occurs, the strength of dithranol cream
can be increased every 2–3 days from 0.1% to 0.25%, to 0.5%, to 1.0% and finally to
2%. When the psoriatic plaques go brown (see Fig. 8.69), stop using the treatment. The
brown colour fades after 7–10 days.
Alternatively, 1% and 3% Micanol cream, or Psorin ointment can be used.
The application of dithranol in Lassar’s paste in a hospital or clinic setting (see p. 230)
will clear psoriasis in about 3 weeks. It is time-consuming and messy, but in some
instances it can lead to prolonged periods of remission.
Fig. 8.66 Psoriasis treated with topical steroids: plaques have become flat with
little scale but they still are red
SCALY RASHES / 229
Topical steroids
The use of topical steroids in psoriasis is controversial. They are effective in clearing
psoriasis without being messy, and are thus the mainstay of treatment in Europe and
the United States, but they are used less often in the United Kingdom. There is no doubt
that very potent topical steroids, if used extensively, can result in worsening of psoriasis
when the treatment is stopped (rebound) or even generalised pustular psoriasis. They
will also cause all the other side effects of topical steroids (see p. 33).
The problem is how to use them without running into problems. We would recommend
the following options.
● Use steroids in the potent group on the body and the moderate potency group on
the face.
● Use at any one site for a maximum of 4 weeks, after which they should be not be
used for a further 2 weeks – use a moisturiser.

● If the psoriasis rebounds or relapses quickly then other treatments need to be
considered. If maintenance treatment is needed, restrict this to two applications a

week (weekend treatment).
● Restrict the amount of steroid to 100 g per week.
Fig. 8.67 Psoriasis treated for Fig. 8.68 Dithranol in Lassar’s paste
4 weeks with Dovobet gel (right leg) being applied to plaques with a
and Dovonex ointment (left leg): the spatula in Ingram’s regimen
plaque on the right leg is flatter and Sun exposure
less scaly than on the left
Recreational sun exposure, provided that burning is avoided, will generally be beneficial.
Topical retinoids and immunosuppressants
Fig. 8.69 Staining of hands A topical retinoid such as 0.05% or 0.1% tazarotene gel or cream (ZoracUK/TazoracUSA)
following application of applied twice a day works by modifying abnormal epidermal differentiation. It can be
dithranol: when the stain
effective but, like all topical retinoids, it produces marked skin irritation. Applying it once
remains on the surface, this
means that the exfoliation daily can reduce this. It is a useful treatment for a few isolated plaques.
caused by psoriasis has ceased 0.1% tacrolimus (Protopic) ointment can also be tried for stable plaques, especially on
and therefore the psoriasis will the face.
have resolved – the stain takes
up to 4 weeks to resolve
TREATMENT: GUTTATE AND SMALL PLAQUE PSORIASIS

3b. Goerckerman’s regimen: 2% crude coal tar in white soft paraffin or Lassar’s paste
Guttate psoriasis will clear in 2–3 months. If it is itchy use an emollient. is applied to the psoriasis and covered by a tubular dressing. The strength of tar is
increased to 20% gradually over a 3- to 4-week period. A treatment of 2% or 5%
Ultraviolet light therapy (see p. 60) is very effective but requires attending a hospital or
crude coal tar in Lassar’s paste is a very effective treatment for psoriasis of the face.
clinic three times a week. For those who cannot do this, a tar cream is the most useful
4. The next morning (or later that day for day treatment) the paste is cleaned off with
treatment.
arachis oil or liquid paraffinUK/petrolatumUSA. Tar ointment can be removed with
Refined coal tars (coal tar solution/liquor picis carbonisUK/liquor carbonis detergensUSA) ordinary soap and water.
mixed with a moderately potent steroid ointment can be effective.
Repeat the process daily until the psoriasis has cleared. It is usually possible to clear
psoriasis in 3–4 weeks by these methods.
TREATMENT: EXTENSIVE PLAQUE PSORIASIS

Ultraviolet light therapy TREATMENT: PSORIASIS – SYSTEMIC THERAPY
Narrowband ultraviolet light therapy or PUVA are effective treatments for extensive Patients who fail to respond to topical therapy or narrowband UVB, or those who
larger plaque psoriasis, but the lifetime dose of treatment should be restricted (see frequently relapse or have very extensive disease, require systemic treatment. The
pp. 60–1). following are available:
● PUVA (see p. 61)
● methotrexate (see p. 52)
Day care or inpatient treatment: Ingram’s or Goerckerman’s regimen ● acitretin (see p. 49)
● ciclosporin (see p. 53)
1. Tar bath: the patient soaks in a bath containing 20–30 mL of a tar emulsion ● hydroyxcarbamide (hydroxyurea, see p. 55)
(Balnatar, LavatarUSA, Polytar, ZetarUSA) for 10–15 minutes. While in the bath the ● fumaric acid esters (see p. 55).
scales can be rubbed off with a soft brush.

These all have serious side effects so should only be initiated by a dermatologist.
2. Ultraviolet light therapy: after getting out of the bath and patting dry the skin, the
patient is exposed to a sub-erythema dose of narrowband UVB (see p. 60). Intolerance or failure of systemic treatment are indications for the use of biologic
3a. Ingram’s regimen: dithranolUK/anthralinUSA in Lassar’s paste is applied carefully agents (see p. 56), monoclonal antibodies that target TNF-α, IL-12, IL-23 and IL-17:
to each psoriatic plaque (see Fig. 8.68) and left on for 24 hours. Over a 3- to ● infliximab
4-week period the concentration of dithranol is gradually increased. Start with ● adalimumab
0.1% dithranol and increase daily by increments of 0.1% up to 1% and then by ● etanercept
increments of 1% up to 10%. Talcum powder is applied to the surface of the paste ● ustekinumab.
to stop it being smudged. The body is covered with Clinifast/Tubifast to prevent

These are extremely expensive but can be very effective, especially when other agents
staining of clothes and bedding. The paste needs to be removed the next day with
have failed. In time, when the price becomes more reasonable and their long-term
arachis oil or liquid paraffin.
effects are known, their use will increase.
SCALY RASHES / 231
CHRONIC SUPERFICIAL SCALY DERMATITIS (DIGITATE CUTANEOUS T-CELL LYMPHOMA (MYCOSIS FUNGOIDES)
DERMATITIS) A T-cell lymphoma is usually confined to the skin. It presents
This is a pink, scaly rash with oblong or finger-shaped plaques as itchy, red, scaly patches (see Figs 8.71a & b) that may mimic
around the trunk. The surface has a fine ‘cigarette paper’ either eczema or psoriasis. The main differentiating feature is
wrinkling. It is usually asymptomatic. It differs from cutaneous that individual lesions are of different colours, so that some
T-cell lymphoma in that the lesions are all the same colour and a patches are pink, others red or orange brown. The patches become
biopsy will show eczema and not a lymphoma. more indurated to form plaques (see Fig. 8.72). These stages of
cutaneous T-cell lymphoma may persist for many years.
TREATMENT: SUPERFICIAL SCALY DERMATITIS
If it itches, narrowband UVB phototherapy will stop the itching temporarily, but it will
not make the rash go away. It is given two to three times a week for 6–8 weeks. Topical
steroids tend not to work.
Fig. 8.70 Chronic superficial scaly dermatitis: note Fig. 8.71a Cutaneous T-cell lymphoma: patch stage Fig. 8.71b Close-up of cutaneous T-cell lymphoma,
finger-like patches patch stage
Late in the course of the disease, tumours develop (see Fig. 8.73) TREATMENT: CUTANEOUS T-CELL LYMPHOMA
from the plaques. The disease may then spread to other organs of
the body and become more aggressive. Progression is, however, All patients should be referred to a dermatologist for confirmation of the diagnosis. In
very variable. The diagnosis is confirmed by skin biopsy and the plaque stage the options are:
● a moderately potentUK/group 4–5USA topical steroid ointment or cream – this may be
polymerase chain reaction to show that the abnormal cells are
monoclonal. all that is needed for many years; it will alleviate the itching and keep the patient
comfortable
● PUVA (see p. 61) given twice weekly for 8–10 weeks may make the rash go away for
a period of months or years.
Once tumours have developed, radiotherapy or chemotherapy will be needed.

For disseminated disease, bexarotene (a retinoid variant), electron beam therapy to
the whole body, extracorporeal photophoresis, monoclonal antibodies and various
chemotherapy regimens are used at specialist centres as required.
Fig. 8.72 Cutaneous T-cell lymphoma: plaque stage Fig. 8.73 Cutaneous T-cell lymphoma: tumour stage
SCALY RASHES / 233
TINEA CORPORIS (RINGWORM)

Ringworm of the body is due to dermatophyte fungi of
the Microsporum, Trichophyton and Epidermophyton species.
Dermatophytes live on keratin, so the clinical picture is of one
or more pink, scaly papules or plaques, which gradually extend
outwards healing from the centre and forming a ring. You should
always consider the diagnosis in any unilateral or asymmetrical
red, scaly rash whether or not it is annular in shape. It is a mistake
to consider all annular rashes as tinea. What should alert you
to the diagnosis is that the lesions tend to be asymmetrical (see
Fig. 5.54, p. 136).
TREATMENT: TINEA CORPORIS
Since the infection is in the keratin layer on the surface of the skin, topical treatment
works better than systemic therapy. The options are: Fig. 8.74 Tinea corporis on the neck: note annular plaque
● an imidazole cream applied twice a day for 2 weeks
● terbinafine (Lamisil) cream applied daily for 7 days.
It is acceptable practice to treat a scaly rash that you think is due to a fungal infection
with an antifungal cream provided you first take scrapings to be sent for mycology (see
p. 20) where the fungal hyphae can be visualised by direct microscopy and cultured. The
patient can be followed up after 4 weeks when the result of the mycology is known. If
the mycology is negative and the rash no better you should reconsider the diagnosis.
It is bad practice to treat scaly rashes with antifungal-steroid combinations to ‘hedge
your bets’. The steroid may make the fungal infection worse, and eczema will respond
better to a topical steroid alone.
Fig. 8.75 Tinea corporis on the back: note the well-defined border
Face, trunk and limbs CHRONIC ECZEMA

Chronic eczema
Begins in Begins in adult life
childhood
Starts on face/ Poorly defined border Well defined border

scalp
Rash behind Rash anywhere Rash on central Lower legs in Rash around Usually limbs Site of contact Forearm, occiput,
knees and in front chest or back elderly ankles over of allergen sacrum, calf
of elbows malleoli
Personal or Scaling around Irregular Varicose veins Scale or Exudate and Patch test Single plaque
family history of nose, ears, fissuring Haemosiderin dried crust wet crust positive Lichenified
atopy scalp pigmentation Excoriated
Yes No
ATOPIC UNCLASSIFIABLE SEBORRHOEIC ASTEATOTIC VARICOSE DISCOID DISCOID ALLERGIC LICHEN

ECZEMA ECZEMA ECZEMA ECZEMA ECZEMA ECZEMA ECZEMA CONTACT SIMPLEX
(Dry type) (Wet type) DERMATITIS
p. 236 p. 235 see p. 205 see p. 384 see p. 384 p. 243 p. 243 p. 242 see p. 219
CHRONIC ECZEMA / 235
CHRONIC ECZEMA/DERMATITIS Chronic eczema is diagnosed by identifying the typical

In this book the term eczema is used for the endogenous eczemas. morphological features of eczema. What you normally see is an
For those due to external factors the word dermatitis is used. In itchy, poorly defined erythematous scaly rash. It is distinguished
the United States the term dermatitis is used for both endogenous from psoriasis by being much less vivid in colour (usually a
and exogeneous causes. nondescript pink), with poorly defined edges and less obvious
scale. Scaling is present but does not become either more obvious
The word eczema comes from a Greek word meaning to bubble or silvery in colour when scratched. Persistent scratching,
through (see Fig. 7.36, p. 189), and the hallmark of eczema (or leads to thickening of the skin, with increased skin markings
dermatitis) is the presence of vesicles. In practice, vesicles are (lichenification, see Fig. 8.81).
only seen in acute eczema (see Fig. 8.76), but the patient will often
tell you that small blisters have been present in the past, and Any symmetrical eczema on the trunk and limbs that does not fit
the remains of these are seen as small pinhead-size crusts (see any of the recognisable patterns (i.e. atopic, seborrhoeic, discoid,
Fig. 7.37, p. 189). varicose, hand and foot) is called unclassifiable eczema.
Fig. 8.76 Acute eczema with vesicles Fig. 8.77 Chronic eczema: poorly Fig. 8.78 Chronic eczema in Fig. 8.79 Lichenified eczema
and erosions defined pink, scaly rash pigmented skin, brown not pink
ATOPIC ECZEMA where the inflammation reduces the barrier, allowing penetration
Atopy means an inherited predisposition to eczema, asthma or of irritants and allergens (especially bacteria), which causes
hay fever, and atopic individuals may have one or all of these further inflammation. Autoimmunity and the production of IgE
manifestations. It is becoming recognised that an inherited antibodies is likely to be a by-product of these factors.
defective skin barrier is important in its cause. The protein The eczema usually begins between the ages of 3 and 12 months
filaggrin helps bind keratin fibres in the stratum corneum, and this (asthma at age 3–4 years and hay fever in the teens) on the scalp
protein has been found to be defective in atopic eczema. The result and face, and may or may not spread to involve the rest of the
of this is that corneocytes are deformed, natural moisturising body. When children get older it may localise in the flexures,
factors are reduced and an increase in skin pH promotes particularly the popliteal and antecubital fossae. It is very itchy so
inflammation. The defective barrier then results in loss of water, excoriations and lichenification (see Fig. 8.81) may be seen, and if
dryness of the skin and penetration of irritants and allergens such children rub rather than scratch, the nails may become very shiny.
as house dust mites, pollen and bacteria. The developing immune 50% of such children will also have ichthyosis (also associated
system in infants becomes unbalanced with Th-2 lymphocytes and with a filaggrin defect) with dry skin and increased skin markings
cytokines predominating over Th-1 cells. A vicious circle develops on the palms and soles. In 90% of children the eczema will clear
Fig. 8.80 Atopic eczema in an adult: note the symmetrical, pink, poorly defined Fig. 8.81 Lichenification on flexor Fig. 8.82 White dermographism
rash – there is little scale, but it is present if you look carefully aspect of the wrist
spontaneously by puberty, but in a small minority it will persist

into adult life or become active again later. A few of these will
have very extensive and troublesome eczema. Less commonly,
atopic eczema may develop in adult life.
In adults a diagnosis of atopic eczema can be made if there is
a history of infantile eczema, or if they also have or have had
asthma, hay fever, ichthyosis, increased skin markings on the
palms (see Fig. 8.85) and soles, or white dermographism (stroke
gently with your fingernail through an area of eczema: after 30
seconds a white line appears, see Fig. 8.82). A history of atopic
eczema, asthma or hay fever in the immediate family (parents,
siblings, children) is further evidence of atopy.
Fig. 8.83 Atopic eczema on a child’s face: note folds under the eyes
Fig. 8.84 Atopic eczema localised to the popliteal fossae Fig. 8.85 Increased skin markings on the palm in a child with ichthyosis vulgaris
TREATMENT: ATOPIC ECZEMA Treatment plan

Prevention of atopic eczema
Consider the following when planning treatment of atopic eczema.
As it is now recognised that the primary cause of atopy in children is a defective skin barrier, 1. Use emollients routinely for moisturising, bathing and washing.
it is critical to apply moisturisers frequently, especially in infants with a strong family history 2. If the eczema is weeping – dry it up with an astringent such as potassium
of atopy. Irritants such as soap, bubble baths and prolonged immersion in water need to be permanganate or aluminium acetate solution (see p. 30).
avoided. The patient should bathe using one of the dispersible bath oils (see Table 2.01b, 3. For the eczema itself – treat with a topical steroid potent enough to quickly
p. 27) for 10 minutes daily. Secondary skin infections can be prevented by cleansing the control the eczema, and then reduce frequency of application and potency to
skin with a low concentration of antiseptic (e.g. Dermol shower/wash/lotion). maintain control.
4. Immune-modulators are useful as steroid sparing or proactive treatment.
Once eczema starts to develop it is very important to treat it immediately with topical 5. If the patient is awake at night – use a sedative antihistamine.
steroids. The benefit from the reduction of the inflammation far outweighs any perceived 6. If there is infection – use a systemic antibiotic for a week only. Do not use topical
risk from topical steroids. Proactive treatment with a twice weekly application of a topical antibiotics or steroid-antibiotic mixtures.
calcineurin inhibitor (e.g. tacrolimus 0.03%) or a moderately potentUK/group 4–5USA topical 7. Wrapping eczematous skin is useful in controlling acute flare ups or in preventing
steroid ointment to previously affected skin has been shown to reduce the occurrence of excessive scratching in young children.
acute flares of eczema. 8. Other considerations – clothing, reduction in house dust mite, stress.
9. UV phototherapy (see p. 60) or systemic agents such as ciclosporin (see p. 53–4)
or azathiaprine (see p. 54) may be necessary if the above fail to control the
Allergy and eczema disease. These can be provided by dermatologists.
Although patients with atopic eczema have elevated IgE levels to foods, grass pollen,
cats and house dust mites, these allergies do not affect the severity of the eczema. Prick 1. Complete emollient therapy
testing is unhelpful because of multiple false positives. A positive specific RAST test also
does not mean that the allergen is the cause of the eczema. The only way to be sure is to The use of emollients on dry and eczematous skin is an important part of the
avoid the allergen for a week (which will result in improvement in the eczema) and then to treatment and prevention of atopic eczema. Emollients should be used liberally
reintroduce it again to establish a rapid relapse in the eczema. and frequently for moisturising, washing and bathing, even if the skin is clear.
Food allergy (cows’ milk, egg, soya, peanut) may also affect children with eczema, but this Everything that goes on the skin should be emollient based so that the skin barrier
will result in acute urticaria or angio-oedema rather than worsening of the eczema. Some is repaired and maintained. Numerous emollients are available (see Table 2.01a,
children under age 3 also have gastro-intestinal symptoms with a good history of a dietary p. 26), and how greasy these need to be is often a matter of patient choice or trial
trigger. This food intolerance may be temporary, and reintroducing the item several months and error. The drier the skin, the more greasy the moisturiser needs to be. Lighter
later may be possible. (cream) emollients can be used for daytime or summer, and heavier (ointment
based) emollients used at night and in winter. Patients should be offered a leave-on
Airborne allergens cause asthma and hay fever, but these are immediate reactions – runny emollient, a product to wash with (soap must be avoided) and a bath emollient. The
nose, swollen eyes, sneezing or wheezing. Environmental allergens (cats, house dust mite) patient can be offered product testers to find which suit him or her best.
are difficult to avoid, and a positive reaction is generally unhelpful.
3a. Topical steroids

Bathing: soaking in a lukewarm bath for 10–15 minutes every day is helpful provided
10–20 mL of one of the dispersible bath oils has been added (see p. 27). Emollient
Topical steroid ointments are still the mainstay of treatment for atopic eczema. Patients
shower/wash formulations (e.g. Doublebase shower gel, E45 wash cream, QV gentle
or parents are often afraid of using topical steroids because of the widespread publicity
wash) or Epaderm cream should be used instead of soap, detergents or bubble bath,
about side effects. Failure to treat active eczema will cause more harm to the patient by
but these should not be used as a leave-on emollient. Aqueous cream is best avoided as
allowing allergens to penetrate the defective cutaneous barrier.
it contains sodium lauryl sulphate, which is a skin irritant.
You will need to explain that there are different strengths of steroids (see p. 32). Start
Moisturisers should also be applied to the skin after getting out the bath, while the
with 1% hydrocortisone ointment applied daily on the face and skin folds, and on the
skin is still warm and moist. Apply the moisturiser starting at the neck, and smoothing
trunk and limbs use a moderately potentUK/group 4–5USA topical steroid ointment. Short
(not rubbing) it in downwards on the trunk, arms and legs. The moisturiser should be
courses (5 days) of potentUK/group 2–3USA steroids for an acute flare may be necessary
applied first, and left on for 20 minutes before applying a topical steroid.
to get the eczema under control quickly, and for lichenified or thickened plaques.
Humectants such as glycerol, urea, polyethylene glycol and lactic acid are often added
By using a steroid with the appropriate potency to quickly control the eczema and
to emollients as they can increase the horny layer’s capacity to retain water (see p 26).
continuing treatment until completely clear will reduce the likelihood of a rebound
Some products such as Doublebase Dayleve and Oilatum cream contain film-forming
flare. Then taper therapy to alternate days before reducing to proactive treatment:
agents that form an additional protective layer over the surface of the skin, helping to
twice weekly applications of a topical steroid to previously affected skin for up to a
reduce water loss and penetration of irritants and allergens.
month. This has been shown to reduce flares of eczema and improve the quality of
Antiseptics. Emollients which contain antiseptic products such as chlorhexidine and life. Continuous long term use of potent steroids on the face and body folds must be
benzalkonium chloride (Dermol cream, Eczmol cream) may help to reduce bacterial avoided, and a topical calcineurin inhibitor may be used instead (see p. 240).
colonisation and infection, which can exacerbate eczema. However these agents may be
Ointments work much better than creams, since the grease forms an occlusive barrier
irritant so need to be used with caution.
preventing evaporation of water and delivers the steroid more effectively to the
Antipruritics such as lauromacrogols have properties of a mild topical anaesthetic and skin. They are best applied after a bath. First apply a moisturiser all over, and after
have an antipruritic effect (Balneum Plus cream, E45 Itch Relief cream). 20 minutes the topical steroid can be rubbed into the eczematous areas.
Allergen-free products such as ointments or products containing no preservative (e.g. It is important to give the patient enough ointment, and to monitor the amount being
Emollin spray) are useful in patients who are allergic to them. Emollient sprays are used (too little may be as bad as too much). To cover the whole body surface twice a
useful in elderly patients who have difficulty in reaching areas of skin (back, lower legs). day, infants will need approximately 10 g a day (70 g/week); a 7-year-old, 20 g a day
(140 g/week); and adults, 30 g a day (210 g/week) – see fingertip units p. 32. A record
of the amount of steroid prescribed and used (ask the patient or parent to bring back
2. Astringents used tubes) will be helpful in monitoring this. Using too little steroid may be as relevant
as using too much.
Astringents (see p. 30) dry up exudate by coagulating protein. Soak the affected areas
in one of these solutions by applying moistened gauze swabs or by emersion in a bath
or hand basin.
4. Topical immune-modulators 6. Treatment of secondary infection
These drugs work by blocking the molecular mechanisms of inflammation in If the eczema becomes suddenly worse, infection with S. aureus may be the cause. There will
the skin (see p. 34). Two drugs are available: 0.1% and 0.03% tacrolimus be associated pustules or yellow crusting. This is best treated with a systemic antibiotic such as
(Protopic) ointment and 1% pimecrolimus (Elidel) cream. Both can cause flucloxacillin 125–500 mg qid (or erythromycin if allergic to penicillin) for one week only. Do not
a burning/stinging sensation when first used, which stops after about use topical antibiotics or topical steroid–antibiotic mixtures, as these are often ineffective and are
20 minutes and disappears altogether after a few days. Use in the following likely to cause an allergic contact dermatitis.
situations:
If the pustules are umbilicated consider eczema herpeticum (see p. 109). In this condition, the lesions
● proactive (preventative) treatment twice weekly to previously affected areas
often are painful and the patient miserable. Treatment is with an antiviral agent (see p. 180).
● patients with facial, periocular or neck eczema
● patients who have not responded, are using too much or too strong a
steroid, or who have developed steroid side effects

● patients with poor compliance with topical steroids because they are afraid
7. Wrapping techniques
of the side effects
● patients with perioral dermatitis (see p. 115) or rosacea (see p. 122) which
Localised wrapping or occlusion will cool, soothe and protect from scratching inflamed,
has been triggered by topical steroids excoriated or lichenified skin. Zinc impregnated bandages (Zipzoc, Fig. 8.86) or dressings (PB7,
● patients in whom you would otherwise be considering systemic treatment.
Icthopaste) can be applied overnight or left on for longer periods. Because the zinc paste is sticky,
it will need to be covered by a tubular bandage or secondary dressing.
Generalised wrapping with a suit consisting of long sleeved vest, leggings, socks and mittens
5. Antihistamines (Fig. 8.87) is useful for treating widespread itching and eczema. It prevents scratching and the
occlusion provided by the garment allows better penetration of the moisturiser. The affected areas
Sedative antihistamines are useful if the child is not sleeping at night and of skin are treated with a topical steroid ointment, and then the whole body surface is covered
is keeping the family awake. They will not stop the itching, but if given in with a suitable emollient (see p. 26). These garments can be washed and used several times. They
adequate dosage the child will sleep through the night. Start with 5 mL of are available made of viscose (Acti-Fast, Comfifast, Easifast, Skinnies, Tubifast) or silk (Dermasilk,
promethazine (Phenergan 5 mg/5 mL) or alimemazine (7.5 mg/5 mL) elixir Dreamskin, Skinnies). The advantage of silk is that it is cooler, requires less moisturiser on the skin,
which should be given around 6pm in the evening. Double the dose each and does not wear out, but it is more expensive.
night until the child sleeps until morning. Alimemazine forte is available as
Wet wrapping is very effective in bringing a generalised flare of eczema in children and adults
30 mg/5 mL. Children surprisingly can tolerate much higher doses than adults.
under control quickly. It cools the skin, improves moisturisation, prevents scratching and reduces
Neither is addictive and both are quite safe.
the need for topical steroids. Two layers of the therapeutic suits (as above) are put on following
In adults, start with 10 mg of promethazine, hydroxyzine or alimemazine and application of moisturiser and topical steroid. The layer adjacent to the skin is moistened with
double the dose as necessary until the patient sleeps through the night. Non- luke-warm water, squeezed dry and then a second dry layer is put on over this. Many children do
sedative antihistamines (see p. 49) are ineffective in treating eczema. They can not like it initially, but once put on the skin feels so much better that they can feel the benefit.
be tried if sedative antihistamines produce unacceptable drowsiness, or during Parents can spray water onto the inner layer to keep it moist. On removal, if the garment sticks to
the day. the open eczematous areas, it should be soaked off in a bath.
Table 8.02 Information sheet and prescription for child with atopic eczema
Rx
1. Leave on emollient (light cream) ________________ 500 g
apply frequently to all dry or inflamed areas during the day
AND/OR
1b. Leave on emollient (heavy oint) ___________________ 500 g
apply all over after bathing and leave on overnight
2. Wash product _____________________ 500 mL
to be used instead of soap, rub onto skin and wash off
3. Bath emollient _____________________ 250 mL
add to bath water, soak daily for 10–15 minutes
4a. Topical steroid for the face 1% hydrocortisone oint 60 g
4b. Moderately potent topical steroid for the body __________________oint 200 g
apply steroids daily for 2 weeks or until clear. Then apply alternate days for
2 weeks, and thereafter only twice weekly up to a month.
5. Potent topical steroid ________________ oint 30 g
apply daily for up to 5 days if eczema flares up, then revert to moderately potent
steroid (4b) Fig. 8.87 Skinnies, viscose suits in
Fig. 8.86 Zipzoc. On left as removed
6. Sedating antihistamine: promethazine elixir (200 mL) from packaging which can be applied blue or pink worn for wrapping;
directly to skin (right leg), and then they are seamless and non-irritant
OR promethazine/hydroxyzine tablets 10 mg
covered with blue line tubifast (left available on prescription (for sizes see
×56
leg). skinniesuk.com).
take 5 mL or 10 mg around 6pm in the evening, increase dose until sleeping
through the night, reduce dose if morning drowsiness
7. Elasticated viscose garments ___________________ 4 sets
Table 8.02 lists the items that should be prescribed for a patient with atopic eczema. It is suggested
long sleeved vest / leggings / mittens / socks that this table can be reproduced and given to the patient as instructions of what to use where. Fill in
Put on after applying moisturisers and steroid ointment. the product recommended on the blue line.
For suggestions: 1. emollients see Table 2.01a, p. 26;
Either apply single layer dry,
2. wash products and 3. bath emollients, see Table 2.01b, p. 27,
Or moisten first layer with luke warm water, squeeze dry, and put on a second dry 4. and 5. topical steroids, see Table 2.02, p 32,
layer over it. 7. see BNF section A5.8.3
Recommended quantities that should be prescribed are listed on the right.
7. Other considerations ALLERGIC CONTACT DERMATITIS

A well-defined plaque of eczema may be due to
Cotton clothing worn next to the skin is comfortable, while wool is irritating. Reduction in contact with contact with an allergen such as nickel in buckles
house dust or pets may be beneficial. The following measures will help to reduce levels of house dust mite. or jean studs, colophony in elastoplast or chrome
● Vacuum all household carpets (especially around skirting boards), fabrics, and sofas daily.
in leather straps. Creams containing parabens,
● Remove dust regularly with a wet duster or damp mop.
antibiotics, antihistamines or even a topical steroid
● Laminated floor coverings are preferable to carpet in the bedroom as they can be damp mopped.
● Duvet and pillows should have synthetic fillings. Use mattress and pillow covers. Bedding and night
may also cause an allergic dermatitis (see also pp. 106
clothing should be made of cotton.
& 415). The patient will need to be patch tested (see
● Keep humidity levels to around 50%. Dry air will dry the skin. Humid air encourages mould and house
p. 21) by a dermatologist with a special interest in
dust growth. A dehumidifier can be used to remove excess moisture. If the air is too dry, place a bowl of contact dermatitis to interpret positive patch tests,
water under the radiator. some of which may not be relevant. Any allergens
Keep pets out of the bedroom particularly at night and do not allow them to sleep on the bed. Only
thought to be causing the dermatitis will need to
avoid contact with animals if definite improvement away from them (and relapse on re-exposure) can be be avoided. In theory avoidance results in a cure,
demonstrated. although in practice this is not always the case. The
dermatitis is treated with a potentUK/group 2–3USA
Where possible stress at school or work needs to be tackled. Patient and parent support can be provided
topical steroid ointment.
by specialised dermatological nurses, the local dermatology department or the National Eczema Society.
Fig. 8.88 Nickel testing kit: a drop of Fig. 8.89 Allergic contact dermatitis to a nickel belt Fig. 8.90 Allergic contact dermatitis to chrome in
dimethylglyoxime and a drop of ammonia on a buckle watch strap: the leather has been chrome tanned
cotton wool bud rubbed onto the buckle stains pink
DISCOID (NUMMULAR) ECZEMA TREATMENT: DISCOID ECZEMA

This differs from other forms of eczema in that it presents as well-
demarcated round, oval or annular red, scaly plaques. It can be ● In the wet form, dry up the exudate with potassium permanganate or aluminium
wet or dry. The wet type consists of plaques made up of numerous acetate soaks (see p. 30).
vesicles that break to produce exudate (see Fig. 8.91) and crust (see ● Use a moisturiser regularly on the dry type.
Fig. 8.92) on the surface. The dry type is similar but has scale (see ● In both then use a potentUK/group 2–3USA topical steroid ointment applied twice a
Fig. 8.94) on the surface. In young adults the commonest site is day. The response is variable – sometimes discoid eczema can be quite resistant to
treatment or it can relapse quickly on stopping topical steroids.
the dorsum of hands and fingers. In older individuals it is more ● Resistant cases will need to be referred to a dermatologist.
usual on the lower legs. Some patients with atopic eczema, allergic
contact dermatitis or unclassifiable eczema also have discoid
plaques of eczema. Do not confuse it with tinea (see p. 233) just
because it is round.
Fig. 8.91 Wet discoid eczema Fig. 8.92 Crust on surface of discoid Fig. 8.93 Plaques of dry discoid Fig. 8.94 Large plaques of dry discoid
eczema eczema eczema on arm
Trunk and limbs

Chronic erythematous rash GENERALISED RASH
Normal or scaly surface
(>50% body surface)
Generalised exfoliation Generalised erythema Generalised itch,
No rash
Well-defined Poorly defined Elderly/mental Islands of Confluent Excoriations only

plaques retardation normal skin erythema
↑ scale on Lichenification Look for mites Thickened

scratching palms
Fig. 8.95 Pityriasis rubra pilaris
PSORIASIS ECZEMA CRUSTED PITYRIASIS ERYTHRODERMA GENERALISED

(NORWEGIAN) RUBRA PRURITUS
SCABIES PILARIS
see p. 225 see p. 235 see p. 250 p. 244 see p. 194 see p. 252
TREATMENT: PITYRIASIS RUBRA PILARIS
The majority of cases resolve spontaneously in

PITYRIASIS RUBRA PILARIS
1–3 years. Treatment with a systemic retinoid such as
Pityriasis rubra pilaris is a rare condition of unknown cause. Red macules appear around acitretin 0.75 mg/kg or isotretinin 1 mg/kg will hasten
follicles and gradually coalesce to areas of widespread erythema. Characteristically there this (see p. 49). Topical steroids are not effective but
are islands of spared normal skin. The palms and soles become hyperkeratotic and orange emollients are useful.
in colour and the nails thickened and discoloured distally.
CRUSTING – NO BLISTERS / 245
Trunk and limbs

Chronic erythematous rash
Surface crust, excoriations CRUST AND EXCORIATIONS – no blisters
Widespread papules/plaques/small erosions
No blisters present, small erosions (<1 cm) only
Coalescing papules Plaques Itching+++ Discrete papules (nodules)
separated by involved skin & excoriations only separated by normal skin
Elbows, knees, sacrum Finger webs, palms and No primary rash Excoriated Papules with Pustules present
and scalp involved genitals involved lesions central punctum
Yes No Yes
Biopsy Biopsy = Biopsy = Isolated Grouped Comedones Staph. present

acantholysis spongiosis papules/ papules Upper trunk
nodules and face
Middle-aged +ve family Scabetic

adult history burrows
DERMATITIS GROVER’S DARIER’S ECZEMA SCABIES GENERALISED PRURIGO INSECT ACNE FOLLICULITIS
HERPETIFORMIS DISEASE DISEASE PRURITUS (Nodular) BITES
p. 246 p. 247 p. 247 p. 248 p. 248 p. 252 p. 252 see p. 198 see p. 116 see p. 185
DERMATITIS HERPETIFORMIS The diagnosis can be confirmed by finding: TREATMENT: DERMATITIS HERPETIFORMIS
This is a disease classically of young ● tissue transglutaminase IgA/IgG
adults and it presents with severe itching, (tTG), anti-gliadin or anti-endomysial Initial treatment with dapsone, 50–150 mg daily is
particularly at night. Grouped vesicles antibodies in the blood. required. This will stop the itching within a few hours
● a subepidermal blister containing and is usually dramatic. Check a full blood count
in the distribution of psoriasis (elbows,
polymorphs on skin biopsy. before starting dapsone, because it causes haemolysis
knees, sacrum, scalp) are quickly scratched
of red blood cells. This normally occurs within a few
away to leave pink excoriated papules and ● deposits of IgA in the upper dermis on
days of starting treatment, so the blood count should
plaques. It is unusual to see blisters and the immunofluorescence of normal skin. be repeated after one week. Most patients will show
rash can be confused with eczema. It is an ● subtotal villous atrophy (as in coeliac
some haemolysis and methaemoglobinaemia. The side
important, if uncommon, disease because disease) on jejunal biopsy. effects can be minimised by giving cimetidine 400 mg
it is associated with a gluten enteropathy. tid with the dapsone.
A gluten-free diet will eradicate the IgA from the
dermal papillae in 9–12 months and the itching will
then stop. Although not pleasant, patients should be
encouraged to stick to a gluten-free diet so that the
dapsone may be stopped and to prevent the long-term
risk of small bowel lymphoma from developing (the
risk is the same as for coeliac disease).
Fig. 8.96 Typical distribution of dermatitis Fig. 8.97 Dermatitis herpetiformis: Fig. 8.98 Dermatitis herpetiformis: typical grouped
herpetiformis excoriated papules on elbows small vesicles on trunk
GROVER’S DISEASE (ACANTHOLYTIC DARIER’S DISEASE TREATMENT: DARIER’S DISEASE

DERMATOSIS) This rare condition is inherited as an
This is a very itchy rash that occurs on autosomal dominant trait. The rash For localised areas use 0.025% retinoic acid cream
the trunk (usually middle-aged men). It is consists of follicular papules that coalesce or a topical steroid–antibiotic mix twice a day. For
extensive disease use acitretin 0.5–1 mg/kg/day
made up of itchy papules with an eroded into plaques affecting the trunk, upper
which will need to be prescribed by a dermatologist.
surface. Individual papules are discrete arms, face and flexures. The surface is
Photodynamic therapy can also be helpful in some
and usually 2–3 mm in size. The rash lasts covered with a yellow-brown, greasy crust. patients.
from 2 weeks to many months and tends to A skin biopsy is diagnostic. Other changes
remit and relapse. Diagnosis is established are longitudinal ridging of the nails with
by skin biopsy, which shows acantholysis V-shaped notches at the ends (see Fig.
(loss of cohesion) of the epidermal cells. 14.07, p. 438), pits on the palms and soles,
Treatment is unsatisfactory, but it is worth and plane wart-like papules on the dorsum
trying anti-itch/anaesthetic emollients of the hands and feet.
(Balneum plus cream, E45 itch cream) and
a moderately potent topical steroid.
Fig. 8.99 Close-up of Grover’s disease: eroded Fig. 8.100 Typical distribution of Darier’s disease Fig. 8.101 Close-up of follicular papules of Darier’s
papules on chest disease
SUBACUTE ECZEMA
The physical signs of eczema are the result of inflammation of
the skin. In the acute phase, vesicles and exudate are seen in
the epidermis (spongiosis, see p. 189). Once the acute phase has
settled, any exudate dries, causing crusting and erosions. We call
this subacute eczema. Intense itching results in excoriations and
erosions. These physical signs can also occur in any very itchy
rash (generalised pruritus, dermatitis herpetiformis), when there
is breakdown of the epidermis (acantholysis – Darier’s disease,
Grover’s disease, pemphigus), or with non-specific inflammation
of the epidermis (scabies or eczematous drug rash). In all these
conditions blisters are unlikely to be seen.
Intact blisters will be seen if the blistering occurs at the dermo-
epidermal junction (pemphigoid) or is intraepidermal on
the palms and soles where the stratum corneum is thickened Fig. 8.102 Subacute eczema: erosions and crusts
(pompholyx eczema). For types of eczema and treatment, see
p. 234.
SCABIES
Scabies is an infestation with the human scabies mite Sarcoptes
scabiei. It is transmitted by prolonged skin-to-skin contact with
someone who has it (usually by lying next to someone in bed
all night or by holding hands). A fertilised female has to be
transferred for infestation to take place. She will then find a
place to lay her eggs (a burrow). Between 4 and 6 weeks later
a secondary hypersensitivity rash occurs. This is characterised
by intense itching, particularly at night. The rash is made up of
excoriated papules scattered over the trunk and limbs but sparing
the face (except in infants). The diagnosis is confirmed by finding
one or more burrows (often there are fewer than 10 in total to be
found). These are linear S-shaped papules, 3–5 mm in length and
usually along the sides of the fingers or on the front of the wrists.
Fig. 8.103 Scabies: typical rash on hands involving the finger webs
Less commonly they can be found along the sides of the feet, around the Fig. 8.105 Dermoscopy
nipples, on the buttocks or on the genitalia. There is almost always a rash of scabetic burrow
showing the ‘jet contrail’
on the hands and, in males, papules on the penis and scrotum. Other
sign: the mite is a small
members of the family or sexual partners may also be itching. Scabies black dot at the head of
in developing countries can be associated with an increased incidence the jet stream (indicated
of streptococcal infection complications such as glomerulonephritis and by arrow) in this picture
rheumatic fever. Although scratching and skin damage makes colonisation and in Fig. 8.106.
with Staphylococcus and Streptococcus more likely, it is probable that the
scabies mite itself may play a part in allowing these streptococcal antigens
to damage the kidney or heart.
Fig. 8.106 Scabies burrow
Fig. 8.108 (above) Scabies: penile papules
Fig. 8.104 Scabies: rash on trunk Fig. 8.107 (left) Scabies mite and egg (×350)
TREATMENT: HUMAN SCABIES CRUSTED (NORWEGIAN) SCABIES

This is an infestation with the human scabies mite in an individual
It is essential to treat not only the patient but also anyone else who has been in close with lowered immunity, mental retardation or sensory loss. The
contact, even if they are asymptomatic. In practice this means all individuals living in the host response is abnormal leading to the presence of thousands
same house and any sexual partner(s). If there are children in the family, grandparents,
of mites all over the skin. These are shed into the environment,
aunts and uncles, babysitters, neighbours and anyone else who has been holding the
eventually infecting other people. Thick hyperkeratotic scale
children will also need treating.
occurs on palms, soles, flexures and under the nails. Eventually
The idea of treatment is to kill all stages of the life cycle of the scabies mite (eggs, a widespread scaly rash occurs all over the body – this is often
larvae, nymphs and adults) at the same time. A single treatment of 5% permethrin misdiagnosed as eczema. The diagnosis usually comes to light
cream (LyclearUK/ElimiteUSA) or 0.5% malathion lotion (Derbac-M) can be used. when those in contact with the patient develop an itchy rash
The cream or lotion is applied to the whole body surface except the face and scalp
(which is diagnosed as ordinary scabies). To confirm the diagnosis
(including the skin between the fingers and toes, under the finger nails, the genitalia
and the soles of the feet). Treatment is applied at night before the patient goes to bed
remove some of the thick scale from the patient and/or collect
and left on for 24 hours. The whole family and other contacts should be treated at the up scales and other debris from the bed, and examine under the
same time. Twenty-four hours later the patient can have a bath and wash the scabicide microscope. Numerous eggs, larvae, nymphs and adult mites
off. The patient should then change his or her underwear, pyjamas and the sheets on will be seen.
his or her bed. The clothes should be washed and ironed to kill any wandering acari,
although in practice it is very unlikely that any will be left alive at this stage. There is no
need to go to elaborate means to fumigate the house or bedding. 15 g of permethrin
cream or 30 mL of malathion lotion will be needed for a single application (for an adult),
so you can work out how much to prescribe for the whole family. Any residual itching
can be treated with calamine lotion or crotamiton (Eurax) cream twice a day.
Treatment failure in scabies is due to:
● the scabicide not being applied over the whole body
● the contacts not being treated
● the wrong diagnosis.
A similar rash without any burrows can be due to animal

scabies, where mites are found on the pet (usually a dog) and the
diagnosis is confirmed by brushing the animal’s fur on to a sheet
and sending the brushings to the local microbiology laboratory to
identify the mites. Treat the pet for scabies rather than the human
contact.
Fig. 8.109 Norwegian scabies: rash on back of hands looks like eczema
TREATMENT: CRUSTED SCABIES BODY LICE

Body lice live and lay their eggs in the seams of clothing, but
TREATMENT IN AN OLD PEOPLE’S HOME they need to bite humans to obtain their blood. The adult louse is
1. Identify the patient with crusted (Norwegian) scabies. 2–4 mm in length. Body lice thrive when humans are not able to
2. Identify a single room where he or she can be isolated and empty that room of all wash and iron their clothes (which would kill the lice). Lice are
furniture and soft furnishings apart from a bed. Clean the room thoroughly and mainly seen in vagrants but are also seen in refugee camps or in
wash the floor and walls with a suitable detergent. Make up the bed with freshly war situations. Infestation is spread by sharing bedding, clothing
washed and ironed bedding.
or by very close contact. You will not find the lice on the patient’s
3. Treat the patient with permethrin (Lyclear) cream as a single application all over
skin – look along the seams of his or her clothing to find the lice
(including the face and scalp). Crusted scabies does not respond well to ivermectin.
4. After treatment put the patient into the cleaned single room.
and nits.
5. The home should be closed to new residents and visitors until steps 6–9 have been
carried out.
6. Explain to the staff (whether or not they have had direct physical contact with the
patient) what is happening. Explain that the patient has Norwegian scabies and
that whether or not they are itching they will almost certainly have caught it and
will need treatment. Explain that the variety they have caught is ordinary scabies
and not the very infectious kind that the patient has. Explain that they are only
infectious to very close contacts, i.e. immediate family or those with whom they
share a bed.
7. To remove any mites from the environment wash and iron all bedding, curtains and
other soft furnishings in the patient’s bedroom and any public rooms that he or she
has used. Wash or spray the floors, walls and other hard surfaces in all the rooms
where he or she has been with 1% lindane emulsion.
8. Explain what is happening to the other residents and tell them that they will not be
able to go out or have visitors until they have been treated. Treat them once with Fig. 8.110 Body louse on seam of clothing, with nits scattered along the seam
5% permethrin cream over the whole of the skin except the face and scalp. Leave it
on the skin for 24 hours.
9. All staff and their husbands, wives, boyfriends, girlfriends and children must be
treated with permethrin cream as directed on p. 250. Ivermectin tablets (200 μg/
kg) given as a single dose is a convenient alternative for everyone apart from the
patient with crusted scabies.
10. Once steps 6–9 on this list have been done, the home can be reopened to visitors.
TREATMENT: BODY LICE Table 8.03 Systemic causes of generalised pruritus and investigations needed to
rule them out
Since the lice live off the body, there is no need to treat the patient. Clothing should be
hot washed and tumble dried, or dry-cleaned, ironed or burnt. The itching will stop once Systemic cause Investigation
the lice have been removed. Anaemia, especially iron deficiency Full blood count, serum iron and ferritin
Polycythaemia rubra vera (itching, especially Full blood count
in a hot bath)
GENERALISED PRURITUS
Uraemia (also seen in 80% of patients on Urea and creatinine
In most instances if someone is itching all over but no rash is seen maintenance haemodialysis)
other than excoriations no cause will be found, but it is important Obstructive jaundice (may occur in patients Liver function tests; autoimmune profile
to exclude the conditions shown in Table 8.03. with primary biliary cirrhosis before jaundice
occurs)
In the elderly, generalised pruritus (senile pruritus) is quite
Thyroid disease, both hypo- and hyperthyroid T4 and thyroid-stimulating hormone;
common and may in part be due to drying out of the skin through autoimmune profile
too-frequent bathing or showering. There may be psychological
Lymphoma, especially in young adults Enlarged lymph nodes clinically and on chest
issues, so look for evidence of depression, anxiety or emotional X-ray
upset. Very often no cause can be found.
Carcinoma, especially in old age Good history, full physical examination, chest
X-ray, occult bloods, abdominal ultrasound
PRURIGO and CAT scan
Prurigo is a rash that is caused by the patient scratching and HIV/AIDS HIV ELISA test
picking his or her skin. Sometimes just excoriations are seen, but
Body lice, likely in vagrants living rough (see Look for lice and nits in the seams of
often numerous discrete intensely itchy pink, mauve or brown p. 251) underwear
excoriated papules or nodules occur (nodular prurigo). They heal Delusions of infestation See p. 254
to leave white scars that sometimes have very obvious follicular
openings within them. Prurigo can sometimes be associated with
eczema.
Prurigo of pregnancy is common, with secondary signs of
scratching. It resolves at term. Check the liver function tests,
since itching can be due to elevated bile salts in the blood, raising
the possibility of intrahepatic cholestasis of pregnancy. In this
condition, itching of the palms and soles is characteristic. It can
be associated with abnormal clotting (treated with vitamin K) and
foetal distress. Early delivery may be necessary.
TREATMENT: PRURITUS AND PRURIGO
Any specific cause found needs treating.

