By

Benjamin Twiri Ampah

Definition
 Inflammation is a localised vascular and cellular
response of the body to injury.
 Types of inflammation
1. Acute inflammation
2. Chronic inflammation
3. Sub-acute inflammation
Acute inflammation
This is the ability of the body to
 Resist attack and damage by microbes and foreign
agents
 Contain an injury or damage
 Prepare the grounds for repair of damaged tissues.
Nomenclature
Inflamed tissues are named by adding the suffix “itis” to the
name of the organ affected.
Example are appendicitis, hepatitis, gastritis which stands for
inflammation of the appendix, liver and stomach
respectively.
There are few exceptions to this rule where the suffix “itis” is
not added to the names of the tissues acutely inflamed.
These include:
Pneumonia: acute inflammation of the lung
Pleurisy: acute inflammation of the pleura
Causes of inflammation
 Physical agents: blunt trauma, penetrating injury,
thermal burns and radiation injury
 Chemical agents: corrosive oesophagitis, acid burns,
alcohol hepatitis
 Microbial agents: viruses, bacteria, fungi and protozoa
 Immune agents: pollen, house dust and
antigens/immunogens.
 Ischaemia/hypoxia: infarct, thrombi, emboli.
The process of inflammation
1. Vascular response
Transient vasoconstriction
 The immediate event after an injury is transient
vasoconstriction due to sympathetic stimulation by
the injurious agent.
 This is to control blood loss from bleeding and to allow
time for clot to form to plug bleeding.
The process of inflammation
Persistent vasodilaltion
 This is due to vasoactive substances released by various
inflammatory cells in response to the injury.
 These vasoactive substances include histamine,
complement C3a-5a, bradykinins.
The process of inflammation
Increased vascular permeability
 The vasoactive substance also cause increased vessel
permeability, widening the gap junctions between the
endothelial cells.
Fluid exudate
 The vasodilation and increased vessel permeability,
fluid exudates into inflamed area resulting in swelling,
increased warmth and reddening of the site.
 These three are part of the cardinal signs of
inflammation namely tumour (swelling), calor
(warmth), rubor (reddening)
Cont’d…
 Tissue distension as a result of accumulation of exudate as
well as nerve endings irritation by the injurious agents
causes pain (dolor), the cardinal sign of inflammation.
 The exudation of fluid to the inflamed area serves to dilute
the injurious and supply neutralising substances to nullify
their effect.
 The fluid is serous but becomes purulent when secondarily
infected or if the injurious agent is bacteria.
 The cellular response is carried out by many immune cells
in the body.
2. Cellular response of acute
inflammation
 Neutrophil movement outside the blood vessel
through the process of margination, pavementation,
and emigration/diapedesis.
 The cells predominant in acute inflammation is
neutrophils. They move to the periphery of the blood
vessel known as margination.
 The neutrophils coat the inside of the blood vessel in a
process called pavementation.
 The neutrophils are able to pass through the widened
gap junction created by increased permeability termed
as emigration or diapedesis.
Cellular response of acute
inflammation
 Neutrophils movement throughout the inflamed area to
where pathogens and foreign bodies are known as
chemotaxis. This is aided by chemoattractants, examples
are C5a and bacteria proteins.
 Once the neutrophils reach the pathogens, they extend
their cytoplasm like pseudopodia of an amoeba and engulf
them.
 For the neutrophils to engulf the pathogen, it is necessary
for the pathogen to be coated with certain substances just
like garnishing of food to make them palatable and
appetising for the neutrophils. This is called opsonisation.
Examples are IgG and C3b
Pathogen killing
 The engulfment of the pathogens by the neutrophils is
termed phagocytosis.
 Inside the neutrophils are certain chemicals
(lysosomes) which are released to kill the pathogen.
This is termed intracellular killing.
 Certain times the pathogens are not engulfed, rather
the neutrophils produce certain chemicals to kill the
pathogens outside. This is called extracellular killing.
