Paediatrics and Child Health Lecture Note

PAEDIATRICS AND CHILD HEALTH
FOR
Health Science students
Lecture Note
Jimma University
Paediatrics and Child Health
For
Health Science students
Lecture Note
Tsinuel Girma (MD), Habtamu Fekadu (MD), Goitom G/Yesus (MD),

Assfawossen Bekele (MD), Mekete Latebo (MD), Wogene Tamire (MD),
Solomon Amsalu (MD), Dula Benti (MD), Yezna Temesgen (MD)
In collaboration with
The Carter Center (EPHTI) and The Federal Democratic
Republic of Ethiopia Ministry of Education and Ministry of
Health
Jimma University
Debub University
University of Gondar
Alemaya University
Acknowledgement
The team of Authors from the department of Pediatrics of various University would
like to thank and express their deep rooted gratitude to The Carter Center (EPHTI)
for its initiation and drive to prepare this teaching material.
The team would like to thank the administration of Jimma Univeristy, Univeristy of
Gondar, Alemaya Univeristy and Debub University for extending support to authors
whenever it was needed.
The Authors are particularly grateful to Dr. Damete Shimeles and Dr. Assaye
Kassaye Assistant Professors Pediatrics in Addis Ababa University for their highly
professional input that shaped this material for the benefit of health science
students.
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Table of Contents
Acknowledgement ................................................................................................. i
Table of Contents ........................................ ....................................................... ii
List of Acronyms ......................................... .......................................................v
PART I
Chapter One: General paediatrics................ .......................................................1
1.1 Child health in Ethiopia..................... .......................................................1
1.2 Immunization .................................... .......................................................3
1.3 Growth and development.................. .....................................................12
1.4 Nutrition and its disorders ................. .....................................................25
Chapter Two: Neonatology .......................... .....................................................78

2.1 Assessment of the newborn ............. .....................................................78
2.2 Neonatal resuscitation ...................... .....................................................87
2.3 Prematurity, low birth weight and small for gestational age....................91
2.4 Respiratory distress in the newborn . .....................................................96
2.5 Neonatal jaundice ............................ ...................................................101
2.6 Neonatal Sepsis and Meningitis ....... ...................................................104
2.7 Congenital infections (TORCH syndrome)............................................107
Chapter Three: Shock.................................. ...................................................115
PART II
Chapter Four: Infectious disease ................. ...................................................118
4.1 Common childhood infections........... ...................................................118
4.2 Typhoid fever.................................... ...................................................134
4.3 Tuberculosis ..................................... ...................................................138
4.4 Tetanus............................................. ...................................................147
4.5 Paediatric HIV/AIDS ......................... ...................................................152
4.6 Viral hepatitis .................................... ...................................................160
4.7 Epidemic Typhus .............................. ...................................................166
4.8 Relapsing Fever ............................... ...................................................167
4.9. Malaria............................................. ...................................................170
4.10 Leishmaniasis................................. ...................................................181
4.11 Schistosomiasis.............................. ...................................................184
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Chapter Five: Diseases of the respiratory system ...........................................187
5.1 Upper Respirotory tract infection ...... ...................................................187
5.2 Acute upper airway obstruction ........ ...................................................190
5.3 Pneumonia ....................................... ...................................................197
5.4 Bronchiolitis ...................................... ...................................................200
5.5 Bronchial Athma ............................... ...................................................202
Chapter Six: Diseases of the cardiovascular system .......................................209

6.1 Approach to congenital heart diseases.................................................209
6.2 Rheumatic fever ............................... ...................................................212
6.3 Infective Endocardites ...................... ...................................................216
Chapter Seven: Diseases of the gastrointestinal system .................................219

7.1 Diarrheal Disease ............................. ...................................................219
7.2 Portal Hypertension .......................... ...................................................227
Chapter Eight: Hematological diseases....... ...................................................230

8.1 Anaemia ........................................... ...................................................230
8.2 Megaloblastic Anemias..................... ...................................................234
8.3 Bleeding disorders............................ ...................................................236
8.4 Leukemia .......................................... ...................................................244
8.5 Lymphoma........................................ ...................................................248
Chapter Nine: Diseases of the renal system ...................................................253

9.1 Introduction....................................... ...................................................253
9.2 Urinary tract infection........................ ...................................................254
9.3 Acute glomerulonephritis .................. ...................................................258
9.4 Nephrotic syndrome ......................... ...................................................261
9.5 Acute renal failure............................. ...................................................265
Chapter Ten: Diseases of the nervous system ................................................271

10.1 Bacterial meningitis ........................ ...................................................271
10.2 Seizure disorders............................ ...................................................277
10.3 Coma .............................................. ...................................................278
10.4 Seizure Disorders ........................... ...................................................283
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Chapter Eleven: Poisoning .......................... ...................................................293
11.1 Organophosphate poisoning ............ ...................................................296
11.2 Carbamate insecticides.................... ...................................................299
11.3 Hydrocorbone .................................. ...................................................300
11.4 Acetaminophen ............................... ...................................................301
11.5 Salicylates........................................ ...................................................303
11.6. Co-Poisoning .................................. ...................................................305
Annex ........................................................... ...................................................307
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List of Acronyms
ABC Airway, breathing and circulation

AC Activated charcoal
Ach Acctylcholine
ANC Antenatal care
AFP Acute flaccid paralysis
AGA Appropriate for gestational age
AGN Acute Glomerulonephritis
ARF Acute renal failure
ARI Acute respiratory infections
CHD Congenital heart disease
CL Cutaneous leishmaniasis
CMV Cytomegalovirus
CNS Central nervous system
CPS Complex partial seizures
CRS Congenital rubella syndrome
EPI Expanded programme on immunization
GA Gestational age
GFR Glomerular filtration rate
HC Head circumference
HSV Herpes simplex virus
HMD Hyaline membrane disease
Hx History
IMCI Integrated Management of Childhood Illnesses
ITP Idiopathic thrombocytopenia purpura
IUGR Intrauterine growth retardation (Infants weighing less than tenth
percentile for gestational age)
LBW Low birth weight
LGA Large for gestational age
LP Lumbar puncture
LRTI Lower respiratory tract infection
MUAC Mid-upper-arm-circumference
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NCHS National Centres for Health Statistics
NAC N – acetylcysteine
NAPQI N-acetyl p-benzoquinonemine
OPs Organophosphates
PCP Pneumocystis carinii pneumonia ()
PEM Protein energy malnutrition
PMTCT Prevention of mother to child transmission of HIV
PPV Positive pressure ventilation
PTT Partial Thromboplastin Time
PT Prothrombin Time
RDA Recommended daily allowance
RES Reticulo endothelial system
RBP Retinal binding protein
RPR Rapid plasma reagin
RSV Respiratory syncytial virus
RX Treatment
SGA Small for gestational age
SMR Sexual maturity rating
SPS Simple partial seizures
TT Thrombin time
UTI Urinary Tract Infection
VAD Vitamin A deficiency
VDRL Venereal Disease Research Laboratory
VLBW Very Low birth weight
WBI Whole bowel irrigation
WHO World Health Organization
VL Visceral leishmaniasis
VZV Varicella zoster virus
VZIG Varicella zoster immunoglobulin
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PART ONE
General Paediatrics and Neonatology
CHAPTER ONE
GENERAL PAEDIATRICS
1.1. CHILD HEALTH IN ETHIOPIA

Tsinuel Girma
Objectives
At the end of this chapter, the student will be able to describe:
 The magnitude of childhood morbidity and mortality in Ethiopia
 Common causes of childhood morbidities and mortalities
 Child health interventions set in place at national level
The world population growth rate is very high compared with the socioeconomic
development, particularly so in developing countries where 80% of the world’s child
deaths occur. This population is largely unhealthy. Each year 14 million children under
five years old die and 2000 children die every hour. Child deaths in low income
countries comprise 98% of the world’s, of which 60% are preventable.
Main causes of morbidity are acute respiratory infections, diarrhoeal diseases, malaria
and neonatal problems like tetanus. Emerging health problems such as substance
abuse, street children and child labour make the situation worse.
Ethiopia is similar to many other low income countries in having a young population:
those under the age of 15 years make up 44% of the population. Basic health indicators
show unacceptably high figures. The infant mortality rate is 96.8 per 1000 live births.
Low birth weight deliveries are 16%.
Neonatal deaths, especially in the first week of life, contribute a large fraction of infant
deaths. Most of these deaths are easily preventable. But still 49 out of 1000 live births
die in Ethiopia.
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Data from health institutions and health surveys show the major causes of morbidity
and mortality are PEM, anaemia and vitamin A deficiency, acute respiratory infections
(ARI), malaria and vaccine preventable diseases.
Almost half of the children under five years of age are stunted and underweight, 52%
and 47% respectively. The rate of wasted children (11%) is also very high. Surveys in
different region show the rate of Bitot’s spot and night blindness to be 5% and 7%
respectively. The rate of breast-feeding is high especially in rural areas but in 60% of
cases colostrum is avoided while 70% neonates get breast-feeding within 24 hours.
ARI causes most deaths because in many of the cases treatment is not sought or
delayed.
HIV/AIDS has had a major impact on maternal and child health survivial. Each year
400,000 children are newly infected. The 2001 estimate for HIV/AIDS infection in
Ethiopia showed 200,000 children living with the infection and 1.2 million orphans. A
recent (2003) study in Jimma showed 9.8% sero-positive pregnant mothers during
routine antenatal care (ANC).The national programme for the prevention of mother to
child transmission of HIV (PMTCT) is at an early stage.
Various health interventions have been set in place to address the most important child
health problems in Ethiopia. Some of these are EPI (expanded programme on
immunization) since 1980, ARI case management (1990) and control of diarrhoeal
disease (1983). EPI was launched with the intention of increasing the coverage by 10%
annually and reach 100% of the people in 1990.The objective was not met for various
reasons: the poor health infrastructure, the low levels of trained man power, the high
turn over of staff and a decline in donor funding. In 2001 the national coverage for BCG,
DPT3, and measles was 63%, 51% and 40% respectively.
The new strategy of integrating most aspects of child health care is the basic principle
of IMCI (Integrated Management of Childhood Illnesses), which was launched since
1998 in three selected regions. The components of IMCI are improving health worker
skills, improving health system and improving family and community practices.
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Further Reading
Health and Related Indicators, Planning and Programming Department. Ministry of
Health, Ethiopia. 1994
Integrated Management of Childhood Illnesses. (IMCI), Ministry of Health, Ethiopia.

1999.
Demographic and Health Survey. 2000.
1.2. IMMUNIZATION
Tsinuel Girma
Objectives
At the end of the topic, the student will be able to describe the:
 Basic mechanism of immunization
 Nature of vaccine antigens
 Route of vaccination and dose
 Major contraindications for vaccination
 Major side effects of vaccination
 EPI for Ethiopia
 Catch-up vaccination
Introduction
Infectious diseases lead to high mortality and morbidity in paediatrics patients. They
range from mild self-limiting diseases to those that result in long-term disability like
blindness, deafness and others. Maintaining good nutrition, environmental and personal
hygiene, access to safe water supply and better living environments help to reduce the
magnitude of communicable diseases. Immunization, pioneered 200 years ago by
Jenner, represents another remarkably successful and very cost effective means of
control. More than 50 immunobiologic products are available for clinical use.
Sustainable financial support, well-organized infrastructure and epidemiology of disease
will determine the type of vaccine used in given country.
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The expanded programme on immunization (EPI), launched in Ethiopia in 1980 is

targeted 6 diseases with the aim of universal coverage by 1990.. Logistics, access and
management constraints contribute to the current coverage of less than 30%.
Definition
Vaccination is the administration of any vaccine or toxoid for prevention of disease.
Immunization is the process of inducing immunity artificially.
It can be active or passive
 Active immunization involves stimulating the immune system to produce antibodies

and a cellular immune response against infectious agent through the use of a
urine vaccine or toxoid.
 Passive immunization provides temporary protection through the administration of

exogenous antibody or maternal antibody transfer to the foetus.
Determinants of the Immune response

The nature and magnitude of the response to a vaccine or toxoid depend on the
following factors:
1. Age – presence of high concentration of maternal antibody and immature response
to some vaccines in the first four months of life impair immunization. The measles
vaccine is given at 9 months of age to reduce this effect.
2. Route of administration.
 Vaccines given orally induce mucosal secretary IgA
e.g. OPV vaccine
 Using an improper route to administer the vaccine may reduce the immune
response e.g. where BCG is administered IM rather than intradermal
3. Nature of vaccine
 Live attenuated vaccines induce immunity with a single dose which lasts longer
than inactivated ones
4. Genetic
 Individuals genetically vary in their ability to respond to the same vaccine.
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5. Potency
Ensuring the potency of a vaccine, especially live attenuated, requires keeping the cold
chain. This helps to determine the quality of EPI program (see Table 2.2).
Biologic nature of immunizing agents

Active immunization uses vaccines with different physical characteristic. They can be
grouped based on their biologic nature (See Table 2.1.)
Table 1 The main antigenic preparations
Type of antigen Vaccine example

Living organism Natural Small pox vaccine.
Attenuated * Polio (sabin) OPV, Measles,
Mumps, Rubella, BCG
Intact but non- Virus Polio (Salk)
living organisms Bacteria Pertussis
Sub cellular Capsular disaccharid Meningococcal
Fragments Surface antigen Hepatitis B.
Toxoids Tetanus, diphtheria
*Live attenuated vaccine (diminished virulence retaining desired antigens)
Live attenuated vaccines, particularly viral ones like measles, confer life long protection
after a single immunizing dose, since they closely simulate natural infection and contain
the greatest number of microbial antigen. Their drawbacks are:
 Reversion to wild type can lead to disease
 They can cause severe disease in immunocompromised children
 Some people exhibit hypersensitivity to viral antigens.
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Vaccines for routine (EPI) use in children
Preparations
The vaccines targeted against the 6 major diseases are presented in different forms
with a need to keep them in specified environmental conditions, particularly the
temperature ranges.
Table 2: Recommended Storage Temperature of EPI
Type of vaccine Storage temperature

Most Oral polio -15oC to – 25oC
sensitive Measles (freeze dried) -15oC to – 25oC
to heat DPT 2oC to 8oC
Least BCG (freeze dried) 2oC to 8oC
sensitive Tetanus toxoid 2oC to 8oC
to heat
Vaccines
Administration
Proper technique of administering vaccines is needed to achieve acceptable immune
response and avoid problems (see Table 2.3).
Injection safety procedures in immunization

Injections are safe when they are not a health threat to the recipient, health worker, the
community or the environment.
Factors that contribute to unsafe injection are:

 Reuse of a single syringe and needle
 Inadequate supply of injection material
 Inadequate disposal of used syringes and needles
Guidelines on injection safety include:

 Use of a single sterile syringe and needle for each dose of vaccine
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 Use of AD syringes preferably

 Provision of safety boxes for disposal of used syringes
 Incineration of full safety boxes
 Removal and proper burial of residue from the incinerator
 No disposal of used syringe, needle or full safety boxes in open garbage or
dumped randomly.
Schedule
The strategies used to give vaccines can be adapted in three ways depending on the
local situation:
1. Primary schedule for infants below one year in static health services:
Birth: OPV; BCG
6 weeks of age: OPV, DPT; BCG (if not given at birth)
10 weeks of age: OPV, DPT
4 weeks of age: OPV, DPT
9 months of age: Measles, Vit A. **
** Children less than 6 months –not recommended
 Children 6-11months -100, 000iu

 Children 12-59 months - 200,000iu
 Record on child’s immunization card
Table 3 - Administrations of Vaccines
ROUTE OF SITE OF
VACCINE DOSE ADMINISTRATION ADMINISTRATION
BCG Infants: 0.05 ml0.1ml for Intradermal Right deltoid region of the
children>1yr arm
DTP 0.5ml Intramuscular Upper, outer portion of the
thigh
Polio 2 drops, or Oral Mouth
Measles 0.5 ml Subcutaneous Outer ,upper part of left
arm
Tetanus 0.5 ml Intramuscular Deltoid region of the
Toxoid upper arm
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For children below 5yr but not vaccinated in the first one year (catch-up vaccination) the
following should be administered:
Visit Vaccination
1st visit DPT
OPV
Mantoux test,
BCG if test negative in 3 days
2nd visit (1 month after 1st visit DPT
OPV
3rd visit (1month after 2nd visit) DPT
OPV
Measles, if not exposed
4th visit (1 year later) DPT
OPV
th
5 visit (4 years later) (adult type)
2. Outreach (Mobile schedule for remote areas): This service gives coverage for
people living within 20 km radius of the health facility.
3. Mass campaigns: National immunization days (NIDs) for polio (currently active) and
measles.
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Side effects of vaccines

BCG:
 Kochs phenomenon – self limiting acute inflammatory reaction four days after
vaccination.
 Indolent ulcer – ulcer persisting 12 wk after vaccination or ulcer more than 10
mm, mainly resulting from deep injection or secondary infection.
 Deep abscess – abscess at site of injection or draining lymph nodes due to
subcutaneous or deep injections.
 Disseminated disease with BCG – 1 per million vaccines results in BCG causing
active disease especially in immunosuppressed children.
OPV: Paralytic polio from vaccine strain poliovirus
DPT: The major side effect is from the pertussis component