In the elderly, prescribe emollients. If no cause is found, treatment will need to be
symptomatic. Try the following measures.
1. Start with 10% crotamiton (Eurax) cream twice a day.
2. If it does not help, use a moderately potentUK/group 4–5USA steroid ointment or
cream.
3. If the topical steroids do not adequately control the itching and it is interfering with
sleep, a sedative antihistamine such as alimemazine (10–20 mg) or promethazine
(Phenergan, 25–50 mg) taken about an hour before going to bed may help. The
patient will, of course, need to be careful about driving the next day.
4. In patients with uraemia or HIV infection, UVB therapy two to three times a week
may help (see p. 60).
5. Other measures worth trying include doxepin cream or 0.5% menthol in aqueous/
hydrophilic cream (Levomenthol).
6. If none of these measures help, you can try a tricyclic antidepressant such as
amitriptyline 10 mg at night. Fig. 8.111 Nodular prurigo on dorsum of hands
TREATMENT: NODULAR PRURIGO
In order to get this better the patient somehow has got to stop scratching and picking
the skin. A potentUK/group 2–3USA topical steroid ointment applied twice a day may help
control the itching. Fluandrenalone (Haelan) tape may be applied to individual lesions
and left on for several days at a time. Sometimes a sedative antihistamine at night may
be needed. If it is confined to the arms and legs, they can be wrapped up in an occlusive
paste bandage (Ichthopaste or Zipzoc) covered with Tubifast for a week at a time.
Unfortunately, when the bandages are taken off the patient will often begin to scratch
again. Severe cases may need systemic steroids (prednisolone 30 mg for 2 weeks to
break the itch–scratch cycle, and slowly reducing the dose by 5 mg per fortnight). Often
this will work, although relapse may occur when the dose of steroid is reduced.
Fig. 8.112 Nodular prurigo in black skin

DELUSIONS OF INFESTATION
This is a psychiatric illness where the patient is convinced that parasites or mites are in
his or her skin. The patient will complain of itching, or a crawling sensation. The skin
shows multiple excoriated papules where the patient has tried to dig out the offending
insect. Often he or she will present with a matchbox or container with bits of skin that
have been scratched off as ‘proof’ of the infestation (see Fig. 8.115). When examined under
the microscope no creatures are found. The patient may become quite angry with you
if you do not take his or her complaint seriously. A similar condition called Morgellons
syndrome is associated with the delusion that fibres are trapped in the skin, and the
Fig. 8.113 Excoriations in a patient with pruritus: no patient attempts to pick them out, resulting in the same clinical picture.
underlying primary rash is seen
TREATMENT: DELUSIONS OF INFESTATION
Treatment is difficult, since it is almost impossible to

convince the patient that the infestation is imagined.
Referral to a psychiatrist generally is not helpful, but
a combined dermatology and psychiatric clinic is. It
is important to keep the patient’s trust that you are
trying to help cure the problem, otherwise the patient
will not return for further appointments. To do this
the possibility of infestation needs to be excluded by
medical tests (such as mycology and bacteriology).
The eventual aim is to persuade the patient to take an
antipsychotic such as pimozide, which in most cases
resolves the problem.
Fig. 8.114 Delusions of infestation: multiple Fig. 8.115 ‘Matchbox sign’: fragments of skin and
excoriations with crusting crust brought by patient
BLISTERS AND LARGE EROSIONS / 255
Trunk and limbs

Chronic erythematous rash BLISTERS and/or LARGE EROSIONS
Surface crust, exudate
Widespread vesicles, bullae and/or large erosions
Large tense blisters Flaccid blisters rupture easily Large erosions Exudate +++ Grouped vesicles
on erythema Erosions/crusts No blisters
Elderly Pregnant Adults Children Infants Adults Adults Adult Children

Age >70 3rd trimester age 40–60 age 20–40 age 3–10
Biopsy and Biopsy and Biopsy and Bacteriology +ve family Square/ Round, oval Elbows, sacrum Blisters in rings
immuno- immuno- immuno- history angular/odd knees, scalp Immuno-
fluorescence fluorescence fluoroscence shape Immuno- fluorescence
fluorescence
IgG basement IgG basement IgG around Staphylococcus Histology Histology Granular IgA in Linear
membrane membrane epidermal cells +++ spongoisis papillary dermis IgA along
basement
membrane
BULLOUS PEMPHIGOID PEMPHIGUS IMPETIGO EPIDERMOLYSIS DERMATITIS DISCOID DERMATITIS CBDC/LINEAR

PEMPHIGOID GESTATIONIS BULLOSA ARTEFACTA ECZEMA HERPETIFORMIS IgA DISEASE
(DYSTROPHIC)
p. 256 p. 256 p. 257 see p. 107 p. 259 p. 260 see p. 243 see p. 246 p. 259
BULLOUS PEMPHIGOID
Bullous pemphigoid is an autoimmune disease that usually begins
with a non-specific itchy rash that does not look quite right for
either eczema or urticaria. Weeks or months later, blisters occur.
The separation of the skin is at the dermo-epidermal junction (see
Fig. 8.119), with localisation of IgG antibodies here (see Fig. 8.120).
Antibodies to basement membrane are also found in the blood.
The roof of the blister is made up of the full thickness of the
epidermis, so blisters may become large and haemorrhagic and
may remain intact for several days. It is often localised to one
part of the body for a while, but like pemphigus will eventually
become widespread. It is the commonest cause of blisters in the
elderly.
TREATMENT: BULLOUS PEMPHIGOID

Fig. 8.116 Bullous pemphigoid: pre-bullous rash
UK USA
Localised areas can be treated with a potent /group 2–3 topical steroid ointment
or cream applied twice a day. Widespread blistering requires treatment with systemic
steroids (e.g. prednisolone 30–40 mg day) until the blistering stops. The dose can then
be reduced by 5 mg weekly down to 15 mg and then by 2.5 mg weekly. If blistering
starts up again the dose is put up and a steroid-sparing agent such as azathioprine (up
to 3 mg/kg in divided doses) is added. Long-term maintenance with around 5–10 mg of
prednisolone is usually necessary.
PEMPHIGOID (HERPES) GESTATIONIS

This is a very rare condition occurring in pregnancy. It is a very
itchy rash looking like either widespread erythema multiforme
or bullous pemphigoid usually with periumbilical involvement.
It needs to be differentiated from the much more common
polymorphic eruption of pregnancy (see p. 206).
Fig. 8.117 Bullous pemphigoid: tense blisters on background erythema

Fig. 8.119 Histology of bullous pemphigoid: blister Fig. 8.120 Immunofluorescence of bullous
at dermo-epidermal junction pemphigoid: IgG antibodies localised to basement
membrane
Fig. 8.118 Bullous pemphigoid: large blisters, some Fig. 8.121 Histology of pemphigus vulgaris: Fig. 8.122 Immunofluorescence of pemphigus
haemorrhagic, erosions and secondary crusting individual epidermal cells have separated from one vulgaris: IgG antibodies localised around individual
another, causing a blister within the epidermis epidermal cells
TREATMENT: PEMPHIGOID GESTATIONIS PEMPHIGUS VULGARIS

This is an autoimmune disease in which circulating IgG antibodies
Treatment with topical steroids is given if the patient is near term. If it occurs earlier and target desmosomal proteins (desmoglein 3 ± desmoglein 1).
itching is intolerable, systemic steroids (prednisolone 30 mg/day) may be needed. The The epidermal cells come apart from one another (acantholysis)
application of ice cubes or bags of frozen peas may also help the itching!
resulting in an intraepidermal blister. These are always very
superficial so are unable to stay intact for very long. Therefore,
you see mainly erosions and crusts. The blisters are never
haemorrhagic. The skin shears easily if rubbed, producing an
erosion (Nikolsky’s sign, see Fig. 8.123). It most commonly begins
with erosions in the mouth and it may be weeks or months before
the telltale blisters appear on the skin. It may spread very rapidly
and be life-threatening. Diagnosis is confirmed by histology (see
Fig. 8.121), immunofluorescence (see Fig. 8.122), and high titres of
serum antibodies.
PEMPHIGUS FOLIACEUS
Here the split is just below the granular layer so the blisters are
very superficial. Clinically, widespread, crusted erosions on the
face, scalp and upper trunk are seen. It is often misdiagnosed
as seborrhoeic eczema, as no blisters are seen. It is less common
than pemphigus vulgaris in Europe and the United Sates, but
Fig. 8.124 Pemphigus vulgaris: flaccid blisters, erosions and crusts
commoner in Africa and South America. Here the antigen is
desmoglein 1. The diagnosis can be confirmed by skin biopsy and
immunofluorescence.
Fig. 8.123 Nikolsky’s sign: skin shears off by tangential pressure Fig. 8.125 Pemphigus foliaceus
TREATMENT: PEMPHIGUS VULGARIS/FOLIACEUS CHRONIC BULLOUS DISEASE OF

CHILDHOOD
Immediate referral to hospital is recommended. Sometimes it is necessary to treat the patient in a burns unit if large areas A rare disease of young children (usually
of skin are eroded. Treatment is started with prednisolone 120 mg daily until the blisters stop. The dose is then gradually begins age 3–5), with grouped blisters
reduced to a maintenance dose of 5–10 mg a day.
around the genitalia, umbilicus and on
What often happens is that the blisters dry up initially but once the dose is down to 50 mg a day, new blisters appear. the face. It is not itchy and it gets better
Steroid-sparing agents such as azathioprine, ciclosporin or methotrexate may well be needed too. Complications caused spontaneously after 3–4 years. Histology
by high-dose steroids or secondary infection can result in considerable morbidity. shows a subepidermal blister and on direct
Pemphigus foliaceus responds better to steroids and may eventually be controllable with topical steroids. immunofluorescence a linear band of IgA
is seen along the basement membrane of
the epidermis.
EPIDERMOLYSIS BULLOSA (DYSTROPHIC)
Linear IgA disease is the adult version
This is a group of inherited diseases where blisters and erosions appear in response to of chronic bullous disease of childhood.
trauma. Dystrophic epidermolysis bullosa is due to a split below the epidermal basement Usually the blisters occur in rings.
membrane. Many patients do not survive the first 2 years of life (see Fig. 8.127), while Immunofluorescence and histology are the
others are disabled by the skin shearing off easily. Secondary scarring, milia formation, same.
infection and binding together of fingers and toes can occur (see Fig. 13.54, p. 429).
Patients will need referral to a dermatology department for confirmation of diagnosis by
skin biopsy and electron microscopy.
TREATMENT: EPIDERMOLYSIS BULLOSA
Treatment is a wound care problem. Raw areas need to be dressed with a non-adherent dressing (see p. 46). The skin
should be moisturised with emollients and protected from injury by hydrocolloid dressings. Shoes and clothing should
not be allowed to rub. Pain and secondary infection need treatment, and genetic counselling and parent support will be
necessary.
DEBRA, the international epidermolysis bullosa charity, has specialist trained nurses based out of London and
Birmingham who cover the entire country and will see all newly suspected patients with epidermolysis bullosa. They will
see the baby, perform a punch biopsy for specialist split skin histology and electronmicroscopy performed in London
to identify the specific epidermolysis bullosa type and instigate the best dressing regimens with carers and family as
required.
Fig. 8.126 Chronic bullous disease of childhood

TREATMENT: CHRONIC BULLOUS DISEASE OF CHILDHOOD/LINEAR IGA DISEASE
Oral dapsone 25–100 mg/day is given until it remits spontaneously. Check the full
blood count regularly for haemolysis. Add cimetidine 400 mg tid if haemolysis or
methaemoglobinaemia occurs.
DERMATITIS ARTEFACTA
These lesions are self-induced. The clue is that instead of being
round or oval, like most naturally occurring rashes, they have
straight sides – square, rectangular, triangular (see Fig. 1.84, p. 17).
They occur anywhere that the patient can reach and damage the
skin with fingernails, scissors, nail files, phenol, acids, household
cleansers, and so forth. The open wounds exude serum then form
crusts.
Fig. 8.127 Dystrophic epidermolysis bullosa in a newborn
TREATMENT: DERMATITIS ARTEFACTA
This is very difficult to treat because the patient (often female) is not willing to admit to
producing the lesion(s) or to the idea that treatment involves facing up to the problem
or conflict in her life that is causing her to damage her own skin. If the lesions are
occluded so that the patient cannot get at them, they will usually heal very quickly.
These patients need psychiatric help. Unfortunately, psychiatrists are not always
interested in helping them. Direct confrontation usually leads to the patient seeking
help elsewhere.
Fig. 8.128 Dermatitis artefacta: note straight rather than round margin to rash
261
Non-erythematous lesions
Normal surface
Skin coloured, pink, yellow
Papules
9
Isolated lesions 262
Multiple similar lesions 263
Plaques 270
Nodules 272
White
Macules and small patches (<2 cm) 278
Papules 278
Large patches and plaques (>2 cm) 281
Brown
Macules and small patches (<2 cm) 288
Small plaques (<2 cm) 300
Present at birth or before age 10 292
Appears after age 10 295
Papules and nodules 300
Blue, black, purple
Macules, papules and nodules 310
Patches present before age 10 292
Red, orange
Macules and papules 314
Nodules see p. 213
Warty surface 316
Scaly/keratotic surface
Multiple lesions/rash 322
Single/few lesions 325
Crust, ulcerated, bleeding surface 329
262 / NON-ERYTHEMATOUS LESIONS

Non-erythematous lesions 1. SKIN COLOURED (PINK): ISOLATED PAPULES
Normal surface
Skin coloured, pink
Pedunculated Dome shape Depressed centre Flat surface
Narrow base Soft palpation Firm/hard palpation Normal/firm Size >2 mm Size <2 mm Normal palpation
<2 mm palpation Gradual ↑ not changed No size increase
Axilla, neck, Any site Trunk, limbs Face Any site Any site Cheeks, forehead Any site
inner thigh, Long history Present for Long history
eyelids (years) a few months
SKIN TAG NEURO- DERMATO- PALISADING INTRADERMAL BASAL CELL SEBACEOUS LICHENOID
FIBROMA FIBROMA ENCAPSULATED NAEVUS CARCINOMA GLAND KERATOSIS
NEUROMA HYPERPLASIA
p. 266 p. 264 see p. 265 p. 264 p. 264 p. 265 p. 265 p. 265

SKIN COLOURED PAPULES / 263

Non-erythematous lesions 2. SKIN COLOURED (PINK, YELLOW): MULTIPLE SIMILAR PAPULES
Normal surface
Skin coloured Brown pink Yellow
Pedunculated Dome shape, Spherical, deep Round, oval Flat-topped Round within
on surface within surface within surface on surface surface
Side of neck axilla, Any site Sides of nose Lower eyelids Axillae, central Neck, trunk Face, dorsum Extensor aspect
inner thighs trunk hands of limbs,
buttocks, trunk
±Elderly/ +ve family history 1–4 mm 1–2 mm 2–10 mm Painful in cold or Linear/grouped ↑ blood lipids
obese Café au lait spots asymptomatic when knocked
SKIN NEUROFIBROMAS ANGIOFIBROMA/ SYRINGOMAS STEATOCYSTOMA LEIOMYOMA PLANE WARTS ERUPTIVE

TAGS TRICHOEPITHELIOMA MULTIPLEX XANTHOMA
p. 266 p. 266 p. 267 p. 268 see p. 274 p. 269 p. 268 p. 269

INTRADERMAL NAEVUS PALISADING ENCAPSULATED NEUROMA

This is a skin-coloured melanocytic naevus. All the naevus cells A palisading encapsulated neuroma is a fairly common
are in the dermis so pigment is no longer seen on the surface asymptomatic, solitary, skin-coloured papule mainly found
(see p. 303). It is a small, round, dome-shaped or papillomatous on the face. It has a distinctive histological appearance with a
papule. Occasionally telangiectasia can be seen on the surface, proliferation of Schwann cells and a large number of axons within
but the lack of growth, long history and symmetrical dome a perineural-derived capsule. It is harmless and not associated
shape distinguish it from a basal cell carcinoma. They are with neurofibromatosis.
sometimes pedunculated, and can be difficult to distinguish from
neurofibromas or skin tags. If necessary they can be removed by SOLITARY NEUROFIBROMA
shaving them off flush with the skin, and cauterising the base with These are dome-shaped or pedunculated soft papules that when
heat or aluminium chloride solution (Driclor, Anhydrol Forte). pressed in the centre have a hole at the base (like a buttonhole).
They are distinguished from intradermal naevi by being softer and
usually larger (5–9 mm).
Fig. 9.01 Multiple intradermal naevi on the cheek Fig. 9.02 (a) Solitary neurofibroma on buttock; Fig. 9.03 Palisading encapsulated neuroma: easily
and temple (b) (inset) central pressure with a finger elicits a confused with a basal cell carcinoma
‘hole’ or soft centre.
DERMATOFIBROMA SEBACEOUS GLAND HYPERPLASIA

Dermatofibromas are easily recognised This is a common benign lesion due to enlargement of sebaceous glands around a single
clinically because they are always firm hair follicle on the face. It is a small (2–5 mm diameter), skin-coloured-yellow papule with
on squeezing between thumb and finger. telangiectasia running over the surface and a central punctum (the opening of the hair
They are pink or skin-coloured papules or follicle). It is sometimes confused with a small basal cell carcinoma, since both occur on
nodules resulting from trauma such as an the face of middle-aged or elderly individuals. They can be removed by cautery under
insect bite or foreign body (see p. 301). local anaesthetic.
BASAL CELL CARCINOMA LICHENOID KERATOSIS

The early growth of a nodular basal cell This is a variety of a solar lentigo, which is a pink papule with a smooth surface. On
carcinoma can look just like an intradermal histology a lichenoid infiltrate is present. It can be confused clinically with an early basal
naevus. However, if you look closely there cell carcinoma.
is always telangiectasia over the surface
(see p. 330). If in doubt, excise for histology.
Fig. 9.04 Dermatofibroma Fig. 9.05 Basal cell carcinoma: note Fig. 9.06 Sebaceous gland Fig. 9.07 Lichenoid keratosis
pink colour with telangiectasia hyperplasia
SKIN TAGS TREATMENT: SKIN TAGS NEUROFIBROMATOSIS (VON

These are small pedunculated, skin- RECKLINGHAUSEN’S DISEASE)
coloured or brown papules around the If the patient wants them removed, snip the tag Multiple skin-coloured, pink or red
neck, in the axillae or sometimes on the off with a pair of sharp scissors without any local papules and nodules appear anywhere
anaesthetic. Bleeding is stopped with aluminium
inner thighs. Single tags are commonly on the skin after puberty. If you press
chloride (Driclor) , a silver nitrate stick or cautery.
seen in the elderly on the eyelids. on the surface, the lesions are found
Alternatively, if they are very small, ablate with the
hyfrecator.
to be soft with a hole at the base (like
a buttonhole). They vary in size from
1–2 mm to several centimetres in diameter.
Some are sessile, some pedunculated.
The patient will also have multiple (more
than five) café au lait patches (see p. 294)
and axillary freckling. Lisch nodules
(pigmented iris hamartomas) are seen on
slit-lamp examination and help confirm
the diagnosis. Various endocrine and
neurological abnormalities can also be
present. This condition is inherited as an
autosomal dominant trait, the gene being
Fig. 9.08 Skin tags around the eyes on chromosome 17.
TREATMENT: NEUROFIBROMAS
Single lesions can be removed by excision or shave

and cautery. It is impossible to remove all the lesions
in von Recklinghausen’s disease, but any particularly
unsightly ones can be excised.
Fig. 9.09 Multiple skin tags around neck Fig. 9.10 Neurofibromatosis
TRICHOEPITHELIOMA ANGIOFIBROMAS (ADENOMA SEBACEUM)

Single or multiple translucent papules around the eyes or on These are multiple very firm, discrete, translucent papules with a
the nasolabial folds appear after puberty. They look similar to telangiectatic surface affecting the nasolabial folds and spreading
angiofibromas but are not red and there is no telangiectasia on out onto the cheeks and chin.
the surface. They are benign hair follicle tumours also known
They appear in early childhood (age 3–4) and are a sign of
as epithelioma adenoides cysticum. They are inherited as an
tuberous sclerosis (epiloa). Tuberous sclerosis is an autosomal
autosomal dominant trait.
dominant disorder affecting many organs. Other skin lesions
TREATMENT: ANGIOFIBROMAS/TRICHOEPITHELIOMAS
are oval or ash leaf-shaped white patches (see Fig. 9.14), which
are present from birth, the shagreen patch (a connective tissue
A few lesions can be removed by shave and cautery under local anaesthetic. Widespread naevus, see p. 270) and periungual and subungual fibromas (see
lesions present a problem. Extensive debridement can be tried using a carbon dioxide Fig. 14.43 and 14.44, p. 449), which appear after puberty. Other
(CO2) laser, shave or curettage and cautery under general anaesthetic. Unfortunately, features of the syndrome include mental retardation, epilepsy and
there is a tendency for the lesions to recur. occasionally tumours affecting the heart and kidneys.
Fig. 9.11 Trichoepitheliomas Fig. 9.12 Multiple angiofibromas in a patient with Fig. 9.13 Angiofibromas in black skin: same
tuberous sclerosis distribution as Fig. 9.12, different colour
SYRINGOMA
These small (1–5 mm), round, dome-shaped, translucent papules
on the lower eyelids are very common and completely harmless.
They are benign tumours of sweat glands that are inherited as
an autosomal dominant trait. They appear after puberty. Cautery
with a fine loop will ablate them. Rarely, multiple lesions may be
seen elsewhere on the face and trunk.
PLANE WARTS
These are small, flat-topped papules but, unlike the papules of
lichen planus, they are not shiny on the surface. They are not
rough to the touch like common warts. They are skin coloured,
Fig. 9.15 Syringomas on lower eyelids in white skin
Fig. 9.14 Tuberous sclerosis: ash leaf macule behind the ear Fig. 9.16 Syringomas around eyes in black skin
pink or brown and may be found in LEIOMYOMA ERUPTIVE XANTHOMA

straight lines at sites of trauma (Köebner This is a benign smooth muscle tumour of Eruptive xanthomas are yellow papules
phenomenon). They occur mainly in the erector pili muscle. Multiple pink, red containing lipid deposits secondary to
children, on the face and dorsum of or brown papules are grouped together hypertriglyceridaemia. They commonly
the hands. Reassurance that they will on the trunk or on a limb in young adults. occur on the buttocks and extensor
eventually resolve spontaneously is They can be painful in the cold or when surface of limbs. Most of these patients are
usually all that is needed. You can try 5% knocked, due to the smooth muscle diabetic, so check the HbA1c as well as
salicylic acid ointment or a light freeze contracting. Diagnosis is confirmed by skin lipid levels. The lesions will clear once the
with liquid nitrogen (few seconds only) but biopsy. They can be removed by surgical underlying diabetes and hyperlipidaemia
treatment tends not to be very effective. excision if the lesions are not too large. is treated.
Fig. 9.17 Plane warts (see also Fig. 1.89, p. 17) Fig. 9.18 Leiomyoma on side of chest Fig. 9.19 Eruptive xanthomas
Normal surface SKIN-COLOURED PLAQUES
Plaques
Skin coloured/pink Yellow
Stretch surface and palpate lesion
Raised rolled edge Papules arranged Well defined, Poorly defined, Upper or lower Fig. 9.20 Isolated seborrhoeic keratosis on lower leg
in ring ‘stuck on’ to within surface eyelid
surface
Gradually enlarging Fixed in size Patient over 40 Present since Patient over 50
childhood
BASAL CELL GRANULOMA SEBORRHOEIC CONNECTIVE XANTHELASMA

CARCINOMA ANNULARE KERATOSIS TISSUE NAEVUS
Fig. 9.21 Multiple skin-coloured seborrhoeic

keratoses on back
see p. 330 see p. 210 p. 270 p. 270 p. 271

CONNECTIVE TISSUE NAEVUS
A connective tissue naevus is a birthmark
SEBORRHOEIC KERATOSIS consisting of a skin-coloured/yellowish
The morphology of these lesions (see p. 320) is very varied depending on the skin plaque with a cobblestone surface. It may
type and degree of pigmentation. In fair-skinned individuals (skin types I and II) they be an isolated naevus or part of tuberous
commonly present as flat skin-coloured or pink plaques. Initially the surface may be quite sclerosis (see p. 267), called a shagreen
smooth, although as they develop the surface may become papillomatous or scaly. patch.
SKIN-COLOURED PLAQUES / 271
XANTHELASMA
These are yellow, flat plaques usually found on the medial
aspect of the eyelids. They are not necessarily associated with
hyperlipidaemia.
TREATMENT: XANTHELASMA
Dip a cotton wool bud in a saturated solution of trichloracetic acid (TCA) and lightly
paint the surface of the xanthelasma, making sure that it does not get onto normal
skin. After a few seconds the surface goes white. Immediately smother the surface with
surgical spirit – this quickly neutralises the acid. Any excess acid can also be washed
away with copious amounts of water. The stinging caused by the acid should stop after
just a few seconds. A week later the treated area scabs over and the skin will heal
normally after about 6 weeks. Recurrences or residual areas can be retreated in the
same way.
Alternatively, they can be removed by excision, or ablated by cautery or laser.
Fig. 9.22 Connective tissue naevus
a b c d
Fig. 9.23 (a) Xanthelasma before treatment: yellow plaques on inner eyelids; (b) treatment of xanthelasma immediately after application of trichloracetic acid; (c) 7
days after treatment – crusts have formed; (d) 2 months after treatment there Is just a faint erythema
Normal surface SKIN-COLOURED (PINK, YELLOW) NODULES
Nodules
Mobile under Fixed to surface
skin
Lobulated Soft, fluid Spherical Firm Firm-hard Bony hard

Compressible filled Compressible
Skin colour Translucent Skin coloured Cream Pink Yellow Pink Pink Skin
skin coloured Knees, Single Single coloured
coloured/ elbows Children Multiple
grey blue lipids ↑
? Punctum on Biopsy Biopsy to establish diagnosis Biopsy Excise Excise X-ray

surface (biopsy) calcium ++
LIPOMA APOCRINE EPIDERMOID/ STEATO- CYLIN- INFILTRATIVE BASAL CELL TUBEROUS DERMATO- PILOMA- CUTANEOUS
HIDRO- TRICHLIEMMAL/ CYSTOMA DROMA TUMOUR CARCINOMA XANTHOMA FIBROMA TRICOMA CALCINOSIS
CYSTOMA DERMOID CYST MULTIPLEX (Lymphoma,
Melanoma,
Metastasis)
p. 273 p. 274 pp. 273, 274 p. 274 p. 274 p. 275 p. 276 p. 277 p. 277 p. 277 p. 276
SKIN-COLOURED NODULES / 273
EPIDERMOID CYST DERMOID CYST

An epidermoid cyst (commonly misnamed a sebaceous cyst) is Dermoid cysts look like epidermoid cysts but they are present
a well-circumscribed papule or nodule derived from the upper from birth or early childhood. They are due to the inclusion
part of the external root sheath of a hair follicle or from a sweat of epidermis and its appendages in the dermis at the time of
duct. The lining of the cyst looks like normal epidermis. The cyst embryonic skin closure. Most occur on the head and neck, either
is situated in the dermis and there is usually a visible punctum in the midline or at the lateral end of the eyebrow. They have an
on the surface. Through this punctum the cyst may become obvious punctum, which may have hairs protruding through it.
secondarily infected.
LIPOMA
Epidermoid cysts are inherited as an autosomal dominant trait
This is a benign tumour of fat cells presenting as soft or firm
but do not appear until after puberty (usually 15–30 years). If they
subcutaneous nodules (you can move the skin over it), round or
occur before puberty they may be associated with polyposis coli
irregular in shape. They may be single or multiple and vary in size
(Gardner’s syndrome) or with the basal cell naevus syndrome.
from 1 to 10 cm in diameter. The overlying skin is normal. Usually
Similar cysts may occur in patients with acne after damage to hair
they are of no significance.
follicles, or after penetrating injuries where bits of epidermis are
implanted in the dermis.
Fig. 9.24 Epidermoid cyst Fig. 9.25 Dermoid cyst Fig. 9.26 Lipoma
TRICHILEMMAL (PILAR) CYST CYLINDROMA

These are derived from the external root sheath of a hair follicle Single or multiple, spherical or lobulated, red, smooth nodules
between the opening of the sebaceous duct and the bulge occur on the scalp or face (see Fig. 9.29). They can grow to quite
(insertion of the erector pili muscle). Most occur on the scalp a large size. Sometimes they occur in association with multiple
(see p. 95), although they can occur anywhere except the palms trichoepitheliomas (see p. 267). Alone or in combination they are
and soles. They do not have a punctum so they do not become inherited as an autosomal dominant trait. They are uncommon.
infected. They are inherited as an autosomal dominant trait.
APOCRINE HIDROCYSTOMA
STEATOCYSTOMA MULTIPLEX This is a solitary smooth, dome-shaped, cystic nodule, which may
Multiple, symmetrical, small skin-coloured, white or yellowish be skin coloured or blue grey in colour. It is found most commonly
papules or nodules occur on the skin of young adults. In females around the eyelids. It is usually misdiagnosed as a basal cell
they are mainly in the axillae and between the breasts. In males carcinoma.
they are mostly on the trunk in a diamond-shaped area between
the xiphisternum and umbilicus or on the back. They are inherited
as an autosomal dominant trait.
Fig. 9.27 Trichilemmal cyst on scalp Fig. 9.28 Steatocystoma multiplex Fig. 9.29 Cylindroma: looks like a Fig. 9.30 Apocrine hidrocystoma
nodular basal cell carcinoma
TREATMENT: LIPOMAS, CYSTS AND APPENDAGE TUMOURS
These can all be excised under local anaesthetic if they are large or a nuisance. Lipomas
are removed by making an incision through the skin and shelling out an encapsulated
tumour of fatty tissue. Pressing down around the lipoma often results in it popping out
easily.
Appendage tumours (hidradenomas, cylindromas, pilomatricomas) can be excised
together with the overlying skin.
When removing cysts first excise an ellipse of skin over the cyst so that the upper
surface of the cyst is visible (see Fig. 3.44, p. 95). You will now be in the right plane to
dissect out the cyst. The amount of skin you need to remove depends on how big the
cyst is and how much redundant skin has been pushed up. The cyst is then dissected
out using a pair of blunt curved scissors. If the resultant hole is large, close off the dead
space with deep dissolving sutures before inserting ordinary interrupted sutures into the
skin.
Fig. 9.31 Metastases on abdomen from carcinoma of ovary
Epidermoid cysts are the most difficult to remove, since they are often stuck down
to the surrounding connective tissue, particularly if they have ever been inflamed.
Trichilemmal cysts shell out very easily once you are in the right plane, since they have
a connective tissue sheath around them. If huge numbers of steatocytoma multiplex
cysts are present, they can be incised with a no. 15 scalpel blade, the contents squeezed
out and the cyst lining removed by pulling out with a pair of artery forceps. You have
to pull quite hard to remove them. This will normally need to be done under a general
anaesthetic.
Do not remove cysts while they are actively inflamed. It is important to remove all of the
cyst wall during the procedure; if any of it is left behind, the cyst will recur.
TUMOURS
Many types of tumour (lymphoma, amelanotic melanoma,
metastases, and so forth) present as skin-coloured or pink nodules
growing within the dermis. They may be difficult to diagnose
clinically, and urgent referral for a biopsy is usually necessary (see
also p. 216). Fig. 9.32 B-cell lymphoma on cheek
BASAL CELL CARCINOMA

A nodular basal cell carcinoma can
grow slowly without ulcerating to
form a large nodule. It usually has
a pearly translucent appearance
with obvious telangiectasia on the
surface (see p. 330).
CUTANEOUS CALCINOSIS
Bony hard papules and nodules
due to the deposition of calcium
within the dermis can occur in:
Localised lesions
● Various cysts (trichilemmal, Fig. 9.33 Basal cell carcinoma: note Fig. 9.34 Cutaneous calcinosis in a patient with CREST syndrome
pilomatricoma, see pp. 95 and the telangiectasia on the surface
277)
● Pinneal (ear) calcification
● Venous disease on the lower
legs (see pp. 391, 398)
● Cutaneous calculus (see p. 280)
● Scrotal calcinosis (see p. 364)
Generalised disease
● Chronic renal failure
● Dermatomyositis
● Hyperparathyroidism
● Sarcoidosis
● Systemic lupus erythematosus
● Systemic sclerosis (CREST
syndrome) a b c
Fig. 9.35 Subcutaneous calcification: (a) in radiation-damaged skin; (b) X-ray of same; (c) on the thumb
PILOMATRICOMA DERMATOFIBROMA TUBEROUS XANTHOMA

A pilomatricoma is a benign tumour of A slow-growing nodule that is firm but not These are firm lobulated tumours
the hair follicle most commonly seen in bony hard growing within or out of the appearing at sites of pressure, usually the
children. It presents as a nodule resembling surface is likely to be a dermatofibroma. extensor surface of the knees or elbows
a cyst, which is usually pink red in colour. It can be shaved or excised under local in patients with hypercholesterolaemia.
It is often calcified so is bony hard on anaesthetic. The lesions will regress slowly once the
palpation. It can be excised under local hyperlipidaemia has been treated.
anaesthesia.
Fig. 9.36 Pilomatricoma on the cheek of a young Fig. 9.37 Dermatofibroma on the leg (inset: Fig. 9.38 Tuberous xanthoma on the elbow
boy (inset: close-up of lesion) close-up of lesion – hard on palpation)
Non-erythematous lesions Non-erythematous lesions

Normal surface WHITE MACULES Normal surface WHITE PAPULES
White colour White colour
Macules Papules
Single or isolated lesion Multiple similar lesions Flat-topped Round shape Irregular/
Isolated Multiple lesions Linear
Round with mole Linear/odd Multiple, small Round/oval

in centre shape round macules coalescing on trunk Hard on Umbilicated in Size 1 mm Associated Previous acne/
(<5 mm size) palpation centre Spherical blackheads injury
Normal skin Loss of Arms and legs Surface scaly if

texture appendages scratched
HALO NAEVUS SCAR IDIOPATHIC PITYRIASIS CUTANEOUS MOLLUSCUM MILIA CLOSED SCAR
GUTTATE VERSICOLOR CALCULUS CONTAGIOSUM COMEDONES
HYPOMELANOSIS
p. 278 p. 279 p. 278 see p. 203 p. 280 p. 279 p. 280 p. 280 p. 279
HALO NAEVUS IDIOPATHIC GUTTATE HYPOMELANOSIS

An immunological reaction against the melanocytes in a mole Numerous symmetrical, small (1–5 mm), white macules on the
produces a halo of depigmentation around it. Eventually the mole arms or legs are extremely common, especially in individuals with
disappears. This reaction is common in children, quite benign and black or pigmented skin. Individual lesions have well-defined
does not indicate that the mole has undergone malignant change. borders and normal skin markings within them. Reassurance that
they are harmless is all that is required.
WHITE LESIONS / 279
SCARRING MOLLUSCUM CONTAGIOSUM

Scars with triangular or rectangular shapes This is a poxvirus infection of the skin usually affecting children. Small 1–5 mm white or
may be due to self-inflicted damage; those pink umbilicated papules (see Fig. 9.42) are found anywhere on the skin and there may
that are crescent-shaped or star-shaped be few or many. They can become inflamed and red in colour. They last 6–24 months and
may be due to tearing of the skin after then disappear spontaneously. In children with atopic eczema, they may be extensive
minor trauma in elderly patients or those particularly at the sites of the eczema. Isolated lesions in adults can be confused with a
on oral steroids or using potent topical basal cell carcinoma.
steroids. Acne can leave white, round,
papular scars on the back
Fig. 9.39 Halo naevus Fig. 9.40 Idiopathic guttate Fig. 9.41 Scars on the forearms due Fig. 9.42 Molluscum contagiosum
hypomelanosis to steroids
TREATMENT: MOLLUSCUM CONTAGIOSUM MILIA

These are very small superficial epidermoid cysts. They are small
Trauma to individual lesions results in their resolution. 5% potassium hydroxide solution (1–2 mm diameter only) white spherical papules protruding
(MolluDab) can be applied twice a day for 3–5 days (until an inflammatory reaction is above the surface on the cheeks and eyelids. They can occur
seen). This is an effective treatment that is not painful and can be applied by the child’s
spontaneously or follow any acute sub-epidermal blister, e.g. after
parents.
burns or other blistering diseases. To remove, open the skin over
each cyst with a sharp needle; press on either side and it will pop
out.
CUTANEOUS CALCULUS
A single white, round, flat-topped papule on the face of a child CLOSED COMEDO
that feels firm to hard on palpation is likely to be a cutaneous
A closed comedo (whitehead) is a single blocked pilosebaceous
calculus. It is due to calcium deposited in the upper dermis and is
follicle in which the follicular opening is not visible (see acne,
quite harmless.
p. 116).
Fig. 9.43 Cutaneous calculus on child’s face Fig. 9.44 Milia Fig. 9.45 Closed comedones on the back
WHITE LESIONS / 281
Normal surface WHITE PATCHES AND PLAQUES
White colour
Patches and plaques
Patch Plaque
Colour change only Thickened dermis
Well defined Poorly defined
Large geographic Single/few Small round areas Irregular outline Press Single plaque Increased
areas (Depigmented) Patient from coalescing ±Surface scale surrounding skin
Asia/Africa (Hypopigmented) skin: blanches wrinkles
same colour
(↓ blood supply)
Since Gradual Surface Surface Surface Previous rash at Child’s face Size <5 cm Size >5 cm Face, back
birth onset anaesthetic scale on wrinkled same site Skin type Age >60 Brown border of neck
Biopsy scratching Skin type IV–VI IV–VI Face Atrophic Skin type
Microscopy centre I–II
+ve
PIE- VITILIGO TUBERCULOID PITYRIASIS LICHEN POST- PITYRIASIS NAEVUS MORPHOEIC MORPHOEA SOLAR
BALDISM LEPROSY VERSICOLOR SCLEROSUS INFLAMMATORY ALBA ANAEMICUS BASAL CELL ELASTOSIS
et HYPOPIGMEN- CARCINOMA
ATROPHICUS TATION
p. 282 p. 282 p. 283 p. 285 p. 285 p. 286 p. 286 p. 287 see p. 331 p. 287 p. 287
VITILIGO PIEBALDISM
Vitiligo is thought to be an This is an inherited condition
autoimmune disease in which (autosomal dominant) where
the melanocytes disappear white patches are present at
from the epidermis. The patient birth and remain unchanged
presents with symmetrical white throughout life. It may be
patches on any part of the skin. associated with a white
The skin is depigmented rather forelock of hair if the skin in
than hypopigmented, which that area is affected. The white
distinguishes it from all other white patches are identical to those of
skin lesions (other than piebaldism). vitiligo.
It is often confused with pityriasis
versicolor, but vitiligo consists
of large patches with no surface
scale. Vitiligo on visible skin Fig. 9.46 Vitiligo: symmetrical areas of depigmentation
can be very unsightly, especially
in dark-skinned individuals.
Sometimes there is a band of
hyperpigmentation at the edge of
the patches, and in patients who are
very fair skinned this may be more
noticeable than the depigmented
areas. On exposed sites vitiligo will
burn in the sun.
In 30% of patients there is a positive
family history of vitiligo, and it may
also be associated with the organ-
specific autoimmune diseases such
as hypo- and hyperthyroidism,
pernicious anaemia, Addison’s
disease and diabetes mellitus. Fig. 9.47 Vitiligo on dorsum of hand: note burning in depigmented areas Fig. 9.48 Vitiligo on face of African
and hyperpigmentation at the edge of the patches girl
WHITE LESIONS / 283
TREATMENT: VITILIGO
In white-skinned individuals the best advice is probably to keep out of the sun and to
apply a high-factor sunblock all over to prevent the normal skin from tanning and the
depigmented skin from burning.
If it is spreading very rapidly you can to switch it off with systemic steroids. In adults,
give three doses of triamcinolone 40 mg intramuscularly at monthly intervals. In children,
give prednisolone 5–10 mg/day for 2–3 weeks. Systemic steroids have no effect on
stable vitiligo.
Repigmentation can be attempted by any of the following treatments.
● Apply a potentUK/group 2–3USA topical steroid cream to the white areas in the
morning followed by half an hour of sun exposure a day (or narrowband UVB at your
local hospital in the winter). After this period of sun exposure, the patient should use
a high-protective-factor sunscreen on any exposed sites to prevent burning. Topical
steroids should not be used for more than 3 months if used daily (6 months if used
on alternate days).
● Topical 0.1% tacrolimus ointment may be used instead of a potent topical steroid,
especially on the face. Both of these treatments can be used in children.

● Narrowband UVB (311 nm) two to three times a week to whole body if more than
15%–20% of the body’s surface involved.