Cardinal signs of inflammation
 Tumour (swelling)
 Rubor (redness)
 Calor (warmth)
 Dolor (pain)
 Functio laesa (loss of function)
Adverse effect of inflammation
 Excessive swelling leading to disruption of tissues
 Disabling pain from excessive swelling and nerve
irritation
 Pressure necrosis on neighbouring structures
 Progression to systemic inflammatory response
syndrome
 Excessive high temperature which may lead to
convulsion especially in children
Benefits of inflammation
 Helps to contain minor infections before they become
overwhelming
 Cause dilution of toxins
 Destroy offending agents
 Alerts the body to the threat injury
 Leads to the production of protective antibodies against
future infections of the same kind
 Leads to fibrin formation to confine and localise the
inflammatory process
 Leads to restriction of injury to the smallest area possible
 Results in killing of foreign microbes
Outcome of acute inflammation
 Resolution
 Progression to suppuration
 Progress to chronic inflammation
Attenuation of the adverse effect
Prevention or reduction of the adverse effects of
inflammation are:
 Tepid sponging
 Administration of anti-pyretics
 Administration of analgesics
 Administration of antibiotics
 Debridement of wounds
 Incision and drainage of abscesses
 amputation of dangerous limbs
Characteristics of acute
inflammation
 Onset is immediate
 Duration is 1-2 days
 Predominant cells involved are neutrophils
 Lifespan of the neutrophil is within 10 hours
 Healing leads to return to normal function
Characteristics of chronic
inflammation
 Onset delayed till after 48 hours
 Durations is 2weeks or more
 Predominant cells are macrophages, lymphocytes
(non-granular leukocytes)
 Usually healing after chronic inflammation leads to
scar formation and deformities especially around
joints
 Healing therefore may not lead to return to normal
function.
Wounds and wound
healing
Definition
 A wound is a break in the continuity of tissues which
may or may not involve the overlying epithelium.
Simply a wound is the disruption of normal tissue
structure.
 A wound is different from an ulcer which is a break in
continuity of epithelium.
 Wound healing is the replacement of damaged tissue
by another tissue which is usually fibrous tissue (scar).
Classification
 Wounds are classified based on the following two
modalities:
1. Mechanism of injury
2. Degree of contamination
3. Degree of visibility
Types of wounds based on
mechanism of injury
 Abrasion: is a superficial wound which involves only
minimal loss of tissue.
 Surgically incised wound: these are planned and
therefore are under sterile conditions. There is
minimal tissue injury and tissue loss. Additionally the
wound edges are well apposed to allow quick healing.
 Contusion: contusion involves blunt injury to tissues.
The tissue is damaged by the impact made by force of
the injury. This may be deep without significant
commensurate injury of the overlying skin.
Types of wounds based on
mechanism of injury
 Laceration: this is similar to surgical incision as they both
involve a cut but here, it is not under sterile conditions and
the edges may be rough and far apart with significant tissue
loss. Laceration occurs commonly following accidental
injury.
 Punctured wound: these are penetrating wounds usually
deeper than wide. These are particularly prone to tetanus
infections due to the anaerobic environment created.
 Avulsion: here there is considerable loss of tissue and the
wound edges are very apart. It may involve loss of skin,
muscle and even bone.
Types of wounds based on degree
of contamination
 Clean wound: These are considered clean wounds.
They show no signs of infection or inflammation. They
often involve the eye, skin, or vascular system. Risk of
wound infection is less than 2%.
 Clean contaminated: this wound may not show signs
of infection, it is at an increased risk of becoming
infected because of its location. For example, surgical
wounds in the gastrointestinal tract may be at a higher
risk of becoming infected. Risk of wound infection is
2-5%.
Types of wounds based on degree
of contamination
 Contaminated: A surgical wound in which an outside
object has come into contact with the skin has a high
risk of infection and is considered a contaminated
wound. For example, a gunshot wound may
contaminate the skin around where the surgical repair
occurs. Risk of wound infection is 5-10%
 Dirty: This class of wound is considered dirty-
contaminated. These include wounds that have been
exposed to faecal material, sand, grass etc.
Types of wound based on degree
of visibility
 A wound is a type of injury which happens relatively
quickly in which skin is torn, cut, or punctured (an
open wound), or where blunt force trauma causes a
contusion (a closed wound).
Replacement of damage tissues
 Naturally the attempt of the body to replace damaged
parts is by two ways, namely:
 Regeneration
 Healing by fibrosis
Regeneration
 Regeneration is the replacement of lost tissue by
exactly the same type such that there is no evidence of
previous damage.
 However the process of regeneration in man is
IMPERFECT!!!
 The closest example of regeneration in man is the re-
growth of the liver post hemi-hepatectomy.
 There are different types of cells with respect to the
ability to regenerate or divide.
 These are grouped as follows: labile cells, stable cells
and permanent cells
Regeneration
Labile cells
 These cells can regenerate fully and actually do so
continuously as long as one lives. Examples are
epithelial cells of the gastrointestinal tract,
genitourinary tract and respiratory tract. Another
example is epidermis of the skin.
Regeneration
Stable cells
 Under normal circumstances, these cells are dormant
but when stimulated can attempt to regenerate.