 Superficial injection can cause injection site abscess a week later.
 Encephalopathy ( 0.3 – 3/100,000 vaccines)
 Convulsion (0.3 – 90/100,000)
 Shock like state or collapse (hypotonic – hypo responsiveness episode) (0.5 –
30/100,000)
 Permanent brain damage (0.2 – 0.6/100,000)
Measles: May have mild reaction likes low grade fever irritability and allergic reactions.
Major side effects include (per 100,000 vaccinations):

 Encephalopathy (0.1)
 Convulsions (0.02 – 100)
 Sub acute sclerosing panencephalitis (0.01 – 0.05)
Contraindication and precautions
There are circumstances in which there should be a judgment of the risk and benefit of
administering a vaccine.
Contraindications: there are circumstances in which a vaccine, either first dose or

repeat, should not be given. The general contraindications for all vaccines include:
9
 Anaphylactic reaction
 Moderate to severe illness
 Live-attenuated vaccines for severely immunosupressed patient (exception is
measles) Not contraindications
 Moderate fever after prior vaccine dose
 Moderate local reaction after inject able vaccine
 Mild acute illness
 Prematurity (same dose as for full-term infants)
 Severe malnutrition (rather strong indication)
 Penicillin allergy (personal or family)
The contraindications for specific vaccines include:

BCG : Symptomatic AIDS
OPV:
 Severe immune suppression
 Diarrhea is not contraindication .Give OPV without registering it and repeat OPV 4
weeks later.
DPT:
 Encephalopathy within 7 days of Previous dose not attributable to another cause
 Seizures if poorly controlled or new onset, defer until control
The following precautions are necessary:

 Temperature  40.5oC within 48 hr. of prior dose
 Collages or shock like state
 Convulsion within 3 days after period close
 Persistent or inconsolable cry ( 3hr), within 48 hr of prior dose
 Gillian – Barrie syndrome within 6 wk after prior dose
The following are not contraindications

 Family history of seizure
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 Well controlled epilepsy

 History of febrile convulsion (personal or family). Give paracitamole for 24 hr after
vaccination
 Measles: the are virtually no absolute contraindications
Vaccines in special circumstances

Disease outbreaks in normal situations or prevention of epidemics in emergency
circumstances such as displacement or war, call for the use of different a schedule and
vaccine antigens. the most common diseases are measles and meningococcal
meningitis. Decisions about measles vaccination may be taken as follows:
Measles target population

Emergency setting
No Yes
Measles outbreak Yes
No Vaccinate all children*

6 mon – 5 yr.
Vit. A if not provided in the

Preceding month
* If limited vaccine supply, prioritize those who are undernourished or sick children
Meningococcal vaccine
The serotype A&C can cause major outbreaks in developing countries. The target
group (population) for vaccination in epidemic situations includes:
 Classically persons aged from 2 to 30 yrs.
 If the attack rate is high among > 30 yrs, vaccinate entire population
Use the bivalent A &C vaccine within the meningitis belt
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Further Reading
Nelson. Text Book of Pediatrics. 16th Ed. W.B. Saunders. 2000
Disease of Children in the Sub Tropics and Tropics, A/e, Edward Arnold, 1991
Manual for routine EPI, MOH, Ethiopia, 2003 (draft)
Study Exercises
1. Explain the concepts of active and passive immunization and compare the two
2. Select the live attenuated vaccine
a) BCG c) Diphtheria e)Polio (Salk)
b) Pertussis d) Tetanus
3. List conditions which are not contraindications for vaccination.
1.3. GROWTH AND DEVELOPMENT

Goitom G/Yesus
Objectives
By the end of this chapter, the student will be able to:
 Define growth and development
 Describe how to assess growth and development
 Describe the normal patterns of growth and development at different ages
 Describe factors affecting growth and development
Introduction
Growth and development in physical, intellectual, emotional and social terms are the
essential biological characteristics of childhood. A child is not a small adult, but is a
developing human being who changes from a new born baby through infancy,
toddlerhood and early school years into an adolescent and finally, a mature adult. One
needs to understand growth and development in three ways:
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An understanding of the normative pattern of physical growth and the emergency of

motor cognitive and emotional competence allows one to monitor children’s progress.
Understanding of how biological and environmental forces interact to shape

development allows one to target factors that increase or decrease risks.
Understanding of how parents conceptualize development facilitates guidance and

intervention.
Definitions
 Growth: Is the process of growing – the increase in size and development of a
living organism from a simple to a more complex form or from its earliest stage of
being to maturity.
 Development: implies an increase in skill and complexity of function.
Factors Affecting growth

Genetic factors
The growth of a child is a result of complex interactions of genetic and environmental
factors. As a result of multiple genetic differences, certain people are taller than others:
for example, pigmies are one of the world’s smallest races and appear to have
genetically determined inability to respond to somatomedin; twin studies have shown
that body size, shape and patterns of growth are strongly influenced by genetic factors.
Neural control of growth

It has been suggested that there may be a growth center in brain that keeps the child in
his or her genetically determined growth curve: thus, if a child deviates from a growth
pattern for a period of time because of malnutrition or illness, a period of accelerated or
’catch-up‘ growth brings him or her back to the ’predetermined‘ curve, implying some
sort of central control mechanism.
Hormonal influence
Most of the endocrine glands influence growth significantly either by promoting protein
synthesis, regulating substrate supply, or enhancing the effect of other hormones on
specific organs. Hormones with a great influence on growth are: growth hormone,
somatomedines, insulin, thyroid hormone, and sex hormones
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Nutrition
Adequate food to provide substrate for energy and synthesis of proteins is essential for
normal growth. Observations of growth in humans during famine and in economically
disadvantaged countries have clearly shown a lack normal growth.
Environmental and social factors

The home, neighborhood, and school environments have profound effect on the child’s
psychosocial development. Socio-economic status also significantly affects the growth
of a child: thus, children in top socioeconomic groups are taller than children of lower
socioeconomic class.
Assessment of Growth and Development
Disease in childhood affects growth and development. Measurement of growth and

development is therefore an essential skill to monitor the health of the individual child
and the community at large.
Assessment of Growth
Growth assessment is an essential component of paediatric health surveillance
because almost any problem with in the physiologic, inter-personal and social domain
can adversely affect growth.
Physical growth varies in rate and pattern in different tissues and different regions of the
body. In practice, several measures such as body weight, height or length, head
circumference, skin fold thickness and mid-upper arm circumference may be used.
The most powerful tool in growth assessment is the growth chart (see Annex 1). The
growth chart provides most of the information needed to assess growth. The standard
charts are based on data collected from 1963 to1975 by the National Centres for Health
Statistics (NCHS) on weight for age, height for age, head circumference for age, and
weight for height.
Separate charts are provided for boys and girls. Each chart is composed of seven
percentile curves, which indicate the percentages of children at a given age on the X-
axis whose measured values fall below the corresponding value on the Y-axis. The
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normal values for age are represented between the fifth and ninety-fifth percentiles, and
the fiftieth percentile represents the median (standard) value.
In children under 5 years old an additional chart (Harvard standard) is used to measure
weight for age as percentages of the median or standard value in the NCHS curve.
Weight for age

Weight is usually measured using beam balance or spring balance for small children
and a standing scale for older children. When weighing, children should be undressed
or wear light clothing. Children falling below the 5th centile of NCHS or below the 80% of
Harvard Standard are labelled as malnourished.
Height or length for age
Height is measured in the upright position for children more than three years of age,
while for those younger than three years, length should be taken. Length in children
less than three years should be taken by two examiners. One should position the child
(with the child supine on a measuring board). Then the child’s head should be held with
the ear/eye plane vertical, the ankles gently pulled to stretch the child, and the feet
turned up vertically.
The older children should stand straight against a wall or the erect measuring scale;
and their head, shoulder, buttocks and heels should touch the wall or scale. Then, they
should take a deep breath to relax the shoulders and with a flat object such as a book,
the upper level of their head should be marked against the scale.
A height for age measure shows linear skeletal growth. A height for age that is below
normal shows stunting and indicates chronic states of malnutrition.
Weight for height
Getting an accurate age may be a problem in countries like Ethiopia, where the majority
of people are from rural areas and illiterate. Weight for height measurements can
overcome this problem. However, it only identifies children with acute malnutrition,
whose height has not been as affected as their weight. Those with weight for height
falling below the 5th percentile of NCHS are labelled as stunted.
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Head circumference for age

Head circumference is measured by crossed tape technique. Placing a measuring tape
just above the brow anteriorly and the occiput, measure the occipito-frontal
circumference. Values below the -3 standard deviation (SD) are labelled as
microcephally and above +3 SD as macrocephally.
Mid-upper arm circumference
The circumference of left upper arm is taken at mid point while the arm is hanging by
the side. This is used as an age independent criterion for detecting malnutrition in
children of age one to five years. A mid upper arm circumference of less than 12.5cm
indicates malnutrition and when less than 11cm, severe malnutrition.
Developmental Assessment
Assessment of development helps to identify children with developmental delay. For

this purpose the following developmental assessments may be used.
Gross motor development
Denotes gross muscular activity and neuro-development including posture, independent

nobilities, progresses from head control when the child is sitting alone to standing,
walking and running.
Manipulation (fine motor development)
Fine motor development denotes the ability of the child to reach for, grasp and
manipulate objects. It follows the loss of the primitive grasp reflex, and progressively
becomes more sophisticated through infancy and childhood.
Cognition and social skill
These include social smile, watching a mirror, waving goodbye, general alertness, and
curiosity about the surrounding.
Language
Development of speech is closely linked with general understanding.
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General principles
 The sequence of each pathway of development does not vary, although the rate of
development is variable
 The rate of development along different pathways is variable
 Motor development proceeds in a cephalo- caudal direction (e.g. Hand control
develops before trunk control)
 Some primitive reflexes must be lost before voluntary movement occurs (e.g.
primitive grasp must disappear before voluntary grasp can develop)
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Growth and developmental milestones at different ages
Infancy (0-12 months)
This is a period of rapid physical growth. Normally this is manifested as follows:

 Physical growth: babies weigh an average of 10 kg at 12 months, length increases
by 25 cm, and head circumference increases by 12 cm.
 Gross motor: at 3 months babies need their head supported when pulled to sit, at 6
months sit without support, at 8 months crawl, and at around 12 months they can
stand without support.
 Fine motor: at 3-4 months babies can grasp objects, at 5-6 months they can transfer
objects from hand to hand, at 9 months they can achieve a thumb-finger (pincer)
grasp, and at around 12 months they start to scribble.
 Cognition and social skills: at 6-8 weeks babies start to smile in response to faces or
voices, at 4 months they laugh, at 6-8 months they develop stranger anxiety, and at
9-12 months they discover that objects are permanent.
 Language: during their first 6 months babies pronounce vowels; at 7 months they
start to voice consonants, at 8-9 months they pronounce “papa” and “mama”, and at
12 months they can say a few words besides “papa” and “mama”.
Toddlerhood (12 - 24 months)
In this period the growth rate slows down compared to infancy. Normal development is
as follows:
 Physical growth: toddlers gain an average weight of 2 kg, height of 12cm, and HC of
3cm.
 Gross motor: toddlers start to walk independently between the age of 12 to 15
months; at 18 months, they can run stiffly and walk upstairs with one hand held, at
24 months they can run well and walk up and down stairs one step at a time.
 Fine motor: at 15 month toddlers can make a line with crayon and insert pellet in a
bottle; at 18 month they can imitate a vertical stroke, and at 24 months they can
imitate a horizontal stroke.
 Cognition and social skills: at 15 month toddlers can indicate some desires by
pointing; at 18 month they can feed themself and they may complain when wet or
soiled; at 24 months they can help to undress and listen to stories with pictures.
18
 Language: at 15 month toddlers start to speak in jargon; at 18 months they can say
10 to 15 words; at the end of 24 months they can say two word sentences (e.g.
mama shoe)
Pre school years (2-5 years of age)
The normal pattern of development in the pre school years is as follows:

 Physical growth: at this time the average weight gain is 2 kg per year and height
increases by 7 cm per year. By the end of three years all primary teeth have
erupted.
 Gross and fine motor: at two and half years children can go upstairs alternating feet,
at 3 years they can ride tricycles, at 4 years they can hop on one foot and throw a
ball overhead, and at 5 years they can skip.
 Cognition and Language: language development occurs most rapidly between the
ages of 2 - 5 years. Vocabulary increases from 50 - 100 to about 2000 words.
Sentence structure advances and usually the number of words in a sentence equals
the child’s age in years. At two and half years most children know their full name
and engage in pretend play, at 3 years they know their age and sex, count three
objects correctly, wash their hands and put on shoes. At 4 years children can tell a
story and play with several children; at five years they can name 4 colors, count 10
objects correctly, and dress and undress.
19
Table 4: Developmental milestones in the 1st yr of life

Average age of Developmental
Milestone Attainment (in implication
months)
Gross motor
Head steady in sitting 2 Allows more visual
intention
Pull to sit, no head lag 3 Muscle tone
Hands together in mid 3 Self discovery
line
Sits without support 6 Increasing exploration
Rolls back to 6.5 Truncal flexion, risk of falls
stomach
Walks alone 12 Exploration, control of
proximity to parents
Runs 16 Supervision more difficult
Fine motor
Grasps rattle 3.5 Object use
Reaches for object 4 Visual motor coordination
Transfers objects 5 Comparison of objects
Thumb -finger grasp 8 Able to explore small
object
Scribbles 13 Visual-motor coordination
20
Communication and
Language
Smile in response to face, More active social participation
voice 1.7
Monosyllabic babble 6 Experiment sound
Follows one step command 7 non verbal communication
gesture
Follows one step out 10 Verbal receptive language
gesture
Speaks 1st real word 12 Beginning of labeling
Speaks 4-6 word 15 Acquisition of object & personal
name
Speaks 10-15 word 18 Acquisition of objects &
personal name
Speaks two word 19 Beginning of grammatization
sentences
Cognitive
Stares momentarily at spot Lack of objective permanence
where object disappeared 2
Uncovers toy (after seeing 8 Object permanence
i.e. hidden)
Egocentric pretend play 12 Beginning symbolic thoughts
School age (6-12 years)

Normal development in the school years is as follows:
 Physical growth: the average weight and height gain per year is 3-3.5kg and 6cm
respectively. Head circumference increases by only 2-3 cm. Loss of primary teeth
starts at 6 years of age.
 Motor: coordination and stamina increase progressively, and children are able to
perform complex movements such as dancing.
 Cognition and language: children start thinking in concrete logical operations.
21
Adolescence
Children undergo rapid changes in body size, shape, physiology, and psychology and
social functioning. Adolescence proceeds across three distinct periods: early, middle
and late, each marked by a characteristic set of salient biologic, psychological and social
issues. The common changes that occur during the early, middle, and late adolescence
period are described in the following table.
Table 5: Changes in early, middle, and late adolescence
Variable Early adolescence Middle adolescence Laye adolescence
Age 10-13 yrs 14-16 17-20 & beyond

Somatic 20 sex char, Height peak, acne & Slower growth
beginning of rapid odor, menarce
growth spermarche
Sexual Sexual interest Sex drive urges Consolidation of
experimentation sexual identity
Cognitive Concrete operation Abstract thought, self Idealism; absolution
and moral conventional centered
morality
Family Bids for Continued struggle for Practical
independence acceptance of greater independences
autonomy family remains
secure base
Peers Same-sex groups, Dating, peer groups less Intimacy, possibly
conformity, cliques important commitment
The sequences of somatic and physiologic changes that occur can be used to assess
developmental maturity according to Tanners ‘Staging: Sexual Maturity Rating (SMR) as
described in the following tables and figures.
22
Figure 1: Sexual changes in boys and girls during adolescence
Table 6: Classification of sex maturity stages in girls
SMR Pubic Hair Breasts

Stage
1. Preadolescent Preadolescent
2. Sparse, lightly pigmented, Breast and papilla elevated as
straight, medial border of small mound; areola diameter
labia increased
3. Darker, beginning to curl, Breast and areola enlarged, no
increased amount contour separation
4. Coarse, curly, abundant, but Areola and papilla form
amount less than in adult secondary mound
5. Adult feminine triangle, Mature, nipple projects, areola
spread to medial surface of part of general breast contour
thighs
23
Table 7: Classification of sex maturity stages in boys
SMR
Pubic Hair Penis
Stage Testes
1. None Preadolescent Preadolescent
2. Scanty, long and, Slight enlargement Enlarged scrotum,
slightly pigmented pink, texture altered
3. Darker, beginning to Longer Larger
curl, small amount
4. Resembles adult Larger; glans and Larger, scrotum dark
type but less in breadth increase in
quantity; coarse, size
curly,
Adult distribution, Adult size Adult size
5. spread to medial
surface of thighs
Exercise
1. What does a centile curve describe in the standard growth charts?
2. How old is a normal child if he can crawl, say mama and has developed stranger
anxiety?
3. Describe the physical characteristics of a boy and girl with SMR stages of 3 and 4
respectively?
References
A.S Paynter and M. Parkin, Growth in Childhood,
P. Stanfield. Diseases of Children in the Subtropics and Tropics. 4th Edition. 1993.
Robert D. Needleman, Growth and Development,
Behrman, Kliegman, Jenson, and Nelson Text Book of Pediatrics, 16th Edition, 2000.
P.K. Barthakur, Principles of Development;
S.V. Kale, Child Psychology and Child Guidance.
24
1.4. NUTRITION
Habtamu Fekadu
Objectives
By the end of this topic, the reader should be able to:
 Describe malnutrition, its magnitude, and consequences.
 Describe infant and young child feeding patterns in Ethiopia.
 Enumerate the benefits of breast feeding.
 Recite optimal breast feeding and complementary feeding behaviors.
 Know feeding options for an infant born to HIV positive mother.
 Describe methods to assess nutritional status.
Introduction
Nutrition is the provision of adequate energy and nutrients (in terms of amount, mix and
timeliness) to the cells for them to perform their physiological function (of growth,
reproduction, defense, repair, etc). Impaired nutritional status is called malnutrition.
There are two types of malnutrition:

1. Undernutrition
Undernutrition is due to inadequate nutrient in terms of quality and quantity. It takes two
forms:
Protein energy malnutrition (PEM) arises from inadequate energy and protein supply to
cells. Currently micronutrient deficiencies are incriminated as one important cause. It
includes mild and moderate malnutrition, and the severe forms kwashiorkor ,marasmus
and marasmic-kwashiorkor.
Micronutrient deficiencies arise from inadequate vitamin and mineral intake. They
include deficiency of vitamin A, iron, iodine, vitamin D, zinc etc. Deficiencies frequently
occur in populations with a high infectious disease burden and monotonous, poor quality
diets characterized by limited consumption of animal products and seasonal and periodic
food insecurity.
25
Most micronutrient deficiencies and the majority of PEM (mild and moderate forms) are
‘hard to see’: i.e they don’t show obvious signs. This is called the hidden hunger. That is
why the enormous consequences of malnutrition are not often appreciated.
If an infant is not properly fed, he or she will grow poorly, be at increased risk of illness
and death, have impaired intellectual development and be less productive in later life.
2. Overnutrition (obesity)
Obesity is due to excess intake of nutrients
Epidemiology
Undernutrition is prevalent in developing countries: one-third to one-half of all children
are stunted and 20-40% are underweight in most countries of eastern, central, and
southern Africa. One out of ten children suffer from acute malnutrition. Fifty four percent
of the deaths in children under-five in developing countries are directly or indirectly
attributable to malnutrition.
In Ethiopia, 51%, 47%, and 11% of under-five children are stunted, underweight and
wasted respectively. Malnutrition is the major cause of child mortality and is responsible
for 58 % of under-five mortality. The peak age for malnutrition is 12 to 24 months.
In Ethiopia, 27% of under 5 children suffer from sub clinical vitamin A deficiency and
17% of childhood deaths are attributable to vitamin A deficiency. Anemia and iodine
deficiency are also very common cause of morbidity and mortality.
The cause of malnutrition is multifactorial. The commonest causes of malnutrition are

suboptimal infant and young child feeding practices such as suboptimal breastfeeding
practices, poor quality complementary foods (too few calories, protein and/or
micronutrients), detrimental feeding practices (inappropriate timing of the introduction of
complementary foods as well as infrequent, unsupervised feedings), and contamination
of food and feeding utensils.. In Ethiopia infant feeding practices are suboptimal.
According to 2000 DHS survey, only 54% of babies are exclusively breast fed from 0-6
26
months and 57% of infants 6-9 months are sub-optimally fed. 24% of infants deaths are
due to poor breast feeding.
Infant and Young Child Feeding
Breast-feeding is an unequalled way of providing ideal food for the healthy growth and
development of all infants.
Optimal feeding of infants and young children means exclusive breastfeeding from birth
to about six months, followed by introduction of complementary foods drawn from the
local diet at about six months. Breastfeeding should be sustained well into or beyond the
second year of life, with increasing amounts of complementary foods.
Children are at highest risk of nutritional deficiency and growth retardation between the
ages of 6 and 24 months. The prevalence of malnutrition usually peaks at 12 to 24
months of age. Micronutrient deficiency, such as anemia, vitamin A deficiency, also
peaks at this age.
Complementary feeding means the provision of other foods or liquids along with breast
milk. At six months of age, breastmlik alone does not provide sufficient calories and
nutrients to sustain optimal growth and at this age infants are developmentally ready to
take soft and semi-solid foods in addition to breastmilk.
Appropriate complementary feeding involves a combination of practices to continue on-

demand breastfeeding and at the same time, improvements in the quantity and quality of
foods, hygienic food preparation and active feeding of the child. The best
complementary foods for children are foods that are:
 High in energy (calories) and protein
 Good in variety
 Easy to digest
 Pure and clean
 Easy and inexpensive to prepare
27
The advantages of breast-feeding

Breast milk is the best nutrition for infants and also young children. For the details of
breast milk composition see Table 8.
The benefits of breastfeeding for the child include:

 It is the best natural food for babies. It contains sufficient amount and the right
mixture of fats, sugars, proteins, minerals, and most vitamins for a growing baby. It
changes in composition to meet baby’s changing needs.
 It is easy to digest and nutrients are well absorbed.
 It contains enough fluids for the first 6 months of life (breast milk is 90 % water)
 It protects the baby from disease. Breast milk, esp colostrum, contains protective
substances against the germs that cause diarrhoea respiratory and other infections.
Breast-fed children have fewer diarrheal, respiratory, and ear infections.
 It is always clean and available 24 hours a day and requires no special preparation. It
does not cost anything.
 It creates bonding between the mother and baby that leads to better psychomotor
and social development.
 It protects against allergies because it contains no substance that could provoke
allergic reactions.
 Because of its above benefits, breast milk promotes normal growth and development
and saves lives of children.
The benefits of breast-feeding for the mother include:

 Breast-feeding provides an efficient contraceptive method during the first 6 months if
breast-feeding is exclusive and frequent. This has health benefits for the mother and
child.
 It reduces the risk of post-partum hemorrhage.
 It prevents breast engorgement and its consequences.
 It reduces the mother’s workload since breast milk is available at any time and
anywhere and it does not need any processing.
28
Table 8 Composition of Mature Human Milk and Cow's Milk
29
Common problems of breast feeding
Retractile nipples: This condition should be detected during prenatal care. The solutions
is to stretch the tip of the breast often during pregnancy and later make a hole in the bra
at nipple level.
Sore nipples: The causes of sore nipples are wrong attachment of the baby’s mouth to
the nipple and candidiasis. The solutions include:
 good attachment and frequent feeding.
 applying breastmilk on the infected zone
 not washing the breast too often.
 treating the candidiasis.
Mastitis and abscess: These conditions are caused by cracks, untreated ductal
obstruction, or engorgement. Solutions include:
 Breast hygiene
 Treat the abscess i.e. antibiotic and drainage
 Warm compress before breast-feeding to let the milk flow
 Cold compress after breast feeding to relief pain and reduce edema
 Treat plugged duct or engorgment if they are the causes.
Cleft lip or palate in the baby

It should still be possible to breastfeed if the health practititoner:
 Tells the mother breast milk is important.
 Tries to fill the cleft (with mother’s finger or special tooth plaque (obturator),
sometimes the mother’s breast can fill the cleft) in order for the child to keep the
nipple and areola in his/her mouth during feeds.
 Expresses milk and gives it to the child using a cup or teaspoon
30
Poor production of milk

It should still be possible to breastfeed if the mother and health practititoner:
 Increases the number and duration of feeds; the more the child sucks, the more
the mother produces milk.
 Breast feeds day and night
 Properly positions and attaches the baby on the breast
 Builds the mother confidence that she can breast feed
Recommended Breastfeeding Practices for Infants and Young Children:
Optimal breastfeeding practices from 0 to 6 months
Optimal breastfeeding practices from 0 to 6 months include:

1. Initiating breastfeeding within one hour of birth.The first milk (colostrum) is of
particular nutritional and health value to the infant because of its high content of
proteins and fat-soluble vitamins and its anti-infective properties.
2. Do not give any prelacteal feeds such as water, other liquids, or ritual foods.
3. Establish good breastfeeding skills, i.e. proper positioning, attachment and effective
feeding. Correct positioning means mother’s back is supported whether sitting or
lying down and the baby is held close to the mother, facing the breast with the
baby’s ear, shoulder, and hip in a straight line. Proper attachment signs are:
 infant’s mouth is open wide
 the lower lip is turned outwards
 the chin touches mother’s breast
 the entire nipple and a good portion of the areola (dark skin around the nipple)
are in infant’s mouth.
 More areola shows above than below.
31
A B
Figure 2 – well attached baby, notice – the Figure 3 this baby is not well attached.Mouth is wide open, the
lower lip turned outward and the chin touches mother’s breast, a good portion of the areola are in the
infant’s mouth.
4. Exclusive breast feeding for the first 6 months. Do not give any fluids such as water,
other liquids and foods other than breast milk before 6 months of age.
5. Frequent and on-demand breastfeeding, including night feeds (as often as infant
wants). Feeding every 2 to 3 hours (8 to12 times per 24 hours) or more.frequent
suckling is important for milk production.
6. Offer second breast after infant empties the first. The infant receives both ’fore‘ milk
(which has a high water content to quench the thirst) and ‘hind‘ milk (which is rich in
fat and nutrients).
7. Mother continues breasfeeding more often when the infant is ill.
8. A mother who will be away from her infant for an extended period expresses her
breast milk and the caregiver feeds the milk from a cup.
Recommended complementary feeding practices

Recommended complementary feeding practices include:
1. Introducing complementary feeding at six months of age.
2. Continuing frequent and on-demand breastfeeding untill 24 months. Breastmilk is
still major source of energy and key source of fat, vitamin A, calcium, riboflavin.
32
3. Increasing food quantity and frequency as the child grows. A healthy breastfed child
needs:
 2-3 meals per day at 6-8 months
 3-4 meals per day at 9-12 months and 1-2 snacks
 3-4 meals per day at 12-24 months and 2 snacks
4. Gradually increasing food consistency and variety as the child gets older:
 Feed mashed and semi-solid (thick gruel) foods by 6 months of age.
 Feed energy-dense soft foods to 6-11 months.
 Introduce snacks that can be eaten by children alone by 8 months and family
foods by 12 months
5. Diversifying the diet to improve quality and micronutrient intake:

 Feed vitamin A rich fruits and vegetables daily.
 Feed meat, poultry, or fish daily or as often as possible
 Use fortified foods or other staples, when available
 Give vitamin-mineral supplements when animal products and/or fortified foods
are not available (see Fig 4).
6. Practising active feeding:

 Feed infants directly and assist older children when they feed themselves
 If they refuse, experiment with different food combinations, tastes, textures and
methods.
 Feed slowly and patiently. Do not force.
7. Frequent and active feeding during and after illness:
 During illness, increase fluid intake by more frequent breastfeeding and patiently
encourage children to eat favorite foods.
 After illness, breastfeed and give foods more often than usual, and encourage the
child to eat more food
8. Practicing good hygiene and proper handling of foods:

 Wash caregivers and children’s hands before and after food preparation and
feeding.
 Serve food immediately after preparation.
 Use clean utensils to prepare and serve food.
33
 Serve using clean cups and bowls, and never use feeding bottles
Additional measures and advice

1. Give iron supplements daily (12.5 mg/day) to infants 6 months to 1 year of age, if
daily vitamin-mineral supplements or iron-fortified foods are not being given. If the
prevalence of anemia is known to be very high (40 percent or more), continue
supplementation until 24 months of age. For low birth weight infants, start
supplementation at 3 months.
2. Give every 6 months, high-dose vitamin A supplements after 6 months (100,000 IU
for infants 6-12 months and 200,000 IU for children 12 months and older)
Infant feeding and HIV

The overwhelming source of HIV infection in young children is mother-to-child
transmission. Infants can acquire HIV infection from their mothers during pregnancy,
labor and delivery or after birth through breastfeeding. Between 25-45% (1 in 4 or 3) of
HIV + women living in resource-poor settings pass on the virus to their babies.
Conversly,55 - 77% (two-thirds) of babies born to HIV+ mothers are not infected, even if
breastfed. Fourteen percent (i.e. 1 out of 7 infants) are infected through breastfeeding.
Timing of mother-to-child HIV transmission with breastfeeding and no ARV.
The risks of not breastfeeding in poor countries include the increased risk of
malnutrition, infectious diseases, and mortality. Failure to breastfeed is associated with
a 3-5 fold increase in infant mortality.In addition, the other benefits of breastfeeding
(psychological, birth spacing etc.) are lost.
This delicate balance between breastfeeding’s lifesaving benefits and the risk of HIV
transmission complicates optimal infant feeding in communities affected by HIV,
especially developing countries. For this reason, counseling on infant feeding is one of
the most important interventions to reduce mother to child transmission (MTCT) of HIV
and to increase HIV-free survival.
34
Up to 6 Months of Ages
 Breastfeed as often as the child

wants.
 Add complementary foods: Mashed
potatoes softened with milk,thick

gruel, porrigge
35
2-3
Figure 4: Feeding recommendations adapted for Ethiopia (IMCI)
The infant feeding options in communities with HIV/AIDS are based on the united
nations policy of informed choice (WHO, UNICEF, UNAIDS 2000).
1. Mothers whose HIV status is unknown or who have been tested and HIV negative
ca fneed their infant as described above in optimal feeding practices:
- Exclusive breastfeeding 0-6 months.
- Introduction of complementary feeding at 6 months.
- Continue breastfeeding to 24 months.
2. Mothers who have been tested and HIV positive should be provided with information
on the risks and benefits of different infant feeding options so that she chooses and
advised to implement the safest feeding option for her situation.
36
Figure 5: Timing of Mother-to-Child HIV Transmission with Breastfeeding and No ARV
Early Antenatal Early Postpartum Late Postpartum

(<36 wks) (0-6 months) (6-24 months)
Antenatal Labor and Delivery Breastfeeding

5-10% 10-20% 10-20%
L Antenatal Adapted from N Shaffer, CDC

(36 wks to labor)
When replacement feeding is acceptable, feasible, affordable, sustainable, and safe,

avoidance of breastfeeding is recommended.
ACCEPTABLE means taking account of:

 Social and cultural norms about infant feeding.
 Concerns about stigma associated women who do not breastfeed, suspicion of HIV
FEASIBLE means means taking account of:

 Economic, behavioral, psycho-social aspects for the care-giver and infant
 Resources and skills that are required
AFFORDABLE means:
 Able to purchase adequate amount of the formula over the duration it is needed
 Able to purchase necessary fuel and equipment
SUSTAINABLE means:
 Formula feeding can be practiced every day and night
 Resources are available throughout
 Formula feeding will be exclusive over first 6 months
37
SAFE means:
 Formula free from contamination
 Nutritious
 Free from stigma
 Does not spillover to general population
38
There are four options if a HIV positive mother chooses breastfeeding:
Option 1- safer breastfeeding
Safer breastfeeding involves:

1. Exclusive breastfeeding from 0-6 months. Avoid completely mixed feeding because
it may increase risk of HIV transmission.
2. Maintain good breast health by correct positioning, attachment etc. because mastitis
and cracked nipples increase risk of HIV transmission.
3. The mother should practice safe sex.
4. Mothers with breast problems (mastitis,sore/cracked nipples,abscess) shpuld stop
breastfeeding from the infected breast and seeks prompt treatment.
5. Stop breastfeeding as soon as complementary feeding is acceptable, feasible,
affordable, sustainable and safe or when the baby is started on complementary
feeding at the age of 6 months.
6. Stop breastfeeding if the mother develops full-blown AIDS.
7. Introduce complementary feeding at 6 months.
39
Option 2 – wet nursing
Wet nursing is breastfeeding by a woman who is not the infant’s mother. If this option is
taken it important to:
1. Ensure the wet nurse is HIV negative.
2. Maintain exclusive breastfeeding for 0-6 months.
3. Introduce complementary feeding at 6 months.
Option 3- Heat treated breast milk
In this option, the mother expresses her breastmilk safely and heats the breastmilk to
boiling point before feeding thebreastmilk to her infant with a cup. The following points
should be observed:
1. The heat treated milk should be used within one hour.
2. Introduce complementary feeding at 6 months or if complementary feeding is
acceptable, feasible, affordable, sustainable, and safe.
Options if the mother chooses not to breastfeed:

If the mother chooses not to breastfeed, the following points are important
1. Replacement feeding from birth with breastmilk substitutes
2. It should be exclusive replacement feeding (never mix-feed)
3. The most important thing is the hygienic preparation.
4. There are 2 groups of breastmilk substitutes options:
 Home prepared formula
 Commercial infant formula
For more detail about the formula read the references at the end of thesection.
An artificially fed baby needs about 150 milliliters of milk for each kilogram of his or her
own weight each day.
If cow's, or goat's, or camel's milk is used for artificial feeding:

 During the first 15 days of life give 1 part of boiled milk diluted with 1 equal part
of boiled and cooled water.
40
 From 2 weeks to 6 months of age give 2 parts of boiled milk diluted with 1 part of
boiled and cooled water.
 After 6 months of age give undiluted boiled and cooled milk.
Nutritional Assessment
Assessment of nutritional status is the primary step in the evaluation of childrens’
growth and should be an integral part of the evaluation and management of children
with acute and chronic disease. This chapter discusses nutritional assessment methods
and their practical application.There is no easy and satisfactory way to measure the
nutritional status of a child or community at a single examination. Four methods that are
widely used are described below. However, none of them is ideal.
Clinical method
The clinical method assesses nutritional status by examining the changes in the skin,
hair, buccal mucosa or thyroid glands which are believed to be due to inadequate
nutrition. It is a cheap, noninvasive and quick method.
The main drawbacks are it is very subjective, less specific (other diseases may have
similar picture e.g. edema can be due to cardiac disease) and usually the signs cannot
be attributed to be deficiency of a particular nutrient (e.g. glossitis may be observed in
riboflavin,vitamin B12,or iron deficiency.)
Table 9: Some clinical signs of malnutrition that are used for nutritional
assessment.
Nutritional deficiency Clinical signs
Edema, easily pluckable and gray hair, flacky
PEM paint dermatosis, muscle wasting etc.
Anemia Pale conjunctivae and palms
VitaminA deficiency Cornealxerosis, Bitot spot keratomalacia,
hypertkertosis of skin
Iodine deficiency Thyroid enlargement
Vitamin D deficiency Wrist widening, rachitic rosary, Harrison’s
(Rickets) sulcus
41
Anthropometric assessment
Anthropometry measures the variations in physical growth at different ages and the
degree of nutrition. It evaluates the long term nutritional history. It is a widely used,
simple, accurate, rapid, quantitative, inexpensive and non-invasive measure of the
general nutritional status of an individual or a population group. It is applicable to larger
sample sizes and it can be used both in clinical set up and fieldwork. If children are
measured more than once, growth velocity data are obtained that can be more valuable
because they reflect change.
The major pitfalls are it cannot detect impaired nutritional status of short duration nor
can it identify specific nutrient deficiencies.
Particular care should be taken to use appropriate equipment and techniques for
measuring stature/length and weight. This can significantly improve the assessments
that are performed.
Length or Stature
Length or stature is the most useful indicator of growth status. In infants and children
younger than 2 years, recumbent length is measured. Two people are required to
accomplish this measurement. The measuring table or board should consist of a fixed
headboard, a movable footboard, and a rule attached at one side. One of the
measurers should hold the crown of the infant's head against the headboard so the
external auditory meatus and the lower margin of the eye orbit are aligned
perpendicular to the table. The second measurer grips both ankles of the infant with
one hand and positions the heels firmly against the footboard, which is manipulated
with the other hand. The knees, which are slightly flexed, are then pressed down on the
table with the lateral edge of the hand. The recumbent length should be recorded to the
nearest 0.1 cm.
Height is measured for children older than 2 years. Measurements of height are made
with the child’s feet bare. The child should stand erect with the heels, buttocks,
shoulders, and head all touching the measuring board. The feet should be positioned at
a 90-degree angle. The child’s axis of vision should be horizontal, with the child looking
ahead and the external auditory meatus and lower margin of the orbit aligned
42
horizontally. The stature is recorded to the nearest 0.1 cm (see the figures on the
following pages).
Weight
Various types of apparatus, such as infant scales, beam-balance scales and readout
scales are available to measure body weight. The type used needs to be regularly
calibrated to maintain accuracy. Weight should always be recorded as nude weight. If
the subject is not weighed nude, then the estimated weight of the clothing should be
subtracted from the total weight.
43
44
45
Head Circumference
Head circumference is a useful measurement until about 3 years of age, when head
growth slows. It must be measured with a narrow and nonstretchable measuring tape.
To obtain an accurate measurement, the tape must cross the forehead just above the
supraorbital ridges, passing around the head at the same level on both sides to the
occiput. It is then moved up or down slightly to obtain the maximum circumference. The
tape should have sufficient tension to press the hair against the skull.
The commonly used four building blocks or measures used to undertake

anthropometric assessment are age, sex, weight and height. When two of these
variables are used together they are called an index/indices. There are many
anthropometric measures including mid-upper-arm-circumference (MUAC), head
circumference, and skin fold thickness but three indices are commonly used in
assessing the nutritional status of children
 Weight-for-age
 Length-for-age or height-for-age;
 Weight-for-length or weight-for-height.
The values of these measurements will be interpreted using standard charts (Harvard
curve, NCHS) of weight-for-age, height-for-age, weight-for-height, and head
circumference-for-age. The three indices are used to identify three nutritional
conditions: underweight, stunting and wasting.
Weight-for-age
For monitoring growth of children over a limited period, weight-for-age is the simplest
method. A low weight-for-age index identifies the condition of being underweight, for a
specific age. The advantage of this index is that it may reflect both past (chronic) and/or
present (acute) under nutrition (although it is unable to distinguish between the two).
Underweight, based on weight-for-age, is a composite measure of stunting and wasting.
46
Height-for-age
This index is an indicator of past undernutrition or chronic malnutrition. It cannot
measure short term changes in malnutrition. For children below 2 years of age, the term
is length-for-age; above 2 years of age, the index is referred to as height-for-age.
Deficits in length-for-age or height-for-age is called stunting. Stunting is an indicator of
past growth failure.
Weight-for-height
The ratio of actual weight to the ideal weight for height (usually referred to as weight for
height in children under 2 years of age or weight-for-height in children over 2 years of
age) helps to identify children suffering from current or acute under nutrition or wasting
and is useful when exact ages are difficult to determine. It can be used to differentiate
stunted growth from wasting and is independent of age. Wasting results from acute or
subacute nutritional deprivation and by acute medical conditions such as diarrhea. Body
weight is depleted out of proportion to length, making the weight-for-height ratio low.
.
Mid upper arm circumference (MUAC)
The mid upper arm circumference is an indicator of muscle growth. It is age
independent, relatively easy to measure and a good predictor of immediate risk of
death. It is used for rapid screening of acute malnutrition in children from 1-5 years of
age. MUAC can be used for acute undernutrition screening in emergency situations and
for estimating prevalence of undernutrition at the population level.
The left arm is usually measured by convention. A point is marked midway between the
acromion (shoulder) and the olecranon (elbow) on the vertical axis of the upper arm
with the arm bent at a right angle and between the lateral and medial surface of the
arm. The child should then stand or sit with the arm hanging loose at the side. The tape
is passed around the arm at the level marked and is tightened so it touches but does
not compress the skin or alter the contour of the arm. Because the arm on cross section
is not an exact circle, some difficulty is usually met in ensuring that the tape touches the
arm on the medial surface. To accomplish this, the middle finger of the examiner’s left
hand can be used to gently press the tape to the skin (see the figure on the next page).
47
Classification
The various methods of classification are described below.
Gomez: Wt. for age = Wt. of subject x 100

Wt. of normal child of same age
Wt. for age Degree of malnutrition

90-109% normal
75-89% mild (grade I)
60-74% moderate (grade II)
< 60 severe (grade III)
The Gomez system is used in public health screening and to evaluate the impact of
public health intervention. Its shortcomings are:
 It relies on age which is usually unreliable, especiallyin developing countries.
 It fails to differentiate acute vs chronic malnutrition.
 It fails to differentiate between types of severe PEM
48
49
Welcome uses the weight for age, measured by the Harvard Curve
Table 10: The Welcome system for measuring weight for age
wt. for age
Edema 60-80% 60%
Absent Underweight Marasmus
Present Kwashiorkor Marasmic-
Kwashiorkor
This system is preferable for clinical setups to distinguish different forms of PEM its
shortcomings includes that it:
 Relies on age
 Does not consider height
 Does not differentiate acute VS chronic malnutrition
Water low
In this system terms suggest the following:
 Wasting suggests acute malnutrition
 Stunting suggests chronic malnutrition
The system has the following advantages:

 It is the best method for screening malnourished children in the community
 It can detect mild forms of PEM
 It can distinguish acute from chronic malnutrition
 It does not rely on age, which is sometimes difficult to ascertain in rural areas
Its short coming is that it does not differentiate severe forms of PEM.
50
Table 11: The Water low system for measuring nutritional status
Wt. for Ht. Nutritional Height for Nutritional
status age status
90-100% Normal > 95% Normal
85-90% Mild wasting 90-95% Mild stunting
75-85% Moderate 85-90% Moderate
< 75 % Severe < 85% Severe
wasting stunting
Biochemical methods
Biochemical methods measure the total amount or concentration of nutrient in body
fluids (blood, serum, urine) and organs (storage sites) of the body. The tests reflect
recent nutritional status and identify specific nutrient abnormalites.They also detect sub
clinical deficiencies.The most commonly used tests are hemoglobin, serum albumin and
others like vitamin A, thiamine in urine, serum ferritin etc.
Dietary survey
Dietary survey is an important component of nutritional assessment. It assesses
through recording the food intake and translating it into nutrients consumed. Dietary
data can be collected at national, household, and individual level. It can be estimated in
individual level by:
 Dietary history: to record the usual food intake pattern over a relatively long period
of time and is obtained by interview.
 24 hours recall: the subject is asked to recall all food consumed during the
previous day
 Food record: the subject keeps a record of the food consumed during a specific
period of 3-7 days, quantities being estimated in household measures. This is the
most accurate method of dietary assessment because it accounts for most of the
daily variation in diet and eliminate the subjectiveness of diet recall records
 Weighed intake: the subject or trained person weighs all food consumed during a
given period of time.
51
Protein Energy Malnutrition (PEM)
Objectives
By the end of this topic, the reader should know:
 the magnitude of PEM.
 the basic, underlying and immediate causes and the pathogenesis of PEM.
 the clinical pictures of marasmus and kwashiorkor.
 the pathophysiological changes and their implication on the manifestations and
treatment.
 the common complications and the principles of management.
Definition
PEM is a clinical syndrome mainly due to deficiency of macronutrients (protein and
energy) and micronutrients.
Epidemiology
PEM is frequently observed in children between 6 months and 5 ears of age.
Marasmus peaks in the first year and Kwashiorkor between 1 and 3 years of age.
Stunting is most common between 2.5 and 3 years of age. PEM is more common
during the weaning period and the rainy season.
Causes
The nutrition status of an individual, including any of the four major forms of malnutrition
(PEM, IDD, vitamin A deficiency and iron deficiency anemia) is an outcome of complex
biological and social processes, as summarized in the conceptual framework of
malnutrition (see Figure 9).
The causes are classified as the follows:
Immediate causes: inadequate dietary intake and disease.
Underlying causes: insufficient food available to families (household food insecurity),

inadequate care of women and children, insufficient health care, and an unhealthy
environment.
52
Basic causes: inadequacies in educational, political, and economic systems and

problems with the availability and control of resources.
Pathegenesis
Pathegenesis is a multi-deficiency state but there are different theories for the exact
pathogenesis. Currently the most accepted pathogenesis, especially for edematous
malnutrition, is the free radical theory.
53
Inequality Drought War

Basic ----------------
poverty and social disadvantage

Underlying -------------------
Immediate ------ Lack of food Infections
Malnutrition
Manifestation -----------
Figure 9 - Conceptual framework for causes of malnutrition.
Protein and calorie deficiency

Marasmus is due to both calorie and protein deficiency, predominantly calorie.
Kwashiorkor is due to more marked protein deficiency than calorie which leads to
hypoalbuminemia and edema. Currently less accepted cause.
Adaptation
Marasmus is well adapted to the deficiency due to the high cortisol and growth hormone
levels and depression of insulin and TH Kwashiorkor is a poorly adapted form of PEM.
Free radical theory

Free radical theory can be described using the figure on the next page:
54
Figure 10: The free radical pathogenesis
Increased production of free radicals (oxidants) - peroxides, epoxides, due to NOXA -

infection, bowel bacteria, contaminated foods, aflatoxin
AND
Decreased scavenger mech. that removes free radicals because of deficiency of
micronutrients (vitamins, zinc, selenium, etc) and glutathione
Accumulation of free radicals
Damage cell memberane and vessels
Kwashiorkor - fatty liver, dermatosis, edema etc.
Classification – There are different classification but only the Welcome has clinical
importance and is mentioned here. For the other classifications, see the nutritional
assessment section (page 52).
Under this system, even if the weight-for-age is more than 80% of what it should be, a
child will be labeled as kwashiorkor if he /she has clinical signs of Kwashiorkor.
It is important in clinical setups to distinguish between different forms of PEM. These

are described beloe.
Severe malnutrition
A child is labeled as having severemalnutrition if any one of the following is present:
 Weight for height less than 70 % of what it should be;
 MUAC less than 11cm for a child with a length less than or equal to 75cm;
 Bilateral edema; or
55
 Based on the Welcome classification, if the child has Kwashiorkor, Marasmus, or

Marasmic-Kwash
Clinical features
Marasmus
The clinical features of marasmus include marked loss of weight, almost no subcutaneous tissue and
atrophic muscles. The child will have the face of an old man, distended abdomen. The child will usually
have a good appetite
Pathophysiological Changes
Body Composition GIT
- TBW and ECF increased - Villi atrophy
- Increased ICF Na+ - Reduced dissachardase
- Decreased body K+ and - Bacterial overgrwth
Magnesium (Mg+) - Decreased biliary
- Marked loss of fat and muscle secretion
- Pancreatic acinar cells
Liver atrophy
- Fatty liver - Decreased digestive
- Reduction in synthesis of pancreatic enzymes
proteins
- Ability to take up, metabolize, Temperature
and excrete toxins is limited - Heat generation is impaired
- Impaired gluconeogenesis - Sweating is also impaired
Diagnostic and therapeutic Hematology

implication - Anemia is common
- Assesement of dehydration is
difficult. Metabolic
- Need large doses of K+ and - Hypoglycemia
magnesium - Decreased BMR
- Hepatomegaly
- Decrease protein load during CVS
initialphase - Atpophied myocardium
- Reduce drugs dose if - Reduced cardiac output
hepatotoxic or needs hepatic and stroke volume.
disposal. - Blood pressure is low
- Predispose to hypoglycemia. - Start low calorie and
This effect is not severe protein
enough to interfere recovery - Limited digestive and
during diet absorpitive capacity.
56
malabsorption eg lactose - Impaired phagocytic

intolerance and diarrhea. function Low complement
- So feed small and frequent
meals Inflammatory response
- Prone both to hypothermia - Impaired acute phase
and hyperthermia. response
- Keep emperature to normal - WBC do not migrate to area
- Vulnerable to both increase of infection
and decrease blood volume
- Easily develop heart failure. - Susceptible for infection
- Restrict IV fluid, rehydrate - Mild and severe infection
slowly spread
- Give antibiotics
Immunity - Signs of infection are subtle
- All aspects of immunity are - Raised WBC and fever are
impaired except humera l- CMI uncommon
profoundly affected:
- Reduced secretory IGA
57
Kwashiorkor
Kwashiorkor is an acute illness. Bilateral edema is a sine qua non for diagnosis.
Bilateral edema is pitting and starts in the lower legs and later involves the upper limbs
and face. Large ascites is uncommon so consider other causes.
The hair is red or brown, straight, sparse, lusterless, easily and painlessly pluckable.
The face appears moon-shaped and puffy (jowls). The skin is hyperpigmented at first
and become dry and peels off leaving hypopigmented and sometimes ulcerated areas
(flaky paint dermatosis): the skin appears like old paint flaking off the surface of the
wood. The lesions frequently occur on pressure areas like the buttocks, flexure areas,
behind the ears and legs.
Hepatomegaly occurs in one third of patients. They are miserable, disinterested to their
environment when undisturbed and irritable when disturbed.
58
Figure 11: A 5 year old child with kwashiorkor
Notice the edema, hair loss and demtosis over the thigh, shoulder, wrist and scalp, the
wasting of the shoulders and arms and the prominent ribs.
Figure 12: The same child with hyperpigmented and hypopigmented dermatosis over the knee
59
Figure 13: The same child with hyperpigmented and hypopigmented dermatosis over the foot
Note the pitting edema.
Investigations
Investigations for kwashiorkor include:
 Hct, blood glucose, urine analysis, blood and urine culture,
 blood film if febrile,
 Serum albumin or protein if edematous malnutrition is suspected.
Complications
The complications of kwashiorkor include:
Hypoglycemia
 All are at risk and most are asymptomatic.
 An important cause of death in the 1st 2 days of treatment.
 impaired gluconeogenesis may lead to infections
 if the patient is not fed for more than 4-6 hours they may suffer from hypothermia.
 Patients may present with hypothermia, limpness, lethargy or convulsions
 possible do random blood glucose
Hypothermia
Hypothermis is diagnosed by a temperature of less than 35.5 C.
Patients with kwashiorkor are highly susceptible to hypothermia. Mostly this is due to a
low environmental temperature and lack of covers. Kwashiorkor patients are
60
suspectible because they have impaired heat production and loss of subcutaneous
tissue. This may lead to infection and hypoglycemia.
Dehydration
Most of the signs of dehydration in normal children occur in a severly malnourished
child who is not dehydrated. Therefore, recent sunkening of the eyes, eagerness to
drink, pulse volume, blood pressure, urine output and lethargy or coma are used to
assess for dehydration.
Giving fluid for a malnourished child who is not dehydrated leads to congestive heart
failure and death because they are very sensitive for excesses sodium and fluid.
Inappropriate fluid therapy is the commonest cause of death especially after 24 hours of
admission.
If there is recent fluid loss (diarrhea or vomiting) and recent sunkening of the eyes, the
child is dehydrated.
In a child with fluid loss, the diagnosis of severe dehydration or shock (if there are signs
of shock) is made:
 fast and weak pulse,
 cold extremities and
 disturbed consciousness (drowsiness, unconscious)
Septic shock is considered if the above signs of shock are present in the absence of
major fluid loss or if the child with severe dehydration or shock does not respond to the
first 15 ml/kg/hr intravenous fluid.
Infections
Nearly all patients have bacterial infection at admission and they are difficult to
detect.They present with apathy, drowsiness, hypothermia, and hypoglycemia.
Common infections include pneumonia, diarrheal diseases, UTI and sepsis
Etiologies follow those of common pathogens in other normal children and E.coli,
klebsiella, Staph. aureus or epidermidis
61
Congestive heart failure