● Localised areas on the face can be treated with the excimer laser at 308 nm.
● PUVA therapy twice weekly (see p. 61). It may need to be given for 12–24 months
for maximum effect.
When the vitiligo repigments, it does so initially from the hair follicles, so you will see Fig. 9.49 Repigmenation around hair follicles in a patient with vitiligo
small brown macules in the white patches.
The cosmetic appearance can be improved using cosmetic camouflage:
● fake tan applied every 3–5 days LEPROSY
● cover creams available on prescription after consultation with the Red Cross (see Leprosy is a chronic bacterial infection due to Mycobacterium
p. 39). leprae. It is spread by droplet infection and has a long incubation
period (anything from 2 months to 40 years). It principally affects
In very extensive vitiligo, depigmentation of the remaining normal skin can be
peripheral nerves and the skin. The clinical features are very
attempted by using the monobenzyl ether of hydroquinone twice a day for several
variable depending on the patient’s cell-mediated immunity to the
weeks. This depigmentation will be permanent.
leprosy bacillus.
In tuberculoid (TT) leprosy (where At the other end of the spectrum, in In between are various forms of borderline
patients have good cell-mediated lepromatous (LL) leprosy, the patient leprosy (BT, borderline tuberculoid;
immunity) few/no bacteria are found in has no cell-mediated immunity and BB, mid borderline; BL, borderline
the skin (paucibacillary leprosy). There consequently there are numerous lepromatous) with clinical features
are one to five hypopigmented anaesthetic organisms in the skin (multibacillary gradually changing from tuberculoid to
patches with a raised red-copper-coloured leprosy). Clinically there are multiple lepromatous.
border. Often this is associated with a papules, nodules and plaques that are not
The diagnosis is made by recognising the
single enlarged cutaneous nerve nearby. anaesthetic, and a ‘glove and stocking’
typical clinical features, doing slit-skin
peripheral neuropathy due to widespread
smears looking for organisms or by doing
nerve damage.
a skin biopsy.
Fig. 9.50 Tuberculoid leprosy: single anaesthetic Fig. 9.51 Lepromatous leprosy: nodules on the face Fig. 9.52 Borderline leprosy: multiple asymmetrical
hypopigmented plaque on arm with a raised border hypopigmented patches
WHITE LESIONS / 285
TREATMENT: LEPROSY
Patients suspected of having leprosy should be referred to a leprologist, since

management requires careful monitoring of the skin and nerve lesions and regular
supervision. All patients must have multidrug therapy.
TT and BT BB, BL and LL

Paucibacillary Multibacillary
Duration of Rx 6 months 24 months
Rifampicin 600 mg monthly 600 mg monthly
Dapsone 100 mg daily 100 mg daily
Clofazimine 300 mg monthly
and 50 mg daily
PITYRIASIS VERSICOLOR
White round or oval macules coalesce to form large Fig. 9.53 Pityriasis versicolor: Fig. 9.54 Lichen sclerosus et
hypopigmented patches occurring on atrophicus: close-up of lesions
hypopigmented patches on the upper trunk and proximal limbs
black skin showing surface atrophy and wrinkled
in young adults with tanned or pigmented skin. The surface is surface
always slightly scaly when scratched (see p. 203).
LICHEN SCLEROSUS ET ATROPHICUS

This condition usually presents with genital itching and is seen
as white atrophic plaques in the perineum (see p. 368). Rarely the
trunk and limbs may also be involved. Small flat white atrophic
macules and papules with a shiny wrinkled surface occur, most
commonly on the upper trunk. Fortunately they are usually
asymptomatic. Trunk lesions tend to be unresponsive to treatment.
Fig. 9.55 (right) Lichen sclerosus et atrophicus: white macules, patches and
plaques on upper back
PITYRIASIS ALBA POST-INFLAMMATORY

Multiple poorly defined hypopigmented, HYPOPIGMENTATION
slightly scaly patches can occur on the face Partial loss of pigment may follow any irregular in outline, and producing little
of children. In Caucasians they may only inflammatory skin condition affecting or no scale on scratching the surface, and
be visible in the summer when the normal the epidermis, e.g. eczema or psoriasis, from vitiligo by being hypopigmented
skin tans. In dark-skinned individuals just as some individuals develop rather than depigmented. Treat the
it is relatively common. It is considered hyperpigmentation in response to the same underlying disease if it is still active, but
to be a form of post-inflammatory stimulus. It is distinguished from pityriasis reassure the patient that the pigmentation
hypopigmentation following mild eczema. versicolor in being more ill-defined and will return to normal in due course.
Fig. 9.56 Pityriasis alba Fig. 9.57 Post-inflammatory pigmentation following Fig. 9.58 Post-inflammatory hypopigmentation
atopic eczema in black skin following eczema: poorly defined macules
WHITE LESIONS / 287
NAEVUS ANAEMICUS MORPHOEA

There is no structural abnormality in the skin. This is a This is a localised thickening of the dermis due to excess collagen
pharmacological naevus with the blood vessels overreacting with loss of appendages (sweat glands and hair follicles). It occurs
to adrenalineUK/epinephineUSA and noradrenalineUK/ at any age (peak incidence from 20 to 40) and is more common in
norepinephrineUSA. Pressure through the edge of the lesion will females. The lesions are firm oval plaques with a shiny smooth
make the naevus disappear as the surrounding blood vessels are surface. The edge is often purple or brown, while the centre is
compressed. It is completely harmless. white or yellow. It feels thickened compared with the surrounding
skin. Rarely it may be linear, going down an arm or leg, or on the
SOLAR ELASTOSIS forehead (see p. 80).
This is a yellowish discolouration of the skin with more obvious
In rare instances, morphoea can be extensive, and when involving
skin creases and follicular openings on the face and neck due to
large areas of the chest wall breathing, may be impeded. It is not
chronic sun damage. This is the first sign of chronic sun damage
related to systemic sclerosis, which is a widespread multi-system
and will always be seen in patients with basal cell carcinomas and
disease. There is a rare and mutilating form of linear morphoea in
squamous cell carcinomas. Both open and closed comedones can
children in which the underlying muscle and bone are involved
be found within solar elastosis (Favre–Racouchot syndrome, see
as well as the skin, causing problems with growth and permanent
Fig. 1.38, p. 10).
deformity.
Fig. 9.59 Naevus anaemicus: white patch due to Fig. 9.60 Solar elastosis on side of face and neck: Fig. 9.61 Morphoea: purple border with white
localised vasoconstriction chronic sun damage in a patient with skin type I atrophic centre
Face, trunk and limbs FRECKLES (EPHELIDES)

Non-erythematous lesions BROWN MACULES AND SMALL PATCHES (<2 cm) These well-demarcated, small (1–5 mm in
Normal surface diameter) orange-brown macules occur
All lesions <2 cm diameter on sun-exposed sites (face, dorsum of
hands and forearms). They appear after
Multiple (>20) Single, few or isolated lesions
similar lesions sun exposure in summer and disappear in
winter. They occur in red-haired, blue-eyed
individuals who burn rather than tan in
the sun. Histologically they contain normal
Sun-exposed sites only Light brown Dark brown Multiple numbers of melanocytes but increased
colours melanin pigment. They do not usually
present a diagnostic problem or need any
treatment.
Lesions No change Appears over Small <7 mm Irregular in outline
appear after after sun age 40 Round/oval and colour LENTIGO
sun exposure exposure Uniform
colour Lentigines are larger and darker than
freckles and may have irregular edges.
Face, trunk Surface Surface Appears No change Recent Long history They occur mainly on the sun-exposed
normal opaque before in size or increase in Elderly on skin of middle-aged and elderly people
age 40 shape diameter sun-exposed and are present all the year round. They
sites
are caused by chronic sun exposure and
if seen on the trunk in younger people
Children Elderly Biopsy Biopsy Biopsy
(age <40) are evidence of too much sun
exposure as a child. They are due to
increased numbers of melanocytes in the
FRECKLE LENTIGO SEBORRHOEIC JUNCTIONAL DYSPLASTIC SUPERFICIAL LENTIGO basal cell layer of the epidermis.
KERATOSIS NAEVUS NAEVUS SPREADING MALIGNA
MELANOMA
p. 288 p. 288 see p. 320 p. 290 p. 290 see p. 305 p. 291

BROWN LESIONS / 289
TREATMENT: LENTIGINES
Skin-lightening creams do not work. Reassure the

patient that lentigines are part of the normal ageing
process. Individual lesions can be frozen with liquid
nitrogen or treated with the NdYAG laser at 532 nm.
SEBORRHOEIC KERATOSIS
These lesions are usually raised; an early
seborrhoeic keratosis may be flat and light
brown, but under close inspection it will Fig. 9.65 (right)
have an uneven surface. Lentigines on
face of elderly
lady with skin
Fig. 9.62 Freckles type I
Fig. 9.63 Lentigines on dorsum of hand Fig. 9.64 Multiple lentigines over back in an Fig. 9.66 Dark star-shaped lentigines – these are
individual who spent his or her childhood in Africa benign
JUNCTIONAL NAEVUS
A flat dark-brown mole that is round or oval in shape is a
junctional naevus. Most are smaller than 7 mm in diameter. They
can occur anywhere on the skin including the palms, soles and
nail matrix (see Fig. 14.15, p. 440). They appear at any age but
usually before the age of 35. Histologically groups of melanocytes
are found in contact with the basal layer, hence the term junctional
naevus (see Fig. 9.102a).
DYSPLASTIC (ATYPICAL) NAEVUS

A dysplastic (atypical) naevus is a flat or slightly raised mole,
often >7 mm in diameter, that looks like a junctional naevus Fig. 9.67 Junctional naevus: round, Fig. 9.68 Dysplastic naevus: irregular
but which has an irregular edge and different shades of brown symmetrical evenly pigmented shape and pigmentation
within it. ABCDDEEE score (see p. 307) = 0 Border irregular, colour variable, dark:
(not dark) score = 3
The atypical mole (dysplastic naevus) syndrome
There are a small number of families where some members have
large numbers of moles (often >100), most of which are dysplastic,
and a family history of malignant melanoma. Such individuals
have an increased risk of developing multiple malignant
melanomas.
TREATMENT: JUNCTIONAL AND DYSPLASTIC NAEVI
Junctional naevi do not need to be removed unless there is doubt over the diagnosis.
Indeed, if lesions on the trunk are excised in young adults, the subsequent scarring can
be unsightly. If the lesion has changed or developed any irregularity in colour, shape or
border it should be excised and sent for histology to exclude a malignant melanoma. In
patients with multiple dysplastic naevi, professional medical photographs taken of the
whole body and given to the patient will help him or her identify any new or changing
naevi.
Fig. 9.69 Atypical mole syndrome: multiple large and irregular naevi on the
trunk
BROWN LESIONS / 291
LENTIGO MALIGNA
This looks very similar to an ordinary
lentigo but is larger (usually >20 mm),
has irregular margins and variation
in pigment colour. It occurs only on
sun-damaged skin, most commonly
on the cheeks of the elderly. It may be
difficult to distinguish from a benign
lentigo, but slow extension over
several years is characteristic. The
diagnosis should be confirmed by a
skin biopsy, which shows a malignant
melanoma confined to the epidermis
(melanoma in situ), see p. 304. These
can sometimes progress to become an
invasive malignant melanoma. Fig. 9.70 Lentigo maligna on cheek Fig. 9.71 Lentigo maligna melanoma arising in lentigo
maligna on scalp
TREATMENT: LENTIGO MALIGNA
Excision is the treatment of choice, although

for very large lesions on the face this may be
impractable. Slow Mohs surgery using routine
histopathology (see p. 332) can be used to
control margins.
Alternatives include:
● topical 5% imiquimod (Aldara) cream
applied three times a week for 12 weeks;

this causes marked inflammation (see
Fig. 9.72b) and the patient should be
warned about this
● cryotherapy.
a b c
Recurrence can occur, so follow-up is essential. Fig. 9.72 (a) Lentigo maligna before imiquimod treatment; (b) treatment with imiquimod has produced an intense
inflammatory reaction; (c) 4 weeks after completion of imiquimod treatment
Non-erythematous lesions NAEVUS SPILUS

Normal surface This is a birthmark where dark, speckled
Brown, blue or grey BROWN LESIONS (>2 cm) before AGE 10 macules or papules occur in a larger pale-
Large patches and plaques (>2 cm) brown pigmented patch.
Present from birth or before age 10
Patch Plaque
Dark-brown Light brown Blue/grey colour Dark brown

macules on
light-brown
background
Single lesion Recent Single/multiple

Present since childhood onset ?
Trauma
Oval/round Irregular Oval/round Around eye Ill defined on Round/oval +

geographic Multiple back hairy
shape
NAEVUS LENTIGINOUS CAFÉ AU NAEVUS OF MONGOLIAN BRUISING CONGENITAL

SPILUS NAEVUS LAIT PATCH OTA SPOT (? Child MELANOCYTIC
abuse) NAEVUS
p. 292 p. 293 p. 294 p. 293 p. 293 p. 293 p. 294

Fig. 9.73 Naevus spilus
BROWN LESIONS / 293
NAEVUS OF OTA
This is blue-grey patch of pigmentation
around the eye and on the sclera on one
side only. It is a type of blue naevus with
the melanocytes situated deep within
the dermis. It is common among the
Japanese and is present from birth or early
childhood. It remains present throughout
life. A similar lesion on the shoulder is
called a naevus of Ito.
MONGOLIAN SPOT
A large blue-grey patch on the back of
an oriental baby is extremely common.
It disappears spontaneously by the end Fig. 9.74 Naevus of Ota Fig. 9.75 Neavus of Ota on the sclera
of the first year of life. It can occur in any
race.
BRUISING (? CHILD ABUSE)

Bruising (see Fig. 9.77) can appear as blue-
grey discolouration as it settles. In children
the possibility of abuse always needs to be
considered.
LENTIGINOUS NAEVUS
This is a flat, pigmented birthmark, light
or medium brown in colour and oval or
geographic in outline. There is no surface
abnormality (see Fig. 9.79).
Fig. 9.76 Mongolian spot on buttocks and lower Fig. 9.77 Bruising
back
CAFÉ AU LAIT PATCH CONGENITAL MELANOCYTIC NAEVUS

These are light-brown patches, round or Congenital melanocytic naevi are moles that are present at birth. They are normally >2 cm
oval in shape, and often large (2–10 cm in diameter. At birth they may be red, rather than brown, but within a few months are
diameter). They are present at birth or obviously pigmented. They may be flat or raised, hairy or warty. They may sometimes
appear in early childhood. If more than six be very large, covering up to half the body surface. For the very large naevi there is a 9%
are found, or the patient also has freckles lifetime risk (greatest before puberty) of developing one or more malignant melanomas
in the axillae and multiple neurofibromas within the naevus.
in the skin or peripheral nerves, the
diagnosis of neurofibromatosis (von
Recklinghausen’s disease) can be made
(see p. 266).
Fig. 9.78 Lentiginous naevus Fig. 9.79 Multiple café au lait patches Fig. 9.80 Congenital melanocytic naevus: large
‘bathing trunk’ naevus with multiple smaller ones
BROWN LESIONS / 295
Normal surface
Brown, blue or grey BROWN LESIONS (>2 cm) after AGE 10
Appear after age 10 years
Poorly defined borders Well-defined border
Side of neck only Female Site of previous rash Lower legs Recent oral Upper trunk/upper arms Slowly Round/oval
Face only ? Previous medication, or enlarging Recurrent same
purpura skin application site
Mottled ?Contraceptive Brown colour Orange-brown Brown/orange/ Unilateral Bilateral ? Skin Previous blister/
Red-brown pill/pregnant blue-grey Geographic Small lesions thickened erythema
See list outline coalescing
POIKILODERMA MELASMA/ POST-INFLAMMATORY HAEMOSIDERIN DRUG-INDUCED BECKER’S PITYRIASIS MORPHOEA FIXED DRUG
OF CIVATTE CHLOASMA HYPERPIGMENTATION PIGMENTATION PIGMENTATION NAEVUS VERSICOLOR ERUPTION
LICHEN AUREUS
p. 296 p. 296 p. 297 pp. 279, 299 p. 298 p. 299 see p. 203 p. 299 p. 297
POIKILODERMA OF CIVATTE MELASMA (CHLOASMA)

Poikiloderma is identified by the Unsightly symmetrical pigmented patches occur in women on the forehead, cheeks
combination of pigment, atrophy and and moustache area that darken after sun exposure. They occur most commonly during
telangiectasia. Poikiloderma of Civatte is pregnancy or on taking the contraceptive pill. The pigmentation usually fades after
the commonest type and occurs in middle- delivery or on stopping the pill, but it may be permanent. Identical pigmentation is
aged and older patients on the sides of sometimes seen in men, and in women who are not pregnant or on the pill.
the neck. The skin becomes a mottled
red-brown colour with atrophic areas. TREATMENT: MELASMA
The area immediately under the chin and
ears is spared. It is thought to be due to If on the contraceptive pill, stop taking it. A mixture of 0.05% tretinoin, 4% hydroquinone and 0.01% fluocinolone
UV exposure, possibly associated with acetonide in a hydrophilic cream base (PigmanormUK, TrilumaUSA – available over the internet with private prescription)
applied twice a day for 8 weeks works well. Once the pigment has gone, the patient must keep out of the sun and/or use
cosmetics acting as photosensitisers. It is
a high factor (15+) sunscreen or it will reoccur.
very common and patients rarely bring
it to the attention of their doctors. No
treatment is available other than using a
sunblock.
Fig. 9.81 Poikiloderma of Civatte Fig. 9.82 Melasma Fig. 9.83 Post-inflammatory pigmentation following
lichen planus
BROWN LESIONS / 297
POST-INFLAMMATORY HYPERPIGMENTATION HAEMOSIDERIN PIGMENTATION

Brown patches on the skin may occur after any inflammatory This is seen following purpura where haemoglobin is broken
process in the epidermis (e.g. eczema, psoriasis, lichen planus). down to haemosiderin. The haemosiderin pigment looks similar
It is commoner in darker-skinned individuals. There is usually to melanin except that it is a more rust-brown colour. It is usually
a history of a rash before the pigment change. No treatment is seen on the lower legs (see p. 400). In cases of varicose eczema the
available but it usually improves with time. The inflammatory pigmentation may be a mixture of melanin and haemosiderin.
phase of a fixed drug eruption (see p. 181) can also be followed by
a dark-brown patch that remains for several months.
Fig. 9.84 Post-inflammatory pigmentation following Fig. 9.85 Post-inflammatory pigmentation following Fig. 9.86 Haemosiderin pigmentation: the colour is
a fixed drug reaction foot eczema a rust-brown rather than dark brown
PIGMENTATION DUE TO DRUGS

The following drugs can cause pigmentation in the skin:
● amiodarone, chloroquine, minocycline, chlorpromazine (and
other phenothiazines), dapsone, gold: blue-grey pigmentation
in sun-exposed sites
● phenytoin and oral contraceptive pill: pigmentation similar to
melasma (see Fig. 9.82)
● clofazimine (red pink)
Fig. 9.87 (right)
● β-carotene (orange)
Carotenemia
● mepacrine (yellow), on right,
● bleomycin: flagellate brown or purple (linear streaks usually on compared with
back) normal on left
Fig. 9.88 Amiodarone pigmentation Fig. 9.89 Minocycline pigmentation. Fig. 9.90 Gold pigmentation Fig. 9.91 Mepacrine pigmentation
(chrysiasis)
BROWN LESIONS / 299
BECKER’S NAEVUS
This is a congenital hamartoma of the skin that is androgen-
sensitive so appears in the mid to late teens and then persists
for life. It is an irregularly shaped patch of hyperpigmentation
containing more hairs than is normal. It most commonly occurs
over the shoulder region but can occur anywhere. No treatment
is available, although the hair can be removed with a laser
(Alexandrite, see p. 67); this can make the hyperpigmentation
worse.
LICHEN AUREUS
A localised form of capilaritis where blood leaks from superficial
vessels and the residual haemosiderin is seen as an orange/
golden-coloured patch.
Fig. 9.92 Becker’s naevus
MORPHOEA
Morphoea can present as a brown patch or plaque with a purple-
brown border (see also p. 287).
Fig. 9.93 Lichen aureus 9.94 Brown patches of morphoea


Non-erythematous lesions BROWN – raised lesions
Normal surface
Papules, plaques, nodules
Soft on Firm-hard Normal on palpation
palpation palpation
Small papules Papule >3 mm Papules <3 mm Papule >3 mm Plaque >1 cm Nodule >1 cm
(<3 mm base) within surface Multiple on surface
Pedunculated Surface dimples on Flat top Dome shape ‘Stuck on’ Irregular shape, Raised rolled Irregular pigment
squeezing Opaque surface Uniform colour Keratin plugs colour and border border and border
in surface
Neck, axilla Pigment around Linear and Appears < age 35 Appears > age 35 Age >20 Age >40 Recent rapid
periphery grouped Size <8 mm Size >7 mm Slow growth growth
SKIN TAGS DERMATOFIBROMA PLANE WARTS COMPOUND SEBORRHOEIC SUPERFICIAL PIGMENTED NODULAR
NAEVUS KERATOSIS SPREADING BASAL CELL MALIGNANT
MELANOMA CARCINOMA MELANOMA
see p. 266 p. 301 see p. 268 p. 302 p. 301 p. 305 p. 309 p. 307
BROWN LESIONS / 301
DERMATOFIBROMA (HISTIOCYTOMA) SEBORRHOEIC KERATOSIS/WART

This is a firm-hard papule situated in the dermis and occurs Seborrhoeic keratoses usually have a warty or keratotic surface
anywhere on the body. It often follows an insect bite, so is (see p. 320). Occasionally they have a smooth surface and can be
most commonly found on the legs. It is usually small (<5 mm), confused with compound naevi or even malignant melanomas if
attached to the skin and mobile over deeper structures. Squeezing very heavily pigmented. If you look carefully at the surface you
the lesion from the sides results in puckering of the skin since may see small keratin plugs, which are specific to seborrhoeic
dermatofibromas are situated very high in the dermis. The colour keratoses. In addition the lesion will tend to be sitting on top of
ranges from skin coloured, to pink to brown, often with a darker the skin and have no deep component at all.
ring at the edge. The surface may be smooth or slightly scaly. It
looks like a compound naevus but is distinguished by being much
firmer on palpation.
Fig. 9.95 Dermatofibroma showing halo of Fig. 9.96 Puckering of the skin over a Fig. 9.97 Seborrhoeic keratosis: note tiny keratin
pigmentation around edge dermatofibroma when squeezed plugs in surface
COMPOUND NAEVUS If a benign mole becomes more elevated and at the same time
These are melanocytic naevi that are raised and pigmented, and lightens in colour, this is the normal change from junctional to
may be hairy. On histology the melanocytes are both at the dermo- intradermal naevus. Sometimes moles can look irregular if part
epidermal junction and within the dermis (hence compound). of the periphery of the mole is flat and brown (junctional) and the
The melanocytes at the dermo-epidermal junction give moles centre raised and lighter in colour (intradermal) (see Fig. 9.101).
their brown colour while the intradermal melanocytes result Malignant change should be thought of if there is lateral spread of
in elevation. The natural history of moles is a maturation from pigment (see Fig. 9.103b).
junctional naevi (flat and dark brown) to compound naevi (brown
and dome-shaped or papillomatous) to intradermal naevi (skin- TREATMENT: COMPOUND NAEVUS AND DERMATOFIBROMA
coloured papules) see Fig. 9.102, p. 303.
Only remove if they are very unsightly or get caught on clothing. For compound
Established benign moles change (see previous paragraph) and naevi removal by shave biopsy will generally leave an acceptable scar, which is flat
new moles occur or get bigger around puberty, during pregnancy and no bigger than the original lesion, although recurrence of pigment may occur.
and after sun exposure. Assuming that all moles that change are Dermatofibromas need to be excised but in young people this can leave ugly scars.
malignant is misleading. It is the type of change that is important. Always send the lesion off for histology.
Fig. 9.98 Compound naevus: dark- Fig. 9.99 Compound naevus with a Fig. 9.100 Compound naevus in Fig. 9.101 Compound naevus with
brown, elevated mole papillomatous surface patient with type I skin peripheral junctional area
ABCDDEEE score (see p. 307) dark, ABCDDEEE score not applicable: warty colour variable, elevated: score = 2 colour variable, diameter >1 cm: score = 2
elevated: score = 2 surface
BROWN LESIONS / 303
a. Junctional naevus (p. 290) b. Compound naevus (p. 302) c. Intradermal naevus (p. 264) d. Combined junctional and
compound naevus
Histological features:
Naevus cells at dermo-epidermal Naevus cells at dermo-epidermal Naevus cells only within dermis. Junctional cells throughout lesion,
junction. junction and within the dermis. intradermal naevus cells centrally
only.
Clinical features:
Flat and dark brown. Raised (dome shaped or papillomatous) Raised (dome shaped or papillomatous) Periphery flat and brown, centre raised and
(ABCDDEEE score, see p. 307) and brown. and skin coloured. brown.
dark: score = 1 dark, elevated: score = 2 elevated: score = 1 colours multiple, elevated: score = 2
Fig. 9.102 Clinicopathological correlation of melanocytic naevi (moles)

a. Lentigo maligna (p. 291) b. Superficial spreading malignant c. Superficial spreading melanoma d. Nodular malignant melanoma
melanoma (p. 305) with nodule (p. 306) (p. 306)
Histological features:
Malignant melanocytes restricted Malignant melanocytes migrating Malignant melanocytes growing Malignant melanocytes migrating
to epidermis only. Has an laterally along dermo-epidermal downwards as well as laterally. vertically downwards only. Has a
excellent prognosis. junction. Has a good prognosis. Has a worse prognosis. poor prognosis.
Clinical features:
Large irregular patch on sun-exposed skin Flat plaque with irregular shape and Black irregular plaque out of which is Black bleeding nodule. No surrounding
in the elderly – long history. pigment, recent increase in diameter. growing a brown nodule. pigmentation.
ABCDDEEE scoring (see p. 307) Asymmetry, border irregular, colour Asymmetry, border irregular, colour Border irregular, diameter >10 mm,
Asymmetry, border irregegular, colour variable, diameter >10 mm, dark: score = 4 variable, diameter >10 mm, dark, elevated: dark, elevated: score = 4
variable, diameter >10 mm: score = 4 score = 6
Fig. 9.103 Clinicopathological correlation of malignant melanoma

BROWN LESIONS / 305
MALIGNANT MELANOMA 2a. Superficial spreading malignant melanoma (SSMM). The initial growth phase of
A malignant melanoma is malignant malignant melanocytes is along the dermo-epidermal junction (radial growth phase).
tumour of melanocytes. Two-thirds arise This change is seen clinically as a flat brown patch enlarging in diameter. Because the
from normal skin and one-third from a radial growth is usually uneven, there will be variation in the degree of pigmentation
pre-existing mole. There are four clinical and an irregular border, often with scalloped edges. There may also be evidence of
patterns of malignant melanoma. inflammation, erythema and sometimes an altered sensation. Tumour cells remain
1. Lentigo maligna. A large (1–3 cm size) high in the dermis and are unlikely to invade blood vessels or lymphatics. As a
brown patch on sun-exposed skin in result superficial spreading melanomas generally carry a good prognosis. If however
an elderly patient. The tumour cells regression has occurred, then the depth of invasion may have been greater previously
are confined to the epidermis (see than it is at removal, raising the possibility that the prognosis based on thickness may
p. 304). Later an invasive melanoma be false.
can develop with a lentigo maligna as
a papule or nodule within the original
patch (see Fig. 9.71, p. 291).
Fig. 9.104 Superficial spreading melanoma: note Fig. 9.105 Small early superficial spreading melanoma on chest: close-up (above left).
size, irregular border and pigment. (Scores 4 points on ABCDDEEE, see p. 307; border irregular, diameter >10 mm, dark, elevated)
(Scores 5 points on ABCDDEEE, see p. 307)
2b. Superficial spreading melanoma with nodular component. surrounding irregular pigmentation. A typical nodular melanoma
Eventually the malignant melanocytes grow downwards (vertical is a black, dome-shaped nodule. The surface of the lesion will
growth phase). A papule or nodule will appear within the flat eventually break down to bleed, ooze and crust over. Sometimes
irregular brown patch (see Figs 9.103c and 9.106). Once this nodules may be red (amelanotic – see also Fig. 8.47, p. 216) rather
happens the prognosis becomes worse because tumour cells are than brown-black. The diagnosis can be delayed as there is no
more likely to have entered dermal blood vessels and lymphatics superficial spread to alert the patient, and prognosis is often poor
leading to metastases. as the lesion will be relatively thick before it has been diagnosed
and removed. The ABCDDEE list may not help with nodular
3. Nodular malignant melanoma. This type needs to be
melanomas. Black or red nodules should be referred for biopsy.
distinguished from the superficial spreading melanoma. Here
there is no radial growth and the malignant melanocytes grow 4. Acral lentiginous melanomas occur on the palms, soles or
down vertically from the start. The lesion is a nodule without any under the nails (see p. 440).
Fig. 9.106 Nodule arising in a lentigo maligna Fig. 9.107 Nodular melanoma with no horizontal Fig. 9.108 Recurrence of melanoma around a large
(scores 6 points with ABCDDEEE – asymmetry, border growth phase skin graft on the back
irregular, colour variable, diameter >10 mm, darkness, (scores 6 points on ABCDDEEE – colour variable, diameter
elevation) >10 mm, darkness, erythema, elevation, exudate)
BROWN LESIONS / 307
Diagnosis of melanoma ● Asymmetry: there will not be an axis of symmetry in any

It is important to diagnose malignant melanomas while they direction
are thin so that removal results in cure. In practice this means ● Border irregular: the border should be definite but irregular
distinguishing them from lentigines, junctional and compound with notches; fade-out of border does not count (see Fig. 9.109)
naevi. Remember that benign moles can change (see Fig. 9.102). ● Colour variable: definite areas of light
Malignant lesions tend to be larger, darker, palpable, and may and dark brown, or black
ooze or bleed. ● Diameter >10 mm
● Darkness of colour (dark brown or
To identify melanomas this checklist (ABCDDEEE) may be black)
helpful. If four or more are present, a melanoma is possible. ● Erythema
Biopsy if three are present. Only apply this check list if the surface ● Elevation
is smooth (i.e. not warty, papillomatous, scale, keratin or crust). ● Exudate: any evidence of serum or Fig. 9.109 Benign naevus
Dermoscopy will also be useful in distinguishing the benign from blood on the surface with border fade-out
malignant (see p. 18).
1. 2. 3 4. 5. 6. 7.
Asymmetry yes yes yes no yes no no
Border irregular yes yes yes no yes no no
Colour variable no yes no no no yes no
Diameter >10 mm yes yes no no yes yes yes
Darkness yes no yes yes yes no yes
Erythema no yes no no no no yes
Elevation no no no no yes no yes
Exudate no no no no no no yes
SCORE 4 5 3 1 5 2 5
Diagnosis: SSMM SSMM Dysplastic naevus Junctional naevus Nodular MM Lentigo (cheek) Ulcerated nodular
MM
Fig. 9.110 Using the ABCDDEEE checklist in diagnosing melanomas

Aetiology of malignant melanoma ● those who have a large number of moles (>50); duration of sun
Malignant melanoma is more likely to occur in: exposure in childhood is linked to number of moles
● those with fair or red hair who burn rather than tan in the sun ● those with a past or family history of malignant melanoma
(skin types I and II) ● those with atypical mole syndrome (see p. 290)
● those who have been badly sun burnt on more than one ● giant congential melanocytic naevus, p. 294
occasion in childhood (< age 18), but not as an adult ● the use of tanning beds before age 35.
Prognosis of malignant melanoma (See Table 9.01.)

Table 9.01 Prognosis of malignant melanoma showing % survival rates at 1–15 The following have been found to accurately predict prognosis.
● Breslow’s thickness (see Fig. 9.111): measure in millimeters the
years
depth from the top of the granular cell layer of the epidermis to
Prognosis of malignant melanoma (% survival rates 1–15 years)
the deepest point of invasion. This is by far the most important
No lymph node involvement or distant metastasis prognostic indicator.
Stage Thickness Ulceration 1 year 2 years 5 years 10 years 15 years ● Ulceration: for any given thickness this worsens the prognosis.
IA <1 mm No 99.7 99.0 95 88 85 ● Involvement of regional lymph nodes or satellite/in-transit
IB <1 mm Yes 99.8 98.7 91 83 72 metastases makes the prognosis worse (stage III). The more
1–2 mm No 99.5 97.3 89 79 72 nodes involved (>3) and if the metastases are clinically
IIA 1–2 mm Yes 98.2 93 77 64 57 apparent, the worse the prognosis.
2–4 mm No 98.7 94 79 64 57 ● Distant metastases and elevated levels of lactic dehydrogenase
IIB 2–4 mm Yes 95.1 85 63 51 44 in the blood imply a very poor prognosis (stage IV).
>4 mm No 95 89 67 54 44
IIC >4 mm Yes 90 71 45 32 29
With lymph node involvement or distant metastasis – any thickness
Stage Nodes Ulceration 1 year 2 years 5 years 10 years 15 years
IIIA 1–3 micro No 95 86 67 60 59
IIIB 1–3 micro Yes 88 75 53 38 31
1–3 macro No 88 75 53 38 31
IIIC 1–3 macro Yes 71 49 27 19 17
>4 or in-transit Yes/No 71 49 27 19 17
IV Distant metastases 50 25 10 7 5
Note: from Balch CM, Gershenwald JE, Soong SJ, et al. Final version of 2009 AJCC melanoma staging Fig. 9.111 Breslow’s thickness: measure in millimeters the depth of invasion
and classification. J Clin Oncol. 2009; 27(36): 6199–206. from the granular layer to the deepest tumour cells
BROWN LESIONS / 309
TREATMENT: MALIGNANT MELANOMA PIGMENTED BASAL CELL CARCINOMA

Occasionally basal cell carcinomas are heavily pigmented and they
All suspicious lesions should be excised with a 2 mm margin of normal skin and sent for may then be confused with a nodular malignant melanoma. The
histology. Having confirmed the diagnosis histologically, wider excision is carried out as typical rolled edge should suggest the diagnosis (see p. 330).
follows (UK and Australian guidelines):
● confined to the epidermis – excise with 0.5 cm margin
● tumours <1 mm thick – excise with 1 cm margin
● tumours 1–2 mm thick – excise with 1–2 cm margin
● tumours >2 mm thick – excise with 2 cm margin.
SENTINEL NODE BIOPSY AND ADVANCED DISEASE

Removal of the nearest lymph node (the sentinel node) to which the lymphatics at
the site of the tumour drain may help predict the prognosis. It is found by injecting a
radioactive tracer and a blue dye. If this node does not contain tumour, the prognosis
is obviously better than if it does. Block dissection of the nodes is usually done if the
sentinel node is positive. Otherwise lymph nodes are not removed unless clinically
involved.
There is no evidence that sentinel node biopsy or removal of lymph nodes improves the
prognosis. It should only be performed to give the patient or physician a better idea of Fig. 9.112 Pigmented
prognosis (usually in clinical trials). basal cell carcinoma:
note pigment in the
Metastatic melanoma can be treated with immunotherapy: ipilimumab (blocks CTLA-4) rolled edge
plus vemurafenib (blocks BRAF), see p. 57.
PREVENTION OF MELANOMAS
Almost all melanomas are induced by sun exposure, particularly short, sharp bursts
leading to sunburn. Everyone should protect themselves from sunburn and in particular
parents should protect their children from sunburn by using a waterproof high-
protective-factor sunscreen (SPF 30+) on all exposed skin and covering as much skin as Fig. 9.113 Pigmented
possible. basal cell carcinoma:
clinically it is not possible
There is no evidence that having a melanoma during pregnancy affects the prognosis;
to distinguish this lesion
likewise, taking the contraceptive pill or hormone replacement therapy do not alter the from a melanoma
natural history of melanoma. except by histology
(scores 7 points with
ABCDDEEE list, see p. 307)

Non-erythematous lesions BLACK, BLUE, PURPLE or GREY LESIONS
Normal surface
Macules, papules and nodules
Rapidly Individual or isolated lesions >5 mm Multiple small lesions <5 mm
growing
Multiple
lesions
Purple Irregular border, Round, papule/nodule Central punctum Black plugs in surface Multiple small
variable colour papules
Papules, Rolled edge ? Previous No change on on firm pressure Empties on firm pressure Teenager or Elderly on Black papules
nodules mole changed elderly nose on cheeks
plaques
HIV +ve Biopsy Dermoscopy Smooth Warty/keratin Dermoscopy Trans- 1–4 mm <1 mm Skin type V
Biopsy surface cysts on illuminates and VI
surface
KAPOSI’S PIGMENTED MALIGNANT BLUE/ SEBORRHOEIC HAEM- APOCRINE COMEDONE TRICHOSTASIS DERMATOSIS
SARCOMA BASAL CELL MELANOMA COMPOUND KERATOSIS ANGIOMA HIDRO- SPINULOSA PAPULOSA
CARCINOMA NAEVUS* CYSTOMA NIGRA
p. 311 see p. 309 see p. 305 p. 311 see p. 301 p. 312 see p. 274 p. 313 p. 313 p. 313
*Seen in heavily pigmented skin

BLACK, BLUE, GREY LESIONS / 311
KAPOSI’S SARCOMA
This is a malignant growth of blood vessels caused by human
herpes virus 8. It is seen mainly in patients with HIV/AIDS. The
lesions begin as small reddish-purple, reddish-brown or purple
macules or papules that grow to form nodules and plaques.
Screening for HIV and a biopsy will confirm the diagnosis.
TREATMENT: KAPOSI’S SARCOMA
In patients with AIDS, the appearance of Kaposi’s sarcoma would be a reason to

introduce HAART (highly active antiretrovirus treatment) even with a normal CD4 count.
For the Kaposi’s sarcoma itself, no treatment is needed unless the lesions are unsightly
or painful. Small lesions can be excised. Lesions localised to a limb can be treated with
radiotherapy. Chemotherapy using vinblastine, doxorubicin, and bleomycin give good
palliation for a while.
BLUE NAEVUS Fig. 9.114 Widespread Kaposi’s sarcoma: macules and papules
This looks like a compound naevus except that it is blue or blue-
black rather than brown in colour. It is dome shaped, usually less
than 10 mm in diameter. Blue naevi appear during childhood
and then remain fixed, a feature that will distinguish them from
a malignant melanoma. In pigmented skin, ordinary compound
naevi may be black in colour rather than brown. No treatment is
needed, as this is a benign lesion.
Fig. 9.115 Nodule of Kaposi’s Fig. 9.116 Blue naevus

sarcoma
HAEMANGIOMA AND ANGIOKERATOMA Angiokeratomas are similar but have a scaly surface. They may be
The terms angioma and haemangioma are interchangeable. Red almost black in colour.
or purple papules and plaques that have been present since
childhood are due to a localised overgrowth of blood vessels. The TREATMENT: ANGIOMA AND HAEMANGIOMA
stagnant blood within the lesion may be compressed partially, but
the colour will never fade completely. Small lesions can be excised or cauterised. Larger lesions are best left alone as the
vascular malformation in the deeper tissue may be extensive.
Those occurring in adult life may be very dark in colour and
mimic an early melanoma. If you look carefully you will
see a lobulated vascular pattern; this is easily seen using a
dermatoscope (see Fig. 1.91, p. 18).
Fig. 9.117 Haemangioma: (a) compressible nodule Fig. 9.118 Black coloured angioma: diagnosis made Fig. 9.119 Angiokeratoma on a child’s leg: differs
on left temple; (b) same lesion after compression by dermoscopy (see p. 18) from an ordinary angioma in having a scaly surface
BLACK, BLUE, GREY LESIONS / 313
TRICHOSTASIS SPINULOSA GIANT COMEDONE

Small blackheads on the nose in elderly Single large comedones can occur on the trunk and face in the elderly. They are much
patients are very common. They are due larger than the blackheads associated with acne in teenagers, but the aetiology is basically
to the failure of shedding of vellus hairs in the same, i.e. a single follicle with a keratin plug at its mouth, filling up with keratin and
the hair follicles of the nose. sebum behind it. Clinically it is a white/cream papule with a central black punctum.
If the patient complains about the problem DERMATOSIS PAPULOSA NIGRA
and wants treatment, 0.05% isotretinoin
Multiple small black or brown papules occur on the cheeks particularly in black skin.
(Isotrex) gel or lotion applied at night
Histologically the lesions are seborrhoeic keratoses. They are inherited as an autosomal
for 6–8 weeks will give a fairly dramatic
dominant trait. They are harmless and best left alone.
improvement. It can be kept clear by using
it twice a week.
Fig. 9.121 Giant comedo Fig. 9.122 Dermatosis papulosa nigra: tiny
seborrhoeic keratoses on cheek in black skin
Fig. 9.120 (left) Trichostasis spinulosa on the nose

Non-erythematous lesions SPITZ NAEVUS

Normal surface These look like moles but they are red/orange in colour.
Red, orange colour RED or ORANGE LESIONS They mainly occur in children. In adults they can be confused
Macules, papules, plaques histologically with malignant melanoma. Reassurance that they
(Nodules see p. 213) are benign is all that is necessary.
Macule Papule Plaque
Red/purple colour Orange colour Red/straw

coloured
Fluid filled
Middle age/elderly Bleeds easily Children Lobulated
CHERRY PYOGENIC SPITZ LYMPHANGIOMA

ANGIOMA GRANULOMA NAEVUS CIRCUMSCRIPTUM
(Cambell de
Morgan spot)
see p. 315 see p. 334 p. 314 p. 315

Fig. 9.123 Spitz naevus
RED, ORANGE LESIONS / 315
CHERRY ANGIOMA (CAMPBELL DE MORGAN SPOT) LYMPHANGIOMA CIRCUMSCRIPTUM

These small (1–4 mm) bright-red or purple papules appear on the This is an uncommon malformation of lymphatics. Grouped
trunk and proximal limbs in patients over the age of 35. Usually straw-coloured papules that look like frogspawn are present in the
there are multiple lesions. They are a normal finding and do not skin. Usually there is some communication between lymphatics
need to be removed. Viewed through the dermatoscope (see p. 18), and blood vessels so some of the lesions can be red or black. The
you can see that they are vascular. lesions may remain static or gradually increase in extent over the
years.
TREATMENT: LYMPHANGIOMA CIRCUMSCRIPTUM
As well as the visible surface component, there is a deep component (muscular cistern)
in the subcutaneous fat. If treatment is required, surgical excision is the treatment of
choice but the deep component will have to be removed to prevent recurrence.
If surgical removal is not possible and the lesions get traumatised and leak, then the
best thing is to produce a superficial scar over the surface to seal them using a carbon
Fig. 9.124 (right) Angioma dioxide or Erbium-YAG laser.
showing lobulated pattern
Fig. 9.125 Multiple cherry angiomas Fig. 9.126 Lymphangioma circumscriptum: close-up of a lesion on the neck
Surface warty/papillomatous WARTY or PAPILLOMATOUS LESIONS
Brown, skin coloured
Papules, plaques
Present at birth Appears age Appears any age
0–10
Pigmented Linear Smooth on palpation Rough on palpation

± hairy
Skin – brown Dome shape Pedunculated Flat top Keratin plugs in Dome shape On stalk
coloured Opaque surface
Grows with Brown colour Skin coloured Multiple Multiple ‘Stuck on’ to Growing out of Multiple
child Axilla/neck Grouped surface surface Often face
CONGENITAL EPIDERMAL COMPOUND INTRADERMAL SKIN TAGS PLANE SEBORRHOEIC COMMON FILIFORM
MELANOCYTIC NAEVUS NAEVUS NAEVUS WARTS KERATOSIS WART WART
NAEVUS
p. 317 p. 317 see p. 302 see p. 264 see p. 266 see p. 268 p. 320 p. 318 p. 320
WARTY SURFACE / 317
EPIDERMAL NAEVUS CONGENITAL MELANOCYTIC NAEVUS

An epidermal naevus is a developmental Congenital melanocytic naevi, unlike
defect that presents as a skin-coloured or acquired moles, are present at birth.
brown linear warty plaque. It often looks They are usually >2 cm in diameter and
like a line of viral warts, but it is present are brown with a warty and sometimes
from birth or early childhood. It may be hairy surface (see also Fig. 9.80, p. 294).
quite small (1–2 cm long) or go down the Malignant melanoma may arise in
length of an arm or leg, or in a line around congenital naevi, and any growing nodules
one side of the trunk. will need to be biopsied.
Fig. 9.129 Congenital melanocytic naevus: present

from birth and grows with age
Fig. 9.127 Warty epidermal naevus on side of the trunk Fig. 9.128 Congenital melanocytic naevus with a papillomatous surface
TREATMENT: CONGENITAL AND EPIDERMAL NAEVI
Small naevi can be excised, although scarring is more

prominent in children’s skin. Giant naevi are too large
to remove surgically. Treatment with a pigment laser
may reduce the colour but is unlikely to produce a
good cosmetic result, and does not reduce the risk of
melanoma.
Surgical removal of epidermal naevi is difficult, especially
if the lesion is large. A compromise is to shave and
cauterise the superficial component. There is a tendency
for the warty papules to regrow but this may take
several years.
COMMON WARTS Fig. 9.130 Multiple common warts on the hand

Warts are an infection of the epidermis with
one of the numerous human papilloma
viruses. They are transmitted from one
individual to another through broken skin
(cuts, grazes, and so forth). They disappear
spontaneously without scarring after weeks
to years (average about 2 years) when the
body has built up enough cell-mediated
immunity. Unfortunately immunity to one
type of wart virus does not confer immunity
to any of the others, i.e. having had an
infection with the common wart virus does
not prevent infection with the plantar wart
or plane wart virus.
Common warts are easily recognised as
firm, rough, skin-coloured or brown papules Fig. 9.131 Multiple warts in and around mouth in Fig. 9.132 Warts on wrist
with black pinpoint dots on the surface. patient with HIV infection
WARTY SURFACE / 319
TREATMENT: COMMON WARTS
Treatment of warts depends on the age of the patient and how many are present.
In young children the best treatment is to leave alone. You will need to explain to
parents that they are a viral infection that will resolve spontaneously.
For older children and adults, if there is a single wart or only a few warts the options
are as follows.
● Cryotherapy. First pare down any hyperkeratosis on the surface and then freeze
with liquid nitrogen until the wart and a halo of normal skin goes white (10–30
seconds). The patient should get a blister at the site within 48 hours as the epidermis
that contains the wart lifts off. It is important that the treatment is repeated every
2–3 weeks until the wart goes. Do not use several freeze–thaw cycles, as you may
get necrosis of the underlying skin. Large warts (>5 mm) diameter do not respond
well to cryotherapy.
● Curettage and cautery under local anaesthetic is very effective and should result in
clearance immediately. This is a very good treatment for single warts on the face and Fig. 9.133 Curettage of a wart using a Volkmann spoon, which allows blunt
dissection of the wart off the skin: the base is cauterised and curetted twice
elsewhere.
For multiple warts the options are:

● leave alone and await natural resolution
● a keratolytic agent (salicyclic + lactic acid) – apply at night before going to bed; pare
down any excess keratin before the agent is applied, and cover with a plaster unless
it contains a collodian gel that sets; this should be carried out for several weeks to
months; you should remind the patient that keratolytic agents do not cure warts
themselves; any effect is probably secondary as an adjunct to the development of
natural immunity
● 20% podophylline applied at night – this is brown and unsightly
● 5% imiquimod cream applied three times a week for 12 weeks – use a keratolytic
agent first to reduce surface keratin to allow better penetration of the imiquimod
● pulsed dye laser – this results in coagulation of the blood vessels within the wart; a
single shot of 8 joules/cm is given to each wart; treatment is expensive but in many
cases two or three treatments will be effective.
Fig. 9.134 Wart treated with liquid Fig. 9.135 Blister after treatment with
nitrogen showing halo of frozen liquid nitrogen
normal skin
FILIFORM WARTS
These are warts with long finger-like protrusions. They occur around the eyelids, on the
nose, lips and beard area.
TREATMENT: FILIFORM WARTS
For single or few lesions curettage and cautery under local anaesthetic is the treatment of choice. Cryotherapy is also
effective. For multiple warts in the beard area, frizzle them up with a hyfrecator.
SEBORRHOEIC KERATOSIS/WART (BASAL CELL PAPILLOMA)

These very common lesions have a flat but warty surface, and typically look as if they
are ‘stuck on’ to the skin. Sometimes small keratin cysts can be seen in the surface (see
Fig. 9.97, p. 301). These can be black or white in colour and easily visualised through a
dermatoscope (see Fig. 1.95, p. 18). Initially seborrhoeic keratoses are skin coloured and
Fig. 9.136 Filiform warts on eyelid
not very noticeable, but gradually become more prominent and deepen in colour from
light brown to jet black. They are usually multiple and occur most commonly on the face
and trunk of middle-aged or elderly people. They are usually easy to diagnose but their
appearance late in life, the black or brown colour and the increase in size are all features
that cause alarm to the patient. Occasionally they may become inflamed, particularly if
they have been caught in clothing and partly torn off (see Fig. 9.165).
They need to be distinguished from moles, solar keratoses, and occasionally from
pigmented basal cell carcinomas and malignant melanomas. Moles (melanocytic naevi)
are more dome shaped and do not have the ‘stuck on’ appearance, while solar keratoses
are rough to palpation, being felt more easily than seen. Basal cell carcinoma has a more
shiny surface and a rolled edge with telangiectasia running over it, while a malignant
melanoma has an irregular edge, colour variation and does not look as if it is ‘stuck on’ to
the surface.
Fig. 9.137 Filiform warts on the beard area

WARTY SURFACE / 321
TREATMENT: SEBORRHOEIC KERATOSIS
Most lesions require no treatment. Unsightly lesions on the face and trunk can be
removed by curettage and cautery under local anaesthesia or by freezing with liquid
nitrogen.
Fig. 9.138 Seborrhoeic keratoses: note the variation in colour (left lesion) and
small keratin cysts within the lesion on the right
Fig. 9.139 Seborrhoeic keratosis: Fig. 9.140 Seborrhoeic keratosis:

non-pigmented lesion with deeply pigmented lesion – might be
papillomatous surface confused with a malignant melanoma,
but ‘stuck on’ to surface and with
papillomatous surface Fig. 9.141 Multiple seborrhoeic keratoses on the back
Surface scaly or keratin SCALE or KERATIN: MULTIPLE LESIONS or DRY SKIN
Papules, patches, plaques
Multiple (more than five) lesions/rash
Widespread dry skin Widespread Multiple isolated lesions
follicular
papules
Onset in childhood Onset as adult Onset in Poorly defined Well-defined lesions

childhood
Elbow and knee flexures spared Outer arms Fair skinned Fine dry scale Greasy scale Warty scale
thighs, (cheeks) Sun exposed sites picks off easily adherent
Yes No Scale/keratin Fine ring of Scale picked Flat top ‘stuck Rounded top
difficult to keratin and flat off easily on’ surface ‘growing out’ of
remove centre surface
Fine white scales Large brown Fine white Follicular Face, scalp, Lower legs, Lower legs
scales scales keratin plugs dorsum of hand forearms Elderly
ICHTHYOSIS X-LINKED ACQUIRED KERATOSIS SOLAR ACTINIC STUCCO SEBORRHOEIC VIRAL

VULGARIS ICHTHYOSIS ICHYTHOSIS PILARIS KERATOSIS POROKERATOSIS KERATOSES KERATOSIS WARTS
p. 323 p. 323 p. 323 p. 324 see p. 326 see p. 326 p. 324 see p. 320 see p. 318
SCALY/KERATIN SURFACE / 323
ICHTHYOSIS VULGARIS X-LINKED ICHTHYOSIS

This is a genetic disorder transmitted as an autosomal dominant trait. It is first noticed This is transmitted by an X-linked
at or soon after birth. The skin is dry with small fine white scales, affecting the whole of recessive gene, so appears in boys but is
the skin except the antecubital and popliteal fossae. There are increased skin markings on transmitted though females. It is much less
the palms and soles (see Fig. 8.85, p. 237), and some individuals will also have keratosis common than ichthyosis vulgaris, from
pilaris and atopic eczema. The patient will complain of the appearance and the associated which is distinguished by the fact that the
itching. It often improves in the sun and with increasing age. scales are large and dirty brown in colour
and the flexures are involved. Sunshine
Acquired ichthyosis is clinically similar to ichthyosis vulgaris but occurs later in life. It
does not help and it does not usually
may be idiopathic or due to an underlying lymphoma.
improve with age.
TREATMENT: ICHTHYOSIS
Since central heating tends to dry out the skin, this

should be kept to a minimum and if the weather
is cold and the humidity low, then this needs to be
increased with a humidifier.
Add a capful of one of the proprietary dispersible bath
oils to the bath water (see Table 2.01b, p. 27) and stay
in the bath for 15 minutes a day. Wash with Dermol
500UK or EpadermUK ointment instead of soap, because
soap removes the natural grease and makes the skin
even drier.
After getting out of the bath, while the skin is moist
and warm, apply a greasy moisturiser. There is a wide
range available. Some contain keratolytic agents such
as urea (AquadrateUK, CalmuridUK, CalmolUSA), salicylic
or lactic acid, which also help remove the excess
keratin (see Table 2.01a, pp. 26).
Severe cases may be improved by systemic retinoids
such as acitretin 10–25 mg/day (see p. 49). These are
available only from a dermatologist.
Fig. 9.142 Ichthyosis vulgaris: fine white scale Fig. 9.143 X-linked ichthyosis: large dark scales
KERATOSIS PILARIS TREATMENT: KERATOSIS PILARIS STUCCO KERATOSES

This is such a common condition in childhood and adolescence This is a term used to describe
that it can be regarded as one end of the normal spectrum of skin If treatment is required, a topical multiple fine scaly papules
changes. Many patients will not notice it or complain about it. keratolytic agent can be applied: 10% scattered over the lower
urea cream (Calmurid) or 2% salicylic
It often improves spontaneously in the summer. Skin-coloured legs in some elderly people.
acid ointment put on once or twice
follicular papules develop on the cheeks, the upper arms and The lesions are seborrhoeic
a day will not cure it but will remove
thighs. Sometimes the papules are red rather than skin coloured. It the rough surface temporarily and
keratoses. They may improve
may be associated with ichthyosis vulgaris or atopic eczema, and make it feel more comfortable. by applying a urea or lactic
is often familial (see also p. 115). acid based moisturiser such as
Calmurid cream.
Fig. 9.144 Keratosis pilaris on upper arm: rough Fig. 9.145 Keratosis pilaris: close-up of follicular Fig. 9.146 Stucco keratoses: multiple small scaly
follicular pink papules on upper arm of young girl plugs papules on lower legs
SCALY/KERATIN SURFACE / 325

Scale, keratin surface SCALE/KERATIN – single/few lesions
Papules and nodules
Single/few (<5) lesions
Cutaneous horn on surface Rough surface Warty surface Scale on surface
Well defined Poorly defined Well defined Situated on Situated within skin
Base indurated? surface of skin
Yes No Irregular Circular ring of keratin Oval/round Flat papule/ Round

shape papule plaque
Very rapid growth Longer history Face, bald scalp, Lower legs Present from Keratin difficult Keratin easily Firm–hard
(<6 weeks) (>6 weeks) dorsum hand (and arms) childhood to remove removed on palpation
KERATO- SQUAMOUS CELL SOLAR ACTINIC POROKERATOSIS COMMON SEBORRHOEIC DERMATO-

ACANTHOMA CARCINOMA KERATOSIS POROKERATOSIS OF MIBELLI WART KERATOSIS FIBROMA
p. 328 p. 328 p. 326 p. 326 p. 326 see p. 318 see p. 320 see p. 301
ACTINIC POROKERATOSIS SOLAR (ACTINIC) KERATOSES

This is problem on the lower legs and forearms mainly in women. A cutaneous horn is a keratotic outgrowth from the skin (see
Numerous small (5 mm), round, slightly scaly macules are seen. Fig. 9.150). At its base will be a solar keratosis, Bowen’s disease or
All have a raised edge like a thread of cotton stretched around, squamous cell carcinoma.
which can be more easily seen if illuminated from the side. The
Solar keratoses are rough, scaly papules on chronically sun-
lesions are caused by chronic sun exposure. Usually the patient
exposed skin. They are most commonly seen on the bald scalp,
only notices the lesions when they itch or become erythematous in
face and dorsum of the hands and forearms in patients over the
the sun. Similar but larger lesions called porokeratosis of Mibelli
age of 50 who have fair skin and other evidence of sun damage
can occur in childhood.
(see p. 287). Generally they are more easily felt than seen due to
TREATMENT: ACTINIC POROKERATOSIS
the roughness of the abnormal keratin. The surrounding skin
may be normal or pink/red. Sometimes scaling is not present
If they are symptomless it is best to leave them alone, although the patient should be and the lesion is just a fixed pink macule (see p. 112). Seborrhoeic
encouraged to wear long-sleeved shirts and trousers to prevent further sun exposure. warts may look similar but are not so rough to the touch, and are
Treatment options include cryotherapy, 5-FU cream, retinoic acid cream or a vitamin D3 generally more easily seen than felt.
analogue, but none are particularly effective.
Fig. 9.147 Porokeratosis: close-up of Fig. 9.148 Solar keratoses: these are Fig. 9.149 Multiple solar keratoses: Fig. 9.150 Cutaneous horn below the
lesions, note collar of scale more easily felt than seen more obvious lesions than in earlobe
Fig. 9.148.
Scaly/keratin surface / 327
Treatment: solar keratosis
A single or a few lesions can be treated with the following.

●● The treatment of choice is cryotherapy. You should freeze them just enough to cause
a blister at the dermo-epidermal junction. This is done by freezing the lesion until a
2 mm halo of normal skin goes white around it (5–10 seconds). Warn the patient that
he or she will develop a blister and that it will crust and drop off after 7–10 days.
●● 0.5% 5-fluorouracil (5-FU) and 10% salicylic acid solution (Actikerall) painted on
daily for up to 12 weeks is a useful alternative if cryotherapy is not available.

●● If there is any doubt over the diagnosis or you suspect a squamous cell carcinoma,
remove the lesion by excision and send for histology.

Large numbers of solar keratoses can be treated with the following.
●● Aqueous cream applied twice daily for several months is useful in improving
widespread keratotic lesions in the elderly.
a
●● 3% diclofenac (Solaraze) gel applied twice a day for 2-3 months. This results a low
grade reaction but is also less effective than other treatments below.
●● 5% 5-fluoro-uracil (Efudix) cream. This is applied twice a day for 4 weeks to localised
areas or the whole of the bald scalp and/or face. After the 3 rd week the area will
become inflamed and sore, and by the 4th week all the solar keratoses (even ones not
clinically apparent) will be red and eroded (Fig. 9.151a). 1% hydrocortisone cream
applied for a further week will settle the inflammatory reaction (Fig. 9.151b). Patients
who do not want the severe reaction can use it twice a day on two days/week for 2
months (2,2,2 regimen). This produces less inflammation but is less effective.
●● Ingenol (Picato) gel comes in two strengths. Apply 0.015% gel on the face or scalp
once daily for 3 successive days or the 0.05% gel for 2 days on the trunk, arms or
legs. A reaction will occur from the fourth day lasting around 2 weeks.
●● 3.75% imiquimod (Zyclara) apply once daily for two cycles of two weeks separated
with a 2-week no-treatment gap to a full face or bald scalp.

●● 5% imiquimod (Aldara) cream applied 3 times a week for 12 weeks. The skin will
become inflamed but does not hurt as it does after 5FU cream (see Fig. 9.72b, p. 291).
●● Photodynamic therapy (PDT). 5% methyl aminolaevulinic ester (Metvix) is applied
b under occlusion to affected skin and irradiated 3 hours later with a red light source
for 12 minutes. Treatment is repeated after 1 week (see p. 63).
Fig. 9.151 (a) Solar keratoses treated with 5-fluorouracil cream for 4 weeks: this
●● Daylight PDT. Apply a SPF30 sunblock to all sun exposed areas. Apply Metvix to the
is the reaction to expect at the end of the treatment; (b) same patient 1 month
later, after the inflammation has settled down affected skin and expose the skin for 2 hours to natural sunlight.
KERATOACANTHOMA
A rapidly growing benign tumour occurring on sun exposed skin.
It grows fast for about 3 months, reaching a size of up to 3 cm
in diameter. It then regresses spontaneously and should have
disappeared within 6 months. It has a symmetrical configuration
with an erythematous or translucent circumference and a horny
volcano-like centre. It looks a bit like a basal cell carcinoma but
it grows too quickly, and a basal cell carcinoma has crust rather
than keratin in the centre. A well-differentiated squamous cell
carcinoma tends to be more irregular in shape, slower growing
and does not regress spontaneously.
TREATMENT: KERATOACANTHOMA
If the patient is prepared to wait, the lesion will resolve spontaneously. In most
Fig. 9.152 Keratoacanthoma: symmetrical lesion with central plug of keratin
instances it is best removed either by excision or curettage and cautery, as it is not
always possible to be certain that it is not a squamous cell carcinoma.
SQUAMOUS CELL CARCINOMA (WELL DIFFERENTIATED)

A squamous cell carcinoma is a tumour of keratin producing cells.
Well differentiated tumours produce keratin on the surface like
a solar keratosis, but as they are invasive into the dermis they
have a thickened or indurated base. Basal cells do not produce
keratin, so a basal cell carcinoma will not have a hyperkeratotic
surface. Squamous cell carcinomas grow more rapidly than basal
cell carcinomas, but both will tend to ulcerate as they get bigger.
Tumours on the scalp, ears and lower lip are squamous cell
carcinomas until proved otherwise. Squamous cell carcinomas
are differentiated from a solar keratosis by being indurated
(thickened) at the base, or becoming ulcerated or tender on
palpation. Any of these signs are an indication for a biopsy or
Fig. 9.153 Well-differentiated squamous cell carcinoma with keratotic surface
removal (see p. 332). and thickened base
CRUST, ULCERATED, BLEEDING SURFACE / 329

Papules, plaques, nodules CRUST / ULCERATED / BLEEDING SURFACE
Single/few (<5) fixed lesions
(Multiple [>5] lesions/rash variable in site and time, see p. 245)
Crust on surface – remove this Bleeds easily after trauma
Erosion underneath Ulcer underneath
Elderly, fair skin Gradual growth (months to a year) Rapid growth Bleeding Very rapid growth
Long history (weeks to a month) surface (days–week)
Poorly defined Well defined Telangiectasia Indurated base Previous ‘mole’ Single Multiple
Rolled edge lesion lesions
No Yes
Rough on Biopsy Biopsy Age over 70 Recent foreign Within skin ‘Stuck on’ Growing out of Previous insect
palpation Sun exposed travel + pigmentation to surface normal skin bites/trauma
Biopsy Biopsy Biopsy Biopsy Biopsy
SOLAR BOWEN’S BASAL CELL SQUAMOUS LEISH- MALIGNANT IRRITATED PYOGENIC ECTHYMA
KERATOSIS DISEASE CARCINOMA CELL MANIASIS MELANOMA SEBORRHOEIC GRANULOMA
CARCINOMA KERATOSIS
see p. 326 see p. 220 p. 330 p. 332 see p. 140 see p. 306 p. 334 p. 334 see p. 187
BASAL CELL CARCINOMA (RODENT ULCER)

This is the commonest malignant tumour of the skin. It usually occurs in middle-aged or
elderly fair-skinned individuals who have worked at out of doors all their lives, or who
have spent a lot of time gardening, fishing, sailing, and so forth. Although due to sun
damage, they do not occur at the sites of maximum sun exposure, i.e. rarely on the bald
scalp, lower lip or dorsum of the hands. Most occur on the face, some on the trunk and
limbs.
There are three growth patterns. A nodular basal cell carcinoma starts as a small
translucent (pearly) papule with obvious telangiectasia over the surface. It gradually
increases in size either to form a nodule or sideways to produce the classic rolled edge.
The centre may then ulcerate and form surface crust. Growth is very slow – some may
reach a diameter of 1 cm only after 5 years. If there is any doubt over the diagnosis, stretch
the skin and you will see the raised rolled edge, like a piece of string around the edge. Fig. 9.156 Ulcerated basal cell carcinoma on cheek
with typical rolled edge
In a superficial basal cell carcinoma the growth is along the base of the epidermis, and
Fig. 9.154 Typical nodular basal cell carcinoma with Fig. 9.155 Ulcerated nodular basal call carcinoma Fig. 9.157 Basal cell carcinoma in nasolabial fold, a
telangiectasia over the edge with telangiectasia over the edge common site – will need Mohs surgery
presents more as a scaly plaque (see p. 220). It may become quite TREATMENT: BASAL CELL CARCINOMA
large (>1–2 cm diameter).
1. Local excision with a 2–4 mm margin is the treatment of choice. If the lesion is
A morphoeic or infiltrating basal cell carcinoma has fine strands of completely excised recurrence is unlikely (<5%).
tumour cells infiltrating into the dermis. These may be difficult to 2. Mohs micrographic surgery (see Fig. 9.159): removal of the lesion and assessment
diagnose early because they present like a scar with an indistinct of the peripheral and deep margins by frozen section results in recurrence rates of
border. Sometimes the lesion may be quite extensive without less than 1%. Since this process is time consuming and requires the assistance of a
obvious surface features. Resection by Mohs surgery where the pathology technician, Mohs surgery should be restricted to:
margins can be assessed histologically is recommended. ● central facial lesions in those requiring a skin flap or graft
● recurrent lesions (especially after radiotherapy) on the face

Pigmented basal cell carcinomas are the same as nodular basal ● lesions with indistinct margins
cell carcinomas except for the increased melanin pigment ● morphoeic (infiltrating) basal cell carcinoma.
(see Fig. 9.112) which makes differentiation from a malignant 3. Curettage and cautery has a higher recurrence rate than excision but is useful in
melanoma difficult (see p. 309). If you look carefully and put the elderly patients with multiple tumours or when there are multiple lesions on the
skin on the stretch, the typical rolled edge is usually present. trunk. The lesion is curetted out and the margin cauterised for 1 mm around. This
is repeated three times to give a 3 mm margin. The subsequent wound will heal by
secondary intention over a period of 2–4 weeks. This should be cleaned daily with
damp cotton wool and a topical antibiotic ointment applied.
4. Radiotherapy is only indicated when surgery is inappropriate, e.g. large lesions in the
elderly. Ten daily fractions of 3.75Gy are given. If the patient is very frail, the time
between fractions can be increased, e.g. 10 fractions are given over 10 weeks. This
will cause virtually no local reaction and will be much more pleasant for the patient.
5. Topical imiquimod (Aldara) cream works for superficial basal cell carcinomas on the
trunk and limbs. The cream is applied to lesions three times a week for 12 weeks
(see pp. 34 and 291).
6. Photodynamic therapy is useful if the patient has numerous tumours. A
photosensitiser is applied and this is irradiated with a red light source (see p. 63).
7. Cryotherapy is not recommended, since the recurrence rate is unacceptably high.
8. Vismodegib, an orally active small molecule inhibitor of the ‘hedgehog pathway’ can
sometimes be used to reduce tumour bulk in inoperable basal cell carcinomas (see
p. 57).
Fig. 9.158 Morphoeic basal cell carcinoma at angle of jaw – will need Mohs
surgery
a. The tumour is debulked using a curette or Volkmann spoon.

b. The debulked tumour is completely removed by bevelling the angle of the
scalpel at 45°.
c. The removed tissue is divided into half or quarter sections and the edges
stained.
d. The sections are numbered and colour of edges recorded on a map.
e. The sections are flattened, inverted and mounted on a cryostat chuck, and
sections cut.
f. These sections are read.
g. The presence of any tumour is marked on the map. This indicates the exact site
of any residual tumour.
h. The residual tumour is resected and steps c–g repeated.
i. When the final reading shows no tumour in the sections, then full clearance of
the basal cell carcinoma has been achieved, and the defect can be repaired.
Fig. 9.159 How Mohs surgery is carried out (adapted with permission from
Rook A. et al. Textbook of Dermatology, Blackwell Science)
SQUAMOUS CELL CARCINOMA

Squamous cell carcinoma arises from previously normal (sun-damaged) skin or from The prognosis of squamous cell carcinoma
a pre-existing lesion such as a solar keratosis or Bowen’s disease. A well-differentiated depends on several factors:
squamous cell carcinoma can be distinguished from a basal cell carcinoma by the ● size of lesion >2 cm diameter
production of keratin (see Fig. 9.153) and its faster growth (it may grow to 1–2 cm in ● depth of invasion >4 mm or Clark level
diameter over a few months). They occur at sites of maximum sun exposure, on a IV (reticular dermis)
bald head, the lower lip, cheeks, nose, top of earlobes and dorsum of hands and in the ● poorly differentiated cell type
elderly (usually over 70). There is always other evidence of sun damage such as solar ● immunosuppression
elastosis (see p. 287) and solar keratoses (see p. 326). Poorly differentiated squamous cell ● perineural invasion
carcinomas tend to ulcerate (see Fig. 9.160), and be may be covered with crust. The edge of ● site: lip, ear, non-sun exposed
the ulcer is craggy and indurated, while the base bleeds easily. On the scalp the crust may ● recurrent lesions.
become matted down with hair, which will hide a pus-filled ulcer (see Fig. 9.162).
The presence of two or more of these
Squamous cell carcinomas can also occur on non-sun-exposed skin – at sites of previous factors indicate a high-risk tumour. None
radiotherapy, or in chronic scars such as in old burn scars, osteomyelitis, lupus vulgaris or of these factors suggest low risk.
leg ulcers.
TREATMENT: SQUAMOUS CELL CARCINOMA
● Low-risk lesions: excise the lesion with a 4 mm margin of normal skin around it.
● High-risk lesions: these require a 6 mm margin. Lesions in patients under 70 years age around the central face should
have their margins checked by frozen section (Mohs surgery, see p. 332).
Most cutaneous lesions do not spread so the prognosis is excellent, but always check the regional lymph nodes.
Radiotherapy is a possibility for primary lesions in the very elderly who cannot tolerate surgery, or when the lesion is too
large to remove surgically. Ten daily fractions of 3.75Gy work well. Electrons rather than superficial X-rays are useful on
the ear and nose, as they are less likely to damage the cartilage.
Fig. 9.162 Crusting on scalp of elderly patient (top):

Fig. 9.160 Squamous cell carcinoma: a rapidly Fig. 9.161 Squamous cell carcinoma: typical always remove the crust to see what is underneath;
growing nodule in 40-year-old patient that needed ulcerated nodule on dorsum of hand of elderly in this case an ulcer was present (below) which on
Mohs surgery to remove patient biopsy showed a squamous cell carcinoma
PYOGENIC GRANULOMA Kaposi’s sarcoma can also ulcerate but IRRITATED SEBORRHOEIC KERATOSIS
This is due to a localised overgrowth there will be other lesions elsewhere. A seborrhoeic keratosis (see p. 320) may
of blood vessels in response to trauma, be caught in clothing, half torn off and
often a graze or a prick. There is very TREATMENT: PYOGENIC GRANULOMA become red and inflamed. It may then
rapid growth over a few weeks, and be easily mistaken for a melanoma.
usually a history of the lesion having bled The best treatment is curettage and cautery under The lesion usually has the ‘stuck on’
local anaesthetic. Sometimes there is quite a large
spontaneously at some stage. The lesion appearance of the original lesion, but will
blood vessel at the base but cautery will eventually
is round in shape, bright red or purple in have surrounding erythema rather than
seal this. Always send the lesion for histology.
colour, and the surrounding skin will be pigmentation. If the diagnosis is in doubt,
quite normal. In contrast an amelanotic it should be removed for histological
malignant melanoma is usually irregular in examination
shape, has some surrounding pigmentation
and grows over a period of months rather
than days or weeks.
Fig. 9.163 Pyogenic granuloma: rapidly growing red Fig. 9.164 Nodular malignant melanoma: note Fig. 9.165 Irritated seborrhoeic keratosis: it has
papule that bleeds after trauma; normal surrounding pigment at edge of the lesion been caught in clothing and partially torn off, hence
skin the bleeding; lesion sits on surface, normal skin
around
335
Flexures
Axilla, groin, natal cleft, sub-mammary folds
Erythematous rash/lesions
10
Papules, patches and plaques 336
Nappy (diaper) rash 341
Dermal papules, nodules and sinuses 344
Skin coloured 346
Brown 346
Abnormalities of sweating 349
336 / FLEXURES
Flexures
Erythematous lesions ERYTHEMATOUS RASH
Papules, patches and plaques
Asymmetrical Symmetrical any/all flexures
Groin/buttocks only
Pink Bright red Orange-brown
Scaling/accentuated Poorly defined edge Well-defined edge Satellite papules/ Uniform fine scale on
edge pustules surface
Central clearing Patchy involvement Uniformly involved Opposing surfaces Surface eroded and Soreness +++ Wood’s light ‘coral
only fissured pink’ fluorescence
Mycology +ve Mycology -ve Pubic area, Obese +ve family history Mycology +ve Microscopy
natal cleft Gram +ve rods
TINEA ECZEMA PSORIASIS INTERTRIGO HAILEY–HAILEY CANDIDA ERYTHRASMA

CRURIS DISEASE
p. 337 p. 338 p. 339 p. 339 p. 340 see p. 343 see p. 348

FLEXURE RASHES / 337
TINEA CRURIS
especially if partially treated. Eczema is usually symmetrical and
Flexural tinea only occurs in the groin; it does not involve the tinea is usually unilateral or asymmetrical (unless treated with
axillae or sub-mammary folds. It is caused by the same organisms topical steroids or in someone who is immunocompromised, see
that cause tinea pedis, i.e. Trichophyton mentagrophytes, Trichophyton Fig. 10.02). Always check the mycology if in doubt (see p. 20).
rubrum or Epidermophyton floccosum.
Infection is nearly always from the patient’s own feet, and men are TREATMENT: TINEA CRURIS
affected more often than women. The rash starts in the fold of the
groin and gradually spreads outwards and down the thigh. The An imidazole (clotrimazole, econazole, ketoconazole, miconazole or oxiconazoleUSA)
cream should be applied to the affected area of the groin (and buttock) and to the toe
leading edge is scaly unless treated with topical steroids, when the
webs twice a day for 2–3 weeks or until it is clear. Alternatively, use terbinafine (Lamisil)
whole area may become red (tinea incognito). The rash is usually
cream for 7–10 days. Almost all groin infections have been acquired from the patient’s
asymmetrical, one side being more involved than the other. own feet, so the feet must always be examined and treated at the same time if they are
The infection may also involve the buttocks and back of thighs. involved.
The genitalia, including the scrotum, are never involved. It may
be difficult to differentiate between eczema and tinea of the groin,
Fig. 10.01 Tinea cruris: rash in one groin only, with Fig. 10.02 Tinea cruris: note extensive symmetrical Fig. 10.03 Dermatophyte fungal hyphae on direct
obvious scaly edge rash in a patient with HIV infection microscopy
338 / FLEXURES
FLEXURAL ECZEMA resins in clothing cause a rash around the edge of the axilla but
Eczema in the flexures looks like eczema elsewhere – a poorly spare the vault. Patch testing will distinguish between these, see
defined pink (scaly) rash that is usually symmetrical. The p. 21. Eczema in the groin often also involves the genitalia, which
eczema may be localised to only the flexures or it may be part of distinguishes it from tinea. Tinea does not occur in other flexures,
seborrhoeic eczema elsewhere. Contact dermatitis in the axillae it is usually unilateral and it does not involve the scrotum. If in
may be due to irritants (depilatories, deodorants) or allergens. doubt, take skin scrapings for mycology, see p. 20.
Deodorants cause a rash in the centre of the axilla; dyes and
Fig. 10.04 Seborrhoeic eczema in axilla Fig. 10.05 Eczema in groin and on scrotum: this Fig. 10.06 Eczema around the edge of the axilla
cannot be tinea because of involvement of the due to allergic contact dermatitis from resins in
scrotum clothes
INTERTRIGO
The word ‘intertrigo’ comes from the Latin word intertrerere,
meaning to rub together. Intertrigo therefore describes painful,
red skin due to two moist surfaces rubbing together. It occurs in
the summer months in the flexures of individuals who are too
fat, usually in the sub-mammary, lower abdominal and groin
folds. Only the areas of skin that are touching are involved. In the
summer it is impossible to prevent intertrigo from developing in
patients who are overweight, because the sweaty skin surfaces
will rub together.
TREATMENT: FLEXURAL ECZEMA AND INTERTRIGO
Use a moderately potentUK/group 4–5USA topical steroid initially daily, such as 0.05%
clobetasone butyrate (Eumovate) or 0.1% hydrocortisone 17-butyrate (Locoid) cream
or ointment. For maintenance, use only two to three times a week. The occlusion that Fig. 10.07 Intertrigo: only skin folds affected
naturally occurs in the flexures will increase the potency of the steroid, so avoid strong
steroids, as they are likely to cause atrophy and striae. Loss of weight is the only real
answer for persistent intertrigo.
PSORIASIS
Psoriasis of the flexures (any flexure) is distinguished from all
other rashes by its bright-red colour and well-defined edge.
Silvery scaling will not be seen on the moist skin of the flexure, but
it may be seen at the very edge of the plaque. Often psoriasis is
present elsewhere to confirm the diagnosis. Characteristically the
pubic area and natal cleft are involved.
Fig. 10.08 Intertrigo in a patient who also has eczema

340 / FLEXURES
TREATMENT: FLEXURAL PSORIASIS HAILEY–HAILEY DISEASE

Also termed chronic benign familial pemphigus, this rare condition is inherited as an
Tar, dithranol and retinoids are likely to make the autosomal dominant trait. The patient complains of soreness in any of the flexures, and
skin sore in the flexures and on the genitalia, so they on examination the surface is red and finely fissured (see Fig. 10.11). As in pemphigus
should not be used. The vitamin D3 analogues calcitriol
vulgaris (see p. 257), there is an abnormality of cohesion of epidermal cells. This disease
(Silkis) and tacalcitol (Curatoderm) are non-irritant and
typically remits and relapses. It is exacerbated by friction, heat, secondary infection with
can be used in flexures twice daily and should be tried
first. If they do not help, then you can use a topical
Staphylococcus aureus, Candida albicans, or herpes simplex, and by stress. The patient
steroid. The weakest possible steroid to clear the skin complains of itching, pain and smell. There may be long periods when the patient is
is required, but 1% hydrocortisone is ineffective and entirely asymptomatic, especially in the winter.
not worth trying. Use a moderateUK/group 4–5USA
topical steroid such as 0.05% clobetasone butyrate
(Eumovate) or 0.1% hydrocortisone 17-butyrate
(Locoid) cream or ointment applied twice a day. Do
not use topical steroids in the flexures for long periods
of time, as steroid atrophy and striae are likely.
Fig. 10.09 Psoriasis in the groin and on scrotum (see Fig. 10.10 Psoriasis of perianal skin and natal cleft Fig. 10.11 Hailey–Hailey disease in axilla: note
also Figs 11.13 and 11.14, p. 360) erosions, crusting and fine fissures
Flexures: under nappy/diaper TREATMENT: HAILEY–HAILEY DISEASE

Erythematous lesions NAPPY/DIAPER RASH
Patches, plaques, erosions If the skin is weeping, wet dressings of aluminium acetate (Burow’s solution) or dilute
potassium permanganate solution (see p. 30) can be applied to the affected areas
No rash elsewhere Rash elsewhere once or several times a day. Topical steroids are often helpful. Use the weakest possible
steroid that is effective so as to reduce the risk of skin atrophy in the flexures. Start with
a moderateUK/group 4-5USA topical steroid bid, and increase the strength when required.
Secondary infection should be treated early. Rarely patients may need systemic steroids,
Patchy rash Outlying Start age Start age methotrexate or superficial X-ray treatment.
papules/pustules <3 months >3 months
NAPPY/DIAPER RASH (CONTACT IRRITANT DERMATITIS)

The common type of nappy/diaper rash is an irritant reaction to
Pink/red + Bright red Bright-red, Pink/patchy urine and faeces held next to the skin under occlusion. Bacteria
erosions/ulcers uniform
in the faeces break down urea in urine into ammonia, which is
very irritant to the skin. Clinically the rash is patchy and tends
to involve the convex skin in contact with the nappy (buttocks,
genitalia, thighs) rather than the skin in the folds (see Fig. 10.12).
Skin folds Skin folds Well defined Poorly defined
spared involved In mild cases there is just erythema, but when severe, erosions or
even ulcers can develop. The affected area is sore and cleaning or
bathing the area produces a lot of discomfort.
Mycology -ve Mycology +ve Not itchy Very itchy TREATMENT: NAPPY/DIAPER RASH
Nappies/diapers should be changed as soon as they are wet or soiled and the skin
cleaned and dried. A moisturiser such as zinc and castor oil cream is then applied to
the area that is covered by the nappy. If the rash is very bad and does not improve
after taking these simple measures, a weakUK/group 7USA topical steroid such as 1%
NAPPY/DIAPER CANDIDA INFANTILE ATOPIC
RASH (Irritant 1º or 2º SEBORRHOEIC ECZEMA hydrocortisone ointment can be applied twice daily for a few days to speed things up.
dermatitis) ECZEMA
p. 341 p. 343 p. 343 see p. 236

342 / FLEXURES
Fig. 10.12 Contact irritant nappy/diaper rash Fig. 10.14 Candidiasis: note bright-red colour with outlying satellite lesions
Fig. 10.13 Infantile seborrhoeic dermatitis Fig. 10.15 Direct microscopy of Candida albicans (spores and short hyphae)
CANDIDIASIS INFANTILE SEBORRHOEIC DERMATITIS

Candida affecting the skin most often occurs in patients at the extremes of life – babies (NAPKIN PSORIASIS)
and old people – but it can occur at any age. There is always a reason for the presence of Infants under 3 months of age may
the pathogenic form of Candida and this should be looked for and treated. The commonest develop an eruption that starts in the
causes are: nappy/diaper area but later spreads
● broad-spectrum antibiotics to involve the scalp, face and trunk. It
● contraceptive pill looks like psoriasis, consisting of well-
● diabetes demarcated bright-red plaques. In the
● iron deficiency nappy/diaper area involvement extends
● obesity into the flexures (unlike the usual nappy/
● pregnancy diaper rash). There is no itching and the
● immunosuppression – AIDS, systemic steroids, cytotoxic drugs, cancer. infant remains unaffected by the rash. The
condition goes away by itself after a few
It affects all the flexures (axillae, groins, sub-mammary area, toe webs) and is usually months. This rash is distinct from adult
symmetrical. The rash is bright red, and the key feature is that outlying papules or seborrhoeic eczema and has nothing to do
pustules occur around the main rash (see Fig. 10.14). In addition, the skin is sore rather with atopic eczema or psoriasis; is a type
than itchy, a feature that may help distinguish it from psoriasis or tinea cruris. of nappy rash secondarily infected with
Scrapings taken from the edge of the lesions can be examined under the microscope (see C. albicans. Once it disappears it does not
Fig. 10.15) for spores and hyphae, or cultured to prove the diagnosis. It is important to do recur; it is good to reassure the parents.
this, because flexural rashes are often assumed to be ‘fungal’ without any evidence.
TREATMENT: INFANTILE SEBORRHOEIC DERMATITIS
TREATMENT: CANDIDIASIS
Parents are usually very distressed because infantile
Take scrapings for mycology before treatment, as treatment ‘failure’ may be due to the misdiagnosis of eczema or seborrhoeic dermatitis looks unsightly. The application
intertrigo as candida. Look for predisposing factors and treat these. of 1% hydrocortisone ointment to the affected
areas two or three times a day will clear it up fairly
An imidazole cream twice daily is most convenient for the patient. In women, if the pubic area or groin is involved also speedily. Usually there is secondary infection with
treat the vagina with a single clotrimazole 500 mg pessary, or a single oral dose of fluconazole 150 mg. Involvement of Candida or bacteria, so use a cream containing
the perianal skin will necessitate oral treatment with nystatin tablets (100 000 units) qid for 5 days to clear the gut. Oral both hydrocortisone and an imidazole, nystatin, or
nystatin is not absorbed from the gut, so is not useful for Candida infection elsewhere. clioquinol (e.g. Daktacort, Vioform HC or Nystaform).
Alternative oral treatments are itraconazole 200 mg for 7 days or fluconazole 50 mg daily for 2 weeks. This is one of the rare instances where combined
steroid/antifungal preparations can be recommended.
344 / FLEXURES
Flexures:
axillae, groins and natal cleft ERYTHEMATOUS LESIONS
Erythematous papules, nodules and sinuses
Painful/tender Itchy
Single episode Recurrent over months Previous scabies
Single/ Multiple Sinus in

multiple sinuses natal cleft
Fig. 10.16 Hidradenitis suppurativa in Fig. 10.17 Hidradenitis suppurativa in

the axilla the perineum
BOIL/ HIDRADENITIS PILONIDAL SCABETIC

CARBUNCLE SUPPURATIVA SINUS NODULES TREATMENT: HIDRADENITIS SUPPURATIVA
Minor degrees of hidradenitis can be controlled by long-term, low-dose antibiotics as

for acne. Erythromycin or clindamycin 250 mg bid, or one to two co-trimoxazole tablets
twice a day, given over a period of years will keep some patients free of disease. If they
see p. 177 p. 344 p. 345 p. 345 do not work, a combination of rifampicin 600 mg/day plus doxycycline 100 mg/day may
work better. Systemic retinoids such as acitretin 10–50 mg daily may also be of benefit,
HIDRADENITIS SUPPURATIVA and in severe cases they can be combined with antibiotics (clindamycin) and steroids
(prednisolone). Surgery is really the last resort. All the apocrine glands in the affected
This is a disease of the apocrine sweat glands that are found in the
area need to be removed. Excision of the abnormal skin together with the underlying
axillae and perineum. Tender papules, nodules and discharging sinuses and abscesses is a major undertaking. In the axillae it is often possible to excise
sinuses occur in the axillae, groins, perianal area and very the affected area and close the defect as a primary procedure. In the perineum that is
occasionally on the breasts. They heal leaving scars. It is thought not usually possible, so the patient will be left with a large, open wound that is left to
to be due to an infection with Streptococcus milleri, but it does not granulate up on its own. This may take many months.
always respond to antibiotics.
FLEXURE LESIONS / 345
PILONIDAL SINUS SCABETIC NODULES

A tender papule or nodule in the midline of the natal cleft may A few patients with scabies develop persistent itchy papules,
be due to a pilonidal sinus, where hairs become buried within especially around the axillae. These may last for weeks or months
the skin. Usually the patient has hairy skin and a sedentary after the patient has been successfully treated for scabies. Their
occupation. The sinus needs to be opened up, laid open and presence does not mean that the scabies is active, so further
allowed to granulate up from the base. This is best done by a treatment for scabies is unnecessary. Treat these lesions with a
surgeon and under a general anaesthetic. topical steroid.
Fig. 10.18 Pilonidal sinuses above the natal cleft Fig. 10.19 Multiple tender boils in axilla due to Fig. 10.20 Scabetic nodules
infection with Staphylococcus aureus: treat with
flucloxacillin
346 / FLEXURES
Flexures
Non-erythematous lesions NON-ERYTHEMATOUS LESIONS
Macules, patches, papules, plaques, nodules
Skin coloured, brown
Brown macules Orange/brown patch Brown plaque Brown papules Skin coloured Skin-coloured nodules
Multiple freckles in Uniform, Papillomatous Pedunculated Superficial papules Multiple, intradermal Single, subcutaneous
axillae fine scale surface in axillae within axilla mobile
Café au lait patches Wood’s light: shows Neck/axilla/groin Isolated 1–2 mm Multiple Itchy+++ ±Punctum Biopsy
elsewhere pink fluorescence Biopsy on surface
NEUROFIBROMATOSIS ERYTHRASMA ACANTHOSIS SKIN TAGS FOX–FORDYCE STEATOCYSTOMA LYMPH NODE

NIGRICANS DISEASE MULTIPLEX
see p. 347 p. 348 p. 349 see p. 266 p. 347 see p. 274 p. 347
FLEXURE LESIONS / 347
FOX–FORDYCE DISEASE NEUROFIBROMATOSIS LYMPH NODES

Very itchy skin-coloured or yellowish ‘Axillary freckles’ or light-brown macules Lymph node enlargement may be reactive
papules occur in the axillae due to are pathognomonic of neurofibromatosis. to a local infection, or due to malignancy,
blockage of the apocrine ducts. The itching In children this sign may predate the either a lymphoma or a secondary
may be precipitated by the emotional development of the neurofibromas (see carcinoma. If in doubt, do a fine needle
stimuli that can cause axillary sweating. p. 266), but there will be café au lait aspiration for cytology or refer to a
It mainly occurs in young women, and patches present on the trunk (see Fig. 9.79, surgeon for biopsy. Non-erythematous
treatment is unsatisfactory. p. 294). nodules in the axilla may also be due to
steatocystoma multiplex (see p. 274).
Fig. 10.21 Fox–Fordyce disease Fig. 10.22 Axillary freckling in neurofibromatosis Fig. 10.23 Steatocystoma multiplex in axilla
348 / FLEXURES
ERYTHRASMA
Erythrasma is caused by an infection with Corynebacterium
minutissimum in the flexures. Symmetrical, orange-brown, scaly
plaques spread across the folds. Usually all flexures are involved
– axillae, groins, sub-mammary areas and toe webs – although the
natal cleft is spared. The condition may be confused with tinea
cruris, but the colour is different, more orange-brown, the scale
is not just at the edge, the axillae are involved and mycology will
be negative. A Gram stain on the scales will reveal Gram-positive
rods, and on Wood’s light (UVA) examination there is bright-pink
fluorescence (see Fig. 10.27).
TREATMENT: ERYTHRASMA
Erythromycin 250 mg orally qid for 14 days will clear erythrasma at any site. Nothing
needs to be applied to the skin (topical imidazoles are ineffective).
Fig. 10.25 Erythrasma in axilla
Fig. 10.24 Erythrasma in both axillae: in patients with black skin the scale is grey Fig. 10.26 Erythrasma in groin Fig. 10.27 Coral-pink fluorescence of
rather than brown erythrasma under ultraviolet light
ABNORMALITIES OF SWEATING / 349
ACANTHOSIS NIGRICANS ABNORMALITIES OF SWEATING

This is a rare condition but it is important, because when it occurs PHYSIOLOGY OF SWEATING
in patients over the age of 40 you should look for an underlying Eccrine sweat glands are distributed all over the body surface, but
malignancy – carcinoma of the lung, stomach or ovary. In they are most numerous on the palms of the hands, the soles of the
younger patients it is usually associated with obesity and insulin feet and in the axillae. The secretary coil (sweat gland) is situated
resistance. It is then called pseudoacanthosis nigricans. The skin deep in the dermis and is linked to the skin surface by a straight
of the flexures becomes dark brown, dry and thickened, with a duct. It produces an isotonic secretion that can be modified as
papillomatous velvety surface. In the malignant form the skin it passes up the duct. Secretion of sweat is controlled by the
changes are often associated with marked itching, and there sympathetic nervous system but the mediator is acetylcholine.
may be widespread lesions that look like viral warts. Treatment
involves finding the cause and treating this. Weight loss is Generalised sweating is usually due to an underlying
necessary for pseudoacanthosis nigricans. medical condition, i.e. thyrotoxicosis, diabetes, menopause,
fever, infections such as tuberculosis and HIV, lymphoma,
phaeochromocytoma and some drugs, e.g. tricyclic
antidepressants and tamoxifen.
AXILLARY HYPERHIDROSIS
Hyperhidrosis is excessive production of sweat. In the axillae it
causes embarrassment because of staining of clothes, the need to
change clothes frequently and the rotting of clothes.
BROMHIDROSIS (BODY ODOUR)