Example are the hepatocytes (liver) and osteoblasts
(bone). These repair themselves after damage with
their own kind and not fibrous tissue.
Regeneration
Permanent cells
 These cells are never able to regenerate. Once they are
damaged they can never re-grow. Instead they replace
damaged parts with fibrous tissue. Example are the nerve
cells.
 That explains the development of paralysis once the brain
is damaged following stroke or cerebrovascular accident.
 The fibrous tissue which replaces the brain cells damaged
by the stroke can never function like the original brain
cells, therefore the parts of the body controlled by affected
part of the brain loses the brains control and paralysed.
The process of wound healing
 The process of wound healing can be achieved by two
main mechanisms, namely:
1. Primary intention
2. Secondary intention
The process of wound healing
 Wound healing by primary intention involves the
following steps:
1. Haematoma and scab formation
2. Epithelialisation and wound contraction
3. Acute inflammation
4. Demolition phase
5. Organisation or granulation tissue formation
6. Maturation phase
7. Remodelling
The process of wound healing
Haematoma and scab formation
 Following injury is bleeding. Subsequently a clot or
haematoma forms together with transient
vasoconstriction to stop further blood loss. When this
clot dries a scab is formed.
 The scab serves to cover the wound surface and
prevent secondary foreign body and bacteria invasion
as well as protects underlying tissues from drying up.
 The scab also allows healing to take place underneath
without any disturbance of the new fragile tissues by
external factors.
The process of wound healing
Epithelialisation
 Epithelial cells at the wound edges grow and advance
towards the centre of the wound. Once they meet, further
growth is halted.
 The process whereby cells growing in a horizontal fashion
stop to grow further once they come into contact with
other cells advancing from the opposite direction is termed
contact inhibition. This is completed by 24 hours from the
onset of injury.
 Wound contraction also occurs to reduce wound size with
the help of myoepithelial cell. These are epithelial cells
with smooth muscle properties and so can contract.
The process of wound healing
Acute inflammation
 Below the new epithelial cells, acute inflammation
occurs to bring in needed inflammatory cells to clean
up the wound and make it ready for healing to start.
The wound therefore manifests all the cardinal signs of
inflammation.
The process of wound healing
Demolition
 The inflammatory cells deployed to the wound site are
neutrophils during the acute inflammatory stage. After
24 hours, macrophages arrive at the wound site to help
with the cleaning up of the wound. They also engulf
foreign bodies, bacteria and debris.
Lag phase
 Up to this point, the wound is said to be in a LAG
PHASE. This takes 3-5 days during which period the
preparations are made prior to actual healing.
The process of wound healing
Organisation or granulation tissue formation
 The whole healing process is initiated and controlled
by growth factors. Fibroblast are another group of cells
recruited to the wound site. They lay down collagen to
bridge the wound edges.
 The growth factors stimulate new blood vessels to
sprout out in loops in the floor of the wound. This
loops of new blood vessels ( capillaries) in the collagen
matrix under the microscope has a granular
appearance hence the descriptive term
GRANULATION TISSUE.
The process of wound healing
Organisation or granulation tissue formation
 Healthy granulation tissue is pink, at the same level as
the surrounding tissue with minimal serous discharge.
Healthy granulation tissue does not bleed easily with
contact and has no slough.
 On the other hand, an unhealthy granulation tissue
has irregular surface, looks beefy red or pale and
usually raised above the surrounding tissues. It may
have slough with offensive copious discharge and
bleeds very easily on contact.
The process of wound healing
Maturation and remodelling
 The initial collagen laid down in the wound is
immature. It undergoes certain processes to mature to
finally cover the wound defect.
 The initial collagen is heaped up in the wound,
subsequently it is REMODELLED, a process of getting
it flattened out to be at the same level as the rest of the
skin or surrounding tissue.
 When this process is ineffective or the collagen is
excessively laid down, it leads to HYPERTROPHIC
scars and KELOID formation.
Clinical application
 The enzymes responsible for the maturation and
remodelling of collagen are hydroxylases and
metalloproteinases. They work best in the presence of
vitamin C and zinc as co-enzymes respectively. Vitamin C
and zinc are therefore essential for wound healing.
 Collagen is formed from amino acids with the most
abundant amino acid in collagen being glysine. Others are
methionine, proline and lysine. Therefore adequate protein
intake is vital for wound healing.
 As collagen is laid down, the wound gains tensile strength
but never to the original level of the non-traumatised
tissue. Scars are therefore weaker than the original cells or
tissue.