- Usually occurs after 24 – 48 hrs.
- Causes - commonly as a complication of over hydration
- Severe anemia
- High Na++ content, calorie and protein diet
The earliest sign is tachypnea. Other signs are weight gain, increased liver size,
engorged neck veins, respiratory distress, tachycardia, gallop etc.
Treatment of PEM
All patients with severe PEM (Wt/Ht< 70%, or bilateral edema or MUAC <11cm) should
be admitted to hospital.
The management includes three phases of treatment

Phase I
 Prevent and RX. Complications
 Start to feed
 Give routine medications
 Monitor the patient
Transition phase
 Continue to feed
 Continue the medication started in the phase I
Phase 2
 Feed
 Start to give iron spplements
 provide psychosocial support
 Monitor the response
 Teach the mother about feeding
62
Phase1
Feeding: Feed the patient with F-75 which has 75 kcal/100 ml. It is low in sodium,
protein, energy, and sodium. Give 100 kcal (130 ml)/Kg/day or use the look up table.
Feed 8 times daily using cup and saucer.
Nasogastric tube is indicated in the following cases:

 Pneumonia with rapid breathing
 Painful oral lesions
 Disturbances of consciousness
 The Patient is taking less than 75% of the daily milk
Routine medication
Routine medication includes:
 Vitamin A given on day 1, 2, and 14. For children 6-11 months of age give 100,000
iu and for children of 12 months or older (more than 8 Kg in wieght) give 200,000
iu
 Folic acid given as a 5 mg single dose
 Antibiotics: During the phase I + 4 days the first line antibiotics are amoxicillin or
cotrimoxazole and the second line antibiotics are gentamicin or chloramphenicol
- Treat orally as much as possible.
- If there are no apparent signs of infection and complication, give oral
cotrimoxazole or amoxicillin
- If there are signs of infection or complication, give ampicillin and gentamicin or
penicillin with gentamicin.
 Measles vaccination if the child is older than 6 months and not vaccinated
 Treat for malaria according to the national guideline
Preventing and treating complications

Hypoglycemiacan be prevented by frequent feeding and keeping temperature normal. If
the patients is conscious, give 50 ml 10% sugar water (5 g or one teaspoon of sugar in
100 ml of water) or F-75 by mouth. If they are unconscious or convulsing, 5 ml/kg of
10% glucose IV or give sugar water by nasogastric tube. Start second line antibiotic.
63
Hypothermia): The environmental temperature must be monitored and kept between 8-

32. Do not wash a severely malnourished child. Treatment includes:
 Keeping the patient warm with kangaroo method for young infants.
 Putting a hat on the child and wrapping the mother and child together with double
blanket.
 Feeding frequently
 Treating for hypoglycemia and starting second-line antibiotic
 Taking the patient’s temperature every 30 minutes.
Dehydration
The treatmentfor dehydration is different from normal children. It involves:
 Rehydrating as much as possible orally.
 Infusions are almost never used unless clearly indicated i.e. severe dehydration or
septic shock.
 ReSoMal, rather than standard ORS, is prefered because it has low sodium, and
osmolarity and high potassium.
 Rehydrate slowly over 12 hrs.
 Before treatment take weight, pulse rate, respiratory rate, liver size.
 Feed during rehydration.
 Monitor closely (every 1 hour) for both under and over hydration.
 If the child has recent sunkening eyes or is eager to drink and conscious, give
ReSoMal 5 ml/kg every 30 min. for the first2hrs PO or NGT and then 5 – 10ml/kg/hr
for 10 hrs.
 If the child is unconscious, start I.V. infusion to give:
- Ringer Lactate or half normal saline with 5% D/W, add 20 mmol Kcl/l
- Rate- 15ml/kg over 1 hr and reassess.If improving give 15 ml/kg over the next 1
hr.
 If the child regains consciousness or pulse rate drops, continue the rest of the
dehydration with 10ml/kg/hr of ReSoMal.
 Monitor weight, Pulse rate, Respiratory rate, liver size, and heart sound (gallop
rhythm)
64
Infections
If there are no apparent signs of infection and complication, give PO cotrimoxazole or
Amoxicillin.
If there are signs of infection and complication, give gentamicin or penicillin +

gentamicin I.M. or IV.
Congestive heart failure

Treatment
Treatment involves
 Stopping all PO intakes and intravenous fluids.
 giving small amount of sugar-water
 Furosemide – 1-2 mg/Kg
Anemia
If hemoglobin is less than 4 gm% or hematocrit is less than 12% and it is within 48
hours of admission, transfuse with 10 ml/kg of packed cell volume or whole blood over
3 hours and give furosemide.
If hemoglobin is equal to or less than 4 gm% or hematocrit is equal to or less than 12%
or any level of hematocrit 2-14 days after admission, give iron during phase II.
Monitoring
Take the patient’s temperature twice daily. Measure/observe their weight, edema,
diarrhea, vomiting, signs of dehydration, cough, respiratory rate, pulse rate and liver
size daily.
Transition phase
Progress to transition phase if the edema starts to decrease, the appetite return and
there are no NGT, infusion, and severe medical problems.
65
For marasmic children, if the patient tolerates the diet for 2 days, the appetite returns
and there are no NGT, infusion, and severe medical problems, treat them in the same
way as phase I (routine medication, feed and monitoring) except F-100 is given instead
of F-75.The same volume is given as F-75 so that the energy intake increases by 30%
and the child starts to gain tissue with out causing fluid overload or congestive heart
failure.
Indication for a return to phase I are as follows:

 Increasing edema
 Rate of weight gain >10g/kg/day which is a sign of fluidretention.
 Any sign of fluid overload, heart failure or respiratory distress.
 Tense abdominal distention.
 Development of complications that require intravenousdrugs or rehydration therapy
or poor appetite.
 Refeeding diarrhea that results in weight loss.
Phase 3
The criteria to enter this phase should all be fulfilled:
 Good appetite
 At least 2 days for wasted (marasmic)
 When the edema disappears
 No other medical problems
Feeding
This phase is the period of catch up growth so the patient needs a high calorie and
protein diet.
Feed the patient F-100 five times per day based on the weight, refer the chart for the
amount. Additionally give porridge if the child’s weight is is more than 8 kg.
66
Routine medication
Routine medication includes the following:
 Start ferrous sulfate.
 Treat with mebendazole or albendazole.
 Give the third dose of vitamin A at day 14.
Monitoring
Monitoring involves measuring/observing the following:
 Weight 3 times/week.
 Temperature daily.
 Diarrhea, vomiting, Dehydration, Cough, pulse, and respiratory rate daily.
A good response is indicted by weight gain of more than 10 gm/kg/day.
Return to phase I there is any sign of morbidity.

Discharge criteria
The child may be discharged if he/she fulfills the following criteria.
 Weight /height ≥ 85%.
 No edema for the last 10 days.
 Complications are adequately treated.
 Education completed.
 Immunization up-to-date.
Vitamin A Deficiency (VAD).
Objectives
By the end of this topic the learner is expected toknow:

 The function and main sources of vitamin A.
 The magnitude of VAD in children in Ethiopia.
 The causes and consequences of VAD.
 The eye manifestations and staging of VAD.
 The principle of treatment and the strategies to eliminate VAD.
67
Vitamin A is a fat soluble vitamin which is required by the body in small amounts. It is
essential for the functioning of the immune system and needed for vision and eye
health. It is now also recognized as a critical factor in child health, growth, and survival.
Any intervention that proves effective in improving vitamin A status in deficient
populations will improve markedly childhood mortality and morbidity.
Epidemiology
Vitamin A deficiency is a public health problem in more than 75 countries including
Ethiopia and affects as many as 228 million children subclinically worldwide, at a severe
or moderate level. It is responsible for as many as one out of four (25%) child deaths
globaly. Vitamin A deficiency is the most preventable cause of of corneal ulceration and
blindness in developing countries.
The prevalence of subclinical vitamin A deficiency in children under five years of age in
Ethiopia is 27%. The prevalence of Bitot’s spots, corneal xerosis and ulceration and
corneal scar in the hyper endemic areas of Bale and Arsi are 5.0%, 0.8%, and 0.5%
respectively.
Vitamin A deficiency and risk of childhood mortality and morbidity

Infants and young children who are vitamin A deficient are at increased risk of more
frequent and severe episodes of diarrhea, ARI and measles. Improving vitamin A
status:
 Improves resistance to common childhood infectionsand decreases severity of
infections.
 Reduces child mortality from measles by 50% and mortality from diarrheal disease
by 40%.
The overall mortality in infants and children between the ages of 6 months and 5
years can be reduced by 23%.
Children who are at high risk for vitamin A include:

 Children 6 to 59 months
 Children witth PEM, measles, diarrheal disease, ARI.
68
 Infants less than 6 months old who are not breastfed.
Biochemistry and Physiology of Vitamin A

Sources
The two most important sources of vitamin A are animal foods and breast milk. The
best sources of preformed retinol (active Vitamin A) are liver, fish, eggs and cheese.
Breast milk is an excellent source for infants but the quality dependent on the mother’s
vitamin A status.
Some plants contain beta carotene or provitamin A which can be converted to retinal in
intestinal wall. Red palm is the best plant source. Others are green leafy vegetables
such as spinach and colored vegetables such as carrot, mango and papaya. Cereals
and roots have little or no vitamin A.
Absorption/ storage
The ingested vitamin A is emulsified and absorbed. In the mucosal cells it will be
esterified with palmitic acid and transported by intestinal lymphatics to the liver and
stored as retinyl palmitate. From the liver it is transported in blood bound to Retinal
Binding Protein (RBP) to the eyes/other tissues.
RDA for infants is 375 μg and for children it is 400 -500μg.
Functions
The functions of vitamin A are as follows:
 Maintain a healthy epithelial tissue
 Has a role in keratinization
 Important for the functioning of the immune system.
 Forms visual pigment so important for night vision
69
Causes
The causes of vitamin A deficiency are mainly nutritional and infectious and include:
 Decreased intake due to too little vitamin A in the foods (dietary deficiency) or
anorexia.
 Decreased absorption because of problems such as diarrhea, chronic GIT
disorder.
 Infections such as measles, diarrhea, ARI etc.
Figure 14: infection and Vitamin Adeficiency interaction
Infection
Reduces resistance - Deceased intake

to infection - Reduced absorption
- Increased metabolic
demand
Vitamin A deficiency
When body stores of vitamin A are lost because of the above causes, blood levels fall,
damaging the immune system and later the eyes are affected.
70
Clinical Features
Ocular signs develop insidiously/ bilaterally. The posterior segment is initially affected.
WHO Classification of Xerophthalmia
Primary Signs Secondary signs

X 1A - Conjunctival Xerosis XN- Night blindness
X 1B - Bitot's spot XF- Xerophthalmia fundus
X 2 - Corneal Xerosis Xs- Xerophthalmia scars.
X3A - Corneal ulceration X 3B - Keratomalacia.
Night blindness (XN)

Night blindness is characterized by poor night vision. It is the most early and sensitive
sign of xerophthalmia.
Conjunctival xerosis (X 1A)

Conjunctival xerosis occurs in bulbar conjunctivae and is characterized by dry
conjunctivae which:
 loses it shiny luster and becomes unwetable
 loses its transparency
 wrinkles when the eyes move is fully reversible with treatment.
Bitot’s spot (x1B)

Bitot’s spot is characterized by a foamy /cheese like plaque which is oval /triangular in
shape on bulbar conjunctivae. It usually occurs on the temporal side and is reversible
with treatment
Corneal xerosis (X2)

Is characterized by a hazy, dull and rough corneal surface, which is a highly specific
sign and indicates greatest risk of corneal damage. Early treatment reverse it.
71
Corneal ulceration (X 3A)

The usual site of corneal ulceration is the central or lower part of the cornea. It is not
fully reversible, but vigorous treatment decreases the extensive ulceration.
Keratomalacie (X3B)
Keratomalacie is characterized by very rapid onset. It is the most severe form of
xerophthalmia. Part or whole cornea is destroyed leading to phthisis bulbi or
staphyloma. It is not reversible and results in blindness.
Note: The above stages reveal the earlier the diagnosis the better the reversibilty. So it
is preferable to diagnose at night blindness, conjunctival xerosis, or Bitot’s spot stages.
Dry and scaly skin, retarded mental and physical growth are other manifestation of
vitamin a deficiency.
Diagnosis
Diagnosis is mainly clinical
Treament
Treatment takes two forms:
1. Massive P.O dose of vitamin A
- 100,000 for children from 6mths to 1year old and 200,000 for children of more than
1year of age on the 1st, 2nd and14th day
2. Local treatment for all with corneal ulcers.
- Topical antibiotics
- Eye pad.
Prevention
VAD is considered as a public health problem if the following biological factors are
present in a community survey:
72
Biological indicators WHO cutoff points

Night blindness ≥ 1.0%
Bitot’s spot ≥ 0.5%
Corneal xerosis/ulceration/keratomalacia ≥ 0.01%
Corneal scars ≥ 0.05%
Serum retinol ≥ 10 % (< 0.35μmol/l
Breas milk retinol ≥ 10 %( 8μ/g milk)
There are 4 strategies for the virtual elimination of vitamin A deficiency and to decrease
child morbidity and mortality.
1. Breastfeeding – exclusive breastfeeding for 0-6 months.
 Continued breastfeeding for 2 years.
 Vitamin A supplementation (200,000 or 400,000 iu) to mothers within the first 8
weeks postpartum
2. Supplementation - Massive P.O dose of vitamin A.
 For children 6-59 months: 2 times a year.
 For children 6-59 months with different diseases:
- Pneumonia, persistent diarrhea: one dose.
- Severe PEM, measles: day 1, day 2, and day 14.
The dose in both cases is:
6-12 months – 100,000 iu.
> 12 months – 200.000 iu.
3. Food diversification – access and consume Vitamin A rich foods.
4. Food fortification
73
Vitamin D Deficiency (Rickets)
Objective
By the end of this topic, the learner will be able to describe:
 The function, main sources and metabolism of vitamin D.
 The causes and consequences of vitamin D Deficiency.
 The clinical manifestations and complication of vitamin D deficiency.
 The principle of treatment and prevention.
Definition
Rickets is the failure of calcification of bone matrix of growing bones.
Osteomalacia is failure of calcification of bone matrix of mature bonea.
Sources of vitamin D
Vitamin D is a fat soluble vitamin and its two main sources are:
1. Dietary: vitamin D2 (ergocalciferol) or vitamin D3 (cholecalciferol):
 Fish liver oil -very rich, others are eggs, milk etc.
 The recommended daily allowance (RDA) is 10μg or 400 I.U. daily.
2. Vitamin D3 is present in the skin as 7 dehydrocholesterol that will be converted to
1,25 dehydrocholecalciferol by the action of sunlight and by undergoing
hydroxylation the liver and kidney.
Function of 1,25 (OH)2 D3 ( 1,25 dihydrocholecalciferol )
Dihydrocholecalciferol functions as a hormone. It:

 Facilitates calcification of bone by increasing Intestinal ca+ & phosphrus (P+)
absorption and reabsorption of p+ in kidney
 Controls serum ca+ & p+ with parathahormone (PTH) and calcitonin.
Causes of Vitamin D Deficiency

Causes of Vitamin D Deficiency include:
 Inadequate exposure to sunlight – the commonest cause in Ethiopia.
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 Inadequate dietary intake

 Others: - Chronic GIT disorders which leads to malabsorption.
- Liver and renal disorders
- Anticonvulsants (phenytoin, phenobarbitone)
- Heriditary (e.g. familial hypophosphatemia)
Children at high risk for rickets include:
 Low birth weight, preterms, twins.
 Breast fed and inadequately exposed to sunlight.
 Infants born from mothers with osteomalacia.
The Effects of Vitamin D Deficiency (Pathology)

Effects on the bone
Deposition of excessive uncalcified osteoid tissue at the metaphysis (rachitic
metaphysis) results in irregular and frayed metaphysis. When the uncalcified osteoid
tissue is compressed, it results in rachitic rosary and enlargment of ends of long bones
(wrist or ankle widening).
Subperiosteal bone demineralization as resorption leads to a thin and less rigid cortex
which results in long bone deformity (bow legs etc) and pathological fracture.
Chemical Changes
The chemical changes in rickets are normal or low serum Ca+, Low serum Phosphorus,
and increased Alkaline phosphatase.
Clinical features
The peak age is 6 months to 2 years.
Early signs.
The early signs of vitamin D deficiency include:
 Craniotabes - ping pong feeling on pressing the skull.
 Rachitic rosary- palpable enlargment of costochondral junction.
 Enlarged ends of long bones of arm and legs (wide wrist, double aleoli)
75
Late/Advanced signs
The late/advanced signs signs of vitamin D deficiency include:
 Frontal bossing, pigeon chest, bow legs/knocked knees, hypotonia, caput
quadratum (box like head), Harrison’s groove, fractures, etc.
 Wide fontanel /delayed closure and delayed teeth eruption.
Diagnosis
Diagnosis is mainly clinical and involves:
 Wrist X-ray – shows decreased bone density and irregular and cuped ends of
bones.
 Normal/low serum ca ++, low phosphorus,elevated alkaline phosphatase
Complications
Complications include the following:
- Pneumonia - Atelectasis
- Hypocalcmic tetany - Corpulmonale
- Pathologic fracture
Treatment
There are two forms of treatment:
 Vitamin D3 (cholecalciferol) is the best treatment
Dose - 600,000, i.m stat.
Heeling occurs after 2-4 wks which can be proved with a wrist X-ray.
 Sunlight exposue is useful if no vitamin D3 is available.
Further Reading
Stanfield, P., Brueton, M. et al. Disease of Children tn the Tropics and Subtropics.
1991.
Golden, M. Management of Severe Malnutrition. 2001.
WHO,UNICEF. Nutrition Essentials, a Guide for Health Managers. 1999.
76
Linkages. Facts for Feeding: Guideline for appropriate complementary feeding of

breastfed children 6-24 months of age. Oct, 2001.
Linkages. Facts for Feeding: Recommended practices to improve infant nutrition during
the first 6 months. Sept, 2001.
Linkages. Breastfeeding and HIV/AIDS..May, 2001.
Linkages, AED. Guidelines for Infant Feeding in Communities Affected by HIV.
WHO Division of Child Health and Development. HIV and Infant Feeding: A guide for
health care managers and supervisors. 2001
Behrman, Kliegman, Jenson. Text Book of Pediatrics; 2000.
Belachew, T. Human Nutrition for Health Sciences Students, Lecture Note Series.
Addis Ababa: Carter Center. 2003. .
Ministry of Health. Managment of Childhood Illness (IMCI), chart booklet.
Cogill, B. Anthropometric Indicators Measurments Guide. Food and Nutrition Technical