Smelly armpits are not due to smelly apocrine sweat but to the
breakdown of the sweat by bacteria on the skin. It can also be
caused by secretion of smelly substances in the sweat such as
garlic. Frequent washing of the axilla with soap and water is all
that is needed. Control of excessive sweating does not help. Avoid
spicy foods.
Fig. 10.28 Acanthosis nigricans

350 / FLEXURES
TREATMENT: AXILLARY HYPERHIDROSIS CHROMHIDROSIS (COLOURED SWEAT)

Apocrine sweat may be coloured yellow, blue or green when it
The options available for treatment are as follows. is secreted. More commonly, colourless apocrine sweat is broken
● 20% aluminium chloride hexahydrate in absolute (or 95%) alcohol: this is available
down to different colours by bacteria on the skin surface or on
commercially as Anhydrol ForteUK, DrichlorUK, DrysolUSA. It works by the aluminium axillary or pubic hair. The main problem is staining of the clothes.
ions migrating down the sweat ducts and blocking them. If applied to a sweaty
axilla it will combine with the water in sweat to form hydrochloric acid, which
TRICHOMYCOSIS AXILLARIS
will make the skin sore. It should be applied before going to bed, after washing
and drying the axillae carefully. It can be applied every night for about a week
This is a superficial infection of axillary or pubic hairs with a
to control the sweating, and thereafter applied only when the sweating reoccurs variety of corynebacteria. White or coloured concretions are fixed
(usually every 7–21 days). Mild irritation of the axilla can be relieved by applying 1% to the hair. Most people do not notice this but occasionally some
hydrocortisone cream in the morning. Commercially available antiperspirants contain complain of it. Treat by shaving off the axillary hair and wash the
aluminium hypochlorite. These work well for normal individuals but are ineffective for axilla with soap and water at least once a day.
excessive sweating.
● Botulinum toxin: up to 50 units of Azzalure, Botox, Xeomin or 125 units of Dysport
dissolved in 2 mL saline is injected intradermally into each axilla. The hairy axillary
vault is divided into 1 cm squares and about 0.05 mL injected into each square. This
will abolish sweating for any time from a few weeks to a year. It is very effective and
safe, but it is expensive and needs to be repeated when sweating reoccurs. It is the
treatment of choice for severe, disabling hyperhidrosis.
● Surgery: removal of the axillary vault will remove most of the eccrine sweat glands
and so stop sweating.
TREATMENT: GENERALISED SWEATING
Treat the underlying cause. If no cause is found it is worth trying propantheline 15 mg

tid, but its anticholinergic side effects are often not tolerated (blurred vision, dry mouth,
constipation, urinary retention, dizziness and palpitations). Glycopyrrolate (Robinul)
1–2 mg tid (named-patient prescription) and oxybutynin 2.5–5 mg bid are better
tolerated. A β-blocker is an alternative, but do not use in patients with asthma or
peripheral vascular disease.
Fig. 10.29 Trichomycosis axillaris

351
Genitalia
Including pubic, perianal and perineal areas
Genital ulcers and erosions 352
11
Penis
Papules and plaques 356
Scrotum and pubic area
Papules, plaques and nodules 357
Vulva
Perineum and perianal skin
352 / GENITALIA
Genitalia
ULCERS AND EROSIONS
Acute Chronic
Single lesion Multiple lesions Multiple lesions Single lesion
Sexual risk Erosion on Sexual risk Grouped Mouth lesions Odd shape Indurated Erosive patch/plaque
erythema linear, nodule
square
Painless Painful ulcer ? Similar Serpiginous Prodromal Erosions/ Ulcers ± Similar Increase in Red, velvety Red, shiny,
ulcer lesion erosions itch/pain scarring of last lesions size surface smooth
elsewhere conjunctiva weeks elsewhere surface
+ve dark Acquired in Recurrent +ve Recurrent Biopsy Biopsy Biopsy Biopsy
ground tropics at same VDRL test same site
examination site
PRIMARY CHANCROID FIXED SECONDARY HERPES MUCOUS BEHÇET’S DERMATITIS SQUAMOUS INTRAEPIDERMAL ZOON’S
SYPHILIS* DRUG SYPHILIS SIMPLEX MEMBRANE DISEASE ARTEFACTA CELL NEOPLASIA BALANITIS
ERUPTION PEMPHIGOID CARCINOMA
p. 353 p. 354 see p. 181 p. 353 p. 355 see p. 146 see p. 147 p. 260 p. 354 p. 354 p. 354
*In patients who have lived in the tropics, think of granuloma inguinale or lymphogranuloma venereum (see p. 354)
ULCERS AND EROSIONS / 353
PRIMARY SYPHILIS SECONDARY SYPHILIS

Primary syphilis presents as a round painless ulcer (1° chancre) Irregular shallow serpiginous erosions on the penis, scrotum
with an indurated base about 3 weeks after infection (can be 10–90 or vulva should suggest secondary syphilis. Similar lesions
days). The chancre is seen on the penis, scrotum, vulva, perianal can occur on the buccal mucosa and tongue. These lesions are
skin or lip, but it may also be found on the cervix or within the very infectious and the spirochaetes can be demonstrated in
anal canal. Suspect the diagnosis in any genital ulcer, and confirm the exudate from such lesions by dark ground microscopy.
by demonstrating Treponema pallidum on dark ground microscopy. Serology (VDRL) will always be positive. The patient will also
Serology (EIA, TPHA, RPR) is helpful because it becomes positive have lymphadenopathy; general malaise; a widespread rash on
within a week of the primary sore developing. the trunk (see p. 207), palms of the hands and soles of the feet;
‘moth-eaten’ alopecia; and flat warty papules and plaques on the
genitalia and around the anus (condylomata lata).
Fig. 11.03 (above)

Secondary syphilis on
shaft of penis and
scrotum: serpiginous
erosions
Fig. 11.04 (right) Dark

ground microscopy
showing spirochaetes
Fig. 11.01 Primary syphilis: two chancres where Fig. 11.02 Condylomata lata: these are much flatter of Treponema pallidum
glans in contact with foreskin than viral warts (×100)
354 / GENITALIA
TREATMENT: SYPHILIS ZOON’S BALANITIS

Zoon’s plasma cell balanitis is uncommon. It usually occurs as a
All patients with syphilis should be seen in a department of genito-urinary medicine single shiny, red plaque on the glans penis of a middle-aged or
so that other sexually transmitted diseases can also be screened for and the patient’s elderly man. Biopsy and histology is required to reach a correct
sexual contacts traced. Early syphilis (up to 1–2 years) is treated with a single dose
diagnosis. Circumcision is usually curative.
of benzathine penicillin, 2.4 megaunits by intramuscular injection. To minimise the
Jarisch–Herxheimer reaction, prednisolone 60 mg is given for 3 days, starting 24 hours
before giving penicillin. If the patient is allergic to penicillin, the treatment is doxycycline
100 mg bid for 14 days. For late syphilis (over 2 years) 3 doses of benzathine penicillin,
2.4 megaunits is given by intramuscular injection at weekly intervals. If allergic to
penicillin, doxycycline 100 mg bid is given for 28 days.
Contacts are treated with penicillin (if serology positive), or doxycyline (if negative).
OTHER SINGLE OR MULTIPLE GENITAL ULCERS

If the patient has multiple ulcers and has been to the tropics,
consider granuloma inguinale (due to Klebsiella granulomatis),
lymphogranuloma venereum (due to Chlamydia trachomatis) or
chancroid (due to Haemophilus ducreyi). The latter two are usually Fig. 11.05 Squamous cell carcinoma Fig. 11.06 Intraepithelial neoplasia
associated with marked local lymphadenopathy. All such patients
should be referred to a department of genito-urinary medicine,
where the diagnosis can be confirmed.
Any indurated ulcer on the genitalia that is negative on dark
ground microscopy should be biopsied to exclude a squamous
cell carcinoma or intraepithelial neoplasia. Genito-urinary
surgeons should manage these conditions. An ulcer that has an
odd shape should make you think of dermatitis artefacta (see
p. 260).
Fig. 11.07 Zoon’s balanitis Fig. 11.08 Herpes simplex under

foreskin
ULCERS AND EROSIONS / 355
GENITAL HERPES SIMPLEX TREATMENT: GENITAL HERPES SIMPLEX

Genital herpes simplex is by far the commonest cause of genital
ulceration and is usually due to infection with herpes simplex PRIMARY INFECTION WITH HERPES SIMPLEX TYPE 1 OR 2
type 2 (HSV-2). About 50% of primary infections with HSV-1 or 2 In both men and women, provided that they present within 48 hours of the appearance
are asymptomatic. The rest present with localised burning, itching of the vesicles, treat with one of the following for 5–10 days:
● aciclovir 400 mg tid
or soreness of the penis, vulva, anus or thighs, together with
● famciclovir 250 mg tid
grouped vesicles that break down to form erosions/ulcers that ● valaciclovir 500 mg bid.
heal in 7–10 days. Pain may be severe and there may be associated
fever, malaise, headache and pain in the back and buttocks. In This will relieve the pain and cut the attack short; it will also decrease the time that the
women there may be dysuria if there are ulcerated lesions on the virus is shed and therefore the time that the patient is infectious.
vulva, and in patients of either sex there can be proctitis with anal
The following may be useful to bring symptomatic relief to patients of either sex:
infections. ● take aspirin or paracetamol for the pain
● apply lignocaine gel to the erosions/ulcers

Recurrent episodes of herpes simplex are common and can be
● urinate in a warm bath if there is dysuria
precipitated by fever, stress and sexual trauma. Not all patients
● leave the affected area open if possible, to avoid clothes rubbing
who have had a primary infection with HSV-2 will get recurrent
● avoid sexual intercourse until the ulcers have healed.
episodes. For those who do, it is usually a lot less severe than
the primary episode. It consists of painful grouped vesicles that
RECURRENT INFECTION WITH HERPES SIMPLEX TYPE 1 OR 2
break down to form erosions/ulcers. Ulcers in patients with
In some patients, recurrent episodes cause a lot of pain and this may ruin their sex life
HIV infection may last for months. Patients should be seen at
by causing dyspareunia, frigidity and impotence. Such patients should have a 2-day
the local genito-urinary medicine clinic. Here the diagnosis supply of oral aciclovir 800 mg tid (or alternatives, see first list in this box) at home to
can be confirmed and the presence or absence of other sexually take at the first sign of recurrence. If they are getting frequent recurrences, long-term
transmitted diseases checked for. prophylaxis with oral aciclovir, 400 mg bid, can be used.
A primary infection with HSV-2 in the first 3 months of pregnancy
can cause infection in the foetus and lead to spontaneous abortion. THE USE OF ACICLOVIR DURING PREGNANCY AND LACTATION
Aciclovir is not teratogenic or mutagenic in animals, so it is probably safe to give during
If there is active infection with HSV-2 at the time of birth, the child
pregnancy. Given during lactation, aciclovir will be present in the mother’s breast milk;
should be delivered by caesarean section to prevent encephalitis.
since it is not harmful to babies this probably does not matter.
There is a considerable body of evidence to suggest that genital
infection with HSV-2 is one of the causative factors in the
development of carcinoma of the cervix. Other factors include
early age of first coitus, multiple sexual partners and infection
with genital warts.
356 / GENITALIA
Penis
Papules and plaques PENILE LESIONS AND RASH
(Note list is not exhaustive: see other chapters if necessary)
Small papules, <2 mm size Large papules 2–10 mm size Plaques >10 mm Foreskin difficult to retract
Pink/mauve White/pink Erythematous/mauve Skin colour/ Erythematous Glans white Glans skin
brown colour
Flat-topped 1–3 rings Itchy rash Flat- Warty/ Well defined Poorly defined Atrophic Normal
encircling on trunk topped papillomatous surface surface
corona
Glans Around Shaft, glans Shaft Shaft, glans Glans, Shaft, glans Shaft Glans Shaft, glans Foreskin
corona foreskin foreskin
Burrows on Annular Uniform Lichenified Exudate on

hands Profuse Slight scale glans
scale
LICHEN PEARLY SCABIES LICHEN WARTS CIRCINATE PSORIASIS ENDOGENOUS BALANITIS BALANITIS PHIMOSIS
NITIDUS PENILE PLANUS BALANITIS ECZEMA XEROTICA
PAPULES OBLITERANS
p. 358 p. 358 see p. 248 p. 358 p. 358 p. 361 p. 360 see p. 235 p. 361 p. 362 p. 362
PENIS AND SCROTUM / 357
Scrotum and pubic area

Papules, plaques and nodules SCROTAL AND PUBIC LESIONS AND RASHES
(Note list is not exhaustive: see other chapters if necessary)
Erythematous Non-erythematous
Itchy, any site On scrotum only
Papules Plaques Bright red/purple White/yellow

papules papules and nodules
Rash confined to Associated Poorly Well defined Multiple Multiple Multiple

scrotum/pubic areas with rash defined 1–3 mm pinpoint X-ray area
elsewhere
Nits/lice on Tender papules/ Burrows No burrows Itchy Scaly +++ Asymptomatic Shooting Calcified No
hairs pustules around between thickened pains in limbs calcification
hair follicles fingers skin
PUBIC FOLLICULITIS SCABIES ECZEMA LICHEN PSORIASIS ANGIOKERATOMA FABRY’S IDIOPATHIC EPIDERMOID
LICE SIMPLEX OF FORDYCE DISEASE CALCINOSIS CYSTS
(Pruritis)
p. 363 p. 363 see p. 248 see p. 235 p. 366 p. 366 p. 364 p. 364 p. 364 p. 364
358 / GENITALIA
LICHEN NITIDUS / LICHEN PLANUS PEARLY PENILE PAPULES WARTS

Lichen planus nearly always affects the Small skin-coloured, pink or pearly Warty lesions on the penis, scrotum,
genital area. The lesions are identical to papules 1–3 mm across occur around the vulva or perianal skin may be due to the
those elsewhere, i.e. flat-topped, shiny, corona in about 10% of males after puberty. following.
mauve polygonal papules. If the papules Many young men go to their doctor when ● Genital warts (condyloma acuminata):
are very small they are called lichen they first notice them, thinking that they these are due to one of the human
nitidus (see Fig. 8.04, p. 198). For treatment are abnormal. Reassurance that they are papilloma viruses (HPV 6, 11, 16, 18)
see p. 198. normal is all that is needed. and are spread by sexual contact. These
single or multiple, skin-coloured, pink
or brown warty papules with a moist
rather than rough surface can occur
anywhere on the genitalia or perianal
skin. The patient’s sexual partner
should also be checked and other
sexually transmitted diseases looked for
and excluded.
Fig. 11.09 Lichen planus on glans penis Fig. 11.10 Pearly penile papules around corona of Fig. 11.11 Genital warts on shaft of penis and
the glans pearly penile papules on the corona
● Common warts (see p. 318) TREATMENT: GENITAL AND PERIANAL WARTS

● Plane warts (see p. 268)
● Seborrhoeic warts (see p. 320) The most important part of the treatment for genital warts is to screen the patient for other sexually transmitted diseases,
● Condylomata lata: lesions that look so referral to the local genito-urinary medicine department is required.
like flat viral warts (see Fig. 11.02) may Modalities of treatment that are commonly used are as follows.
occur in secondary syphilis. They 1. For non-keratinised genital warts: 0.5% podophyllotoxin in an alcohol base or as a cream (Warticon) is applied to
are teeming with spirochaetes which each wart twice a day for 3 consecutive days with a 4-day break weekly for 4 weeks. If warts still present, try points 2
can be demonstrated by dark ground and 3 below. It can be done by the patient himself but he needs to be able to see the warts so that it is applied
microscopy (see Fig. 11.04). Think of this carefully to the wart and not the surrounding skin, otherwise it can cause erythema, oedema and erosions.
if the patient is unwell and check the 2. For ano-genital and other keratinised warts: imiquimod (Aldara) cream. This has replaced podophyllotoxin as the
VDRL. treatment of choice. It is applied three times a week for up to 16 weeks (see p. 34). Each application is left on for
12 hours and then washed off with soap and water. It should be washed off before sexual intercourse, as it can
produce a lot of irritation, inflammation and swelling.
3. Freezing with liquid nitrogen is a suitable treatment if there is a single wart or only a few warts present. It is the
treatment of choice for meatal warts. The skin around the wart is put on the stretch so that the liquid nitrogen can be
applied accurately to the wart and not to the adjacent normal skin. Treatment can be repeated every week until the
wart has gone. Use with extreme caution for warts on/near the clitoris or frenum to avoid permanent scarring.
4. Surgical removal under a general anaesthetic is a useful treatment if there are very extensive warts, particularly if
the anal canal is involved as well as the skin. Between 50 and 75 mL of 1:30 000 adrenaline in physiological saline
is injected subcutaneously underneath the warts. This causes the skin to swell up like a balloon so that the warts are
separated from one another and stick out like fingers. Taking hold of the warts with a pair of fine-toothed forceps,
they are then snipped off with a pair of sharp-pointed scissors. The presence of adrenaline means that there will be
very little bleeding; any persistent bleeding points can be diathermied.
Fig. 11.12 Genital warts on vulva in a patient with

HIV
360 / GENITALIA
PSORIASIS TREATMENT: PSORIASIS OF THE GENITALIA

The diagnosis of psoriasis on the glans or shaft of the penis is not
usually difficult, since the bright-red colour is just like psoriasis Tar, dithranol and calcipotriol are likely to make the skin sore in the flexures and on
elsewhere. On the glans, scaling may be absent, but on the shaft the genitalia, so they should not be used. Calcitriol (Silkis) is the treatment of choice
at these sites, since it produces less irritation than other vitamin D3 analogues. Topical
the plaques often have the typical silvery scaling. In boys between
steroids can also be used to clear the skin, but 1% hydrocortisone is ineffective and is
the ages of 5 and 15 years, psoriasis may first appear on the penis
not worth trying. Start with a moderately potentUK/group 4–5USA topical steroid cream or
and cause considerable anxiety to the parents. In adults it often ointment applied twice a day. Whether the patient will prefer a cream or ointment you
is a problem because of pain and embarrassment during sexual will have to discover by trial and error.
intercourse.
Fig. 11.13 Psoriasis on penis, pubic area and groins Fig. 11.14 Psoriasis on glans penis Fig. 11.15 Balanitis: you will need to biopsy this
lesion to exclude Zoon’s or neoplasia; histology
showed it to be inflammatory and it responded to a
weak steroid cream
BALANITIS CIRCINATE BALANITIS

Balanitis means inflammation of the glans penis. It is uncommon This occurs in some patients with Reiter’s syndrome (arthritis
in those who have been circumcised. It is usually an irritant [sacroiliitis ± polyarthritis], urethritis or dysentery, and
dermatitis, which may be due to poor hygiene (particularly if conjunctivitis). A red scaly or eroded area occurs on the glans and
the foreskin is tight and difficult to retract), urethral discharge or spreads outwards in phases with a grey circinate edge. On the
trauma. Always check for Candida albicans, which may not have soles of the feet, tender keratotic papules or pustules can occur
the typical appearance with outlying pustules as in the groin, by (keratoderma blennorrhagicum). Some or all of these symptoms
taking a swab and sending it to the lab. If Candida is present, check usually occur 1–3 weeks after an infection of the genito-urinary
a fasting blood sugar or HbA1c, since this may be a presenting tract (often with Chlamydia), or a bacterial gastro-intestinal
sign of diabetes mellitus in middle or old age. If it occurs very infection causing diarrhoea. Predisposed individuals are usually
acutely, consider an allergic contact dermatitis due to latex HLA B27-positive young males. Patients should be screened for
condoms, spermicidal foams or applied medicaments. other sexually transmitted infections if at risk.
Fig. 11.16 Keratoderma blennorrhagicum: tender keratotic papules and pustules Fig. 11.17 Circinate balanitis in a patient with Reiter’s syndrome
on the soles of feet in a patient with Reiter’s syndrome
362 / GENITALIA
TREATMENT: BALANITIS TREATMENT: BALANITIS XEROTICA OBLITERANS
● If Candida is not present (check by taking a swab) and the patient is not diabetic, If the man has not been circumcised, circumcision is probably the treatment of choice.
soaking the penis in normal saline (1 tablespoon of salt in one pint of water) for 10 If the problem is itching or soreness, a topical steroid in the form of 1% hydrocortisone
minutes twice a day for a week will clear the problem in 80%–90% of patients. If it cream applied twice daily is all that is needed. If that does not work, or if there is a
recurs this can be repeated. problem with urethral stenosis, a very potentUK/group 1USA topical steroid cream will be
● If the patient is diabetic or Candida is present, after soaking in saline, the patient required. It is applied twice a day to the affected area (and to the urethra if necessary)
should apply topical nystatin cream or ointment or one of the imidazole creams (e.g. and produces a very rapid and dramatic improvement. This should not be continued
miconazole cream) two or three times a day until it clears. for more than 2–3 weeks. Once the disease is under control, a weaker topical steroid
● If neither of these measures work, a urethral swab should be taken looking for usually works just as well.
anaerobes. If they are not found, the patient’s sexual partner should also be
examined. If anaerobes are found in the patient or his sexual partner, treatment is
with oral metronidazole 400 mg tid for 10 days. PHIMOSIS
● If no infection is present, then 1% hydrocortisone cream is usually effective. Difficulty in retracting the foreskin in a young adult without any
● If none of the above points work, then refer to a dermatologist for a biopsy. clinical signs may be due to a congenitally tight foreskin, repeated
trauma or underlying balanitis xerotica obliterans.
BALANITIS XEROTICA OBLITERANS (BXO)
This is the same condition which in females is called lichen
sclerosus et atrophicus (see p. 368). It most commonly affects
young adults. It can present in a number of ways. The patient may
notice white discolouration of the glans or prepuce, blistering
or haemorrhage, difficulty in retracting the foreskin or the urine
spraying out uncontrollably during micturition. On examination,
ivory-white macules, papules or plaques are present on the glans
with or without obvious atrophy. Blisters or haemorrhage may
also be seen (see Fig. 11.18).
Fig. 11.18 Haemorrhagic erosions in Fig. 11.19 Phimosis due to balanitis

balanitis xerotica obliterans xerotica obliterans: note atrophic area
on glans and foreskin
PUBIC LICE
Pubic lice (crab lice) like other lice live on human blood. They
grip the pubic hair and feed on blood through the pubic skin. The
eggs are laid on the pubic hair. These look identical to the nits
that are found in the scalp: oval, white, shiny capsules 1–2 mm
long and firmly attached to the pubic hairs. In Negros the nits are
sometimes very dark in colour but are otherwise the same. If no
nits are present, look for other evidence of eczema or scabies to
confirm the diagnosis of these. In individuals who are very hairy,
pubic lice can also be found in the axillae, on the body hair and in
the eyelashes (see Fig. 11.20).
FOLLICULITIS/BOIL
Small, red papules around a hair follicle, some of which have pus
in the centre, are due to folliculitis. Larger nodules are boils. Both
are caused by infection with Staphylococcus aureus (see pp. 177, 185
Fig. 11.20 Pubic (crab) louse and nits on eyelashes and 187). With both there may be painful lymphadenopathy in the
groin. Bacteriology culture will confirm the diagnosis.
TREATMENT: PHIMOSIS TREATMENT: PUBIC LICE
If there is no obvious infection present the patient will need to be circumcised; he ● Shaving the pubic hair is the simplest solution.
should be referred to a surgeon. ● 0.5% Malathion lotion (Derbac-M), 0.5% phenothrin lotion or 5% permethrin cream
are applied to the pubic hair and washed off 12 hours later. Treatment is repeated
If a urethritis is present (urethral discharge), the commonest causes are non-specific
after 7 days to kill any adult lice that have hatched since the first application.
urethritis and gonorrhoea. The patient should be referred to a genito-urinary medicine
Alcoholic solutions are not suitable for applying to the pubic area.
department so that the diagnosis can be confirmed. Sometimes the penis is so tender
● In individuals who are very hairy, pubic lice can also be found in the axillae, on
that it is impossible to take urethral swabs. In that case the patient’s sexual partner
the body hair and in the eyelashes. These areas should always be checked and, if
should be examined and the diagnosis confirmed from her. If no infection is found, ice
involved, the whole body should be treated.
or 1% hydrocortisone cream applied twice a day can be helpful.
● Lice and nits on the eyelashes should be picked off with the fingers and petroleum
jelly applied three or four times a day so that the lice cannot hold on!
● All sexual contacts must also be treated.
364 / GENITALIA
ANGIOKERATOMA OF FORDYCE EPIDERMOID CYSTS AND IDIOPATHIC CALCINOSIS

Numerous small, bright-red or purple non-itchy papules on the Single or multiple white papules confined to the scrotal skin are
scrotum are quite common particularly in the elderly. They are most commonly due to epidermoid cysts. In women, similar cysts
usually asymptomatic, but occasionally they bleed. The diagnosis occur on the labia majora. Histologically they are identical to
can be confirmed by skin biopsy. They are quite harmless. epidermoid cysts elsewhere, with a lining that looks like normal
epidermis and the centre filled with keratin.
FABRY’S DISEASE (ANGIOKERATOMA CORPORIS DIFFUSUM)
Sometimes lesions that look exactly the same as epidermoid cysts
This is a very rare X-linked disorder in which tiny angiokeratomas
are found not to be cysts histologically but lumps of calcium
occur on the skin in the area usually covered by the underpants.
lying in the dermis. There is no capsule around them and there
They occur just before puberty and are associated with
is no indication of why they are there. They are not associated
excruciating pains in the limbs and with renal failure. If this
with hypercalcaemia or deposition of calcium elsewhere. If the
diagnosis is suspected, a specialist opinion should be sought.
diagnosis is thought of before excision, the calcification can be
shown on X-ray. Both conditions are completely harmless.
Fig. 11.21 Angiokeratoma of Fordyce on the Fig. 11.22 Multiple epidermoid cysts on the scrotum Fig. 11.23 X-ray showing idiopathic calcification of
scrotum the scrotum
VULVA, PERIANAL AND PERINEAL SKIN / 365
Vulva, perianal and perineal skin

Papules, plaques and nodules
Erythematous No rash White
Nodules Papules Plaques
Acute Chronic Well defined Poorly

defined
Tender Discharging Papillomatous Single Bright red Soreness Thickened Soreness Excoriated Flat atrophic Thickened
sinuses lesion White Lichenified Discharge No rash surface surface
vaginal Excoriated
discharge
Staphylococcus -ve Gradual Psoriasis Mycology Itching Mycology Itching Biopsy

aureus bacteriology increase in elsewhere +ve +++ -ve +++
size
BOIL/ HIDRADENITIS WARTS BOWEN’S PSORIASIS CANDIDA LICHEN VULVO- PRURITIS LICHEN LEUKOPLAKIA,
INFECTED SUPPURATIVA genital, PAGET’S SIMPLEX/ VAGINITIS ANI/ SCLEROSUS et SCC
CYST common VIN ECZEMA VULVAE ATROPHICUS
TUMOURS
p. 366 see p. 344 see p. 358 p. 368 p. 366 p. 369 p. 366 p. 369 p. 366 p. 368 p. 367
366 / GENITALIA
HIDRADENITIS SUPPURATIVA Rashes presenting with perianal, scrotal or vulval itch

This is an uncommon condition where Psoriasis
painful papules, nodules, discharging When psoriasis is itchy the diagnosis is often missed. If the plaque is bright red rather
sinuses and scars occur at sites where than pink or mauve, whether scaly or not, it is probably psoriasis. Look at the natal cleft,
apocrine glands are present, i.e. in the the rest of the skin, the scalp and the fingernails for other signs of psoriasis (see p. 225).
axillae, pubic area, labia majora, scrotum,
groins, perianal skin, buttocks or the Lichen simplex
areolae of the breasts. If such lesions are Lichen simplex is a single lichenified plaque with or without obvious excoriations caused
confined to the perianal skin, think of by continual rubbing or scratching. The scrotum and vulva are common sites for this
Crohn’s disease and, much less commonly, condition (see p. 219).
tuberculosis. A biopsy will be needed to
establish these diagnoses (see also p. 344).
BOILS AND INFECTED CYSTS

An acutely painful red nodule on the
vulva, pubic area or scrotum may be
an abscess of a hair follicle (boil) due
to infection with S. aureus or in women
a similar lesion can be an infection of
a Bartholin gland due to gonorrhoea,
C. trachomatis or Gardnerella vaginalis.
PRURITIS ANI OR VULVAE

When a patient complains of perianal,
scrotal or vulval itching, you need to know
whether there are any other symptoms
such pain or vaginal discharge, whether a
rash is present on the vulva or elsewhere,
and whether anyone else in the family has
the same or similar symptoms.
Fig. 11.24 Scrotal lichenifiction from persistent Fig. 11.25 Lichenification of vulva
scratching
Eczema Contact irritant eczema occurs in babies (nappy/diaper rash,

Atopic eczema or unclassifiable endogenous eczema may present see p. 341); an identical rash can occur in the elderly if they are
with vulval itching. In the former, intolerable genital itching incontinent. Applied irritants can also cause an irritant eczema or
may be the final straw that makes it impossible for the patient to an acute vulvitis.
cope with her eczema. In the latter, sexual infidelity or anxiety Allergic contact dermatitis is often due to medicaments
about possible venereal disease may be the precipitating factor. (containing lanolin, parabens, antibiotics or local anaesthetics
Both conditions are clinically identical to eczema elsewhere, with bought over the counter or prescribed by a doctor), deodorants,
poorly defined itchy pink papules and plaques with excoriations, contraceptives or other preparations. It usually presents acutely
scaling and no vesicles. with vesicles, weeping and crusting, and it may be extremely sore
rather than itchy. Patch testing once the acute reaction has settled
down will sort out the cause.
Pubic lice
The diagnosis is confirmed by finding nits or adult lice on the
pubic or labial hair (see p. 363).
Scabies
There should be an itchy rash all over the body except on the face,
and the telltale burrows will be found between the fingers. Other
members of the family or sexual contacts may also be itching (see
p. 248).
Herpes simplex
This often causes pain as well as itching. Patients should be
referred to the local department of genito-urinary medicine so that
other sexually acquired diseases can be excluded (see p. 355).
Vaginal intra-epidermal neoplasia (VIN)

White plaques on the vulva that are thickened rather than
atrophic may be due to VIN (leukoplakia). If in doubt, histology
will distinguish between leukoplakia and lichen sclerosus et
Fig. 11.26 Allergic contact dermatitis Fig. 11.27 Perianal eczema with atrophicus.
to a local anaesthetic cream erythema and excoriations
368 / GENITALIA
Lichen sclerosus et atrophicus Tumours

This is a very itchy condition that principally occurs on the vulva or perianal skin. It A single red, scaly plaque unresponsive to
occurs in little girls or in middle-aged women. In children itching, soreness or blisters treatment should be biopsied to exclude
are the presenting symptoms; it gets better spontaneously at puberty. In older women, Bowen’s disease (VIN), extramammary
intolerable itching, soreness or dyspareunia are the reasons for seeking help. White Paget’s disease or a squamous cell
atrophic papules and plaques with or without follicular plugging or haemorrhagic blisters carcinoma.
are seen on the vulva and/or perianal skin. Occasionally lesions may occur elsewhere on
the skin where they are very similar to lichen planus, with flat-topped, shiny, polygonal
papules, but white in colour rather than mauve and with a wrinkled atrophic surface
(see p. 285).
Fig. 11.28 Lichen sclerosus in a child Fig. 11.29 Lichen sclerosus in an Fig. 11.30 Vulval intraepithelial Fig. 11.31 Bowen’s disease of
adult neoplasia (biopsy sites marked) perianal skin
Vulvo-vaginitis Anal discharge

This is inflammation of the vagina primarily with secondary A discharge or liquid faeces can cause itching due to the perianal
involvement of the vulva. It can be caused by: area being continually wet. Mucous discharge, bleeding or
● C. albicans: soreness rather than itching is usually the diarrhoea can all cause problems and a rectal examination is
presenting symptom on the vulva. An acute vulvitis with a essential to exclude haemorrhoids, a fistula-in-ano or carcinoma
red, glazed appearance is characteristic and there may be an of the rectum. Patients with poor perianal hygiene, particularly if
associated thick, white vaginal discharge. The diagnosis can be they have diarrhoea or soft stools, may itch because faeces are left
confirmed by direct microscopy (see p. 343), or culture of the on the skin after defecation. You can check for this by looking; if it
discharge. Remember to check for diabetes is not obvious, try wiping the perianal skin with a gauze swab –
● bacterial vaginosis due to Gardnerella vaginalis (a vaginal any trace of brown or yellow indicates that the hygiene of the area
discharge with a fishy smell is usually the clue to the is not ideal.
diagnosis); wet smears of the discharge show clue cells –
multiple organisms stuck to the epithelial cells. Gram staining Idiopathic
shows Gram-negative rods Perianal and vulval itching is quite common and a specific cause
● Trichomonas vaginalis infection (a frothy, greenish-white may not be found.
vaginal discharge); direct microscopy of the discharge will
show the protozoae VULVODYNIA AND SCROTODYNIA
● a retained foreign body in the vagina. Localised superficial dyspareunia and point tenderness within
the vestibule at the 5 o’clock and 7 o’clock positions is termed
When no rash is present consider the following diagnoses localised vulvodynia, and occurs in young premenopausal
Threadworms women who experience discomfort on penetration. Generalised
These usually cause pruritis ani in children, but in females they vulvodynia and scrotodynia presents as a burning pain.
may wander forward to the vulva, causing itching there too. Symptoms can occur all the time, and may spread over all the
Scratching leads to the ova being transferred to the patient’s genitalia and down the thighs; they are present without anything
fingers and fingernails and thence to the mouth (directly, or touching the area, and can worsen on sitting or climbing stairs.
indirectly on food eaten with unwashed hands). Inside the The appearance of the skin is normal. There may be associated
patient’s large bowel the ova mature and the cycle starts again. depression, fibromyalgia or irritable bowel syndrome.
The diagnosis is made by seeing the worms wriggling out of the Patients should be referred to a dermatologist with a special
faeces (tell the patient or the mother to look), by seeing them interest in these conditions (see p. 370).
on the perineum, or by the Sellotape test (apply some sticky
transparent tape to the perianal skin, place on a glass slide and
look for the eggs).
370 / GENITALIA
TREATMENT: PRURITIS ANI OR VULVAE
Any coexisting disease should be treated. of 2 are treated with piperazine 50 mg/kg body weight daily for 7 days. As well as the
drug treatment, the patient should be told to wash the perianal skin first thing in the
Psoriasis (see p. 340) morning to remove any ova laid during the night, and to wash her hands and scrub
Eczema (see p. 339) under her fingernails with a nail brush after going to the toilet and before meals.
Lichen planus (see p. 198)
Idiopathic group. There remain a large number of patients for whom no physical cause
Scabies (see p. 248)
can be found.
Pubic lice (see p. 363)
Genital warts (see p. 359) Pruritis ani. Whatever the original cause of the itching, scratching damages the skin and
Herpes simplex (see p. 355) makes it itch more. Wearing loose-fitting cotton underpants to keep the area as cool
as possible is often helpful, and it is important to pay particular attention to keeping
Lichen sclerosis et atrophicus. In little girls, 1% hydrocortisone cream or ointment the perianal skin clean and dry. He should wash his bottom with a mild soap and
applied twice a day is usually sufficient. In adult women, a very potentUK/group 1USA water after defecation. A bidet is very helpful in this respect and if the patient does not
topical steroid cream will be required to dramatically improve the symptoms and make have one, he might find it helpful to buy a plastic one (from a boat shop or a surgical
the patient believe that there is some hope for the future. It is applied twice a day to the appliance department) that can be placed over the toilet. Meanwhile, the application
affected area and produces a very rapid and dramatic improvement. Once the disease is of hydrocortisone (1%) or hydrocortisone-17-butyrate (Locoid) cream is likely to be
under control, reduce the frequency of application to two to three times a week. Control helpful in stopping the itching. It is important to use this especially at night to break
of the disease is important to prevent the development of squamous cell carcinoma in the itch scratch cycle, and to reassure the patient that ‘something can be done’. Once
the atrophic skin. the itching is controlled, the cream should only be used if required for intermittent itch.
If these measures do not work he should be referred to a dermatologist so that any
Candidiasis. An imidazole pessary placed high in the vagina at night: clotrimazole
other diagnosis can be ruled out and patch testing carried out. Very often such patients
(500 mg) single dose or miconazole (1200 mg) single dose.
become allergic to the numerous ointments and creams that they have used to treat the
T. vaginalis infection. The patient should be given metronidazole 400 mg bid for condition (especially local anaesthetics).
5–7 days, or 2 g as a single dose (alcohol must be avoided while taking metronidazole).
Pruritis vulvae. Like pruritis ani it may be due to some psychosexual problem. It is a
Bacterial vaginosis. Both the patient and her sexual partner should be given mistake to think that it is just a question of finding the right cream or ointment to use.
metronidazole 400 mg orally tid for 7 days (alcohol must be avoided while taking It is worth exploring with the patient whether there is some anxiety at the bottom of
metronidazole). it (guilt about her own or her partner’s adultery or impotence, a previous abortion or
Surgical problems. Haemorrhoids, fistula-in-ano or carcinoma of the rectum can all sexual abuse in childhood) and if possible sort this out.
present with pruritis ani and will need dealing with surgically. Vulvodynia and scrotodynia are difficult to manage and are best referred to a specialist
Threadworms. The whole family should be treated with mebendazole 100 mg orally dermatology clinic. These patients require detailed counselling, and treatment with
as a single dose (except for pregnant women and children under the age of 2). If re- regular application of bland emollients. In localised vulvodynia, local anaesthetic applied
infection occurs, treatment can be repeated after 2–3 weeks. Children under the age before intercourse may be helpful. Antidepressants can sometimes be helpful.
371
Lower legs
Erythematous lesions/rash
Acute
Patches, papules, plaques, blisters 372
12
Ulcers 385
Chronic
Normal surface 375
Scale, crust, exudate
Large patches and plaques (>2 cm) 382
Papules, small plaques and nodules see Chapter 8
Ulcerated surface
Surrounding skin affected 385
Surrounding skin normal 386
Purple, orange, brown rash 399
Other lesions see Chapter 9
372 / LOWER LEGS
Lower legs
Acute erythematous rash/lesions ACUTE RASH/LESIONS
Normal/exudate/crust surface
Patches, papules, plaques, blisters
Necrosis Blisters/exudate No exudate/blisters Generalised swelling
High fever No fever Papules and/or plaques Rapidly Tender red Unilateral Bilateral
Patient unwell Not ill expanding nodules/
plaque plaques
Dusky Large Isolated Discrete Vesicles/ Bilateral Unilateral Individual Tender calf See ‘Chronic’,
swelling, blisters blisters papules exudate on Poorly Hot to touch lesions last muscle p. 375
rapid spread Intervening erythema defined 7–10 days
skin normal
Yes No
Necrosis Well defined Grouped Patch test Pain and Arthralgia Duplex Doppler Ultrasound
developing erythema Central tenderness and fever or venogram
punctum
-ve +ve
NECROTISING ERYSIPELAS INSECT ACUTE ALLERGIC CELLULITIS ERYTHEMA DEEP VEIN RUPTURED
FASCIITIS BITES ECZEMA CONTACT NODOSUM THROMBOSIS MUSCLE/
(Endogenous DERMATITIS BAKER’S CYST
or varicose)
p. 374 p. 373 see p. 198 see p. 383 see p. 383 p. 373 see p. 378
ACUTE RASHES / 373
ERYSIPELAS Stratum Impetigo: infection under the

corneum stratum corneum
This is an infection of the upper half of the dermis with a
group A β-haemolytic streptococcus (Streptococcus pyogenes). Ecthyma: infection of full thickness
Epidermis
The patient becomes suddenly unwell with a high fever and of epidermis
rigors, associated with a well-defined red swollen area with
central blistering. No obvious portal of entry for the bacteria Upper Erysipelas: affects upper half of
dermis epidermis
is seen, which distinguishes it from cellulitis.
CELLULITIS Lower Cellulitis: affects lower half of

dermis epidermis
This is an infection of the lower half of the dermis by a
group A, C or G β-haemolytic streptococcus. There is
usually an obvious portal of entry for the organism such as Fat
Necrotising fascitis: infection of the
a leg ulcer, tinea between the toes, or eczema on the feet or Fascia
subcutaneous fat and deep fascia
legs. It looks like erysipelas except the area of erythema is
less well defined. There are no blisters and there is associated Fig. 12.01 Sites of infection of with a group A β-haemolytic streptococcus
lymphangitis and lymphadenopathy. The patient is less
unwell.
Fig. 12.02 Erysipelas: large bullae on well-demarcated erythema Fig. 12.03 Cellulitis: erythema with no blistering
374 / LOWER LEGS
TREATMENT: CELLULITIS AND ERYSIPELAS Measuring the antistreptolysin O titre is not helpful, as it is always
normal.
β-haemolytic streptococci are always sensitive to penicillin, but as there may be
associated infection with staphylococci, current practice is to give both intravenous It can be an acute fulminant illness, with the patient dying
benzyl penicillin, 600 mg and flucloxacillin 500 mg every 6 hours. As an outpatient, almost before you can think of the diagnosis, or it can be a much
high-dose flucloxacillin (1 gm 6-hourly) may be used. Treat erysipelas for 7 days and slower process, with the necrotic tissue gradually separating
cellulitis for at least 2 weeks, otherwise relapse is likely. For patients who are allergic to from the surrounding normal skin. In children and young
penicillin, oral erythromycin/clarithromycin 500 mg or clindamycin 300 mg 6-hourly can adults, streptococci are the common pathogen, but in the elderly,
be used instead. Do not use ampicillin because it does not work. If the infection is slow especially after surgery, other organisms may be implicated such
to settle, check that the patient is not diabetic. Cellulitis is always slower to resolve than as staphylococci, Escherichia coli and clostridium.
erysipelas, which usually responds within 24 hours.
As well as treating the cellulitis, you must also treat the co-existing eczema, tinea TREATMENT: NECROTISING FASCIITIS
pedis or leg ulcer that has allowed entry of the streptococcus into the skin. Otherwise
recurrent cellulitis will occur and this leads to chronic lymphoedema. If there have been Patients should be admitted urgently to hospital so that wide surgical debridement of
more than two episodes of cellulitis within 6 months, long-term prophylactic penicillin is the affected skin can be carried out. Antibiotics alone are not sufficient treatment. This is
needed. You can use oral phenoxymethylpenicillin (penicillin V) 250 mg bid. because the streptococci produce a toxin, which causes the blood vessels in the affected
area to thrombose. This not only causes the necrosis of the skin, which is the hallmark
of the disease, but also prevents the antibiotics from getting to where they are needed.
NECROTISING FASCIITIS Without surgery some patients with necrotising fasciitis will die and others will spend
many months in hospital.
Necrotising fasciitis is an acute fulminant infection of the
subcutaneous fat and deep fascia, usually by a group A
β-haemolytic streptococcus. A toxin released from the organism
causes thrombosis of the blood vessels in the skin and thence
necrosis. Initially it looks like cellulitis or erysipelas but purple
areas followed by frank necrosis occur within 2–3 days. The most
important thing here is to think of the diagnosis in any patient
who has what looks like erysipelas or cellulitis that does not
begin to improve with penicillin or erythromycin after 24–48
hours, or who has dusky-purple areas appearing within the larger
red, swollen area. Think of it in patients with co-morbidities
such as immunosuppression, diabetes, alcohol excess, cancer
or penetrating injury (e.g. road traffic accident) or orthopaedic
surgery. High levels of anti-desoxyribonuclease B and anti-
hyaluronidase in the patient’s serum will confirm the diagnosis. Fig. 12.04 Necrotising fasciitis
CHRONIC RASH/LESIONS / 375
Lower legs
Chronic erythematous rash/lesions CHRONIC RASH/LESIONS
Normal surface
Patches, papules, pustules, plaques, nodules and swelling
Patch/plaque Nodules Papules Generalised swelling
Pustules
Mottled Well defined Poorly Capillary Non-pitting Pitting

network lesions defined malformation oedema oedema
pattern in skin
Accentuated Centre yellow Flat topped Patient has Tender Non-tender Starts in Fixed Variable
by cold Edge mauve Mauve exophthalmos/ lesions lesions childhood indurated swelling
or brown hyperthyroidism swelling
Surface Biopsy ‘Peau-de- Indurated

atrophy orange’ surface nodules/
plaques
LIVEDO NECROBIOSIS HYPERTROPHIC PRETIBIAL ECZEMA see Table see Ch 8 KLIPPEL– LYMPH- PITTING
RETICULARIS LIPOIDICA LICHEN MYXOEDEMA 12.1 TRÉNAUNAY OEDEMA OEDEMA
PLANUS
p. 376 p. 377 p. 377 p. 376 p. 383 p. 378 see p. 195 p. 380 p. 381 p. 381
376 / LOWER LEGS
LIVEDO RETICULARIS PRETIBIAL MYXOEDEMA