Clinical application
 Re-sutured wounds heal faster because they have
already gone through the lag phase. However, the scar
is weaker than fresh wound’s scar.
 The maximum rate of gain of tensile strength is
between 10-14 days from the start of the process of the
wound healing. This explains the removal of the
stitches after 10th post operative day.
 The head and neck have very rich blood supply and
heal much faster than other parts of the body so
stitches can be removed as early as the 3rd post-
operative day.
Healing by secondary intention
 Bigger wounds that involves a lot of tissue loss with the
wound edges wide apart heal by secondary intention. The
process of wound healing by secondary intention is similar
to what pertains in primary intention but it is more intense
and takes a longer period of time.
 The inflammatory process in secondary intention wound
healing is more intense because there is more damaged
tissue and contaminants to clean up. There is clinically
significant wound contraction much more than in healing
by primary intention to try and narrow the gap created.
 Healing by secondary intention results in bigger scars than
healing by primary intention. Contractures and deformities
are also more likely to occur especially around joints.
Factors affecting wound healing
Systemic factors
1. Nutrition
2. Co-morbid states/chronic diseases
3. Radiotherapy
4. Chemotherapy
5. Steroids
6. Age
Factors affecting wound healing
Local factors
1. Blood supply
2. Oxygen supply
3. Foreign bodies
4. Infection
5. Mobility
6. Surgical technique
Diabetes and wound healing
 Diabetes suppresses the immune system. The
inflammatory cells are not effective in cleaning
wounds in diabetic patients as they are in non-
diabetics.
 Chemotaxis is sluggish, opsonisation is not effective
and phagocytosis is impaired.
 The high glucose level in the tissue also makes a good
medium for bacteria to invade and multiply. For all
these reasons, the lag phase is prolonged and whole
healing process is sluggish.
Wound debridement
 Debridement is the removal of all devitalised tissues at an
inflamed or wound site. Debridement cleans up the wound
and facilitates healing.
Debridement is achieved by the following means:
1. Mechanical debridement is surgically cutting with scalpel
blades, high pressure irrigation and wet-dry dressing.
2. Biological debridement makes use of leeches and
3. Sterile worms/larvae (maggots) therapy to gradually
clean up wounds.
4. Chemical debridement is the use of chemicals like
fibrinolysin, collagenase to remove all dead and dying
tissues from wounds.
Wound dressing
 The first layer of wound dressing must be non-
adherent like Vaseline gauze. The non-adherent
dressing does not damage the fragile new tissues
formed and also limits blood loss during change of
dressing.
 Absorbent layer is the second layer of dressing added.
These are usually cotton wool, soff barn and tonsil
swabs. They are used to absorb from the wound.
 Crepe bandage which is expandable is used next to
cover the dressing. The expansion of crepe bandage
accommodates swelling from fluid exudation.
Wound drains
 Drains are used to allow flow of fluid, exudate and
blood out of wound sites. It helps to prevent
haematoma and seroma formation.
 The drainage may be passive or under suction. It may
also be closed or open. Closed and suction drains are
preferred to minimise infection.
 Examples of wound drains are nelation drains,
corrugated drains and sump drains.
Wound drains
Care of wound drains involves:
 Daily chart of quantity, colour, state of drain site and
odour of the fluid drained.
 Change of the dressing as often as necessary
 Strict asepsis
Complications of wound healing
Early complications
1. Bleeding
2. Haematoma
3. Infections
4. Dehiscence
Late complications
1. Weak scars
2. Incision hernias
3. Implantation cyst
4. Hypertrophic scars
5. Hyper or hypo-pigmentation
6. Keloid
7. Contractures and deformities
8. Chronic ulcers
9. Malignant change.
Grafts and flaps
 Grafts and flaps are tissues borrowed from other parts
of the body or from other humans or even different
species ( animals like pigs) to cover wound defect.
These are needed for huge defects and areas where
wound contractures is likely to occur.
 Grafts have no blood vessels of their own so they get
blood from recipient sites. Flaps have their own blood
vessels taken together with them from the donor sites
to the recipient sites.
Modern trends in wound healing
Growth factors
 Recombinant human platelet-derived growth factor
(PDGF) is approved elsewhere for use in the treatment
of wounds especially diabetic wounds.
Skin equivalents
 Tissue-engineered skin equivalents are available for
wounds like venous leg ulcer and diabetic foot ulcer.
Autologous keratinocytes cultured in humans is used
in covering large defects.
Current research
 There is a research going on to determine the limits of
devitalised tissue to accurately guide debridement.
This includes testing tissue pH, PO2 and perfusion.