Assistance. June, 2001.
77
CHAPTER TWO
NEONATOLOGY
Solomon Amsalu
2.1 PHYSICAL EXAMINATION OF THE NEWBORN
Objectives:
By the end of this section, readers will be able to
 Discuss steps in examining the newborn
 Identify life-threatening conditions in the newborn
 Identify common malformations that occur in the new born
 Estimate postnatal gestational age of a new born
The initial examination of a newborn infant should be performed as soon as possible

after delivery to detect abnormalities.
Table 12: Neonatal growth and normal birth measurements

Neonatal growth parameters Normal birth measurments
weight 2500gm – 4000gm
Height
Head circumference
Pulse (normal 120-160 beats/min), respiratory rate (normal 30-60 breaths/min),

temperature (normal 36.5 37.50C), weight, length and head circumference should be
recorded.
General appearance
 Observing the infant is the most important aspect of physical examination.
 The state of alertness, the muscle tone, the activity, obvious anomalies or injuries,
respiration, and the skin are assessed during inspection.
 The muscle tone should be sufficient for the hips, knees, and elbows to be flexed
while the infant is lying supine.
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 Some spontaneous movement should be evident, and the well infant should appear
alert at some point during the examination.
Skin
Vernix usually covers the skin, especially in the skin folds of the axillae, neck and groin
at birth. Post term infants characteristically have little vernix, and the skin is dry,
crackled and wrinkled.
Generalized cyanosis may indicate significant heart or lung disease. Pallor may
represent severe asphyxia (asphyxia pallida) or anemia. Erythema toxicum, which is a
benign small, white occasionally vesiculopustular papules on an erythematous base
appear 1 to 3 days after birth. It may persist for as long as one week.
Head
 The commonest abnormalities are caput succedaneum and cephalhematoma.
 Caput succedaneum is edema of the scalp skin and crosses suture lines.
 Subgaleal hemorrhage is bleeding below the aponeurosis, It is a boggy swelling
that crosses suture lines.
 Cephalhematoma is a subperiosteal hemorrhage and does not cross suture line.
 Macrocephally, microcephaly, hydrocephalus.
 Craniosynostosis is the premature fusion of sutures. There is a hard non-movable
ridge over the suture and an abnormally shaped skull.
 Craniotabes (softening of the skull) are occasionally found in the parietal bones at
the vertex near the sagittal suture. It is commonly a normal variant.
Eyes
 Conjunctival and retinal hemorrhages are usually benign.
 The cornea should be clear.
 The presence of bilateral red reflexes suggests the absence of cataract or of
intraocular pathology/.
 Leukokoria (white papillary reflex) suggest cataract, tumor or chorioretinitis.
79
Nose
 The naris should be symmetric and patent. Newborn infants breathe preferentially
through the nose so that bilateral choanal atresia may cause severe respiratory
distress.
 Passing a catheter through each naris to the stomach excludes the diagnosis of
choanal atresia.
Mouth
 The soft and hard palate should be inspected for cleft lip or cleft palate.
 Natal teeth occur rarely and are usually shed in a few days.
 On the hard palate on either side of the raphe may be temporary accumulations of
epithelial cells called Epstein pearls.
Neck
 The neck of newborn always seems short. Very short and webbed neck may be
associated with Turner syndrome.
 A thyroglossal duct cyst is usually palpable in the midline and retracts with tongue
protrusion.
 The infant may have congenital torticollis with or without a fibrous mass in the
sternocleidomastoid muscle, associated with head tilt.
 A cystic hygroma is a spongy mass that may increase with increased intrathoracic
pressure.
 Hemangiomas are similar to hygromas upon palpation but are frequently
associated with skin discoloration.
 Thyroid masses are usually visible and easily palpable with the head extended.
Chest and Lungs

 The appearance of flaring, grunting, tachypnea or retractions (lower chest
indrawing intercostal retractions) is called respiratory distress
 Look for chest deformity. Breast hyperthrophy, under maternal hormonal influence,
is common. Milk may be present for a few days or weeks.
 A respiratory rate consistently over 60/min during periods of regular breathing
usually indicates pulmonary, cardiac or metabolic disease.
 Look for apnea whicsh is cessation of breathing for more than 15 seconds.
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Heart
 The pulse rate may vary from 90/min in relaxed sleep to 180/min during activity.
 Radial, brachial and femoral pulses should be palpated and compared. Poor or
diminished quality of pulses is an indication of inadequate cardiac output.
 Heart murmurs may be transient or may indicate significant heart disease.
Abdomen
 The liver is usually palpable and less commonly the tip of the spleen may be felt.
 The abdomen should be palpated for masses. Renal pathology is a usual cause of
neonatal abdominal mass.
 Abdominal distention may be due to intestinal obstruction.
 A scaphoid abdomen in a newborn suggests diaphragmatic hernia
 The umbilical vessels should be inspected to exclude the presence of single
umbilical artery. Approximately 10-15% of infants with a single umbilical artery
have other major congenital malformations.
Genitalia
 Males should be checked for hypospadias, to determine the location of the testes
and to exclude inguinal hernias or hydrocele.
 Non purulent vaginal discharge may be present in females secondary to
transplacentally passed maternal hormones.
 A large penis or clitoris should raise the question of adrenogenital syndrome.
Anus
 Some passage of meconium usually occurs within the first twelve hour after birth.
Imperforate anus should be excluded by gentle insertion of the little finger.
Musculoskeletal system
 The hips should be examined to rule out congenital dislocation
 Barlow Test should be undertaken: as the knees are brought together (adducted)
the examiner pushes laterally on the upper inner thigh. A click or clunk indicates
that the femoral head slips over the lateral ridge of the acetabulum.
 Ortolani test should be undertaken: the thigh is flexed and abducted, and the
femoral head is lifted in to the acetabulum. If reduction is possible, the relocation
will be felt as a clunk.
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 The feet should be checked for the presence of clubfoot.
Neurologic system
Examination should include:
 Level of consciousness
 The cry (high piched or inconsolable)
 Posture of the newborn
 Muscle tone
 Spontaneous motor activity
 Neonatal (primitive) reflexes
Neonatal reflexes
Testing the neonatal reflexes allows an assessment of CNS integrity in the newborn.
They are primitive reflexes that should disappear as the baby’s CNS develops and
matures .Asymmetry, absence or persistence beyond a given time frame signifies
dysfunction of the CNS or CNS immaturity (prematurity).
Sucking reflex
When an object is placed in the infant’s mouth or touches the lips,a sucking reflex is
elicited. This reflex disapears by 12 months of age.
Rooting reflex
Stimulating one corner of the mouth or the lower lip causes the infant to turn towards
the touch and open his/her mouth. This reflex disapears by 4 to 7 months of age.
Moro reflex
The infant is placed in a semi-upright position. The head is momentarily allowed to fall
back wards, with immediate resupport by the examiners hand. A complete response
consists of abduction of the upper limbs at the shoulder, extension of the forearms at
the elbow and extension of the fingers followed by adduction and flexion. This reflex
disapears by 4 to 6 months of age.
Absent or weak moro response indicate serious CNS disturbance.
Asymmetries occur with Erb palsy and clavicular fractures.
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Plamar grasp reflex

The plamar grasp reflex is elicited by placing a finger in the open palm of each hand;
normal infants grasp and hold the object. This reflex diminishes by 3 to 4 months of
age.
Estimation of post natal gestational age

The Ballard scoring system for the estimation of post natal gestational age uses 6
neurologic and 6 physical criteria:
 Neurologic criteria include posture, square window (wrist), arm recoil, popliteal
angle, scarf sign and heel to ear test.
 Physical criteria includes assessment of the skin, lanugo hair, plantar creases,
breast, ear and genitalia
 Assessment of gestational age using physical and neurologic criteria is accurate
only + 2 weeks.
 If the discripancy of gestational age by LMP and post natal asssessment is less
thanor equal to 2 weeks, take the gestational age obtained by LMP.If it is greater
than 2 weeks, take the gestational age determined by post natal assessment.
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Physical Score Record
Maturity 0 1 2 3 4 5 score
sign here
Skin Gelatinous, Smooth, pink, Superficial Cracking, Parchment, Leather
Red, visible veins peeling and/or pale areas, deep cracking, y,
translucent rash, few veins rare veins no vessels cracked,
wrinkled
Lanugo None Abundant Thinning Bald areas Mostly bald
Plantar No Crease Faint red Anterior Creases on Creases over
Creases markds transverse ant. 2/3 entire sole
crease only
Breast Barely Flat areolano Stripped areola, Raised Full areola, 5-
perceptible bud 1-2 mm bud areola, 3-4 10 mm bud
mm bud
Eye/ear Pinna flat, Slightly Well-curved Formed & Thick cartilage,
stays folded curved pinna; pinna, soft but firm. Instant ear stiff
soft; slow ready recoil recoil
recoil
Genitals Scrotum Testes Testes Testes
male empty, no descending, few down, good pendulous,
rugae rugae rugae deep rugae
Genitals Prominent Majora & Majora Cilloris and
female clitoris and minora equally large, minora
labia minora prominent minora completely
small covered
Total Physical
Maturity score
Physical criteria for maturity rating, Ballard scoring.
Neuromuscular Maturity (Ballard). (From Ballard J et.al: J pediatr 95:769, 1979.)
Maturity rating
Score Weeks
-10 20
-5 22
0 24
5 26
10 28
15 30
20 32
25 34
30 36
35 38
40 40
45 42
50 44
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Maturity rating as calculated by adding the physical and neurological score, thus
calculating the gestational age (Ballard scoring)
Classification of the newborn

Classifying neonates based on their weight and gestational age is important beacause
newborns, in the different classifications, differ in the cause, expected complications
and prognosis.
Newborns are classified based on gestational age and birth weight.

Based on gestational age they are classified as:
Term – if the baby is born after 37 and before 42 completed weeks.
Post term – if the baby is born after 42 completed weeks.
Preterm - if the baby is born before 37 completed weeks.
Based on birth weight, babies are classified as:
Normal weight – if the birth weight is between 2500gm and 4000gm.
Low birth weight (LBW) – if the weight is between 2500gm and 1500gm.
Very Low birth weight (VLBW) – An infant with a birth weight of less than 1500gm.
LBW and VLBW includes preterm and small for gestational age.
Finally, newborns are classified by comparing the birth weight and gestational age
using the weight for gestational age graph.
A newborn is classified as:
Appropriate for gestational age (AGA) if the birth weight lies between 10%- 90% for the
specified gestational age.
Large for gestational age (LGA) if the weight lies above 90% for the specified
gestational age, the newborn has a high weight for gestational age.
86
Small for gestational age (SGA) if the weight lies below 90% for the specified
gestational age, the infant has a low weight for gestational age. Intaintrutrine growth is
retarded
LGA
LGA
4000gm
LGA
AGA
Birth weight
AGA
AGA
2500gm SGA
SGA
SGA
Preterm 37 Term 42 Postterm
Figure 15: Chart showing weight for gestational age
Exercise
1. What is the aim of examining newborn?
2. How do you assess gestational age of a newborn baby?
2.2 RESUSCITATION OF THE NEWBORN

Objectives
By the end of this section the reader should be able to:
 Identify newborn babies needing resuscitation
 Know the steps of neonatal resuscitation
Goals of neonatal resuscitation include:

 Prevention of morbidity and mortality associated with hypoxic - ischemic tissue
(brain, heart, kidney) injury
 Establishment of adequate spontaneous respiration and cardiac output.
 Prevention of heat loss (hypothermia).
87
The Apgar score is a practical method of systematically assessing the newborn infant
immediately after birth to help identify infants requiring resuscitation for hypoxic
acidosis.
Assessment is carried out in the first minute and resuscitation measures are made (if
necessary) to improve the score at 5 minutes.
88
Table 14: The Apgar Score

___________________________________________________________
Sign 0 1 2____
Heart rate absent <100/min. >100/min.
Resp. rate absent slow, irregular good, crying
Muscle tone limp some flexion active motion

of extremities
Response to no grimace cough or

nasal catheter response sneeze
Color blue, pale body pink completely

extremities blue pink__
A score of 0-3  endotrachial intubation (if no skilled health worker bag and mask
assistance is usually adequate)
A score of 4-6  bag and mask assistance
A score of 7-10  minimal interference
Infants who are born limp, cyanotic, apneic or pulseless require immediate resuscitation
prior to the assessment of 1-minute Apgar score. Waiting until a one minute Apgar
score is assigned before initiating resuscitation only increases the chance of permanent
damage in a severely asphyxiated infant.
The elements of resuscitation include the following:

1. Initial steps: thermal management, clearing the airway, tactile stimulation
2. Establishment of ventilation
3. Chest compression
4. Medication
89
Initial steps
Immediately after birth the neonate should:
 be placed under a radiant heater, dried, positioned down and slightly extended,
 the airway cleared by suctioning and
 gentle tactile stimulation provided
If after suctioning and tactile stimulation there is no respiration or the heart rate is less
than 100/min, positive pressure ventilation (PPV) with 100% oxygen must be initiated.
Positive pressure ventilation

 Usually can be provided quickly by bag and mask.
 Endotrachial intubation should be performed in any infant who does not respond to
initial bag and mask ventilation or who was born apneic, pulseless, cyanotic, and
limp with signs of fetal distress.
 In the vast majority of cases ventilation alone will be sufficient to resuscitate the
infant.
 If after 30 seconds of positive pressure ventilation (PPV) with 100% oxygen the
heart rate remains low, chest compression may be needed to assist a hypoxic and
a failing myocardium.
Chest compression
Chest compression is recommended if:
 after ventilation with 100% oxygen for 15 - 30 seconds the heart rate is below 60
or
 between 60 and 80 and not rising.
The chest should be compressed between 100-120 times per minute with ventilation
occurring 40 to 60 times per minute.
If chest compressions and ventilation do not raise the heart rate above 80 within 30
seconds, support for the cardiovascular system with medications is needed.
90
Medications
Epinephrine, 1:10,000 (0.1- 0.3 ml/kg) intratracheal or intravenous, should be the first
drug to be given. The dose may be repeated every 5 minutes. Epinephrine stimulates
the heart and increases non-cerebral peripheral vascular resistance.
10 to 20 ml/kg of volume expanders (normal saline, ringers lactate or blood) should be

given for hypovolemia, history of blood loss, hypotension or poor response to
resuscitation.
Sodium bicarbonate (1-2 meq/kg) should be given slowly (1 meq/kg/min) if there is a

documented metabolic acidosis or if there is no adequate response to proper
ventilation.
Dopamine and dobutamine (5-20 g/kg/min) and volume expanders should be started
after the initial resuscitation effort to improve cardiac output in an infant with poor
peripheral perfusion, weak pulses, hypotension, tachycardia and poor urine output.
If resuscitative efforts do not result in spontaneous respiration within 30 minutes the

prognosis is uniformly bad with respect to gross neurologic impairment. It is therefore
entirely appropriate to discontinue active resuscitative efforts after 30 minutes if no
spontaneous respiration has been observed, provided that the baby has been given
intermittent opportunities to demonstrate spontaneous breathing.
EXERCISE
1. First minute evaluation of a newborn showed that he is bradycardic, has slow and
irregular breathing, limp, no response to nasal catheter and is cyanosed. What is the
Apgar score? How would you resuscitate this newborn?
2.3. Preterm, Low Birth Weight and Small for Gestational Age Infants
Objectives
At the end of this topic, the student will be able to:
 Describe problems of a preterm newborn
 Discuss the care of a preterm newborn
 Discuss discharge criteria for a preterm newborn from a hospital
91
In developing countries 20% and more of newborns are low birth weight.
Causes of preterm birth

Causes of preterm birth include the following:
Fetal - Fetal distress
- Multiple gestation
- Erythroblastosis
Placental - Placenta previa
- Abruptio placentae
Maternal - Preeclampsia
- Chronic medical illness
- Infections
Other - Premature rupture of membranes
- Polyhydramnios
- Iatrogenic
Main problems of preterm newborns

The problems of preterm newborn babies include:
- Hyaline membrane disease - Hypothermia
- Hemorrhagic disease of the newborn - Apnea
- Hyperbilirubinemia - Hypocalcemia
- Bacterial sepsis - Hypoglycemia
- Necrotizing enterocolitis - PDA
- Intraventricular hemorrhage - Anemia
- Asphyxia
In addition preterm infants frequently have