Livedo reticularis is a mottled reticular discolouration of the skin, Pink, skin-coloured or yellow, waxy plaques or nodules
usually on the legs, but can be seen on arms and trunk. It is due are seen on the anterior shins of around 10% of patients
to stagnation of blood in capillaries of the skin at the margins of with hyperthyroidism. It is associated with diffuse thyroid
supply between adjacent arterioles. Any reduction in the blood enlargement, exophthalmos, and thyroid acropachy. The surface of
flow of skin arterioles may cause this pattern. The causes are: the skin has a ‘peau d’orange’ effect.
1. congenital – cutis marmorata telangiectasia congenita
2. physiological – seen in children and adults in the cold
3. idiopathic – occurs in adults, cause unknown
4. vasculitic – polyarteritis nodosa, autoimmune connective tissue
diseases
5. intravascular – cryoglobulins, thrombocytopenia,
hypercoagulability states.
Patients should be referred to a specialist to rule out vasculitic and

intravascular causes.
Fig. 12.05 Livedo reticularis Fig. 12.06 Pretibial myxoedema in Fig. 12.07 Hypertropic lichen planus
black skin in Asian skin
TREATMENT: PRETIBIAL MYXOEDEMA TREATMENT: HYPERTROPHIC LICHEN PLANUS
Treat the skin with a very potentUK/group 1–2USA topical steroid under occlusion. The Hypertrophic lichen planus on the legs may last for years rather than months and is
thyroid disease will need to be treated with antithyroid drugs or thyroidectomy. often extremely itchy. A very potentUK/group 1USA topical steroid cream or ointment, such
as 0.05% clobetasol propionate (DermovateUK/TemovateUSA), will frequently be effective
when less potent topical steroids have not helped. Occasionally steroids will have to be
HYPERTROPHIC LICHEN PLANUS injected intralesionally in order to be effective (triamcinolone 10 mg/mL).
Multiple itchy, thickened, pink-purple, violaceous or
hyperpigmented plaques on the lower legs may be due to lichen
planus (see Fig. 12.07). The surface may be slightly scaly or warty. NECROBIOSIS LIPOIDICA
The presence of typical lichen planus elsewhere will suggest the Well-defined round or oval plaques on the front of the shins
diagnosis, but an isolated plaque needs to be distinguished from are characteristic of necrobiosis lipoidica. The plaques have a
lichen simplex by skin biopsy. raised mauve or brown edge, while the centre is yellow in colour
with obvious telangiectasia. Seventy per cent of patients with
this condition are diabetic but there seems to be no relationship
between the appearance or spread of the skin disease and control
of the diabetes. The affected areas of skin are atrophic and
occasionally may ulcerate after trauma (usually obvious trauma
such as being kicked or knocked with a supermarket trolley).
TREATMENT: NECROBIOSIS LIPOIDICA
Always check for underlying diabetes mellitus. Treatment is aimed at stopping the
plaques from enlarging. If the disease is active (raised mauve border), treat with a
potentUK/group 2–3USA topical steroid cream twice a day until the edge has flattened
off. The patient should be warned that the treatment will not get rid of the marks
altogether. If the edge is not raised, and the area of skin merely discoloured, treatment
with topical steroids will not help.
It can be very difficult to get ulceration to heal. The legs should be carefully protected
from further trauma, and a non-stick hydrocolloid or foam dressing applied (see
Table 2.05, p. 43, and Table 2.08, p. 46). The dressings can be changed twice a week
until the ulcer(s) heal.
Fig. 2.08 Necrobiosis lipoidica Fig. 2.09 Necrobiosis lipoidica (close (cont.)
up)
378 / LOWER LEGS
ERYTHEMA NODOSUM
Systemic steroids such as prednisolone 30 mg/day for a few weeks may induce healing Tender red nodules (plaques) appear on the front of the shins
but may upset diabetic control. Alternatively, a skin graft may be required but with a mainly in young women. Individual lesions are 1–10 cm in
poor cosmetic result. If an area of necrobiosis lipoidica has been ulcerated in the past, diameter and initially bright red in colour but fading through the
the patient should take every care to protect the legs from further injury in the future. colour changes of a bruise over 7–10 days. Lesions come in crops
This may involve wearing shin pads under the trousers and avoiding trauma.
for 3–6 weeks. There may be associated general malaise, fever and
arthropathy.
TENDER RED NODULES (PLAQUES) ON LEGS Common causes of erythema nodosum:
One or several tender red nodules or indurated plaques on the ● drugs, e.g. sulphonamides and the oral contraceptive pill
lower legs are distinguished by a careful history, examination and ● pregnancy
a biopsy. A referral to a specialist is usually necessary except for ● streptococcal sore throat
erythema nodosum. ● sarcoidosis
● ulcerative colitis
Table 12.1 Causes of tender nodules and plaques on the lower legs ● Crohn’s disease
● tuberculosis
Erythema nodosum Tender red nodules on front of shins
Individual lesions only last 7–14 days ● numerous other viral, bacterial and fungal infections.
Associated fever and arthralgia, mainly young women
Panniculitis Single or multiple red nodules, mainly on lower legs but can be any TREATMENT: ERYTHEMA NODOSUM
area of subcutaneous fat
Lesions last weeks or months First, treat the underlying cause. Non-steroidal anti-inflammatory drugs (NSAIDs) such
Heal with scarring as indomethacin 50 mg qid are the most useful treatment. Give regular oral analgesics
Nodular vasculitis Impossible to distinguish from panniculitis except on biopsy of an for the pain (paracetamol, co-codamol) if required. Tell the patient to rest with the feet
early lesion up as much as possible, and to wear elastic support stockings when walking around.
Mainly lower legs, lesions last weeks or months
Polyarteritis nodosa Benign cutaneous form associated with livedo reticularis and/or
ulceration on lower legs
Generalised form: patient unwell with involvement of lungs and
kidneys; high erythrocyte sedimentation rate
Superficial Red papules over superficial veins
thrombophlebitis No deep involvement
NODULAR VASCULITIS/PANNICULITIS
One or several red nodules/indurated plaques on the lower legs
that persist for weeks or months are due to a nodular vasculitis
(inflammation around the blood vessels in the deep dermis
or subcutaneous fat) or a panniculitis (inflammation in the
subcutaneous fat itself). These can be distinguished by a deep
biopsy of an early lesion.
Panniculitis can be caused by:
● cold, especially in the newborn
● trauma to heavy breasts and buttocks
● release of enzymes by pancreatic disease (e.g. pancreatitis or
Fig. 12.10 Erythema nodosum: multiple tender nodules and plaques on the
lower legs carcinoma of pancreas)
● discoid lupus erythematosus (lupus profundus)
● artefact from self-injection of oily liquids (look for the needle
mark in the centre!).
In nodular vasculitis, look for a focus of infection such as

tuberculosis.
TREATMENT: NODULAR VASCULITIS/PANNICULITIS
Look for the cause and treat that. Where none is found, treatment is symptomatic
with analgesics or NSAIDs and compression stockings. Systemic steroids may be
needed, starting with prednisolone 30 mg daily and gradually reducing as soon as the
disease comes under control to a maintenance dose of 7.5–10 mg daily. Ciclosporin,
azathioprine or cyclophosphamide can be tried as steroid-sparing agents. It is often a
case of trial and error to find something that will work for a particular individual.
Fig. 12.11 Nodular vasculitis in a Fig. 12.12 Panniculitis

patient with tuberculosis
380 / LOWER LEGS
KLIPPEL–TRÉNAUNAY SYNDROME a b
Limb enlargement is associated with congenital
vascular abnormalities such as a capillary
malformation (port wine stain), deeper cavernous
vessels, arteriovenous fistulae or venous-lymphatic
malformations. The limb enlargement is due to
increased blood flow resulting in soft tissue and
sometimes bone overgrowth. Typically, a port wine
stain is obvious at birth or in early childhood. The
limb hypertrophy occurs gradually later on.
Fig. 12.13 Pitting oedema: (a) firm pressure; (b) slow filling of indentation
Fig. 12.14 Klippel–Trénaunay Fig. 12.15 Congenital lymphoedema Fig. 12.16 Lymphoedema with Fig. 12.17 Chronic lymphoedema due
syndrome in the right leg secondary polypoid hyperplasia and to filariasis
pigmentation
PITTING OEDEMA TREATMENT: LYMPHOEDEMA complications of lymphoedema include

Oedema is due to accumulation of fluid in discomfort and ‘heaviness’ in the limb,
the dermis and is demonstrated clinically Because the lymphatics are permanently absent or reduced mobility, leakage of fluid from
by firm pressure producing a depression damaged, the condition is incurable. Simple hygiene breaks in the skin, secondary streptococcal
measures such as washing with soap and water and infection (cellulitis) and tinea pedis
in the surface that only slowly fills in again
moisturising the skin can prevent recurrent bacterial between the toes.
(see Fig. 12.13). Pitting oedema is seen
infections. Deep breathing for 10 minutes before
in the most dependent areas – ankles in getting out of bed in the morning helps to empty the Causes of primary lymphoedema:
someone who is ambulant, and over the lymphatics in the chest and abdomen. Massaging the ● absence or hypoplastic lymphatics.
sacrum in someone who is bedridden. It limb regularly and applying a compression bandage
will resolve with diuretics or if the affected is helpful (see p. 389). It is important to keep the The age the lymphoedema becomes
area is elevated. limb moving and when seated to elevate the limb. apparent is determined by other factors
Complications should be prevented by the use of
Unilateral oedema can be due to: such as infection and venous insufficiency.
prophylatic penicillin V (250 mg bid) and antifungals
● a deep vein thrombosis applied every night between the toes. Hyperkeratosis Causes of secondary lymphoedema:
● chronic venous disease (see p. 387) can be treated with 5% salicylic acid ointment and ● Infection: recurrent streptococcal
● severe skin disease (e.g. eczema, excessive papillomatosis can be removed by curettage infections
psoriasis, cellulitis, erysipelas). (see p. 391). ● Filariasis: Wuchereria bancrofti
Bilateral oedema can be due to: microfiliariae are transmitted by
● cardiac failure mosquito bites; they mature into adult
LYMPHOEDEMA
● hypoproteinaemia worms, which obstruct the lymphatics
Damage to lymphatics results in retention
● obesity – think of it in patients from the tropics
of protein-rich interstitial fluid in the
● nephrotic syndrome (see Fig. 12.17)
affected limb, leading to swelling (see
● early lymphoedema ● Inflammation: chronic eczema or
Fig. 12.15) and fibrosis, so that the oedema
● immobility psoriasis
becomes non-pitting and non-dependent
● drugs causing salt and water retention ● Neoplasia: cancer infiltrating lymph
(i.e. will not improve with diuretics or on
(e.g. hormones, antihypertensives, nodes
elevation of the limb). The skin becomes
calcium-channel blockers, monoamine ● Trauma:
thickened (you will not be able to pinch
oxidase inhibitors, systemic steroids) — surgical removal of lymph nodes
a fold of skin over the base of the second
● venous outflow obstruction in — radiotherapy to lymph nodes
toe) with accentuated skin creases.
pregnancy and abdominal masses. — artefactual – restrictive band applied
Hyperkeratosis and papillomatosis occur
to leg.
after a few years (see Fig. 12.32). Secondary
382 / LOWER LEGS
Lower legs
Chronic erythematous rash/lesions SCALE, CRUST, EXUDATE
Scale, crust or exudate on surface
Large patches and plaques (>2 cm diameter)
(For lesions <2 cm size see Chapter 8, pp. 202 and 245)
If scaly surface, scratch firmly with nail
Profuse silver scaling Slight/no increase in scale or crust/exudate on surface
Multiple large Single/few Single/few Accentuated Coalescing papules, ‘Crazy paving’

bright red small, fixed large plaques edge > centre poorly defined pattern of
plaques lesions erythema
Symmetrical Long history Lichenified Medial/lateral Well defined Unilateral or Symmetrical Elderly
Knees ± Skin type I & II and excoriated malleolus scaly/crusted asymmetrical Any site Dry skin
elsewhere Lateral calf plaque(s)
Mycology Patch test
Biopsy -ve +ve -ve +ve
PSORIASIS BOWEN’S LICHEN VARICOSE DISCOID TINEA ATOPIC/ ALLERGIC ASTEATOTIC

DISEASE SIMPLEX ECZEMA ECZEMA CORPORIS ENDOGENOUS CONTACT ECZEMA
BASAL CELL ECZEMA DERMATITIS
CARCINOMA
see p. 225 see p. 220 see p. 219 p. 384 see p. 243 see p. 233 p. 383 p. 383 p. 384
ECZEMA ON THE LOWER LEGS

Poorly defined, red scaly papules or plaques on the lower legs
are likely to be due to eczema. It is possible to classify the eczema
by the distribution and appearance.
● Acute weeping eczema suggests an allergic contact dermatitis.
● Varicose eczema occurs around the malleoli in patients with
other evidence of venous disease.
● Asteototic eczema is seen in elderly patients where the skin has
been allowed to dry out (see p. 384).
● Atopic eczema elsewhere (previous or present flexural eczema
in the antecubital or popliteal fossae or on the front of wrists).
● Symmetrical eczema that does not fit any of the above is an
unclassifiable endogenous eczema. Fig. 12.18 Acute allergic contact dermatitis from bandages: erosions and
exudate but no ulceration
Well-defined plaques may be due to:
● varicose eczema around medial or lateral malleoli
● discoid eczema – either the wet type, if surface exudate and
crust present, or the dry type, if scaly (see p. 243)
● lichen simplex if situated on the lateral calf or ankle and
associated with itching and excessive scratching (see p. 219).
These will need to be distinguished from psoriasis (scratching the

surface leads to profuse silver scaling).
ALLERGIC CONTACT DERMATITIS

Allergic contact dermatitis on the lower legs is usually due to
medicaments applied in the treatment of venous eczema or
ulcers. The common sensitisers are various antibiotics (neomycin,
soframycin, fucidin), lanolin in various ointments, parabens and
MCI (methylchloroisothiazolinone) in creams and paste bandages,
and occasionally the rubber in elastic support bandages.
Fig. 12.19 Varicose eczema around a small ulcer

384 / LOWER LEGS
TREATMENT: ACUTE ALLERGIC CONTACT DERMATITIS
Dry up the exudate with potassium permanganateUK or aluminium acetateUSA soaks (see
p. 30). Treat the eczema with a potentUK/group 2–3USA topical steroid ointment twice a
day (not a cream, as the preservative in a cream can itself be the causative allergen).
Once the rash is better, identify the allergen by patch testing so that it can be avoided
in the future.
ASTEATOTIC ECZEMA (ECZEMA CRAQUELÉ)

Asteatotic eczema is due to drying out of the skin especially in the
elderly. It occurs in winter or when patients are hospitalised and
made to bathe more frequently than they are used to. The skin
is dry or scaly with irregular erythematous fissures like ‘crazy
paving’. The associated itching usually brings it to the attention of
the doctor.
Fig. 12.20 Asteatotic eczema
TREATMENT: ASTEATOTIC ECZEMA
The patient should either bathe less often or use one of the dispersible bath oils in
TREATMENT: VARICOSE ECZEMA
the bath water each day and a greasy (water-in-oil) emollient (see p. 26) can then
be applied to the dry scaly skin twice a day. Occasionally a weakUK/group 7USA topical
More important than what is put onto the eczema itself is treatment of the underlying
steroid such as 1% hydrocortisone ointment may be needed.
problem (chronic venous stasis due to incompetent valves in the deep veins of the calf)
with proper elastic support. It is probably best to use bandages (see p. 389) until the
eczema is better and then change to elastic stockings, because the treatment for the
VARICOSE/STASIS ECZEMA eczema may otherwise ruin the stockings.
Eczema may occur in patients with venous hypertension (see
For the eczema itself, a moderately potentUK/group 4–5USA topical steroid ointment can
p. 387). It is distinguished from other types of eczema by being
be applied twice a day. The patient may prefer a cream to an ointment, particularly since
confined to the lower legs in a patient with other signs of venous
that will make less of a mess of his or her bandages. This should be resisted though,
disease. Acute-on-chronic varicose eczema should suggest a because many patients are allergic to parabens (from the use of creams or paste
superadded allergic contact dermatitis rather than cellulitis, which bandages). All patients with varicose eczema should be patch tested to make sure that
is unilateral and feels hot. you do not make things worse by applying ointments, dressings and bandages that they
are allergic to.
ULCERS / 385
Lower legs, feet (any site)

Ulcerated surface ULCERS: ACUTE, & CHRONIC (surrounding skin abnormal)
1. Acute – rapid onset
2. Chronic: surrounding skin affected
Rapid (acute) onset Chronic (>2 weeks) slow onset Surrounding skin
Dusky discolouration of skin normal, see next
→ large necrotic ulcer page
Surrounding skin abnormal
Unwell Patient Child, Associated Surrounding erythema, Yellow plaque Skin atrophic
Toxic feels well malnourished purpuric papules/ scaling, pigmentation telangiectasia telangiectasia
vesicles
Lower legs, Any site Legs and feet Legs and feet Around ankles Afro-Caribbean Front of shin Previous therapy
hands, face ? Associated Tropical climate BIOPSY Large, shallow +ve sickle cell BIOPSY
systemic disease painless (usually)
NECROTISING PYODERMA TROPICAL VASCULITIS/ VENOUS/STASIS SICKLE CELL NECROBIOSIS STEROIDS or

FASCIITIS GANGRENOSUM ULCER POLYARTERITIS ULCER ULCER LIPOIDICA RADIOTHERAPY
NODOSUM
see p. 374 p. 396 p. 397 p. 401 p. 387 p. 397 see p. 377 p. 396
386 / LOWER LEGS
Lower legs, feet (any site)

Ulcerated surface CHRONIC ULCERS – surrounding skin normal
Surrounding skin normal
Absent foot Reduced Immobile Normal pulses and sensation
pulses sensation patient
Deep ulcer Single small ulcer Single/multiple large ulcer Multiple small ulcers
Deep Callosity over/ At site of Skin type I and II Recent Varicose Undermined Odd shape, Pus
Painful around ulcer pressure Sun exposed sites foreign veins violaceous edge straight underneath
travel edges surface
crust
Toes, feet, Soles, heel, Heel, Slow growth Rapidly Exposed Lower ¹/³ leg Any site Any site Common in
heel, shin fingers buttocks growing sites – Slow onset Large rapid hot climate
Skin feels face and growth
cold hands
Dopplers Biopsy Biopsy Biopsy Underlying Doppler A/B Swab

A/B index bruit index >0.9 Staph. ++
<0.7
ARTERIAL NEUROPATHIC PRESSURE BASAL CELL SQUAMOUS LEISH- A-V VENOUS PYODERMA DERMATITIS ECTHYMA
ULCER ULCER SORE CARCINOMA CELL MANIASIS ANASTOMOSIS ULCER GANGRENOSUM ARTEFACTA
CARCINOMA
p. 392 p. 393 p. 394 p. 395 p. 395 see p. 140 p. 398 p. 387 p. 396 p. 395 see p. 187
ULCERS / 387
VENOUS ULCERS Venous ulcers occur on the lower third of the leg, over either
The cause of venous ulceration is loss of the valves in the deep or the medial or the lateral malleolus. They are large, superficial
perforating veins. The venous blood returns from the lower legs and painless; if painful, then there may be an element of arterial
back to the heart by the calf muscle pump. Compression of the insufficiency. There will be other evidence of venous disease
calf muscles (by walking or running) squeezes blood up the legs. such as oedema, varicose veins (see Fig. 12.22), venous flare (see
Blood is drawn from the superficial veins and pushed upwards Fig. 12.26), pigmentation (orange brown due to haemosiderin
by valves, which prevent back flow. Loss or incompetence of or dark brown due to melanin, see Figs 12.27 and 12.28), eczema
these valves results in enormous pressure (venous hypertension) (see Fig. 12.19), atrophie blanche (white scars with telangiectasia
in the superficial veins that is transmitted back to the capillaries, on the surface, see Fig. 12.25) and fibrosis around the ankle
resulting in venous disease and ulceration. (lipodermatosclerosis, see Fig. 12.23), which results in narrowing
around the ankle with lack of skin mobility (the opposite to
oedema).
Fig. 12.21 Anatomy of veins in lower leg showing Fig. 12.22 Varicose veins Fig. 12.23 Lipodermatosclerosis (inverted
deep, superficial and perforating veins with one-way champagne bottle shape)
valves
388 / LOWER LEGS
Complications of venous ulceration are relatively rare and include

cellulitis, haemorrhage, soft tissue calcification (see p. 391) and
malignant change (see p. 395). Infection of the ulcer itself is of
little consequence and mixed organisms are often present. Taking
swabs for bacteriology should be discouraged, as this tempts the
physician to treat with potentially sensitising topical antibiotics.
Cellulitis should be treated promptly, but this diagnosis is made
on clinical grounds (see p. 373). Venous ulcers may be complicated
by arterial insufficiency; pain and poor healing with compression
bandages suggest this.
Fig. 12.25 Atrophie blanche around the ankle
Fig. 12.24 Venous leg ulcer: large, superficial and painless, situated on the lower Fig. 12.26 Venous flare: tiny dilated veins visible on the surface
third of the lower leg – note both post-inflammatory hyperpigmentation and
haemosiderin pigmentation around the ulcer
ULCERS / 389
TREATMENT: VENOUS LEG ULCERS
1. Clean and debride the ulcer (see Table 2.05, p. 43)

2. Apply an emollient to the skin around the ulcer (see Table 2.01a, p. 26)
3. Apply a dressing to absorb any exudate (see Table 2.07, p. 45) and protect the ulcer during healing (see Table 2.08,
p. 46)
4. Assess arterial blood flow to leg (feel pulses and do Dopplers, p. 393)
5. Compression bandaging or stockings – see next box
6. Treat any associated complications and consider skin grafting
7. Elevate the leg when at rest; the ankle should be at the level of the pelvis
Fig. 12.27 Post-inflammatory hyperpigmentation Compression bandaging

secondary to venous disease and varicose eczema
The only effective way of treating venous hypertension is by external compression of the leg by bandaging or support
stockings. This compresses the superficial veins so that blood must flow in the deep veins (see Fig. 12.21).
Two-layer bandaging (see Fig. 12.29) has replaced four-layer bandaging because the dressings are less expensive and
patients can wear normal footwear, improving compliance. A tubular stockinette is applied over the skin and any ulcer
dressings and the two layers are as follows.
1. Orthopaedic wool: it is applied as a spiral with 50% overlap. This is absorbent and pads out any bony protuberances.
2. Compression bandage: short-stretch bandages, where the bandage is pulled to full stretch (e.g. Actico, Comprilan),
are preferred – this is easier for patients to apply themselves but should be used only in mobile patients; long-stretch
bandages, where the bandage is pulled to 50% stretch (e.g. Tensopress, Setopress, Surepress), can be used on mobile
or non-mobile patients.
Four-layer bandaging (see Fig. 12.30) is best used in immobile patients, as it provides constant pressure to the leg. It
needs to be applied by a nurse with the appropriate training. It will remain in place and be effective for a full week.
The four layers come as a pack (Ultra Four, Profore) and consist of the following:
Fig. 12.28 Haemosiderin pigmentation on lower 1. orthopaedic wool (Ultra Soft, Profore#1) as a spiral with 50% overlap
leg, secondary to venous stasis with areas of 2. crepe bandage (UltraLite, Profore#2) as spiral at mid-stretch
atrophie blanche
3. high-compression long-stretch bandage (Ultraplus, Profore#3)
4. cohesive lightweight elastic bandage (UltraFast, Profore#4).
Profore is the only system available for calf size of 25–30 cm and above.
(cont.)
390 / LOWER LEGS
Once the ulcer has healed, bandaging should be continued for at least 4 weeks to allow
the healed skin to stabilise. Dopplers should be repeated every 6 months if compression
is continued.
Elastic support in the form of compression stockings is necessary for the rest of the
patient’s life, since the missing leg valves cannot be replaced. Support is achieved by
wearing a below-knee elastic stocking. Decide on the compression level required (see
Table 12.02). For treatment of venous disease, UK class 2 (EU/US class 1) is usual.
Table 12.03 gives an indication of the size the patient requires. Styles of stocking vary.
Pulling on stockings can be helped by using a glide sheet, which is put on the leg first,
over which the stocking then easily slides, and is then removed; alternatively, a metal
stocking donner aid can be used.
Tubinette 1. Orthopaedic 2. Long- or short-

Table 12.02 Compression levels for stockings stockinette wool stretch bandage
Indication Prolonged Varicose Moderate Severe Fig. 12.29 Two-layer bandaging

sitting, veins, healed lymphoedema, lymphoedema
pregnancy leg ulcers severe varicose veins
Compression Light Moderate Firm Extra-firm
UK Class Class 1 Class 2 Class 3
EU/US class Class 1 Class 2 Class 3
UK range (mmHg) 14–17 18–24 25–35
US range (mmHg) 15–20 20–30 30–40
EU range (mmHg) 18–21 23–32 34–46
Table 12.03 Measuring for compression stockings

Measure circumference at calf and ankle
Stocking size Small Medium Large X-Large XX-Large
Calf circumference (cm) 30–37 33–40 35–43 37–46 40–49
Ankle circumference (cm) 19–23 22–25 24–28 28–30 30–34
Tubinette 1. Orthopaedic 2. Crepe 3. High-compression 4. Cohesive lightweight
Measure height below kneecap to floor stockinette wool bandage bandage elastic bandage
Floor to below-knee height (cm) <42 = Regular >42 = Long
Fig. 12.30 Four-layer bandaging
Note: sizes are approximate, as individual brands vary.
ULCERS / 391
Skin grafting
Pinch grafts or partial thickness skin grafts can be used to hasten the healing process.
Small islands of skin are placed on the clean ulcer bed and the area covered with a
non-adherent dressing. The patient will need to remain on bed rest for 2 weeks with leg
elevation to allow the graft to take.
TREATMENT: COMPLICATIONS
● Associated arterial disease (see pp. 393–4).

● Overgranulation of the ulcer: too much granulation tissue will delay healing. This can
be removed by applying a silver nitrate stick to the area before applying compression.
Some patients find this extremely painful, and if this is the case apply a gauze swab
soaked in 0.25% silver nitrate solution instead. Alternatively, granulation tissue can
be curetted off. Fig. 12.31 Split skin grafts applied to a large leg ulcer
● Secondary infection of the ulcer. Only two infections in leg ulcers matter:
—Pseudomonas infection causes an unpleasant smell. This can be eradicated with
5% acetic acid (use ordinary household vinegar diluted 50% in water). Cut a
piece of gauze to the size of the ulcer and soak it in the vinegar. Apply the gauze
daily to the ulcer until the smell goes. Alternatively, a 0.25% solution of silver
nitrate can be used (see Table 2.06, p. 44). These are much more effective than
intravenous piperacillin or ticarcillin and clavularic acid.
—Group A β-haemolytic streptococci in an ulcer causes cellulitis. This is diagnosed
clinically. Taking swabs from leg ulcers is to be discouraged. Treat with
intravenous benzyl penicillin (see p. 374).
● Eczema around the ulcer (see p. 384).
● Nodular polypoid hyperplasia: the excess tissue can be scraped off using a curette
(see Fig. 12.32). No anaesthetic is needed. It will not reoccur if the patient wears
compression bandages.
● Subcutaneous calcification: some venous ulcers will not heal because of calcium
deposition in the subcutaneous fat, which can be confirmed by X-ray (see Fig. 12.50).
Because it is difficult to treat, refer to a dermatologist.
Fig. 12.32 (a) Nodular polypoid hyperplasia associated with lymphoedema; (b)
after excess tissue removed by curettage
392 / LOWER LEGS
ARTERIAL ULCERS
These are due to a reduction in arterial blood supply to the
lower limb usually due to atherosclerosis. They are typically
painful, punched out and relatively deep (sometimes revealing
the underlying tendons). They occur where the arterial supply
is poorest – on the tips of toes, the dorsum of the foot, the heel
and the front of the shin. The absence of peripheral pulses and
a history of intermittent claudication will confirm the diagnosis.
Other signs to look for are cold feet, blotchy erythema of the
feet, loss of hair and thickened toenails. Untreated, gangrene
will eventually follow. The patient may have evidence of more
widespread arterial disease, e.g. a past history of coronary
thrombosis or stroke.
Fig. 12.34 Arterial ulcer on side of Fig. 12.35 Arterial ulcer on front of
toe shin with tendon visible
TREATMENT: ARTERIAL LEG ULCERS
A patient with an arterial ulcer should be referred to a vascular surgeon. If it is not

possible to improve the arterial blood supply, it is very unlikely that the ulcer will heal,
and gangrene will eventually occur. Early rather than late amputation is advised before
the pain becomes intolerable.
Treatment of the ulcer itself. If there is any slough present, it should be removed either
with a pair of sharp scissors or a scalpel or with a desloughing agent (see p. 43). Once
the ulcer is clean it should be covered with a non-adhesive dressing (see p. 46). This can
be left in place for a week at a time so that any new epithelial cells will not be removed
as soon as they have formed. The dressing is covered with a light bandage simply to
keep it in place. Do not apply tight bandages or any kind of elastic support, because
they can impede the arterial supply further. Adequate analgesics must also be given
during the healing process since these ulcers are always painful.
Fig. 12.33 Gangrene of toes due to arterial disease
ULCERS / 393
NEUROPATHIC ULCERS
INVESTIGATIONS TO DETERMINE THE EXTENT OF ARTERIAL DISEASE INCLUDE:
These ulcers result from trauma to anaesthetic feet, so occur over
1 Feeling the pulses and listening for bruits
2 Measurement of the blood pressure in the arm and at the ankle with a Doppler bony prominences, particularly the first metatarsophalangeal
probe joint, the metatarsal heads or the heel, or at any other site of
injury. Classically they are deep, painless, and often covered with
Systolic blood pressure ankle = Resting ankle/brachial (A/B)
thick callous. The diagnosis is confirmed by finding sensory loss
Systolic blood pressure arm pressure index
and some associated disorder that has caused it, e.g. diabetes,
If it is >0.9 there is no arterial disease leprosy, paraplegia, peripheral nerve injury, polyneuropathy,
If it is <0.9 there is arterial disease syringomyelia.
Compression should not be used if <0.8
If it is <0.7 there is clinically significant arterial disease
If it is <0.5 the patient will be getting rest pain
3 Duplex imaging Doppler: this combines the handheld continuous wave Doppler
together with real-time B-mode imaging to give picture images of the blood flow
and measurement of blood flow
4 Arteriogram to find out where the problem is, how extensive it is and whether the
disease is amenable to surgery
Fig. 12.36 Measurement of the systolic blood pressure at the ankle using a
Doppler probe: shaded area usual site for venous ulcers – place cuff above this Fig. 12.37 Neuropathic ulcer over first Fig. 12.38 Treatment of a neuropathic
on calf metatarsal head ulcer by protecting it in a plaster cast
394 / LOWER LEGS
TREATMENT: NEUROPATHIC ULCERS ULCERS IN A DIABETIC PATIENT

Patients with diabetes mellitus can have both arterial and
Loss of sensation means that patients may not notice an injury to their anaesthetic feet neuropathic ulcers. It is important to sort out which of the two
or legs. Rubbing from shoes, treading on a nail, being bumped into by a supermarket is the main culprit and treat accordingly. The arterial disease can
trolley, having the toes accidentally trodden on, or burning by hot water are some of the
be due to atherosclerosis of the major limb vessels or small vessel
common sources of injury. If the patient does not notice what has happened and does
disease (in which case the treatment options may be limited).
not protect the area from further damage, an ulcer can form. On the sole of the foot,
callous often builds up around the injury, making an ulcer seem smaller than it really is
Either type of ulcer (or both) can be complicated by bacterial
or sometimes completely covering it. It is essential to remove the callous with a scalpel infection. It is important to deal with this promptly with systemic
to see how big the ulcer is. If nothing is done at this stage, repeated trauma will cause antibiotics. Necrobiosis lipoidica (see p. 377) can also ulcerate.
the ulcer to enlarge, and secondary infection is likely to occur (sometimes leading to
osteomyelitis). The foot should be X-rayed and bacteriology swabs taken. If osteomyelitis PRESSURE SORES
is present the patient should be admitted to hospital so that high doses of intravenous Sustained pressure over pressure points in immobile patients
antibiotics can be given. leads to localised ischaemia and eventual ulceration.
To get the ulcers healed, further injury/friction must be avoided. The simplest way
of achieving this is by the patient resting in bed but this is not usually practical. An
alternative is to apply a below-knee walking plaster for 2 months at a time (see Fig.
12. 38). This removes any friction and allows the ulcer to heal. After 2 months when
the plaster is removed the ulcer is usually healed; if it is not, it is put back on for a
further 2 months. If the ulcer is very dirty and there is a lot of exudate, the plaster can
have a window cut in it to allow the ulcer to be cleaned regularly and to minimise the
unpleasant smell for the patient.
Removing the slough (see p. 43) and applying non-adherent dressings (see p. 46) is
the same as for venous ulcers. There is no need for elastic support. The idea is simply to
keep the ulcer clean and free of friction while it heals.
The same principles apply to the treatment of pressure sores. Pressure on bony areas
should be minimised by frequent changes of position and the use of a wool fleece or
ripple bed.
Fig. 12.39 Pressure sores on buttocks: note deep ulcer over posterior iliac crest
ULCERS / 395
SKIN NEOPLASM DERMATITIS ARTEFACTA

Basal cell carcinomas (see p. 330) are a common cause of leg Any ulcer with straight edges (linear, square or triangular), or at
ulcers in the elderly with fair skin. They are usually small, slow an unusual site is likely to be artefactual unless proven otherwise
growing and can be anywhere on the lower legs (see Fig. 12.41). (see p. 260). Treatment depends on preventing the patient
A squamous cell carcinoma (see p. 332) can arise in sun-damaged damaging the site, e.g. by covering it with a bandage or plaster
skin but also in a chronic venous ulcer or burn scar. Occasionally a cast.
tumour around the ankles can be misdiagnosed as a venous ulcer
and can be treated for a long time by compression bandaging. Any
chronic non-healing ulcer, especially one with a proliferative base
(see Fig. 12.40) should be biopsied to exclude a skin tumour. Any
red or pigmented lesion that ulcerates should be urgently biopsied
to exclude a malignant melanoma.
Fig. 12.40 A large squamous cell carcinoma that had been treated as a venous Fig. 12.41 Basal cell carcinoma on the Fig. 12.42 Dermatitis artefacta:
ulcer for over a year: note the proliferation of tissue in the centre (compare with shin: biopsy confirms diagnosis bizarre straight edges
Fig. 12.24)
396 / LOWER LEGS
PYODERMA GANGRENOSUM TREATMENT: PYODERMA GANGRENOSUM

A rapidly growing ulcer with a violaceous overhanging edge
and a yellow, honeycomb-like base should make you think of Patients with pyoderma gangrenosum should be referred urgently to a dermatologist
pyoderma gangrenosum. It is associated with ulcerative colitis, or gastroenterologist for investigation of the underlying cause. The ulcer is treated
with large doses of systemic steroids, beginning with prednisolone 60 mg daily. Once
Crohn’s disease, rheumatoid arthritis and multiple myeloma.
the ulcer is healed the dose can gradually be reduced, and eventually the patient will
In patients with ulcerative colitis, the activity of the pyoderma
be able to come off the steroids. Other immunosuppressive agents such as ciclosporin
gangrenosum reflects the activity of the bowel problem, but 3–5 mg/kg/day or azathiaprine 3 mg/kg/day can also be tried in addition to or instead of
with the other diseases the two conditions seem to behave oral steroids.
independently of each other.
Other possible treatments are a very potentUK/group 1USA topical steroid such as 0.05%
clobetasol propionate applied twice a day to the ulcer, oral clofazamine, dapsone or
minocycline. Biologics such as the anti-TNF therapies (see p. 56) can be trialled in severe
recalcitrant cases.
STEROIDS OR RADIOTHERAPY
Topical or systemic steroids used over a long period, or previous
radiotherapy, may result in thinning of dermal collagen and
ulceration after minor trauma.
Fig. 12.43 Pyoderma gangrenosum Fig. 12.44 Pyoderma gangrenosum in Fig. 12.45 (right) Ulcer on shoulder at
with violaceous overhanging edge black skin site of previous radiotherapy
ULCERS / 397
TROPICAL AND BURULI ULCERS SICKLE CELL ULCERS

The most likely cause of ulcers developing in a tropical climate is Patients with sickle cell anaemia who are homozygous for the
ecthyma, a staphylococcal infection of the epidermis and dermis sickle cell gene develop ischaemic ulcers on the legs and feet in
from an insect bite or scratch (see p. 187). childhood and early adult life. They look like venous ulcers but
are due to blockage of small arterioles in the legs and feet by the
A tropical phagedenic ulcer is a fast-growing, painful ulcer on the
sickled red blood cells. Confirm the diagnosis by haemoglobin
lower legs and feet in malnourished children from Africa, India,
electrophoresis. Keep the ulcer clean until it heals.
South East Asia, Central and South America or the Caribbean.
It can grow 5 cm or larger in 2–3 weeks and usually has a rolled
edge. It is due to fusiform bacilli and treponemes.
A Buruli ulcer begins as a firm, painless, subcutaneous nodule
that either heals spontaneously or ulcerates. Ulcers can remain
small and heal without treatment, or spread rapidly undermining
the skin over large areas, even an entire limb. It is due to
Mycobacterium ulcerans, which is found in water bugs in swamps.
The organism enters the skin through a cut or abrasion, usually
in children who play in and around swamps in tropical Africa or
Mexico. The diagnosis can be confirmed by taking a smear from
the necrotic base of the ulcer and finding acid-fast bacilli on Ziehl–
Neelsen stain.
TREATMENT: TOPICAL ULCERS
● Ecthyma: see p. 188.

● Phagedenic ulcer: clean the ulcer and give antibiotics orally for 1–2 weeks
(phenoxymethylpenicillin, erythromycin or metronidazole).
● Buruli ulcer: rifampicin at 10 mg/kg body weight by mouth daily for 8 weeks
and streptomycin at 15 mg/kg body weight by intramuscular injection daily for
8 weeks (contraindicated in pregnancy) remains the World Health Organization’s
recommended standard antibiotic treatment.
Fig. 12.46 Buruli ulcer Fig. 12.47 Sickle cell ulcer: looks like
an ordinary venous leg ulcer but the
patient is Afro-Caribbean and has no
evidence of venous disease
398 / LOWER LEGS
ATYPICAL ULCERS
Leg ulcers are most commonly due to
venous disease, arterial insufficiency or
sensory loss. If an ulcer on the leg (or
elsewhere) is not healing with recognised
treatments or does not fit any of the
common patterns or appearances, it should
be biopsied to exclude a skin tumour or
one of the rare causes illustrated on this
page.
Fig. 12.48 Leg ulcer over an arteriovenous Fig. 12.49 Very rapidly growing ulcer due to tertiary
anastomosis: warm leg with an obvious bruit – can syphilis
be congenital or follow a fracture
Fig. 12.50 (a) Non-healing ulcer on calf found to be full of calcium; (b) X-ray to Fig. 12.51 This ulcer looked as if it should have been a venous ulcer but it is
demonstrate subcutaneous calcification beneath ulcer situated on the front of the shin: biopsy revealed tuberculosis with involvement
of the tibia on X-ray (right)
PURPURIC DERMATOSES / 399
Lower legs (and trunk, arms)

Non-erythematous rash lesions PURPURIC DERMATOSES
Normal surface
Purple, orange, brown colour
Purple red; no change in colour on pressure Orange brown Dark brown
Papules ± Macules/patches Macules/patches

vesicles ±
ulcers
Rash on other parts of body as On trunk and thighs Confined to lower legs only Preceding rash
well as legs
Polymorphic Check FBC Normal Skin type III–VI

Rash ↓ platelets platelets
Short history Arms, Hands Multiple Single Preceding Venous disease Widespread
macules patch rash present macules and
patches
CUTANEOUS THROMBO- 2º PURPURA CAPILLARITIS LICHEN HAEMOSIDERIN VENOUS PIGMENTED POST-INFLAMMATORY

VASCULITIS CYTOPENIC (Old age, AUREUS PIGMENTATION ECZEMA PURPURIC HYPERPIGMENTATION
PURPURA steroids) ERUPTION
p. 401 p. 400 p. 400 p. 400 p. 400 see p. 297 see p. 384 p. 400 see p. 297
400 / LOWER LEGS
PURPURA PIGMENTED PURPURIC ERUPTION

Purpura is due to leakage of red blood cells from blood vessels This presents as rusty-brown pigmentation, starting on the feet
into the skin. When compressed with the finger, the red colour and gradually working its way up the lower leg over a period of
does not disappear as it would if the blood were still inside the months to years. If you look carefully you will see tiny purpuric
blood vessels (as in erythema, see Figs. 1.60 and 1.61, p. 14). The macules within the pigmented areas, which are the result of
extravasated blood is broken down to haemosiderin, causing the deposition of haemosiderin following the purpura. There is no
colour to change from purple to orange brown. Purpura may obvious cause for the condition and no effective treatment.
be due to a platelet disorder (thrombocytopenic) or a vascular
disorder (non-thrombocytopenic).
Thrombocytopenic purpura
If the platelet count falls below 50 000/mm3 bleeding may occur.
In the skin this is seen as tiny purpuric macules and papules
(petechiae) and larger patches (ecchymoses). There may be
bleeding elsewhere too. Thrombocytopenia may be due to
bone marrow disease (pancytopenia, leukaemia, drug-induced
marrow failure), systemic infections, splenomegaly or idiopathic
thrombocytopenic purpura.
Non-thrombocytopenic purpura
Non-thrombocytopenic purpura can be due to the following:
● leaky blood vessels (capillaritis) – uniformly small, orange-
brown macules occur anywhere on the skin; the cause is
unknown and no treatment is available; when this is localised
to a single area it is known as lichen aureus
● lack of connective tissue support for blood vessels, occurring
in old age (senile purpura) or after topical or systemic
corticosteroid therapy; bruising occurs after minor trauma;
large purpuric patches are seen, especially on the forearms and
dorsum of the hands (see Figs. 12.54 and 2.05, p. 33)
● pigmented purpuric eruption
● cutaneous vasculitis (see p. 401). Fig. 12.52 Pigmented purpuric Fig. 12.53 Close-up of pigmented
eruption purpuric eruption
PURPURIC DERMATOSES / 401
PURPURIC DRUG RASH VASCULITIS

Some drugs cause thrombocytopenia with purpura and larger Vasculitis is an inflammation of the blood vessels in the skin,
ecchymoses. All such patients should be referred urgently to usually due to deposition of immune complexes in their walls.
hospital for investigation. Drugs that can cause a fall in platelet There are several different patterns dependent on the size and site
count include: of the vessels involved:
● all cytotoxic drugs ● chlorpromazine ● capillaries in the superficial and mid dermis (leucocytoclastic
● co-trimoxazole ● furosemide vasculitis; Henoch–Schönlein purpura, see p. 402); there
● gold ● indomethacin will be a polymorphic rash with palpable purpura as well as
● rifampicin. macules, papules, vesicles and pustules (see Fig. 12.56)
● arteries at the junction of the dermis and subcutaneous
Other drugs can cause a non-thrombocytopenic purpura due to fat (cutaneous polyarteritis nodosa); there will be livedo
an underlying vasculitis. This is likely to be mainly on the lower reticularis, nodules and/or ulceration on the lower legs (see
legs. Drugs that do this include: p. 378)
● allopurinol ● barbiturates ● arteries and veins in the subcutaneous fat (nodular vasculitis;
● thiazide diuretics ● carbimazole. erythema nodosum); there will be tender red nodules or
plaques deep in the subcutaneous fat (see p. 378).
Fig. 12.54 Steroid purpura on forearm Fig. 12.55 Severe vasculitis: rash with blisters and early skin necrosis
402 / LOWER LEGS
Causes of cutaneous vasculitis: TREATMENT: HENOCH–SCHÖNLEIN PURPURA

● distant focus of infection, e.g. streptococcal infection
● collagen vascular disease (systemic lupus erythematosus, If it follows a streptococcal throat infection, treat with phenoxymethyl penicillin.
rheumatoid, systemic sclerosis) Otherwise, bed rest will stop new lesions from occurring, and most cases will get better
● plasma protein abnormality, e.g. cryoglobulinaemia spontaneously after 3–6 weeks. Use analgesics (paracetamol syrup) for the joint and
● drugs (see p. 401) abdominal pain. Renal involvement may be more serious. Proteinuria or microscopic
haematuria without impairment of renal function will normally get better spontaneously
● idiopathic (no cause found).
in less than 4 weeks. If acute nephritis or progressive renal failure occur, the patient
should be referred urgently to a renal physician.
TREATMENT: CUTANEOUS VASCULITIS
Look for an underlying cause and treat this if possible. It is worth checking the urine
for protein, blood and casts, and the blood urea and creatinine to make sure that the
kidneys are not involved. If there is renal damage, specialist help should be sought,
because treatment with systemic steroids or cyclophosphamide may be needed. If no
cause can be found the patient can be reassured that it is a self-limiting condition that
will get better after 3–6 weeks. Bed rest will stop new lesions from developing on the
skin. Treatment is symptomatic, with analgesics for pain.
HENOCH–SCHÖNLEIN PURPURA
This form of leucocytoclastic vasculitis occurs mainly in young
children and is associated with arthralgia and abdominal pain.
Leucocytoclastic is a histological term describing dead white
blood cells seen around blood vessels. The rash consists of
erythematous and purpuric macules and papules together with
vesicles and pustules. It should be thought of in any child with
purpura and a normal platelet count. It may follow a streptococcal Fig. 12.56 Henoch–Schönlein purpura: note polymorphic nature of lesions,
sore throat. macules, papules, vesicles and crusts
403
Hands and feet

Hands
Dorsum of hand and wrist
Acute erythematous rash/lesions 404
13
Chronic erythematous rash/lesions
Papules, plaques, erosions, blisters 407
Nodules 410
Macules, patches, papules, plaques see Chapter 9
Nodules 410
Palm
Acute erythematous rash/lesions 404
Chronic erythematous rash/lesions 412
Non-erythematous rash/lesions 412
Hand eczema/dermatitis 413
Feet
Dorsum of foot
Erythematous rash/lesions 419
Sole
Scaling, hyperkeratosis, maceration
Instep and weight-bearing areas 420
Toe webs (between third and fourth toes and fourth and fifth toes) 421
Vesicles, pustules, erosions 421
Ulcers see pp. 385, 386
404 / HANDS
HANDS
Hands
Dorsum and palm HANDS – ACUTE
Papule Nodule Papules Blisters/erosions Patch/plaque Weal
Bright red Tender Not tender 8–48 hours Vesicles with Grouped Ill defined Isolated Occurs after Within
after strong red margin vesicles Itchy Circular exposure to minutes of
sun exposure cold wearing latex
glove
Bleeds on Punctum in Looks like Other sites Children (also Painful ++ Multiple ‘Target’ Red/purple on Prick or RAST
trauma/ centre blister but no (face, chest, mouth and Reoccurs at blisters/ lesions rewarming test positive
spontaneously discharge arms) feet) same site? exudate
PYOGENIC BOIL ORF/MILKER’S POLYMORPHIC HAND, FOOT HERPES ACUTE ERYTHEMA CHILBLAINS CONTACT
GRANULOMA NODULE LIGHT AND MOUTH SIMPLEX ECZEMA MULTIFORME URTICARIA TO
ERUPTION DISEASE (WHITLOW) LATEX
see p. 334 see p. 177 p. 405 see p. 100 p. 405 p. 406 see p. 415 see p. 174 p. 406 p. 405
ACUTE RASH/LESIONS / 405
ORF AND MILKER’S NODULE HAND, FOOT AND MOUTH DISEASE

Orf is a pox virus infection of lambs. It causes sores around This is a mild infection due to Coxsackie A16 virus that occurs in
the mouth so that they have difficulty in suckling. It can be children, where small grey vesicles with a red halo occur on the
transmitted to those bottle-feeding affected lambs, especially if fingers and toes together with small erosions in the mouth (see
they have a cut on the finger. A red, purple, or white round nodule Fig. 6.02, p. 143). It gets better spontaneously after a few days so
develops on the finger and looks like a blister, but when pricked no treatment is necessary.
with a needle no fluid comes out. It gets better spontaneously after
3–4 weeks and the patient is then immune for the rest of his or CONTACT URTICARIA TO LATEX
her life. Natural latex is the sap from the rubber tree (Hevea brasiliensis).
Latex gloves or condoms are made from water-based natural
Milker’s nodules are another pox infection, acquired from the
rubber latex (NRL) emulsions, and these can cause type I
teats of cows or the mouths of calves. It is seen as small papules
hypersensitivity (contact urticaria, angio-oedema, asthma or
or vesicles on the fingers of those involved in milking cows or
anaphylaxis). Powdered NRL gloves cause more problems than
feeding calves. Like orf, it gets better spontaneously and confers
the non-powdered ones. Contact urticaria presents with weals
immunity for the future.
within a few minutes at the site of contact with the rubber.
Fig. 13.01 Orf on side of finger Fig. 13.02 Orf on a lamb’s mouth (courtesy of Fig. 13.03 Hand, foot and mouth disease
Coopers Animal Health)
406 / HANDS
Patients who react in this way may also get problems with eating
bananas, avocado pears, kiwifruit and/or chestnuts. NLR used
to be responsible for intra-operative anaphylactic reactions, but
widespread use of non-latex gloves has made this less likely. The
diagnosis can be confirmed by a positive prick test, or if this is
negative and the history is suggestive, by a ‘use test’ – wearing a
finger from a NLR glove on wet skin for 15 minutes. Dry rubber
latex (in household rubber gloves, elasticated bandages, balloons,
shoes, car tyres, and so forth) cause a type IV hypersensitivity
reaction, i.e. allergic contact dermatitis, from chemicals used to
cure the latex. This must not be confused with true latex allergy,
which is an immediate hypersensitivity reaction.
TREATMENT: CONTACT URTICARIA TO LATEX
Avoid direct contact with NRL gloves and condoms. Use non-latex gloves instead of Fig. 13.04 Herpetic whitlow on finger
latex gloves and use condoms made of polyurethane. It is essential to warn surgeons of
the possibility of latex sensitivity before surgery is undertaken.
HERPETIC WHITLOW
Pain, swelling and vesicles on the fingers are usually due to a
herpes simplex infection, which may be the result of inoculation
of virus in medical or dental personnel (type 1) or from genital
contact (type 2). It may be confused with a fixed drug reaction if
recurrent (see p. 181).
CHILBLAINS
Tender mauve papules or nodules occurring on the hands or feet
from the cold, which become painful on rewarming (see p. 161).
Fig. 13.05 Chilblains on the toes

Dorsum hands and wrist

Chronic erythematous rash/lesions DORSUM HANDS – CHRONIC RASH/LESIONS
Papules, plaques, erosions and blisters
Blisters and/ Well-defined plaques Poorly defined papules/plaques
or erosions
Isolated Crust or exudate on surface Scaly surface Normal surface Finger webs not involved Finger webs involved
lesions
Only Other sites Lichenified Silvery Slight scale Annular Linear Rough on Scaly patches S-shaped White
dorsum of involved surface scales lesion erythema palpation burrows erosions
hands
Check Itchy +++ Psoriasis Active edge Papules in Proximal Elderly Contact with Rash on Sore
urine for elsewhere Mycology ring muscle Chronic sun irritants, soap trunk and Mycology
porphyrins +ve weakness exposure Previous genitals +ve
eczema
PORPHYRIA DISCOID LICHENIFIED PSORIASIS TINEA GRANULOMA DERMATO- SOLAR ECZEMA/ SCABIES CANDIDA
CUTANEA ECZEMA ECZEMA MANUUM ANNULARE MYOSITIS KERATOSIS DERMATITIS
TARDA
p. 408 see p. 243 p. 417 see p. 424 p. 408 p. 409 see p. 132 see p. 326 p. 413 see p. 248 p. 409
408 / Hands
Porphyria cutanea tarda

This is an acquired porphyria and the one most likely to be seen in
clinical practice. It is due to reduced levels of uroporphyrinogen
decarboxylase in the liver resulting in increased levels of
uroporphyrins in the urine and plasma. It is caused by excessive
alcohol intake (2% of alcoholics develop porphyria cutanea
tarda), hepatitis C, subclinical haemochromatosis or the use
of oestrogens or hormone replacement therapy. The patient is
usually a middle-aged or elderly male (less common in females),
who presents with blisters, scars and milia on sun-exposed skin
– dorsum of hands and forearms, face and bald scalp. There may
also be hypertrichosis on the face. The patient rarely associates
the development of skin lesions with sunlight. The diagnosis is
made by finding increased porphyrins in the urine. The urine
can be screened using a Wood’s (ultraviolet) lamp when a coral-
pink fluorescence is seen. Acidifying the urine or adding talc to
it makes the fluorescence more obvious. Detailed analysis of the
various porphyins by a specialist laboratory will confirm the type
of porphyria. Check also the liver enzymes, hepatitis C antibodies,
serum ferritin and look for the haemochromatosis gene mutation.
Fig. 13.06 Porphyria cutanea tarda: blisters and erosions on dorsum of hand
Treatment: porphyria cutanea tarda
Stop alcohol or the contraceptive pill (the most likely causes). If symptoms do not Tinea manuum
improve, remove 500 mL blood fortnightly until the serum ferritin is back to normal or Ringworm infection should be considered in any red, scaly rash
symptoms abate, usually after 2–3 months. The patient should avoid sun exposure (even affecting only one hand. This can be confirmed or excluded
through window glass – porphyrins absorb long-wave ultraviolet [UVA] radiation), wear
by mycology (see p. 20). The source of the infection is often the
a long-sleeved shirt, hat and opaque sunscreen. Oral chloroquine 200 mg twice a week
patient’s own toe webs or nails, so look at the feet as well. Three
improves the skin fragility within 6 months by complexing the porphyrins and promoting
excretion.
patterns of infection can occur:
1. an annular plaque on the dorsum of the hand (see Fig. 13.07)
2. fine scaling picking out the creases on one palm only (see
Fig. 13.49)
3. scaling or vesicles on one hand only.
Fig. 13.07 Tinea manuum Fig. 13.08 Granuloma annulare Fig. 13.09 Knuckle pads Fig. 13.10 Candida infection of finger
webs
CANDIDA INFECTION OF FINGER WEB GRANULOMA ANNULARE

Infection with Candida albicans occurs in the finger webs as well Small, skin-coloured or mauvish-pink papules form rings on the
as the toe webs, especially if the hands are always in water. The dorsum of the fingers, hand or foot. It is usually asymptomatic,
finger webs become macerated and are usually white in colour. although it can be tender if knocked. It is distinguished from
ringworm by not being scaly (see also p. 210).
TREATMENT: CANDIDA
KNUCKLE PADS
Dry the hands thoroughly after washing, especially in the finger webs. Apply a topical These are thickened plaques that occur over the interphalangeal
antifungal such as nystatin ointment or an imidazole cream or 0.5% gentian violet paint joints in young adults for no apparent reason. There is no
twice daily until it is better.
treatment.
410 / HANDS
Dorsum of wrist, hand, fingers or dermatomyositis. The diagnosis can be

1. Chronic erythematous DORSUM HAND – NODULES confirmed by X-ray. Gout results in tophi
2. Non-erythematous (deposits of uric acid crystals, associated
(Acute erythematous, see p. 404) with joint deformity. A ganglion is a
synovial cyst associated with the wrist
Erythematous Non-erythematous
joint (see Fig. 13.14).
Myxoid cysts (see p. 448) are seen
on the dorsum of the fingers, as soft
Ulcerated/hyperkeratotic Smooth surface Warty surface cystic papules due to herniation of the
interphalangeal joint capsule.
FISH TANK GRANULOMA

Tropical fish infected with Mycobacterium
Elderly Contact with ↑ Uric X-ray shows Over Over wrist Usually child marinum die. In removing the dead fish
Sun exposure tropical fish Acid calcium interphalangeal joint
joints the owner can scrape the back of his or
her hand on the gravel at the bottom
of the tank and so implant the atypical
Biopsy Biopsy = Thickened skin Attached
mycobacterium into the skin. Pink/purple
granuloma to tendon nodules occur at the site of implantation.
Occasionally the lesions may ulcerate.
Similar lesions can occur proximally up the
arm due to spread along the lymphatics
SQUAMOUS FISH TANK GOUTY CUTANEOUS KNUCKLE PADS GANGLION VIRAL WART (see Fig. 13.11b).
CELL GRANULOMA TOPHI CALCINOSIS
CARCINOMA TREATMENT: FISH TANK GRANULOMA
Treatment is with co-trimoxazole 960 mg bid, or

minocycline 100 mg bid until the skin heals (usually
see p. 322 p. 410 p. 410 p. 410 p. 409 p. 410 see p. 318
6–12 weeks). Advise the patient to wear rubber gloves
when removing dead fish in the future.
NODULES ON DORSUM OF HAND
White, hard papules or nodules containing calcium (cutaneous calcinosis, p. 276 and
Fig. 13.13) can occur on the fingers or dorsum of the hand in patients with scleroderma
a b
Fig. 13.11 Fish tank granuloma: (a) on dorsum of hand and wrist; (b) lesions spreading up arm proximally (sporotrichoid spread)
Fig. 13.12 Gouty tophi over interphalangeal joints Fig. 13.13 Cutaneous calcinosis Fig. 13.14 Ganglion
412 / HANDS
Palms
1. Chronic erythematous rash/multiple lesions (for single/few lesions, see Chapter 8, p. 195) PALMS
2. Non-erythematous rash with scaling, peeling or increased skin markings
3. Sweating, see p. 59
1. Erythematous 2. Non-erythematous
Pustules present Scaling, hyperkeratosis Vesicles present Increased scaling Thick keratin Increased skin
markings
Pustules Yellow Lesion well Rash poorly Single vesicles Multiple In skin Peeling Onset in Generalised dry
different pustules defined defined coalescing creases, fingertips childhood skin
colours Unilateral and palms
On scaly red Previous Red scaly Look for burrows Soles/ Soles also Elbow/knee
plaque eczema plaque toe webs/ affected flexures spared
toenails also
involved
Present Absent Mycology Family history Family history

+ve
PALMAR INFECTED PSORIASIS SCABIES DERMATITIS ECZEMA TINEA KERATOLYSIS KERATODERMA ICHTHYOSIS
PUSTULAR ECZEMA (Exogenous: (Atopic/ MANUUM EXFOLIATIVA VULGARIS
PSORIASIS irritant, endogenous) (Palmar
allergic) peeling)
see p. 424 p. 417 see p. 424 see p. 248 p. 413 p. 413 see p. 408 p. 413 see p. 429 see p. 323
HAND ECZEMA/DERMATITIS / 413
KERATOLYSIS EXFOLIATIVA (PALMAR HAND ECZEMA/DERMATITIS

PEELING) Types of hand eczema/dermatitis
Peeling of the palms and fingers is
common, often occurring about once a Exogeneous = DERMATITIS Endogenous = ECZEMA
(external cause) (constitutional cause)
month. It is usually asymptomatic but
there may be increased sensitivity to touch.
The cause is not known and there is no
specific treatment. History of occupational No obvious precipitating factors
exposure to chemicals
Finger webs Poorly defined red, scaly Well-defined plaques Multiple

involved plaques coalescing
blisters
Patch test Previous history of flexural or Lichenified Exudate, Palms and/or

childhood eczema Itch ++ erosions, soles
crusting
-ve +ve No Yes
IRRITANT ALLERGIC ENDOGENOUS ATOPIC LICHEN DISCOID POMPHOLYX

CONTACT CONTACT ECZEMA ECZEMA SIMPLEX ECZEMA (Dyshidrotic
DERMATITIS DERMATITIS eczema)
p. 414 p. 415 p. 417 see p. 236 see p. 219 see p. 243 p. 417
In practice the cause of the eczema is often multifactorial, with external factors precipitating eczema in a
constitutionally predisposed individual.
Fig. 13.15 Keratolysis exfoliativa
414 / HANDS
DERMATITIS = EXOGENEOUS ECZEMA In women, detergents are the main culprit. The rash begins under
1. Irritant contact dermatitis a ring or in the finger webs, where the alkaline detergent particles
Irritant contact dermatitis is due to weak acids or alkalis (e.g. in get trapped. A lot of young mothers will get eczema on their
detergents, shampoos, cleaning materials, cutting oils, cement hands when their children are small. Hairdressers commonly
dust) coming into contact with the skin. It occurs in everyone develop this kind of eczema when they first begin work because
who has enough contact with these. It is the commonest type of of the frequent shampooing. Cooks and nurses are also at risk
hand eczema. Poorly defined pink scaly patches or plaques with a because of repeated hand washing.
dry, chapped surface occur at the site of contact with the irritant. In men this kind of eczema is mainly on the dorsum of the hands
Usually there are no vesicles or crusts. from contact with cement dust or soluble oils used for cooling the
moving parts of machinery in the engineering industries.
Fig. 13.16 Irritant contact dermatitis Fig. 13.17 Irritant dermatitis on Fig. 13.18 Irritant contact dermatitis Fig. 13.19 Irritant contact dermatitis
from paint stripper dorsum of hand: dry, chapped surface under a ring in finger webs
2. Allergic contact dermatitis ● centre of palm and flexor aspects of fingers – from rubber,
Allergic contact dermatitis is a type IV allergic reaction and affects nickel or plastic handle grips
only a very small proportion of the population. The rash occurs at ● whole hand (palm, dorsum and wrist) – from rubber gloves
the site of contact with the allergen, but on the hands it is difficult ● in lines on flexor aspect of wrist or dorsum of hand and
to predict the cause from the site involved because the hands come forearm – from the leaves of the plants (see p. 182)
into contact with so many things during the day. ● flexor aspect of the wrist from nickel in watch buckle or PTBP
formaldehyde resin in the watch strap.
Nevertheless there are several well-recognised patterns:
● fingertips – from formalin in laboratory workers and
It is probably wise to patch test (see p. 21) anyone with hand
secretaries (from formaldehyde resins in cardboard folders), eczema who does not get better quickly with topical steroids.
local anaesthetics in dentists, garlic and onion in cooks, tulip
bulbs and less commonly Balsam of Peru in orange peel
Fig. 13.20 Allergic contact dermatitis Fig. 13.21 Allergic contact dermatitis Fig. 13.22 Allergic contact dermatitis Fig. 13.23 Allergic contact dermatitis
on fingertips from garlic (usually on from PTBP formaldehyde resin in the from rubber gloves, extending onto on palm from the nickel in coins
the non-dominant hand) watch strap the wrist
416 / HANDS
Allergic contact eczema may develop explosively with vesicles,

exudate and crusting. If it develops more slowly, then the rash is a
poorly defined red, scaly rash just like eczema elsewhere.
Occupational dermatitis has medico-legal implications. The
assessment of each patient depends on whether the patient could
have reasonably expected to have developed eczema if he or she
had not been engaged in that particular job or occupation.
Patients with atopic eczema in childhood should be discouraged
from going into hairdressing or jobs that involve contact with
cutting oils or cleansing agents.
Fig. 13.25 Pompholyx on fingertip Fig. 13.26 Pompholyx: tiny erosions

on fingertips where the vesicles have
broken
Fig. 13.24 Allergic contact dermatitis from nickel in scissors in a hairdresser Fig. 13.27 Pompholyx: intact vesicles under the thick stratum corneum of the
palm
POMPHOLYX ECZEMA
Acute eczema resulting in blistering on the palms and soles is termed pompholyx (or
dyshidrotic eczemaUSA). Because of the thickened stratum corneum, the epidermal blisters
persist and appear as tiny grey-white ‘grains’ within the skin. Eventually they burst and
erosions occur. Sometimes pompholyx can occur as an isolated episode that then resolves
spontaneously.
Fig. 13.29 Endogenous eczema on dorsum of hand:

note lichenification and excoriations
Fig. 13.28 Histology of pompholyx:

epidermal blister underneath the thick
stratum corneum
ENDOGENOUS ECZEMA
Endogenous eczema can occur on both the palm and dorsum of the hand. You should
think of this diagnosis if the patient has symmetrical eczema, particularly if there is a
past history of atopic eczema in childhood. The eczema is itchy and continual scratching
and rubbing will lead to lichenification. If it becomes secondarily infected with bacteria
(Staphylococcus aureus), pustules may occur. On the palms this differs from pustular Fig. 13.30 Infected eczema on palm
psoriasis because all the pustules are the same colour (yellow). Some hand eczema
becomes hyperkeratotic, resulting in fissures over the finger joints, along the skin creases
and over fingertips. These are painful and can be very disabling.
418 / FEET
● Chronic eczema. The patient will require a potentUK/group 2–3USA topical steroid
ointment or cream applied once or twice a day. It will often be a question of trial and
error to find the one that will suit this particular patient best. If the skin is very dry
or there are a lot of fissures, start with an ointment. If it is not too scaly the patient
may prefer to use a cream. If the eczema is on the hands, prevent further damage
by wearing cotton gloves for doing housework and rubber gloves or cotton-lined
PVC gloves for all wet work. Manual labourers also will need to protect their hands
from irritants as much as possible by wearing surgical latex gloves, which should be
provided at work. Often wearing gloves is not practicable, and it may be necessary
to have time off work if the eczema will not settle down. In many cases, once the
dermatitis is established, it will not resolve without a change in occupation (e.g.
trainee hairdressers, machine workers, chefs and nurses may have to change jobs). If
the eczema is on the feet, white cotton socks and leather shoes are likely to be more
Fig. 13.31 Fissures on fingers that can be treated with Haelan tape
comfortable than man-made fibres, unless of course the eczema is an allergic contact
eczema due to chromate in leather.
TREATMENT: HAND AND FOOT ECZEMA ● Hyperkeratotic eczema. Both the eczema and the hyperkeratosis need treating. The
thickened keratin will prevent applied topical steroids getting through the skin, and
With eczema on the hands it is always worth doing patch tests, because the hands any fissures will be painful when the hyperkeratosis cracks. The hyperkeratosis can
touch a lot of things during the course of a day. If the cause can be found and contact be reduced by 2-5% salicylic acid ointment, either applied alone or mixed with a
with it stopped, the eczema may be cured. Otherwise, the patient will be condemned to topical steroid, e.g. Diprosalic ointment. If the salicylic acid is used alone, it can be
using ointments or creams indefinitely. applied either in the morning or at night, and a topical steroid ointment used alone
● Acute weeping eczema. Initially rest will be required to get the eczema better. the other time. One of the potentUK/group 2–3USA steroid ointments will be required.
For the hands stop washing up, cleaning, shampooing, and so forth. Resting the Haelan tape may also be useful for hyperkeratotic or fissured eczema on the fingers
feet in practice means bed rest. Dry up the exudate by soaking the hands/feet for and feet. Patients like it because it is not messy. A strip of tape is applied to the area
10 minutes twice a day in an astringent such as 1:10 000 potassium permanganate and left on for 12 hours at a time. This usually results in the cracks healing. Applying
solutionUK or aluminium acetate (Burow’s solutionUSA), see p. 30. After drying the superglue (bought from a hardware store) to the cracks is another good way of
skin apply a moderateUK/group 4–5USA topical steroid ointment that does not contain healing the fissures and reducing pain. Once the fissure has healed, the superglue
lanolin. Always use an ointment rather than a cream until the cause of the eczema will fall out.
is sorted out. Once the eczema is better, try to find the cause by patch testing (see
p. 21). FAILURE OF TOPICAL TREATMENT
● Pompholyx eczema. A potentUK/group 2–3USA topical steroid ointment will be needed Severe disabling hand or foot eczema may require treatment with systemic
to penetrate the thick stratum corneum, which should be applied twice a day. immunosuppressive agents such as azathioprine (see p. 54) or ciclosporin (see
When the vesicles break, potassium permanganate soaks may be needed to dry any p. 53). Alitretinoin 30 mg daily (see p. 50) given for a 2-month trial may be useful in
exudate. hyperkeratotic eczema.
ERYTHEMATOUS LESIONS / 419
FEET
Dorsum of the foot
Erythematous rash/lesions DORSUM OF FOOT
Well-defined patches/plaques Poorly defined papules/plaques Serpiginous linear
lesions
Single/few circumscribed plaques Dorsum involved with defined border Widespread Lesion moves
proximally diffuse around over a few
involvement days
Normal surface Crust/exudate Profuse silver Adjacent to 1st Adjacent to 4th Involved up to Symmetrical Asymmetrical
scale and 2nd toes and 5th toes level of shoe Dorsum or sole
Circular shape Itchy ++ Symmetrical Lichenified Asymmetrical Patch test Recent travel to
Children Mycology tropical beach
-ve +ve +ve -ve
GRANULOMA DISCOID PSORIASIS ATOPIC TINEA ALLERGIC ENDOGENOUS LARVA

ANNULARE ECZEMA ECZEMA PEDIS CONTACT ECZEMA MIGRANS
DERMATITIS
see p. 210 see p. 243 p. 424 p. 422 p. 426 p. 422 p. 422 p. 428
420 / FEET
Soles: instep and weight-bearing area

Scaling, hyperkeratosis, maceration SOLES: SCALING, MACERATION
Forefoot, Instep Weight-bearing part of sole ± side of heel
under toes
Glazed White scaling Coarse scaling Hyperkeratosis Maceration

surface + only in skin
fissures creases
Widespread Localised
Children Toenails/ Poorly Well defined No family Family history Pare down with scalpel Holes in the
Age <14 toe webs defined history From childhood keratin
involved Adult
Mycology Patch test Psoriasis elsewhere Palms also ∇-shaped Pinpoint Hole/ulcer Associated
affected keratin over bleeding exposed hyperhidrosis
pressure point Painless
+ve +ve -ve No Yes
JUVENILE TINEA CONTACT ENDOGENOUS PSORIASIS PALMOPLANTAR CORN PLANTAR NEUROPATHIC PITTED
PLANTAR PEDIS ALLERGIC ECZEMA KERATODERMA WART ULCER KERATOLYSIS
DERMATOSIS DERMATITIS
p. 428 p. 426 p. 423 p. 423 p. 424 p. 429 p. 431 p. 432 see p. 393 p. 430
Soles Soles
Vesicles, pustules, erosions SOLES: VESICLES, BLACK between 3rd/4th or 4th/5th toes
(for ulcers see pp. 385-6) EROSIONS, PUSTULES LESION Plaques, nodules
Surface normal, exudate, crust Scaling, hyperkeratosis
Blisters/erosions Pustules Black macule or Peeling/fissures/maceration
patch
(see also p. 310)
Unilateral Bilateral
Wood’s light (see p. 18)
Large isolated Multiple Localised to All same Different Oval black
coalescing instep colour colours dots in surface
Occurs after Bilateral Unilateral Swab On Pare down Painful Itchy No Pink
minimal trauma S. aureus++ erythematous surface fluorescence fluorescence
background
Appears Small Grouped Black colour in

childhood coalescing vesicles keratin
vesicles Mycology
Circular Mycology Mycology Gram +ve
firm area +ve, only spores and diphtheroids
-ve +ve in 4th+5th hyphae hyphae
toe cleft
EPIDERMOLYSIS ECZEMA/ TINEA INFECTED PLANTAR BLACK HEEL/ SOFT TINEA CANDIDA ERYTHRASMA
BULLOSA POMPHOLYX PEDIS ECZEMA PUSTULAR HAEMATOMA CORN PEDIS
SIMPLEX PSORIASIS
p. 429 p. 423 p. 426 p. 423 p. 424 p. 430 p. 431 p. 426 see p. 343 see p. 348
422 / FEET
ECZEMA ON THE FOOT ● Allergic contact dermatitis: a rash up to the level of the shoe
A symmetrical, red scaly rash on the foot in which vesicles have and sparing the toe webs is usually due to an allergic contact
been present at some stage is likely to be eczema (for treatment, see dermatitis to chrome in the leather of the shoe uppers, or azo
p. 418). dyes in nylon socks/stockings. A rash at the site of contact with
flip-flops is due to mercaptobenzothiazole, a rubber additive.
Dorsum of the foot ● Endogenous eczema: symmetrical eczema on the dorsum of
Eczema here can be due to the following. the foot can be due to endogenous eczema. Patch testing is
● Atopic eczema: eczema affecting the dorsum of the big toe in negative.
a child aged 7–10 years is one of the patterns of atopic eczema. ● Discoid eczema presents as a well-defined, round or oval,
Note tinea pedis affects the fourth and fifth toes, not the red scaly plaque with obvious vesiculation and crusting (see
big toe. p. 243).
Fig. 13.32 Atopic eczema on Fig. 13.33 Allergic contact dermatitis from Fig. 13.34 Allergic contact dermatitis Fig. 13.35 Endogenous foot eczema;
the dorsum of the foot in a shoe uppers, note the cut-off at the level of to the rubber in flip-flops symmetrical distribution
child the shoe
Sole of the foot of keratin on the soles, rashes are much more difficult to
Hyperkeratosis occurs when eczema affects the weight-bearing distinguish from one another at this site. Eczema tends to have
areas of the soles. Painful fissures occur if the thickened keratin a less well-defined border. There may be evidence of eczema
splits. The causes of eczema on the soles are as follows. or psoriasis elsewhere. Often both hands and feet are involved,
● Allergic contact dermatitis: symmetrical eczema on the which suggests an endogenous cause.
weight-bearing area of the soles is due to an allergic contact ● Pompholyx (dyshidrotic eczema): vesicles often remain
dermatitis until proven otherwise. It is usually due to rubber in intact for days or weeks on the soles and look like tapioca.
the soles of shoes, PTBP formaldehyde resin (the glue used to When they are present alone with no redness or scaling it is
stick layers of leather together) or the azo dyes in nylon socks/ called pompholyx (see hands, p. 417). This is usually due to
stockings. The diagnosis can be confirmed by patch testing. endogenous or atopic eczema but can occur as a reaction to
● Endogenous eczema: an identical rash can occur in tinea between the toes (‘id’ reaction). Unilateral vesicles on one
endogenous eczema or psoriasis. Because of the thick layer instep are usually due to tinea (see p. 426).
Fig. 13.36 Allergic contact dermatitis Fig. 13.37 Allergic contact dermatitis Fig. 13.38 Hyperkeratotic foot Fig. 13.39 Pompholyx; vesicles on
due to PTBP resin to shoe rubber sparing the insteps eczema with deep fissures the sole
424 / FEET
PSORIASIS OF HANDS AND FEET you a clue to the diagnosis, although the scale. There may or may not be a
Psoriasis of the hands and feet can be of the plaques are often well defined. background erythema and scaling. It
four different patterns. Usually there is more typical psoriasis differs from eczema or tinea that has
1. Plaque psoriasis: there are well- elsewhere. become secondarily infected, because in
defined, bright-red scaly plaques 3. Pustular psoriasis, where there are these conditions the pustules will all be
with silver scaling just like psoriasis pustules of different colours. Individual the same colour (yellow).
elsewhere (see p. 225). pustules dry out as they pass through 4. Rupioid psoriasis affects the ends of
2. Hyperkeratosis of the central palm the keratin layer, changing in colour the fingers and toes. There are bright-
or weight-bearing area of the sole (see from white to yellow to orange brown red, thickened scaly plaques with
Fig. 13.45). There is no redness to give to dark brown before peeling off in involvement of the nails as well.
Fig. 13.40 Psoriasis on dorsum of Fig. 13.41 Psoriasis affecting the Fig. 13.42 Pustular psoriasis on the Fig. 13.43 Rupioid psoriasis affecting
hand central palm: note well-defined border instep: pustules of different colours ends of fingers and nails
TREATMENT: PSORIASIS OF HANDS AND FEET
● Ordinary plaque psoriasis on the palms and soles: the treatment of this is the same
as treatment of plaque psoriasis anywhere else (see p. 226).
● Thick hyperkeratotic psoriasis: treatment is the same as for hyperkeratotic eczema
(see p. 418). Use the keratolytic agent (see p. 36) at night, if necessary under
occlusion, and white soft paraffin/petrolatum in the daytime. Once the thick keratin
has been removed, use a specific psoriatic agent during the day. You can try coal
tar and salicylic acid ointment but the tar will make a mess so may not be tolerated.
Alternatively, try a vitamin D3 analogue ointment, a potentUK/group 2–3USA topical
steroid ointment or a combination of both (Dovobet).
● Pustular psoriasis of the palms and soles is a very difficult condition to help. A
potentUK/group 2–3USA topical steroid ointment or cream applied twice a day may
provide relief. If it does not, then referral to a dermatologist may help.
FAILURE OF TOPICAL TREATMENT FOR HAND AND FOOT PSORIASIS Fig. 13.44 Psoriasis involving the side of the foot and the sole
Sometimes no topical agents will help patients with hand or foot psoriasis, in
which case either patients have to learn to live with it or you will need to refer to a
dermatologist for a systemic treatment.
● Acitretin (see p. 49).
● PUVA. There are special hand and foot machines for PUVA, with small banks of light
tubes (emitting UVA) about the size of an X-ray viewing box. The patient takes the
8-methoxypsoralen as he or she would for ordinary PUVA treatment and 2 hours later
puts the hands or feet on the box emitting the UVA. He will still need to protect both
his eyes and his skin in the same way as if he had been irradiated all over, because
of the circulating psoralens. For details about the precautions to be taken with PUVA
and the side effects see pp. 61–3.
● Topical PUVA is an alternative: the hands and/or feet are soaked in a 1% solution of
5-methoxypsoralen for 15 minutes, patted dry and then irradiated with UVA using a
hand and foot machine.
● One of the cytotoxic drugs: methotrexate, ciclosporin, azathioprine or
hydroxycarbamide. Obviously the disease will need to be seriously interfering with the
patient’s life to consider using drugs like these. For how to use them, see pp. 52–5.
Fig. 13.45 Hyperkeratotic psoriasis
on soles: note sparing of insteps
426 / FEET
TINEA PEDIS 4. White scaling on the soles: this may be unilateral or bilateral,
There are five different patterns of tinea on the feet. and is often associated with discolouration and thickening of
1. Scaling or maceration between the toes, usually between the the toenails; it is due to one particular fungus, Trichophyton
fourth and fifth toes. Here the web spaces are narrow and the rubrum. It may be found by chance when examining a patient’s
humidity high. It begins on one foot only and results in itching. feet, or the patient may complain of burning or itching of the
With time it may spread medially but never as far as the space soles. Rarely a similar pattern can be found on the palm, in
between the first and second toes. Later it may spread to the which case it is usually on one side only.
other foot and/or the toenails. 5. Vesicles on the instep: unilateral vesicles are due to tinea until
2. Typical plaques of tinea on the dorsum of one foot with a proven otherwise. Sometimes they may be present on both feet,
raised scaly edge (see, for example, Fig. 13.07, on the hand). It but usually there will be more on one foot than the other. The
usually starts laterally near to the fourth and fifth toe cleft. fungus is in the roof of the blisters. To confirm the diagnosis,
3. Scaling on the sides of the foot in the shape of a ‘moccasin’ cut off the roof of the blister with a pair of fine scissors and
shoe. examine under the microscope for fungal hyphae (see p. 337) or
send the blister roof for mycology culture (see p. 20).
Fig. 13.46 Tinea pedis: maceration of cleft between fourth and fifth toes – the Fig. 13.47 Tinea pedis: ‘moccasin’ pattern on side of foot
same pattern may also be due to candida or erythrasma
TREATMENT: TINEA PEDIS CANDIDA AND ERYTHRASMA

Symmetrical maceration or scaling between the lateral toe webs
For tinea between the toes or for blisters on the instep, use an imidazole cream twice may be due to candida or erythrasma and not a dermatophyte
a day for 2 weeks, or 1% terbinafine cream daily for 7–10 days. fungus. Erythrasma will fluoresce bright pink under a Wood’s
For the white scaling on the soles due to T. rubrum, terbinafine 250 mg orally once a
(ultraviolet) light (see p. 348). If there is no fluorescence, then take
day for 2 weeks should clear it up. Often the nails will be involved and these should be
scrapings to examine under the microscope (see Fig. 10.15, p. 342)
treated by continuing with terbinafine for a further 3 months (see p. 443).
and for culture, which will distinguish tinea from candida. (For
treatment of candida, see p. 343; for treatment of erythrasma, see
p. 348.)
Fig. 13.48 Tinea pedis: unilateral vesicles on the Fig. 13.49 Tinea pedis: white scaling of the skin Fig. 13.50 Tinea incognito: tinea treated with
instep creases due to Trichophyton rubrum topical steroids causing a symmetrical red rash
428 / FEET
LARVA MIGRANS JUVENILE PLANTAR DERMATOSIS

The larva of the dog hookworm (Ancylostoma This condition occurs only in children, usually between the ages of 7 and
braziliense) burrows into the skin and migrates under 14. The plantar surface of the forefoot is bright red and shiny, and children
the skin producing a serpiginous track. Sometimes complain of itching or painful fissures. It is thought to be due to modern
blistering can occur within the track. The patient footwear – nylon socks and synthetic soles, which do not allow sweat to
notices itching and can see the track extend over a escape through the shoe. It gets better spontaneously after puberty.
period of a few days. It is acquired by walking or
sitting on a tropical beach where dogs have been TREATMENT: JUVENILE PLANTAR DERMATOSIS
defecating (Africa or West Indies, usually). The tracks
can be found on the feet, buttocks, back of legs or back. Nylon socks and trainers should be discouraged, and cotton socks and leather shoes worn if possible.
Charcoal or cork insoles inside the shoes will also help the sweat to evaporate. Medical treatment on the
TREATMENT: LARVA MIGRANS whole is unsatisfactory. Topical steroids are not usually of any help. Try one of the following:
● white soft paraffin applied two or three times a day; alternatively, use one of the less greasy
Oral albendazole 400 mg daily for 4 days or a single dose of ivermectin moisturisers (see p. 26)
● a mild keratolytic agent, e.g. 10% urea cream (Calmurid) or 2% salicylic acid ointment applied twice
200 μg/kg body weight will cure it.
a day.
Fig. 13.51 Larva migrans Fig. 13.52 Juvenile plantar dermatosis

EPIDERMOLYSIS BULLOSA SIMPLEX TREATMENT: EPIDERMOLYSIS BULLOSA SIMPLEX

Epidermolysis bullosa (EB) is a group of inherited conditions
where blisters occur in response to trauma. There are three main Apply a moisturiser such as aqueous cream to the feet twice a day to keep the skin
types, depending on where the site of the split is in the skin. soft. Gradually wear in new shoes and avoid excessive walking. Cotton socks are more
comfortable than nylon ones. Most patients can lead a normal life.
EB simplex is the mildest form, and blisters appear on the feet
spontaneously or after minimal trauma, e.g. on wearing a new
pair of shoes or joining the Army and having to march. Junctional
PALMOPLANTAR KERATODERMA
EB is usually lethal in the first 2 years of life. Dystrophic EB (see
This is a genetically determined condition inherited as an
p. 259) results in recurrent blisters and erosions throughout life.
autosomal dominant trait. Thickening of the keratin on the palms
and soles is present from birth or early infancy. There are many
variants of this condition, some with striate or punctate patterns.
Fig. 13.53 Epidermolysis bullosa Fig. 13.54 Dystrophic epidermolysis Fig. 13.55 Striate keratoderma Fig. 13.56 Plantar keratoderma
simplex: blisters on the soles bullosa with loss of toenails and
webbing of toes
430 / FEET
TREATMENT: PALMOPLANTAR KERATODERMA TREATMENT: PITTED KERATOLYSIS
Salicylic acid ointment (5%–20%) applied at night may keep the hyperkeratosis down. Treating the sweaty feet works better than specifically removing the causative organism
Regular chiropody will almost certainly be needed. If it is very severe it may be necessary (see p. 59). Alternatively, apply 3% fusidic acid cream or clindamycin lotion (Dalacin T)
to use acitretin by mouth. This is only available in hospitals. The dosage is the same as in twice a day.
psoriasis (see p. 49).
BLACK HEEL/HAEMATOMA
PITTED KERATOLYSIS It is quite common for bleeding to occur into the skin on the back
Pitted keratolysis is a condition that only occurs in patients with of the heel or the sole in teenagers and young adults engaged
sweaty feet. A corynebacterium eats into the keratin on the sole, in sporting activities. It is due to rubbing from shoes or direct
which becomes covered with shallow pits. trauma. A painless dark-red or black patch is seen over the
heel. The sudden appearance may alarm the patient and make
the patient think that he or she has a malignant melanoma.
When pared down, dried blood is seen within the keratin layer.
Reassurance is all that is needed.
Fig. 13.57 Pitted keratolysis on Fig. 13.58 Pitted keratolysis on heel Fig. 13.59 Black heel due to bleeding into the keratin layer (inset shows
forefoot close-up) (compare with Fig. 13.60)
HYPERKERATOTIC LESIONS / 431
Fig. 13.60 Acral lentiginous melanoma on sole of foot: note pigment at edge Fig. 13.61 Soft corn: maceration on medial aspect of fifth toe
and ulceration
CORN
A corn is a localised ∇-shaped area of hyperkeratosis over a
pressure point on the foot. When pared down with a scalpel, no
bleeding points are seen (see Fig. 13.66b and c, p. 433).
SOFT CORN
Scaling between the fourth and fifth toes on one foot may be due
to a soft corn (see Fig. 13.61). If you remove the surface keratin
with a scalpel you will quickly come to firmer keratin underneath,
just like a corn elsewhere. Soft corns are due to wearing shoes that
are too tight around the toes. The problem can be explained very
simply to the patient by making him or her stand on a piece of
paper on the floor in bare feet. Draw around the affected foot with
a pencil and then put the patient’s shoe on the drawing. It will
be immediately obvious that the shoe is too tight for the foot (see
Fig. 13.62). Fig. 13.62 Compare the size of foot and shoe into which it must fit!
432 / FEET
TREATMENT: CORN the wart thrombose – this

causes the wart to go black
If a bony exostosis is present or there is an obvious anatomical abnormality of the foot, and within a few days drop
the help of an orthopaedic surgeon may be needed. off.
The patient should wear shoes that fit properly. 2. Children with verrucae
are not allowed to swim.
The area of hyperkeratosis can be pared down regularly with a scalpel by the patient
This may be overcome
or a podiatrist and the central core of keratin removed. Alternatively, 5%–10% salicylic
acid ointment can be applied every night to soften the keratin and make it easier to
by wearing a sock on the
remove. Salicylic acid plasters left on for a week at a time will do the same thing. affected foot to prevent
Wearing a corn pad or circle of orthopaedic felt around the corn will take the pressure spread of virus from one
off it and make walking more comfortable. Alternatively, a proper orthotic appliance can person to another.
be made to fit into the shoe.
For soft corns, keep the affected toes apart with a piece of foam or a silicone wedge to
reduce the sideways pressure. It is most important that the patient wears shoes that are
not too small around the toes. Fig. 13.63 Multiple plantar warts
PLANTAR WART (VERRUCA)

Verruca is the proper name for a wart. In common usage, warts
on the hands are called warts and those on the feet verrucae.
On the feet individual lesions are discrete, round papules with
a rough surface surrounded by a collar of hyperkeratosis. They
may be very numerous and join together to form mosaic warts
(see Fig. 13.67). If the diagnosis is in doubt, pare down the surface
with a scalpel and very soon tiny bleeding points will be seen (see
Fig. 13.66a).
Two problems arise from warts on the feet.
1. They hurt. This is not due to the wart growing into the
foot when it is situated on weight-bearing areas, but to the
hyperkeratosis that occurs around the wart. This grows
outward and causes pain just as a stone in the shoe does. Less
Fig. 13.64 Large corn over metatarsal Fig. 13.65 Thrombosed wart causing
commonly, very severe pain occurs if the blood vessels in
heads pain
HYPERKERATOTIC LESIONS / 433
a) Plantar wart b) Corn

Hyperkeratosis
Dilated capillaries
Cone-shaped
Proliferation of hyperkeratosis over
epidermis due a pressure point
to viral replication
Paring down produces Paring down produces

pinpoint bleeding once a decreasing cone of
the hyperkeratosis has keratin with no capillary
been removed and the bleeding.
capillaries reached.
Fig. 13.67 Mosaic plantar warts
a b c
Fig. 13.66 Differentiation between plantar wart and corn by paring down the surface keratin: (a) plantar wart showing bleeding points; (b) corn before paring;
(c) corn showing cone of solid keratin in centre
434 / FEET
TREATMENT: PLANTAR WARTS
SINGLE/FEW PLANTAR WARTS Surgery

Keratolytic agents Any kind of surgery is contraindicated on the feet. The most likely outcome is recurrence
These work by reducing pain from the hyperkeratosis that forms around a verruca. They of the wart, and there is always the risk that scarring will lead to the formation of
do not on their own get rid of the wart, so the patient needs to be aware of this. The permanent callosities, especially over pressure points.
verruca will only go if the body’s immunity gets rid of it.
The most important thing is for the patient to pare down the hard skin every night with MOSAIC WARTS
a scalpel or to rub it flat with a pumice stone so that it does not hurt. A wart paint or These do not respond as well to treatment as single warts. You can try the following
gel is then applied carefully just to the warts, left to dry and then covered with a plaster options.
● One of the salicylic and lactic acid paints applied every night.
overnight. In the morning the plaster is removed to allow the wart to harden up again
● Formalin or glutaraldehyde soaks. Get the patient to soak the affected part of the
before the wart is pared down the next night.
foot in a 5% solution of formaldehyde BP or Glutarol once a day. First apply a
Wart paints (suitable for use on the feet) are:
thickish layer of white soft paraffin (Vaseline) around the warts, so that the formalin
● salicylic acid 50% in paraffin (Verrugon)
does not make the normal skin sore. Then pour the formalin into a saucer or shallow
● salicylic acid/lactic acid mixtures in collodion (Cuplex, Duofilm, Salactol, Salatac);
bowl and soak the warts in it for 10 minutes each day. The next day, rub down any
26% salicylic acid only (Occlusal) hard skin with a pumice stone or foot scraper before repeating the treatment.
● podophyllotoxin preparations (Warticon cream)
● Apply 40% salicylic acid plasters cut to the same size as the warts. These are stuck
● 10% glutaraldehyde solution (Glutarol).
onto the warts shiny side down, taped securely in place with Hypafix (or something
similar), and left for a week at a time. When they are removed the soggy keratin is
Whichever paint (or gel) is chosen, it should be used each night before the patient
removed with a sharp scalpel blade before putting on a new plaster. This can be done
goes to bed. A fair trial of a treatment is to use it for 12 weeks before giving up and
once a week by the nurse or podiatrist until no wart is left.
changing to something else. If the plaster is left on for too long the wart becomes soggy
and painful. If this occurs, treatment will have to be left off for a few days. One of the
reasons why the treatment does not work is that the patient stops using it if the foot
becomes sore.
Freezing with liquid nitrogen

This is not a good treatment for plantar warts, because you need to freeze for quite a
long time to produce a blister (because of the thick layer of keratin on the sole of the
foot) and this will be too painful for the patient.
Fig. 13.68 Verruca treated with a

keratolytic agent
435
Nails
Anatomy of the nail 436
Examination of the nail 436
Abnormalities of the nail matrix
14
Pitting 437
Transverse ridging 437
Longitudinal ridging 438
Abnormalities of the nail bed
Discolouration under the nail 439
Abnormalities of the nail plate
Discolouration of the nail plate 440
Thickening of the nail plate 442
Splitting of the ends of the nails 443
Abnormalities of the hyponychium
Onycholysis 444
Subungual hyperkeratosis 445
Abnormalities of the cuticle
Paronychia 445
Abnormally shaped nails
Overcurvature 446
Spoon-shaped nails (koilonychia) 446
Wedge-shaped nails 446
Ingrowing toenails 447
Loss of nails
Without scarring (temporary) 447
With scarring (permanent) 447
Lumps and bumps around the nail 448
436 / NAILS
ANATOMY OF THE NAIL

Nails are keratin produced by a modified epidermis called the
nail matrix. From this grows the nail plate, which lies on the
nail bed. Nails protect the end of the digits and on the fingers
they are useful for picking up small objects and for scratching.
Abnormalities can arise from any part of the nail apparatus.
EXAMINATION OF THE NAIL Fig. 14.01 Anatomy of the nail

When looking at nails, examine the following in turn.
1. The nail from above 2. The nail from end on 3. The nail from the side
SURFACE OF THE NAIL THICKNESS OF THE NAIL SHAPE OF THE NAILS

● Pitting, p. 437 ● Thickening of nail plate, p. 442 ● Overcurvature, p. 446
● Transverse ridging, p. 437 ● Splitting of nail plate, p. 443 ● Spoon-shaped nails, p. 446
● Longitudinal ridging, p. 438 ● Subungual hyperkeratosis, p. 445 ● Wedge-shaped nails, p. 446
● Shiny, see p. 236 ● Ingrowing toenails, p. 447
DETACHMENT OF THE NAIL from nail bed

COLOUR OF THE NAIL ● Onycholysis, p. 444 LOSS OF NAILS
● Discolouration of the nail bed, p. 439 ● Without scarring, p. 447
● Discolouration of the nail plate, p. 440 ● With scarring (permanent), p. 447
NAIL FOLD AND CUTICLE LUMPS AND BUMPS AROUND THE NAILS, p. 448
● Loss of cuticle – paronychia, p. 445
● Nail fold telangiectasia, see p. 132

ABNORMALITIES OF THE NAIL MATRIX / 437
ABNORMALITIES OF THE NAIL MATRIX

TRANSVERSE RIDGING
PITTING Causes of transverse ridging:
Inflammatory conditions affecting the matrix cause abnormal 1. Eczema – some pits are so broad as to form transverse ridges
keratin to be formed, which becomes detached from the nail plate 2. Chronic paronychia due to pressure on the nail matrix (see
leaving pits or ridges. Pits are more easily seen in the fingernails Fig. 14.05 and Fig. 14.32).
than in toenails. 3. Beau’s lines – a single line at the same place in all the nails
Causes of pitting: is due to cessation of growth of the nail matrix at the time
1. Psoriasis – small regular pits of a severe illness; when this is over, the matrix will begin to
2. Eczema – larger and more irregular pits, associated with function normally again and the nail will grow out with a line
eczema on the skin around the nail in it; fingernails grow at a rate of approximately 1 mm/week
3. Alopecia areata – small, regular pits may be a poor prognostic (toenails at about a third of that speed), so you can tell how
sign for regrowth of the hair long ago the illness was (see Fig. 14.08).
4. Twenty-nail dystrophy – all finger- and toenails have parallel
pitting, which may merge to form ridges; cause unknown
5. Normal finding – isolated pits may be found in normal nails.
Fig. 14.02 Nail pitting in psoriasis Fig. 14.03 Larger and more irregular Fig. 14.04 Twenty-nail dystrophy Fig. 14.05 Transverse ridging
pits and ridging in eczema secondary to paronychia
438 / NAILS
LONGITUDINAL RIDGING
Causes when all nails are affected:
1. A few ridges are seen in normal nails
2. Lichen planus – fine regular lines (see also p. 447, pterygium)
3. Darier’s disease – regular fine lines with V-shaped notching at
the end of the nails (see also p. 247).
Causes when a single nail is affected:
1. Median nail dystrophy looks like an upside-down
Christmas tree; it is a temporary abnormality and gets better
spontaneously after a few months; the cause is unknown
2. Habit-tic deformity – here there is a broader groove made up
of numerous concave transverse ridges; it is due to picking or
biting the cuticle, which damages the nail plate as it grows out
3. A single wide groove may be due to myxoid cyst or fibroma
over the posterior nail fold that presses on the underlying Fig. 14.08 Beau’s lines: a transverse ridge in all nails due to interruption of nail
matrix (see p. 448). growth secondary to a systemic illness
Fig. 14.06 Longitudinal ridging seen Fig. 14.07 Darier’s disease: Fig. 14.09 Medial nail dystrophy Fig. 14.10 Habit-tic deformity on a
in lichen planus longitudinal ridging with V-shaped thumbnail
notches
ABNORMALITIES OF THE NAIL BED / 439
ABNORMALITIES OF THE NAIL BED Red, purple, black

DISCOLOURATION UNDER THE NAIL 1. Splinter haemorrhages are small, red, longitudinal streaks
The nail bed is the epidermis underneath the nail. In normal classically seen in subacute bacterial endocarditis. In fact, they are
circumstances it does not produce keratin. Problems in the nail very common so are an unreliable clinical sign.
bed cause areas of discolouration under the nail.
2. Subungual haematoma results from bleeding under the nail
White following trauma. It can occur on finger- or toenails. Initially,
Pallor of the nail bed occurs in hypoalbuminaemia or chronic the area is exquisitely painful and dark-red or purple in colour.
renal failure. With time, if the blood is not released immediately by puncturing
the nail, the area is discoloured black or brown. It can be
Orange-brown distinguished from a subungual malignant melanoma by making
This is due to psoriasis in the nail bed (salmon patches). a small horizontal nick on the nail plate at the distal end of the
discolouration and watching for a week. A subungual haematoma
Brown will grow out at the same rate as the nail so the nick will still be at
A round or oval area is a junctional naevus of the nail bed. If it is the distal end of the discolouration; a melanoma does not grow at
growing or made up of different colours, consider a malignant such a regular rate.
melanoma (see Figs 14. 17 and 14.18, p. 440).
Fig. 14.11 White nail bed due to Fig. 14.12 Salmon patch due to Fig. 14.13 Splinter haemorrhages Fig. 14.14 Subungual haematoma
hypoalbuminaemia psoriasis
440 / NAILS
3. Malignant melanoma arising in the nail bed or nail fold is very

uncommon. There will be secondary signs, such as destruction
of the nail plate (see Fig. 14.17) or spread of pigment into the
adjoining nail fold (see Fig. 14.18).
Pink, mauve
A glomus tumour is a rare benign tumour that presents as a
mauve area under the nail that is tender, particularly on pressure
or in the cold.
ABNORMALITIES OF THE NAIL PLATE

DISCOLOURATION OF THE NAIL PLATE
Fig. 14.15 Thin brown line due to a Fig. 14.16 Subungual pigmentation
junctional naevus in the nail matrix resulting from a low-grade The following are causes of discolouration of the nail plate.
haematoma under the nail due to
minor trauma 1. External staining‚ especially from nicotine and medicaments
(e.g. KMnO4 [see Fig. 2.02 p. 30] and dithranol). It occurs less
commonly from hair dyes or nail varnish.
2. Drugs: all the nails will be equally affected, e.g.

● chloroquine, azidothymidine (AZT) and gold stains nails
blue-grey
● penicillamine stains nails yellow.
3. Brown lines in a nail: a thin line down the entire length of the
nail is due to a junctional naevus of the nail matrix. A broad
line under the nail plate that is expanding in width or extending
up through the nail should make you think of a malignant
melanoma. Light-brown pigmentation, especially at the edge of
the nail plate, is likely to be due to a low-grade haematoma from
Fig. 14.17 Malignant melanoma Fig. 14.18 Malignant melanoma in minor trauma or pressure from footwear (see Fig. 14.16).
arising in nail bed with destruction of nail bed and involving the nail fold
the nail plate
ABNORMALITIES OF THE NAIL PLATE / 441
4. White nails: 7. Yellow nails:

● small white streaks due to minor trauma occur in most people ● yellow nail syndrome – all the nails are yellow or green in
at some time colour and are excessively curved in both longitudinal and
● in familial leuconychia the whole of the nail is white; this is transverse directions; the rate of growth is slowed almost
inherited as an autosomal dominant trait to a standstill and sometimes onycholysis can also occur;
● white discolouration that affects nails irregularly is often due it is thought to be due to a congenital abnormality of the
to tinea infection (see p. 442). lymphatics, although the nail changes do not occur until adult
life and often not until middle or old age; there may be other
5. Green discolouration occurs with pseudomonas infection. abnormalities of the lymphatics, such as lymphoedema of the
legs or bilateral pleural effusions
6. Blue discolouration occurs in patients with HIV/AIDS ● localised yellow or brown discolouration can be due to tinea.
infection and this may be a useful indicator of the disease. Similar
discolouration can be due to AZT.
Fig. 14.19 White streaks in nail plate Fig. 14.20 Green discolouration due Fig. 14.21 Blue discolouration due to Fig. 14.22 Yellow nail syndrome
due to minor trauma to pseudomonas infection HIV infection
442 / NAILS
THICKENING OF THE NAIL PLATE

1. Tinea unguium – dermatophyte fungi live on keratin so
multiply within the nail plate, causing it to become thickened
and discoloured white or yellow. They can only become
established in nails that are growing slowly, so they affect
toenails much more readily than fingernails. Once established,
the rate of growth slows down even more, so that cutting
the affected nails becomes an infrequent necessity. It can be
difficult on the feet to distinguish clinically between thickening
of the nails due to tinea and onycholysis and subungual
hyperkeratosis due to psoriasis. First look at the fingernails: the
changes of psoriasis will be more obvious there with associated
pits, salmon patches and onycholysis. If the fingernails are
not involved, tinea is more likely. On the toes, tinea does not Fig. 14.23 Tinea unguium showing thickening and discolouration of nail plate
affect all the nails and usually affects one foot before the other.
You can also look between the toes or on the instep for other
evidence of tinea of the feet (see p. 426). Nail clippings for
direct microscopy (see Fig. 10.03, p. 337) or fungal culture will
confirm the diagnosis.
2. Chronic trauma to toenails (in patients who play football,
tennis, etc.) can produce thickened nails.
3. In old age the nails become thickened, curved and difficult to
cut.
4. Wedge-shaped nails occur in pachyonychia congenita (see
p. 446).
5. Chronic malalignment of big toenails. A congenital disorder
where the big toenails become thickened, ridged and over-
curved, growing at an angle laterally. This condition is
probably quite common and leads to ingrowing toenails.
Fig. 14.24 Tinea unguium with yellow Fig. 14.25 White nail due to tinea
discolouration and patchy involvement unguium
ABNORMALITIES OF THE NAIL PLATE / 443
TREATMENT: TINEA UNGUIUM
Many patients have tinea of their toenails without being aware of it. Treatment is only needed if the patient is
complaining of the problem or if he or she is getting recurrent tinea infections elsewhere (feet, groin, body). Cure rates
from treatment may be as low as 30%.
Topical treatment with 5% amorolfine (Loceryl) nail lacquer applied once or twice a week after nail filing is suitable
if there are only two or three nails involved, with no more than 50% of the distal nail plate affected and lack of
matrix involvement. Other indications for topical treatment are children, if systemic therapy is contraindicated and for
prophylaxis. Amorolfine also works for toenail infections with the saprophytic moulds, Hendersonula toruloidea and
Scopulariopsis brevicaulis. Fig. 14.26 Chronic malalignment of the big toenails
Systemic treatment is recommended when:
● more than 50% of the plate is involved
● there is involvement of the matrix
● multiple nails are involved.
Terbinafine 250 mg is given once daily by mouth for 6 weeks for fingernails and 3–4 months for toenails. Liver function
tests should be checked at baseline and every 4–6 weeks. An alternative is itraconazole 200 mg orally/day. This can be
given continuously (as for terbinafine) or 400 mg/day pulsed (1 week on and 3 weeks off). It is contraindicated in heart
failure and liver disease. Liver function tests should be monitored if given continuously (but not for pulsed treatment).
Terbinafine gives a better cure rate (55% at 72 weeks).
The efficacy of oral therapy can be improved by combination with amorolfine topically. Failure of oral treatment
necessitates the removal of the affected toenail(s) plus oral terbinafine 250 mg daily for 3–6 months. Fig. 14.27 Lamellar splitting at the distal end of the
nail plate
SPLITTING OF THE ENDS OF THE NAILS

1. Lamellar splitting occurs when the distal portion of the nail plate splits into
horizontal layers. It is mainly seen in women who have their hands wet for long
periods of time. Water and detergents damage the keratin. It is treated by keeping the
hands out of water or by wearing rubber gloves.
2. Longitudinal splitting may occur along a longitudinal ridge, especially in Darier’s
disease (see Fig. 14.07).
444 / NAILS
ABNORMALITIES OF THE HYPONYCHIUM

ONYCHOLYSIS
Onycholysis is separation of the nail plate from the nail bed. It is
due to an abnormality of the hyponychium where the nail plate is
less firmly stuck down onto the nail bed. It can be due to:
1. Trauma – on the hands the commonest cause is over-
manicuring; the hyponychium is damaged by cleaning
underneath the nails with a nail file; on the feet it usually
follows a subungual haematoma
2. Psoriasis – onycholysis is more obvious on fingernails than
toenails; once the nail has lifted off, subungual hyperkeratosis
occurs and it may be difficult to distinguish from thickening of
the nail plate due to tinea (compare Fig. 14.29 with Fig. 14.23)
3. Poor peripheral circulation Fig. 14.28 Onycholysis in psoriasis Fig. 14.29 Subungual hyperkeratosis:
4. Thyrotoxicosis note the nail plate is of normal
5. Allergic contact dermatitis to substances that penetrate thickness
through the nail plate (e.g. methacrylate used as a glue for
sticking on artificial nails)
6. Doxycycline taken orally can cause a photo-onycholysis in the
summer; the patient experiences severe pain in all fingernails,
and then the nails lift off; this is becoming more common since
doxycycline is being used for malaria prophylaxis; it can occur
simultaneously in the toenails if the patient is wearing open-
toed sandals.
Fig. 14.30 Photo-onycholysis due to doxycycline: all fingernails involved equally

ABNORMALITIES OF THE CUTICLE / 445
SUBUNGUAL HYPERKERATOSIS ABNORMALITIES OF THE CUTICLE

This is a build-up of keratin under the end of the nail. It needs PARONYCHIA
to be distinguished from nail thickening. The cause is usually The cuticle is an area of keratin joining the posterior nail fold to
psoriasis. the nail plate, preventing bacteria and yeasts from getting into the
soft tissues around the nail. If the cuticle is lost (usually due to
TREATMENT: PSORIASIS OF THE NAILS
chronic trauma to hands that are continually wet, or to eczema),
infection can occur under the posterior or lateral nail folds to
There is no topical treatment that will help psoriatic nail changes (pitting, salmon
cause paronychia. There are two types.
patches, onycholysis or subungual hyperkeratosis). Coloured nail varnish will hide
onycholysis in a woman, and keeping the nails cut short will stop onycholysis getting Acute paronychia: this is due to infection with Staphylococcus
worse. Fortunately, patients do not often ask for treatment for their nails. If the skin aureus (less commonly Streptococcus pyogenes). There is exquisite
psoriasis is bad enough to be treated with a systemic agent (see pp. 227 and 230), the pain, a bright-red swelling and pus formation. Rarely herpes
nails will also improve.
simplex may be the cause, but grouped vesicles over the distal
phalanx will be seen.
Chronic paronychia: Candida albicans produces a more chronic
infection with less swelling, a duller red colour and no pus.
The nail plate may show transverse or longitudinal ridges from
chronic pressure on the matrix (see Fig. 14.32).
TREATMENT: PARONYCHIA
Acute: flucloxacillin or erythromycin, 250 mg qid for 7 days. If there is obvious pus
present, it should be lanced to let it out.
Chronic: the real cause is the loss of the cuticle. The paronychia will only get better
permanently if a new cuticle can be induced to grow. The patient must keep the hands
dry by wearing rubber or cotton-lined rubber or PVC gloves for all wet work until a new
cuticle has grown (3–4 months). A protective film of Vaseline can be applied around the
nail several times a day to keep water out.
Fig. 14.31 Acute paronychia Fig. 14.32 Chronic paronychia with

associated nail dystrophy
446 / NAILS
ABNORMALLY SHAPED NAILS SPOON-SHAPED NAILS (KOILONYCHIA)

OVERCURVATURE Spoon-shaped nails are most often seen in association with iron
This can be due to: deficiency anaemia (although most patients with iron deficiency
1. Clubbing – this is an apparent overcurvature of the nail due do not have this change). It may be a normal finding in young
to loss of the angle between the posterior nail fold and the children.
nail plate; if there is any doubt, put the distal phalanges of the
two thumbs together and there should be a diamond-shaped WEDGE-SHAPED NAILS
gap between them – this disappears if the nails are clubbed; Pachyonychia congenita is a rare genetic abnormality present
clubbing is due to chronic chest disease, carcinoma of the from birth. The nail grows both vertically and horizontally,
bronchus or congenital heart disease causing a thick, wedge-shaped nail that is unsightly on the fingers
2. Resorption of the distal phalanx in hyperparathyroidism – the and causes pain from pressure of shoes on the toes.
nail curves over the end of the finger
3. Yellow nail syndrome, see p. 441
4. Malalignment of big toenails, see p. 442.
Fig. 14.33 Clubbing Fig. 14.34 Koilonychia Fig. 14.35 Pachyonychia congenita
LOSS OF NAILS / 447
INGROWING TOENAILS LOSS OF NAILS

Penetration of the lateral nail fold by the nail itself or a spicule WITHOUT SCARRING (TEMPORARY)
of the nail causes redness, tenderness, pus formation and later ● Trauma especially to the great toenails. It can occur to
the development of granulation tissue. The great toenail is most fingernails too after a large subungual haematoma.
commonly involved. It is due to wearing shoes that are too tight ● Beau’s lines after a severe illness. The nail may break off at the
and cutting the nails in a half-circle instead of straight across. line (see p. 437).
Similar changes can occur as a side effect of the retinoid drugs.
WITH SCARRING (PERMANENT)
TREATMENT: NAIL LICHEN PLANUS
● Lichen planus: the cuticle grows down over and through
the nail plate, resulting in permanent scarring. This is called
Longitudinal ridging (see p. 438) needs no treatment. If pterygium occurs, which will
pterygium.
cause permanent scarring of the nails, prednisolone 30 mg/day started as soon as
possible will often switch it off. Give this dose for 2 weeks and then gradually tail it off
● Genetic abnormalities: all rare.
over the next month.
Fig. 14.36 Ingrowing toenail Fig. 14.37 Ingrowing toenail with Fig. 14.38 Pterygium of thumbnails
infection of nail fold due to lichen planus
448 / NAILS
LUMPS AND BUMPS AROUND THE NAIL

1. Viral warts: small skin-coloured, grey or brown papules with a rough,
warty surface may occur on the skin around the nail. At this site these
are difficult to remove and may grow under the nail. The best way to
remove them is by curettage and cautery, but sometimes some of the
nail plate may need to be removed.
2. Myxoid (mucous) cyst: a round, skin-coloured papule on the dorsal
surface of the distal phalanx. If pricked it discharges a sticky clear fluid.
These are due to the joint capsule herniating into the surrounding skin.
It is best that a hand surgeon carries out the removal, since recurrence
is likely unless the capsular defect is sealed. If a fibroma or myxoid
cyst occurs over the nail matrix, the pressure on the matrix can cause a
longitudinal groove in the nail plate (see Fig. 14.42).
3. Swelling of the distal interphalangeal joint can occur in gout or Fig. 14.39 Bowen’s disease around the nail fold
osteoarthritis (Heberden’s nodes).
Fig. 14.40 Viral warts around nail fold Fig. 14.41 Myxoid cyst lying over distal Fig. 14.42 Groove in nail due to pressure on matrix
interphalangeal joint by a myxoid cyst
LUMPS AND BUMPS AROUND THE NAIL / 449
4. Subungual and periungual fibroma: 5. Subungual exostosis: this is a localised 6. Tumours: rarely squamous cell
small firm pink or skin-coloured outgrowth of bone that presents as a carcinoma and malignant melanoma
papules protruding from the posterior subungual skin-coloured papule. If in can occur around the nail. Any
nail fold or from under the nail occur doubt, X-ray the digit. inflammatory condition around a
in patients with tuberous sclerosis (see single nail that does not improve with
p. 267). They appear after puberty. treatment is an indication for biopsy.
Fig. 14.43 Subungual fibroma Fig. 14.45 Subungual exostosis Fig. 14.47 Malignant melanoma in nail bed
Fig. 14.44 Periungual fibromas in patient with Fig. 14.46 X-ray of subungual exostosis Fig. 14.48 Tumour under nail: a biopsy will be
tuberous sclerosis (see also p. 267) needed to make a diagnosis
459
List of drugs and associated drug reactions

ACE inhibitors Erythrodermic β-blockers Lichenoid
Exanthematous Psoriasis
Lichenoid β-carotene Orange discolouration
Lupus erythematosus bleomycin Flagellate erythema
Pemphigus Pigmentation
ACTH Acne bromides Acne
allopurinol DRESS busulphan Hyperpigmentation
Erythrodermic calcium-channel blockers Lower leg oedema
Purpura (amlodipine etc.) (eczema)
Toxic epidermal necrolysis Lupus erythematosus
Vasculitis Pruritis (elderly)
aminophylline Eczematous carbamazepine Erythrodermic
amiodarone Hyperpigmentation Exanthematous
Phototoxic carbimazole Hair loss
ampicillin Erythrodermic Purpura
Exanthematous Toxic epidermal necrolysis
Vasculitis chloroquine Bleaching of hair
androgens Acne Blue nails
anticonvulsants DRESS Erythrodermic
antifungals Lupus erythematosus Hyperpigmentation of skin
aspirin Histamine release Lichenoid
(urticaria) Phototoxicity
barbiturates Erythrodermic chlorpromazine Erythrodermic
Fixed drug reaction Lupus erythematosus
Purpura Photoallergic
Toxic epidermal necrolysis Purpura (thrombocytopenia)
benzodiazepines Exanthematous chlorpropamide Eczematous
Fixed drug eruption Lichenoid
460 / LIST OF DRUGS AND ASSOCIATED DRUG REACTIONS
ciclosporin Hypertrichosis isotretinoin Dry lips, nose and eyes

Non-melanoma skin cancers Hair loss
Sebaceous gland hyperplasia Photosensitivity
cimetidine Erythrodermic lithium Acne
clofazimine Pigmentation – red/pink Psoriasis
codeine Histamine release (urticaria) mepacrine Lichenoid
contraceptives Erythema nodosum Yellow discolouration
Pigmentation of face (chloasma) of skin
coumarins Skin necrosis methyldopa Lichenoid
cytotoxics Hair loss Lupus erythematosus
Purpura (thrombocytopenia) minocycline DRESS
dapsone DRESS Pigmentation – blue/grey
Pigmentation – blue-grey Lupus erythematosus
diazoxide Hypertrichosis minoxidil Hypertrichosis
diclofenac Pemphigoid nalidixic acid Erythrodermic
doxycycline Photosensitivity Phototoxic reaction
furosemide Exanthematous nitrofurantoin Serum sickness (urticaria)
Phototoxic NSAIDs Erythema multiforme
gold DRESS Exanthematous
Erythrodermic Fixed drug reaction
Lichenoid Phototoxicity
Pigmentation of face – blue-grey Pseudoporphyria
Purpura (thrombocytopenia) Toxic epidermal necrolysis
Vasculitis Vasculitis
heparin Hair loss opiates Histamine release
Vasculitis (urticaria)
hydralazine Lupus erythematosus penicillamine Hypertrichosis
Vasculitis Lichenoid
imatinib Lichenoid Pemphigus
iodides Acne penicillins Anaphylaxis (urticaria)
isoniazid Acne Exanthematous
Erythrodermic Serum sickness (urticaria)
Pellagra phenolphthalein Fixed drug eruption
LIST OF DRUGS AND ASSOCIATED DRUG REACTIONS / 461
phenothiazines Exanthematous Fixed drug eruption

Phototoxic Lichenoid
Serum sickness (urticaria) Purpura
phenytoin Acne Serum sickness (urticaria)
Erythrodermic Toxic epidermal necrolysis
Hyperpigmentation Vasculitis
Toxic epidermal necrolysis sulphasalazine Lupus erythematosus
procainamide Lupus erythematosus tetracyclines Photo-onycholysis
promethazine Photoallergic Phototoxic
protease inhibitors DRESS thiazides Eczematous
Stevens–Johnson syndrome Exanthematous
Toxic epidermal necrolysis Lichenoid
psoralens Hypertrichosis Purpura
Phototoxic Serum sickness (urticaria)
retinoids Dry lips, nose and eyes Vasculitis
(acitretin) Hair loss thioureas Hair loss
(alitretinoin) Photosensitivity Vasculitis
rifampicin Pemphigus tyrosine kinase antagonists Acne
Purpura (thrombocytopenia) Palmar hyperkeratosis
steroids, anabolic Acne Rosacea
cortico- Acne vancomycin Anaphylaxis (urticaria)
Easy bruising Red man syndrome
Perioral dermatitis Stevens–Johnson syndrome
Skin atrophy and striae Toxic epidermal necrolysis Ashton
Telangiectasia vemurafenib Keratoacanthomas and squamous
sulphonamides DRESS cell carcinomas
Eczematous Photosensitivity
Erythrodermic warfarin Hair loss
Exanthematous Skin necrosis
462
Emollient products: how and when to use

Type Class Oil (%) Examples (this list is not exhaustive) Definition Usage Patient groups
Leave-on Ointment (no water) 100 White soft paraffin (Vaseline), 100% paraffin base (no Very dry skin Severe atopic eczema
emollients 50/50 white soft/liquid paraffin, preservative required) Use twice a day Ichthyosis
Use as routine Diprobase ointment, Useful at night-time Sprays useful in the elderly
moisturiser Epaderm/Hydromol/Emulsifying oints, Greasy – may put off some and in hard-to-reach areas
anywhere patients
Aerosol spray Dermamist, Emollin spray
Occlusive cream 30–70 Oily cream/hydrous ointment (lanolin), Water-in-oil emulsion (oily/ Dry skin Moderate atopic eczema or
QV intensive, Unguentum M, cold creams) and 100% lipid Trunk and limbs psoriasis
Lipobase (used as a diluent in Lipocream). ointments 2–3 times a day
Emollient gel 30 Doublebase gel, Water and oil emulsion with Very dry skin Very dry skin
containing glycerol Doublebase Dayleve gel humectant Use 3–4× a day, or 2× a day Psoriasis,
Water held in stratum corneum for Dayleve Ichthyosis
Emollient cream 5–10% Aquadrate, Balneum cream, Calmurid, by humectant (glycerol or urea) Dry skin Useful in older patients and in
containing urea urea E45 Itch Relief, Eucerin intensive, Use twice a day psoriasis
Hydromol intensive, Nutraplus.
Emollient cream 11–30 Aquamax, Aquamol, Oil-in-water emulsion (vanishing Normal to dry skin conditions Mild/moderate atopic eczema
(others without urea) Aveeno cream (colloidal oatmeal), cream) Face and flexures Other dry skin conditions such
Cetraben, Diprobase cream, (Note: tubs can become Good patient compliance as psoriasis and endogenous
Epaderm cream, E45 cream (lanolin), contaminated – prescribe 3–4x a day eczema
pumps)
Hydromol cream, Oilatum cream
QV cream (contains glycerol), Ultrabase
Zerocream, Zerobase cream, Zeroguent
with antimicrobial Dermol cream, Eczmol cream Product contains benzalkonium Useful in preventing flares of Infected/colonised atopic
Emollient lotion 5–14 Dermol lotion chloride, and/or chlorhexidine atopic eczema eczema
with antimicrobial Use lotions as a soap Healthcare workers
substitute Folliculitis
without antimicrobial Aveeno lotion (colloidal oatmeal), Oil-in-water emulsion with low Easy to apply 4x day Poor compliers (teenagers,
E45 lotion (lanolin), oil content Hairy areas (e.g. trunk, scalp) men)
QV lotion Lighter than creams Summertime use
Antipruritic emollient Balneum Plus cream, Product contains antipruritic Pruritus, especially if due to First-line therapy for itching
E45 Itch Relief cream agents (lauromacrogols) dry skin (especially in the elderly)
Adapted from Moncrieff G, Cork M, Lawton S, et al. Use of emollients in dry-skin conditions: consensus statement. Clin Exp Dermatol. 2013; 38: 231–8.
463
Wash and bath emollient products:

how and when to use
Type Class Oil (%) Examples Definition When to use Patient groups
Wash Emollient wash 15–30 Aquamax cream wash, Products contain emulsifiers Instead of soap, which is an irritant Atopic eczema
products products Doublebase shower gel, Should NOT contain harsh and therefore should be avoided in Hand dermatitis and psoriasis
Use only for E45 wash cream, detergents such as sodium lauryl any dry skin conditions
washing, do Hydromol bath and shower emollient, sulphate (e.g. aqueous cream)
not leave on
QV gentle wash,
the skin
Oilatum shower emollient.
Antimicrobial wash 2–30 Dermol shower/wash/lotion, Emollient wash product containing Useful in managing and preventing Recurrent infections or
products Eczmol cream. topically active antimicrobial agents flares of atopic eczema relapses in atopic eczema and
(such as benzalkonium chloride and/ hand dermatitis
or chlorhexidine)
Bath Bath oil: 50–91 Aveeno (colloidal oatmeal), Deposits a layer of oil on the surface All patient with moderate-very dry Use as part of complete
emollients Semi-dispersible oil Balneum, Cetraben, Dermalo, of the water that leaves a slick skin (atopic eczema, ichthyosis) emollient therapy in all dry
Add to bath or Diprobath, around the bath; non-foaming and Bathing in water alone is drying; skin conditions (see p. xx)
water, can be fragrance free bath oils should not be rinsed off
dispersible Doublebase bath additive.
used to wash emulsion Oil disperses evenly through the
E45 bath oil,
with bath water
LPL 63.4, Oilatum,
QV bath oil, Zerolatum, Zeroneum
Antimicrobiol 50–55 Dermol bath, Bath oil containing topical Prevention of infection. Atopic eczema with recurrent
bath oil Emulsiderm, antiseptic agent infections
Oilatum Plus, Zerolatum Plus
Antipruritic bath 85 Balneum Plus bath oil (soya oil) Bath oil containing topical Protection of the skin barrier during Should be used in conjunction
oil antipruritic agent bathing if pruritus is a problem with an antipruritic emollient
464
Classification of topical steroids by potency

Group UK brands USA brands Clinical indication
UK
Weak Hydrocortisone 0.5%, 1.0%, 2.5% (Dioderm, Hydrocortisone 0.5%, 1.0%, 2.5% (numerous Eczema on the face
Group 6–7USA Mildison) products) Eczema at any site in infants
Potency = 1% hydrocortisone Fluocinolone 0.0025% Alclometasone 0.05% (Aclovate)
(Synalar 1:10) cream Desonide 0.05% (Desowen/Tridesilon)
Medium potentUK Group 4–5USA Betamethasone valerate 0.025% (Betnovate RD) Clocortolone pivalate 0.1% Eczema (atopic) on the trunk and limbs, or flexures
Potency = 2.5 Clobetasone butyrate 0.05% (Eumovate) Desoximetasone 0.05% (Topicort LP) (both adult or children)
(×1% hydrocortisone) Fluocinolone .00625% (Synalar 1:4) Fluocinolone 0.025%* Seborrhoeic eczema on trunk
Fluocortolone 0.25% (Ultralanum plain) Fluticasone 0.005% (Cutivate) Flexural psoriasis
Fludroxycortide 0.0125% (Haelan) Flurandrenolide 0.05%
Hydrocortisone 17-butyrate 0.1% (Locoid) Hydrocortisone butyrate 0.1% (Locoid)
Hydrocortisone valerate 0.2%*
Hydrocortisone probutate 0.1%
Prednicarbate 0.1%
Triamcinolone 0.025%* (Kenalog)
PotentUK Betamethasone dipropionate 0.05% (Diprosone) Amcinonide 0.1% (Cyclocort) Lichenified atopic eczema
Group 2–3USA Betamethasone valerate 0.1% (Betnovate) Betamethasone dipropionate 0.05% (Diprolene) Discoid eczema
Potency = 10 Diflucortolone valerate 0.1% (Nerisone) Betamethasone valerate 0.1% (Beta-Val) Varicose eczema
(×1% hydrocortisone) Fluocinolone acetonide 0.025% (Synalar) Desoximetasone 0.05% (Topicort) Scalp eczema
Fluocinonide 0.05% (Metosyn) Diflorasone diacetate 0.05% (Apexicon) Hand and foot eczema or psoriasis
Fluticasone propionate 0.05% (Cutivate) Fluocinonide 0.05% (Lidex) Lichen planus
Mometasone furoate 0.1% (Elocon) Halcinonide 0.1% (Halog)
Mometasone furoate 0.1%* (Elocon)
Triamcinolone 0.5%, 0.1%*
Very potentUK Clobetasol propionate 0.05% (Dermovate) Clobetasol propionate 0.05% (Temovate) Lichen simplex
Group 1USA Diflucortolone valerate 0.3 (Nerisone forte) Fluocinonide 0.1% (Vanos) Resistant discoid eczema
Potency = 50 Halbetasol propionate 0.05% (Ultravate) Discoid lupus erythematosus
(×1% hydrocortisone) Lichen sclerosus et atrophicus
Note: *cream in a lower potency group; the ointment and cream base may result in differing groups for same molecule.
465
Index of algorithms
Erythematous lesions
Surface changes Type of lesion Number of lesions Face/bald scalp Truck/arms, thighs Axilla/groin Lower legs Dorsum hand Dorsum foot
Acute erythematous lesions/rash
Normal/smooth Macules/patches/ papules/ Progressive rash 166 166 166 166/372 166 166
plaques Multiple lesions/rash 98 170 170 372 404 170/372
Transient lesions 171 171 171 171 171/404 171
Papules/nodules Single/few (2–5) 177 177 177 177 177/404 177
Generalised rash 190 190 190 190 190 190
Crust/exudate Vesicles/bullae 104 179 179 179/372 404 179
Pustules 183 183 183 183 183 183
Erosions/ulcers 104 186 186 186/385 186/404 186
Chronic erythematous lesions/rash
Normal/smooth Macules 112 202 202 202 202 202
Papules, small (<0.5 cm) Single/few (2-5) 262 262 344 262 262 262
Multiple lesions/rash 114 196 336 196 196 419
large (>0.5 cm) Single/few (2–5) 262 213 344 213 213 213
Multiple lesions/rash 114 202 336 202 202 419
Pustules 114 201 201 201 201 201
Patches & plaques All lesions <2 cm 126/130 202 336 336 407 419
Some lesions >2 cm 126/130 208 336 375 407 419
Nodules 126 213 344 375 410 213
Scaly/ Papules 133 222 336 222 407 222
hyperkeratotic Patches & plaques Single/few (2–5) 133 218 336 218 218 218
Multiple lesions 224 224 336 224 224 419
Nodules 329 325 344 325 325 325
Generalised rash 244 244 244 244 244 244
Crust/exudate/ Papules, plaques & small erosions (no blisters present) 138 245 245 202/245 245 245
excoriated Vesicles/bullae/large erosions 255 255 255 382 407 255
Nodules 329 329 329 329 329 329
Ulcers 138 329/386 386 385/6 386 385/6
466 / INDEX OF ALGORITHMS CONTINUED
NON-ERYTHEMATOUS LESIONS
Surface changes Colour of lesion(s) Type of lesion(s) Face/bald scalp Truck/arms, thighs Axilla/groin Lower legs Dorsum hand Dorsum foot
Normal/smooth Skin coloured/light Papules – isolated lesions 262 262 262 262 262 262
pink/yellow – multiple similar lesions 263 263 346 346 346 346
Plaques 270 270 270 270 270 270
Nodules 272 272 346 272/375 410 272
White Macules & small patches (<2 cm) 278 278 278 278 278 278
Papules 278 278 278 278 278 278
Large patches & plaques (>2 cm) 281 281 281 281 281 281
Brown Macules & small patches (<2 cm) 288 288 346 346/399 288 288/399
Large patches & plaques (>2 cm)
present at birth/before age 10 292 292 292 292 292 292
appears after age 10 295 295 346 399 295 346
Papules & nodules 300 300 346 300 300 300/399
Blue/black/ purple Macules, papules & nodules 310 310 310 310 310 310
Patches present before age 10 292 292 292 292 292 292
Red/orange Macules & papules 314 314 314 399 314 314
Nodules 213 213 344 213 213 213
Warty Brown/skin coloured Papules & nodules 316 316 316/346 316 316 316
Scale/keratin Multiple lesions / rash 322 322 336 322 322 322
Single/few lesions 325 325 325 325 325 336
Crust/ulcerated Papules, plaques, nodules 329 329 329 329/387 329 329/387
bleeding surface
DERMATOLOGY FOURTH EDITION
DIFFERENTIAL DIAGNOSIS IN
“Brilliant... Take for granted the superb colour photographs, the comprehensive and
readable text, the clinical accuracy and acumen of the authors... what’s special is the
DIFFERENTIAL DIAGNOSIS
diagnostically and educationally helpful structure. This book understands that most of us do
not have photographic memories, and panic when we don’t immediately recognise a skin
lesion. Provided we can establish a few simple features of the rash – where it is, what colour,
how long it has been there, surface characteristics – we turn to the appropriate algorithm,
IN DERMATOLOGY
look at the picture for confirmation and come up with the right answer. It is such a relief I
could burst into tears of gratitude.”
Postgraduate Education for General Practice, on the First Edition
FOURTH EDITION
Revised and updated for its Fourth Edition with specially added images of pigmented skins,
the key aim of Differential Diagnosis in Dermatology remains the same – to allow primary
care physicians to diagnose quickly and confidently with the patient present. Chapters are
divided into different body areas and contain over 750 illustrations, combining excellent
clinical photography with practical text and clear diagrams throughout.
By looking inside the front cover at the intuitive “How To” guide and using the index RICHARD ASHTON, BARBARA LEPPARD and HYWEL COOPER
AND HYWEL COOPER
RICHARD ASHTON, BARBARA LEPPARD
of algorithms found at the back, diagnosis can be effectively reached by identifying the
relevant clinical features. High quality images of white and pigmented skins illustrate each
condition, with a concise description of the clinical features and treatment options.
Other titles of related interest

An Atlas of African Dermatology
Barbara Leppard
EMQs in Ophthalmology, Dermatology and ENT:
An essential revision guide with comprehensive answers
Mukhtar Bizrah and Manaf Khatib
The Pictorial Atlas of Common Genito-urinary Medicine
Shiv Pareek
K28636
ISBN: 978-1-90936-872-9
6000 Broken Sound Parkway, NW 90000
Suite 300, Boca Raton, FL 33487
711 Third Avenue
New York, NY 10017 9 78 1 909 368729
an informa business 2 Park Square, Milton Park
Abingdon, Oxon OX14 4RN, UK w w w. c rc p r e s s . c o m

Differential Diagnosis in Dermatology

Uploaded by

Copyright:

Available Formats

Differential Diagnosis in Dermatology

Uploaded by

Document Information

Original Description:

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Differential Diagnosis in Dermatology

Uploaded by

Copyright:

Available Formats

DERMATOLOGY FOURTH EDITION

Other titles of related interest

1. Site: dorsum hand 1. Site: face 1. Site: trunk

Boca Raton London New York

CRC Press is an imprint of the

No claim to original U.S. Government works

International Standard Book Number-13: 978-1-4987-8473-3 (eBook - PDF)

List of drugs and associated drug reactions 459

BASIC BIOLOGY OF THE SKIN

Fig. 1.02 Melanocyte in basal layer inserting melanosomes into keratinocytes

DIAGNOSIS OF SKIN DISEASE Table 1.01 Skin types

Relationship to physical agents Itching

PAST, FAMILY AND SOCIAL HISTORY DESCRIBING SKIN LESIONS

Single Fig. 1.03 Lymphoma Multiple Fig. 1.04 Lichen planus

FEEL THE LESIONS

a. Flat lesions Raised solid lesions

Papule Any solid lesion (≤ 1 cm size) that

c. Fluid-ﬁlled lesions Blisters (vesicles and bullae)

Loss of some or all of the

Loss of dermis (from any cause)

e. Other terms used

8. SURFACE FEATURES AND TEXTURE b. Abnormal keratinisation

e. Black-purple f. Yellow g. Blue-grey

10. BORDER OF LESION OR RASH

11. SHAPE OF LESION

PRICK TESTING PATCH TESTING

Allergen Source of allergen Allergen Source of allergen

Table 2.01a Emollient products: how and when to use

Ointments Organic hydrocarbons are subdivided by their melting points:

Pastes When to use which kind of vehicle

For wet rashes, use an astringent that will coagulate protein

ACTIVE INGREDIENTS Absorption of topical steroids

Side effects of topical steroids

For these reasons it is rarely prescribed,

Vitamin D3 analogues Keratolytic agents

SUNSCREENS particles that will scatter as well as absorb ultraviolet light

Table 2.04a Summary of types of wound and what dressings to use

Table 2.04b Summary of types of wound and what dressings to use

Table 2.05 Debriding agents

Table 2.06 Reducing bacterial counts and odour

Table 2.07 Absorption of exudate

Table 2.08 Wound and ulcer dressings

SYSTEMIC TREATMENT the skin with conventional courses of flucloxacillin or

ANTIHISTAMINES not been effective. Cimetidine (Tagamet) can also be given

● suppression of the pituitary-adrenal axis leading to adrenal IMMUNOSUPPRESSIVE AGENTS

Side effects: Azathioprine

Complications Biologics in skin cancer

Cryotherapy with dimethyl ether/propane

Determining the patient’s sensitivity to UVB or PUVA

Table 2.10 Diseases that may respond to ultraviolet

High voltage power supply

How lasers work

Table 2.11 Types of dermatological laser

Type of laser λ nm Pulse time Function Comments

Hair and hairy scalp

HAIR PHYSIOLOGY HAIR CYCLE

HYPERTRICHOSIS TREATMENT: HYPERTRICHOSIS

biopsy Positive Negative

ALOPECIA ALOPECIA TRICHO- TRACTION FRONTAL SECONDARY SCALP LICHEN