 Weak and uncoordinated ability to feed
 Prolonged failure to gain weight and
 Late metabolic acidosis
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Main causes of death in low birth weight infants

The main causes of death in low birth weight infants are:
 Hyaline membrane disease
 Intraventricular hemorrhage
 Septicemia
 Asphyxia
Problems of SGA or IUGR infants

The problems of SGA or IUGR infants include:
 Perinatal asphyxia
 Hypoglycemia
 Hypothermia
 Meconium aspiration
 Necrotizing enterocolitis
 Polycythemia
Nursery care
At birth the measures needed for clearing the airway, initiating breathing, care of the
cord and the eyes and administering vitamin K are the same in immature infants as in
those of normal weight and maturity.
Additional considerations
There is a need to
 monitor temperature, and respiration
 for increased oxygen
 pay special attention to the details of feeding
Thermal management
The preterm newborn encounters the problem of severe heat loss for several reasons:
 the baby’s large body surface area relative to body mass
 the tiny baby's small size presents a much smaller heat sink to store thermal
reserve
93
 minimal shivering during exposure to cold and

 poor reserve of brown fat
Heat loss can be minimized by keeping infants in a thermoneutral environment. This

could be achieved by using radiant warmers, blankets, heating lamps and by controlling
the temperature and humidity of the room.
Kangaroo mother care is one method of keeping the baby warm. It involves placing the
LBW/VLBW infants between the mother’s breasts, covered and held in a prone or
vertical position by the woman’s clothes.its advantages are:
 It provides a physiological thermoneutral environment and protect the newborn
from hypothermia,
 It encorages early contact between mother and newborn and early breast
feeding and
 It prevents apnea because the mother breathing movement stimulates the baby
Supplementation with oxygen

Administering oxygen is indicated in newborns with respiratory distress or recurrent
apnea.
Initiation of Feeding
The main principle in feeding premature infants is to proceed cautiously and gradually.
Weight less than 1500 g

Infants weighing less than 1500 g and GA less than 34 weeks require tube feeding
because they are unable to coordinate breathing, sucking and swallowing.
Intestinal tract readiness for feeding may be determined by:-

 active bowel sounds
 passage of meconium
 absence of abdominal distention and
 no bilious aspirate or emesis
For these infants feed breast milk every 2-3 hrs. If breast milk is not possible, give
preterm formula.
94
Weight more than 1500 g

Start breast milk within one hour of birth and feed at least 8 times per day.
Weight gain may not be achieved for 10-12 days because of the physiologic loss of
weight for the first 10 -12 days.
Fluid requirements
Fluid therapy is indicated for preterm newborns as follows:
 Day 1: 70 -100 ml/kg/d
 After day 2: 150 ml/kg/d
 Type of fluid: day 1 - 10 % dextrose, thereafter, normal saline in 10 % dextrose.
This higher fluid requirements in preterms in due to high insensible water loss and they
are less able to concentrate urine; thus, their fluid intake required to excrete solutes
increases.
Discharge from Hospital

Prerequisites for discharge from a hospital include that the baby:
 is able to breast feed
 has sustained steady increments in weight of approximately 10-30 g in 24 hours
 stabilization of body temperature
 resolution of acute life-threatening illnesses
The required weight for discharge is 1500 grams
Exercise
1. What are the main problems of a preterm newborn?
2. What nursery care does a preterm newborn require?
3. Describe fluid management in a preterm newborn
95
2.4. Respiratory distress in the newborn
Objectives
By the end of this section the reader will be able to:
 Discuss main causes of respiratory distress in the newborn
 Know their clinical manifestation and management
Hyaline Membrane Disease

Hyaline membrane disease (HMD) is one of the most important causes of mortality and
morbidity in preterm neonates.
An increased frequency is associated with infants of diabetic mothers, delivery by

cesarean section, multiple pregnancies, precipitous delivery, asphyxia, cold stress and
a prior history of affected infants.
Etiology
Surfactant deficiency is the primary causes of HMD. The failure to develop a functional
residual capacity and the tendency of affected lungs to become atelectatic correlate
with high surface tensions and absence of pulmonary surfactant.
Clinical features
 Signs of HMD usually appear with in minutes of birth, although they may not be
recognized for several hours in larger premature infants.
 The late onset of tachypnea should suggest other conditions.
 Characteristically, tachypnea, nasal flaring, subcostal and intercostal retractions,
cyanosis and expiratory grunting are noted.
 Decreased bilateral air entry may be noted on auscultation.
 The natural course is characterized by progressive worsening of cyanosis and
dyspnea. In most cases, the symptoms and signs may reach a peak within 3 days,
after which improvement is gradual.
Investigation
96
CXR - The typical roentgenographic features consist of a diffuse reticulogranular

pattern in both lung fields with superimposed air bronchograms.
Treatment
Thermoregulation
Infants with respiratory difficulty require an optimum thermal environment to minimize
oxygen consumption and oxygen requirements. Body temperature should be
maintained between 36.5 and 370C.
Fluid
Maintenance of fluid requirements usually begin at 60 to 80 ml/kg/days as a 10 %
dextrose solution and increases gradually to 150 ml/kg/day by the fifth day of life.
Antibiotics
The potentially fulminant course of congenital pneumonia and the difficulty in
distinguishing it from HMD have led to the recommendation that all infants with
significant respiratory distress receive antibiotic after appropriate cultures.
A penicillin combined with an aminoglycoside is the antibiotic regimen of choice.
Ventilatory support
Warm humidified oxygen should be provided to keep arterial levels between 55 and 70
mmHg.
Infants with severe HMD or those who develop complications resulting in persistent
apnea require assisted mechanical ventilation.
Surfactant therapy
Multi-dose endotracheal instillation of exogenous surfactant for the treatment of HMD
has dramatically improved survival and reduced the incidence of pulmonary air leaks.
Prevention
97
 Most important is the prevention of prematurity

 Administration of dexamethasone to women 48 hours before delivery of fetuses less
than 34 weeks of gestation significantly reduces the incidence and the mortality and
morbidity of HMD.
Meconium Aspiration Syndrome

Definition
Meconium staining of the amniotic fluid is usually considered to be indicator of fetal
distress.
The passage of meconium in utero accompanies 8 to 20% of all deliveries and is seen
predominantly in small for gestational age and post mature infants. Five percent of such
infants develop meconium aspiration pneumonia.
Clinical features
The infant frequently exhibits the classic signs of post maturity with evidence of weight
loss together with nails, skin and umbilical cord that are heavily stained with a yellowish
pigment.
The infants are often depressed at birth secondary to the hypoxic insult precipitating the
passage of meconium.
Respiratory distress with cyanosis, grunting, flaring, retractions and marked tachypnea
soon ensues.
Characteristically the chest acquires an over inflated appearance, and rales may be
audible on auscu
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Figure 16: Pathophysiology of meconium aspiration syndrome

Intrauterine asphyxia
Meconium aspiration
Mechanical obstruction Chemical inflammation
Air trapping Atelectasis
Uneven Intrapulmonary
ventilation shunting
Air leaks Hypoxemia Persistent

Acidosis fetal circulation
Investigation
Chet X-ray is indicated by coarse, irregular pulmonary densities, increased anterior
posterior diameter and flattening of the diaphragm.
Treatment
Depressed infant should undergo endotracheal intubation and suction should be applied
directly to the endotracheal tube to remove meconium from the airway.
Treatment includes supportive care and standard management for respiratory distress.
Supportive management may include the use of antibiotics, because bacterial sepsis
may have precipitated the passage and subsequent aspiration of meconium and
bacterial pneumonia may be indistinguishable roentgenographically from meconium
aspiration syndrome. Further, meconium enhances bacterial growth in vitro.
A vigorous infant with lightly stained amniotic fluid may not require treatment.
Prevention
The risk of meconium aspiration syndrome can be decreased by:
 Paying careful attention to fetal distress and initiating prompt delivery in the
presence of fetal distress.
 Careful, thorough suctioning of the oropharynx after the head in delivered.
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 Suctioning via endotracheal tube is indicated for depressed infants before initiation
of positive pressure ventilation.
Pneumonia
Pneumonia could be acquired in the following ways:
Transplacentally
 Cytomegalovirus, rubella, toxoplasma gondii, listeria or treponema pallidum
Natally
 By aspiration of infected amniotic fluid or birth canal secretions.
 Onset occurs during the first few days of life.
 Commonly associated with group B streptococci, gram negative enteric bacilli,
chlamydia and herpes simplex virus.
Postnatally
 It may be caused by a nosocomial or community acquired infection.
 Etiologies: Staphylococcus aureus, Pseudomonas aeruginosa, Klebsiella, Serratia,
B. pertussis and respiratory viruses.
Congenital pneumonia
 Is pneumonia acquired transplacentally or perinatally.
 Frequently associated with premature rapture of membranes (PROM),
chorioamnionitis, labor, premature labor or fetal distress.
Clinical features
The clinical geatures include respiratory distress, poor feeding, lethargy, irritability and a
rise or a drop in temperature.
Chest X-Ray may be typical for bronchopneumonia or show diffuse atelectasis.
Treatment
Teatement is with parenteral ampicillin or penicillin and gentamycin for 7 to 10 days.
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Supportive treatment includes giving intravenous fluids and oxygen and keeping a
thermo neutal environment.
EXERCISE
1. What is the cause of hyaline membrane disease?
2. What are the manifestations of meconium aspiration syndrome?
3. How do you manage a newborn with congenital pneumonia?
2.5. Neonatal Jaundice and Hyperbilirubinemia
Objectives:
 Discuss the etiology of jaundice in the newborn
 Identify physiologic and pathologic jaundice
 Discuss manifestations of kernicterus and management of hyperbilirubinemia
Introduction
Hyperbilirubinemia is a common and in most cases a benign problem in neonates.
The most common type is unconjugated (indirect reacting) hyperbilirubinemia. It is the

type of pigment found in physiologic jaundice and in pathologic states in which there is
increased production, decreased hepatic conjugation, or decreased hepatic uptake of
bilirubin.
Conjugated hyperbilirubinemia (direct reacting) is far less common in neonates and most
often denotes potentially serious disorder. However, it is not neurotoxic.
The unconjugated form is neurotoxic.
Definition
Neonatal jaundice - it is visible jaundice due to elevated serum level of bilirubin.
Hyperbilirubinemia - It is a markedly elevated serum bilirubin usually >15 mg/dl which
predispose neonates to kernicterus.
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Causes
Causes of unconjugated hyperbilirubinemia include:
 Increased load of bilirubin eg. hemolytic anemia following Rh or ABO incompatibility
disease, polycythemia, subgaleal hemorrhage.
 Damage or reduction of the activity of transferase enzyme (genetic deficiency ,
hypoxia, prematurity, and infection)
 Blockage of the transferase enzyme (drugs)
 Absence or decreased amount of the enzyme (genetic defect, prematurity)
Causes of conjugated hyperbilirubinemia include:

 Sepsis
 Intrauterine infection
 Biliary atresia
 Hepatitis
Clinical Manifestations
 Jaundice may be present at birth or may appear anytime in the neonatal period.
 Jaundice usually begins on the face, and as the serum level increases, progresses to
the abdomen and then the feet.
 Affected infants may appear lethargic or may feed poorly.
Physiologic Jaundice
 Physiologic jaundice is the result of increased bilirubin production following
breakdown of fetal red blood cells combined with transient limitation in conjugation of
bilirubin by the liver.
 Jaundice becomes visible on the second or third day, usually peaking between the
second and fourth days at 5 to 6 mg/dl, and decreasing between the fifth and seventh
day of life.
Pathological Jaundice should be considered if:-

 It appears in the 1st 24 hours of life
 Serum bilirubin is rising at rate greater than 5 mg/dl/24 hr.
 Serum bilirubin is greater than 12 mg/dl in full term or 14 mg/dl preterm infants
 Jaundice persists after 10-14 days of life or
 Direct reacting bilirubin is greater than 2 mg/dl
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Investigation
Investigation involves testing for blood group, Rh,Hct, reticulocyte count, peripheral
morphology, billirubin (total and direct) and coomb’s test.
Kernicterus
Defintion
Kernicterus is a neurologic syndrome resulting from the deposition of unconjugated
bilirubin in the brain cells.
The risk of kernicterus increases with a rise in serum unconjugated bilirubin. Preterms
and newborns with infections (sepsis, meningitis) have a greater susceptibility to
kernicterus.
Clinical manifestation
Signs and symptoms usually appear 2 to 5 days after birth in term infants and as late as
seventh day in preterm infants.
Common initial manifestations include lethargy, poor feeding and loss of moro reflex.
Subsequently, the infant appears gravely ill with diminished deep tendon reflexes and
respiratory distress.
It is manifested by opisthotonus, bulging fontanel, a high pitched cry and convulsions

occur in advanced cases. Many infants who progress to these severe neurologic signs
die.
Treatment
The goal of therapy is to avoid kernicterus. The principles of treatment are:
 Phototherapy
 Exchange transfusion
 Treatment of underlying disease.
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Exercise
1 What is the difference between physiologic and pathologic jaundice?
2 What are the causes of pathologic jaundice?
2.6 Neonatal Sepsis and Meningitis
Objectives
 Know the etiologies of sepsis and meningitis in newborns
 Discuss the clinical manifestations
 Describe the management of sepsis and meningitis
Neonatal Sepsis
Definitions
Bacteremia is bacteria in the blood.
Septicemia is caused by bacteremia and is a constellation of signs and symptoms

caused by microorganisms or their toxic products in the circulation.
Neonatal sepsis (sepsis neonatorum) is a clinical syndrome resulting from the

pathophysiologic effects of local or systemic infection in the first month of life.
Epidemiology
Predisposing factors for neonatal sepsis:
 Presence of maternal (obstetric) risk factors such as:
- prolonged rapture of membranes (more than 18 hrs)
- maternal chorioamnionitis (maternal intrapartum fever, maternal leukocytosis,
uterine tenderness, fetal tachycardia)
- Prolonged labor that lastes for moe than 24 hours
- Repeated vaginal examination
 Fetal risk factors include:
- prematurity, LBW
- asphyxia
- developmental or congenital immune defects
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- congenital anomalies
Etiology
Group B streptococci and escherichia coli are the leading causes of early and late onset
neonatal sepsis. Other causes include listeria monocytogenes, klebsiella and
enterococci.
Nosocomial infections are often related to the use of procedures, intravenous lines and
other risk factors. They are most often due to coagulase negative staphylococci,
staphylococcus aureus and gram-negative enteric organisms.
Early onset sepsis presents at birth, or within the first 7 days of life, usually within the
first 3 days and is associated with obstetric risk factors.
Late onset sepsis: the onset is from 8 - 28 days of life and may extend to 60 days.
 Obstetric risk factors are unusual.
 Frequently associated with meningitis.
Clinical features
The initial signs of infection are often subtle or minimal.
There may be temperature instability (hypo or hyperthermia), poor sucking, depressed
reflexes, irritability, lethargy and/or convulsion.
Late manifestations include apnea, cyanosis, hypotension, sclerema, and DIC.
The clinical signs of infection in the newborn are often nonspecific, vary greatly in
intensity and severity and are seen in many non-infectious disorders as well.
Investigations
Evaluation includes blood culture, lumbar puncture (not indcated for those less than 12
hours), urinalysis and urine culture and total WBC count and differential
Immature neutrophil to total neutrophil ratio (more than 0.16) suggests bacterial
infection)
Chest x-ray is indicted for those with respiratory problems
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Treatment
 Initial empiric therapy of early and late onset community acquired infections should
consist of parenteral ampicillin or penicillin and an aminoglycoside (usually
gentamycin).
 In nosocomial infection, an anti-staphylococcal drug like cloxacillin should be
substituted for ampicillin.
 Once the pathogen has been identified and antibiotic sensitivities determined, the
most appropriate drug(s) should be selected.
 Third generation cephalosporins are valuable additions for treating neonatal sepsis
and meningitis but have modest activity against staphylococcus aureus and listeria
monocytogens, and enterococci are uniformly resistant
 Therapy should be continued for a total of 10 to14 days.
 Supportive therapy includes should be carefully monitoring and correcting fluids,
electrolytes, and glucose. The newborn should be kept in thermoneutral environment.
Neonatal Meningitis
Neonatal meningitis is often associated with sepsis and is a cause of significant
morbidity and mortality. Agents that produce sepsis also commonly cause neonatal
meningitis.
Initial signs and symptoms may be indistinguishable from those of neonatal sepsis.
Neurologic manifestations include lethargy, bulging fontanel, seizure, nuchal rigidity and
signs of increased intracranial pressure.
The diagnosis is confirmed by examination of the CSF and the identification of bacteria,
virus or fungus by culture or antigen detection.
Blood culture is positive in 70-85% of neonates with meningitis.
Contraindications for doing a lumbar puncture (LP) include:

 Increased intracranial pressure
 Infection on the lumbar space
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 Severely ill infant if the lumbar puncture will further compromise the respiratory
status.
CSF findings suggestive of meningitis include:

 WBC > 30/mm3, particularly with an increased in the number of PMNL.
 CSF protein > 150 mg/dl.
 CSF glucose < 50% of blood glucose.
CSF should be gram stained and cultured. Appropriate latex agglutination test can be
done.
Therapy
Therapy will include intravenous ampicillin and gentamycin or ampicillin and
cephalosporin for 21 days for gram’s negatives or unknown status and for 10-14 days for
group B strptococcus.
Exercise
1. Describe risk factors for neonatal sepsis.
2. What is early and late onset neonatal sepsis?
3. What is the difference in terms of management between neonatal sepsis and
meningitis?
2.7. Congénital Infections (TORCH syndrome)
Objectives
By the end of this section the reader will be able to
 Know congenital infections that are commonly transmitted from the mother to the
infant
 Discuss the manifestation of common congenital infections
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TORCH stands for:

T - toxoplasmosis
O - other (includes other viruses and congenital syphilis)
R - rubella
C - cytomegalovirus
H - herpes simplex virus
Toxoplasmosis
Toxoplasmosis is caused by the protozoa toxoplasma gondii. Infection may be
transmitted from the mother to the fetus transplacentally or during vaginal delivery.
Overall risk of transmission from the mother to the fetus is about 50%.The incidence of
transmission is least in early gestation and greater later in gestation. The most severe
involvement results from maternal infection that occurs during the first and second
trimesters.
Clinical manifestations
Toxoplasmosis may present as mild or severe disease. Manifestations include IUGR
(intrauterine growth retardation), prematurity, hepatosplenomegaly, jaundice and
thrombocytopenia.
The classical triad consists of hydrocephalus, chorioretinitis and cerebral calcification.
Diagnosis
Diagnosis is usually based on:
 Toxoplasma dye test
 Immunofluorescent IgG toxoplasma antibody test or
 IgM antibody test.
Treatment
A combination of pyrimethamine and sulfonamide (sulfadiazine or triple sulfonamides)
should be given for one year.
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Prevention
The best way to prevent congenital toxoplasmosis is by preventing acute maternal
infection in pregnancy.These includes:
 Avoid contact with cats
 Avoid eating undercooked meat in pregnancy
 Wash vegetables thoroughly before eating
 Wear gloves when handling meat and vegetables
Rubella
The risk of a congenitally infected infant varies with the gestational age of the fetus when
maternal infection occurs. Between 50 and 80% are infected if maternal infection occurs
prior to the 8th week of gestation, but fetal infection is uncommon if maternal infection is
in the third trimester.
Rubella may produce
 Transient neonatal manifestations,
 Permanent organ malformations and tissue injury or
 Delayed late onset disease.
Manifestations include IUGR, microcephaly, microphthalmia, cataract,

thrombocytopenia, congenital heart disease (patent ductus arteriosus and peripheral
pulmonary artery stenosis), linear bone lesions, retinitis, convulsions and sensorineural
deafness.
The majority of manifestations however present much later in life. These include:
 Hearing loss (87%)
 Congenital heart disease (46%)
 Mental retardation (39%) and
 Cataract and glaucoma (34%)
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Diagnosis
 Viral isolation from nasopharygeal secretions, urine or CSF
 Detection of rubella specific IgM
Treatment
 There is no specific treatment for rubella infection.
 Seronegative women of childbearing age should be offered vaccination either after
pregnancy test or immediately postpartum.
Prevention
Prevention includes:
 Rubella vaccine for all nonimmune individuals 12 months of age and older and child
bearing age mothers. Conception also should be avoided for 3 months following
immunization and it is containdicated during pregnancy.
 Avoid contact with anyone known to have acute or recent rubella infection.
 Termination of pregnancy if active maternal infection is detected
Cytomegalovirus (CMV)
CMV is a member of the herpes group of viruses.
Mode of transmission include:

 transplacentally
 through genital secretions
 breast milk and
 blood transfusion
CMV produces characteristic intranuclear and intracytoplasmic inclusion bodies and an

enlarged cell size (cytomegalic).
Fetal damage may follow primary infection or recurrent infection at any stage of
pregnancy
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In about 40% of primary infections of the mother, the fetus will be infected but the
majority of neonatal infections are asymptomatic.
Clinical manifestations include IUGR, jaundice, hepatosplenomegaly, petechial rash,

chorioretinitis, pneumonia, periventricular calcifications and microcephaly.
Infants who have symptoms in the newborn period nearly always have subsequent
handicap, the most common problem being sensory neural hearing loss.
Diagnosis
Diagnosis involves:
 Isolation of the virus from the urine or saliva
 Demonstration of CMV specific IgM antibodies
Treatment
There is no specific therapy. The use of ganciclovir is being studied.
Herpes simplex virus (HSV)

Three quarters of HSV neonatal infection is due to HSV type 2 and the rest is due to
type 1.
Modes of infection include

 Mostly from maternal genital tract infection
 Intrauterine infection (5%)
 Postpartum (10%)
 Transmission from a primary lesion is about 50%
 Transmission from recurrent lesions is only 1-3%.
There are three major categories
1. Disseminated form commences at about 1 week of age with constitutional signs and
symptoms of sepsis and the characteristic erythematous based vesicles
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2. Skin, eye or mouth disease

3. Encephalitic form
- Usually of later onset (3 wks)
- Has a lower incidence of viremia and vesicles
Diagnosis
Diagnosis is based on:
 cytologic examination,
 direct viral culture of skin, mouth or eye lesions or
 analysis of IgM specific antibody response
Treatment and prevention

Treatment and prevention involves intravenous acyclovir for 14 -21 days.
Prevention
Delivery by cesarean section may reduce the risk of neonatal infection.
Congenital syphilis
Syphilis is a chronic, generalized infectious disease caused by a slender spirochete,
treponema pallidum.
Congenital syphilis results from transplacental transmission of spirochetes.
Pregnant women with 10 or 20 syphilis and spirochetemia are more likely to transmit
infection to the fetus than are women with latent infection.
Transmission may occur throughout pregnancy. Syphilis during pregnancy has a

transmission rate approaching 100%. Fetal and perinatal deaths occur in 40% of
affected infants.
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Early congenital syphilis
Early congenital syphilis appears during the first 2 years of life.
Approximately two-thirds of the infants are asymptomatic at birth, if they are untreated,
symptoms develop with in weeks or months.
Manifestations include hepatosplenomegaly, lymphadenopathy, hemolytic anemia,

thrombocytopenia and mucocutaneous rash. Rhinitis (snuffles) and condylomatous
lesions are highly characteristic features of mucous membrane involvement. CNS
abnormalities, failure to thrive, chorioretinitis, nephritis and nephrotic syndrome may also
be seen. Roentegenographic abnormalities include:
 Multiple sites osteochondritis at the wrist, elbow, ankle and knees and
 Periostitis of the long bones.
Late congenital syphilis

The manifestations result primarily from chronic inflammation of bone, teeth, and the
CNS. Skeletal changes include frontal bossing, thickening of the sternoclavicular portion
of the clavicle and an anterior bowing of the mid portion of the tibia (Saber shins).
Hutchinson's triad includes:

 Hutchinson's teeth (peg shaped upper central incisors)
 8th nerve deafness and
 interstitial keratitis
The clutton joint represents synovitis involving the lower extremities (usually the
knee).Saddle nose is a result of rhinitis.
Diagnosis
Serology: Non treponemal tests include:
 VDRL (Venereal Disease Research Laboratory)
 RPR (Rapid Plasma Reagin)
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These tests are rapid and non-expensive but they are not specific. Maternal antibody
crosses the placenta and accordingly a false positive VDRL can occur in an uninfected
infant delivered to a VDRL positive mother. This passively transferred antibody is not
demonstrable by 3 months of age.
Treponemal tests include:

 TPI (Treponema Pallidum Immobilization test)
 FTA-ABs (Fluorescent Treponemal Antibody Absorption test)
Dark field microscopy or direct fluorescent antibody test of scrapings from primary
lesions can reveal T. pallidum and often permits a definitive diagnosis.
Because doing these investigation is not always possible, it is recommended:

1. A presumptive diagnosis of congenital syphilis should be made and be treated in an
infant whose mother had untreated or inadequately treated syphilis or whose
treatment status is unknown. Inadequate treatment means she was treated ≤ 30 days
before delivery or treated with non penicillin regimen.
2. All infants with a presumptive diagnosis of congenital syphilis should be treated with
regimen effective for neurosyphilis because this cannot be reliably excluded.
Treatment
Treatment involves:
 Crystalline penicillin (100,000-150,000 IU/kg/d iv) or
 Procaine penicillin (50,000 IU/kg/d im) for 10-14 days.
Treatment is recommended for any infant if maternal treatment is unknown, inadequate

or given during the last 4 wks of pregnancy or if the treatment was by any drug other
than penicillin.
Exercise
1. What are the manifestations of congenital rubella?
2. What is the difference between early and late congenital syphilis?
3. Describe the management of congenital syphilis?
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CHAPTER THREE
SHOCK
Goitom G/Yesus
Definition
Shock is an acute syndrome characterized by inadequate circulatory perfusion of tissue
to meet the metabolic demands of vital organs.
Etiology
Most common triggering conditions are hypovolemia, sepsis, cardiac failure, trauma
and toxin.
Epidemiology
Shock is a clinical state which may result in high mortality rate of 20 to 50%. Most
patients die in the acute hypotensive or hypoxemic phase of shock, as a result of one or
more complications associated with shock states. Multiple organ system failure
increases the probability of death. In developed countries, the mortality rate of shock in
children has declined as result of educational efforts and pediatric advanced life
support, which emphasizes early recognition and intervention.
Pathophysiology
Shock may result in tissue injury through a number of pathways and factors such as:
 loss of fluid from the body,
 decreased myocardial contraction or obstruction to out flow of the heart,
 shift of fluid from intravascular to extra-vascular compartment, or
 accumulation or stasis of body fluid in the periphery as a result of vasodilation
This may result from the different etiologies of shock leading to inadequate tissue
perfusion. In the early phase of shock, a number of compensatory physiologic
mechanisms act to maintain blood pressure and preserve tissue perfusion. These
responses include increase of heart rate, stroke volume and vascular smooth muscle
tone to help preserve blood flow to vital organs such as the brain, heart and kidneys.
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When the compensatory mechanisms cannot maintain adequate tissue perfusion, the
resulting hypoxia and ischemia causes cell injury and ultimately cell death results.
Shock is classified clinically as shown below:
 Hypovolemic: characterized by loss of body fluid; e.g. diarrhea and hemorrhage
 Cardogenic: cardiac dysfunction; e.g. congenital heart disease, arrhythmias,
myocarditis, cardiomyopathy and mechanical defects.
 Obstructive: obstruction to inflow or outflow of blood to or from the heart; e.g.
cardiac tamponade, pulmonary embolism and pneumothorax.
 Distributive: abnormal vasodilation or increased permeability due to loss of
sympathetic vasomotor tone and/or presence of vasodilating substance in the
blood; e.g. anaphylaxis, sepsis and trauma.
The clinical manifestations of shock depend, in part, on the underlying causes.
General manifestations are tachycardia, weak or impalpable pulses, low blood

pressure, cold extremities, mottled extremities, sluggish or absent capillary refill,
tachypnia, reduced urine output, irregular respiration or apnea, peripheral or central
cyanosis and lethargy ranging up to coma.
Specific manifestations are:

 In hypovolemia- poor skin turgor. Sunken eye balls, dry mouth, signs of multiple
trauma
 In sepsis- fever, flushed appearance, hepatomegally, chest crepitations
Investigation
The investigations that are needed are usually specific to the suspected underlying
cause and may include:
 Complete blood count,cross-match, and culture of blood, urine, and cerebro spinal
fluid, coagulation profile and serum electrolytes may be needed
 Renal function test
 Chest X-ray and EKG
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Management
Early recognition of shock is a key step in the success of treatment.
Initial step include:
 Early attention to patency of airways and breathing
 Give oxygen.
 Maintain intra-venous access and give 20ml/Kg of Normal Saline or Ringer Lactate
as rapidly as possible. Reassess the patient and repeat another 20ml/Kg if
needed. Give subsequent deficit replacement therapy.
 In a patient not responding to the 40ml/Kg dose of fluid or if there is loss of blood,
give 10ml/Kg of blood, 5% albumin, or plasma.
 Catheterize the patient to monitor urine output.
 If sepsis is suspected, give empiric antibiotic coverage.
 Assess response to therapy by checking vital signs, and signs of end organ
perfusion such as skin color and warmth, mental status, and urine out put.
 In patients cardiogenic or septic shock if there is no response to fluid therapy
vasoactive drugs such as Dopamine, Epinephrine, or Dobutamine may be needed
 Treat the underlying cause of shock.
Exercise
1. Define shock.
2. What is the clinical classification of shock?
Further Reading
Cleary, T.G.. Shock. Behrman, Kliegman, Jenson, Nelson Text Book of Pediatrics, 16th
edition, 2000.
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PART TWO
Specific Paediatrics
CHAPTER FOUR
INFECTIOUS DISEASES
Objectives
At the end of this chapter, the student will be able to:
 describe epidemiology of infectious diseases, emphasising on Ethiopian context
 identify etiologic agents and their basic nature
 explain pathogenesis
 describe the diagnosis and important lab investigations
 describe the treatment, preventive measures as well as prognosis
4.1. COMMON CHILDHOOD INFECTIONS

MEASLES
Habtamu Fekadu
Definition
Measles is a highly contagious viral disease characterized by fever, coryza, conjunctivitis
and maculopapular rash.
Etiology
Measles is caused by an RNA virus that belongs to the polymyxoviridae family
Epidemiology
Measles is a leading cause of morbidity and mortality among vaccine preventable
diseases and is endemic in most countries. It accounts for 42 million cases and 1 million
deaths each year. Most occur in developing countries. The highest incidence is between
9 months and 2 years of age and 80% occurs in children under 5. Both sexes are
equally affected. Measles is severe and carries a high fatality rate in malnourished and
immunocompromised children.
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Measles is spread by the respiratory route via small droplets. It is highly contagious:
90% of susceptible contacts contract measles if they are exposed to infected patient.
The infected child is infectious 1 week before and 5 days after the rash appears.
Neutralizing antibodies and activated lymphocytes control infection and provide life long
immunity against subsequent infection.Transplacental immunity is protective for 6 to 9
mths.
Important features for the eradication of the measles include:

 Humans are the only reservoir and there are no carriers
 Vaccination is effective
 Measles’ charestrictic clincal feature is it is only one serotype
Figure 17: Pathogenesis and pathology
Inhalation of virus
Invade respiratory tract cells and multiply
Spread to regional lymphoid tissue and reticuloendothelial system (Primary

viremia)
Infected cells coalesce into multinucleated cells and the virus multiply further
Infected cells release more virus

Blood (secondary viremia)  spread to lungs, CNS, GIT, kin and mucous
membrane causing interstitial pneumonitis, encephalitis, diarrhoea, rash and koplik spot
respectively.
Clinical features
The incubation period lasts 10 – 12 days. Typically, measles has 2 phases:
1. Prodromal phase lasts 3 to 5 days. During this phase the child presents with fever,
cough, coryza and conjunctivitis. Koplik spots appear. These are greyish or whitish
spots surrounded by red base that appear on the buccal mucosa opposite to lower
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molar on the second day and disappear 2 days after onset of the rash. It is
pathognomonic of measles.
2. Eruptive phase during whichthe child is very sick and manifestd with fever, which
rises markedly as the rash appears and peaks by the second or third day and then
starts to decrease. The rash is initially faint erythematous macules that progresses
to a maculopapular rash, first appearing behind ears, along hairline and cheek and
spreading centrifugally to involve the neck, trunk and lastly the feet by the second
or third day day. This fades in 4 to 7 days in the same sequence in which it
appeared, leaving desquamation. Diarrhoea and cough are common especially in
infants and young children
Figure 17: The natural course of measles
Exposure
(IP) Illness
Viral shedding
Days
10 – 14 1 2 3 4 5 6 7 8 9 10
O
T
Rash
Koplik spot
Conj.
Cough.
Diagnosis
Typically, the diagnosis of measles presents no difficulties so it is mainly clinical: a child
who has generalized rash and one of coryza symptoms (cough, runny nose or red
eyes) may be assumed to have measles. It is rarely that a laboratory test is needed.
Complications
The complications from measles include:
 Respiratory complications are the most common complication and cause of death.
Pneumonia is the most common and carries a high mortality. Pneumoniais caused
120
by measles interstitial pneumonitis (giant cell pneumonia) caused by the measle

virus or bacterial pneumonia (pPneumococcus, H. influenzae, staph. aureus) which
has a high moratality. Otitis media is also common.
 Gastroenteritis is the second commonest complication. The child present with
diarrhoea, vomiting, or persistent diarrhoea.
 Malnutrition is a common sequel of measles due to anorexia, oral lesions, persistent
diarrhoea or increased catabolism. Measles often precipitates acute kwashiorkor.
 Corneal ulceration can be caused by the exacerbation of xerophthalmia or direct
viral keratoconjuctivitis and leads to blindness.
 Encephalitis is a rare complication which presents with fever, seizure, neck
 Other complications include measles croup and the reactivation of tuberculosis
stiffness, confusion, and coma.
Treatment
Treatment is symptomatic and includes:
 Bed rest
 Antipyretic
 Increase fluid intake
 Vitamin A on first, second and fourteenth day decreases corneal ulceration and
morbidity and mortality from measles
 Treat complications with antibiotics for pneumonia and otitis media and treat croup
as any croup
Prognosis
Most children recover completely but young and malnourished children and those with
encephalitis have a poor prognosis. The commonest cause of death is pneumonia.
Prevention
Prevention involves
 Isolation for the infectious period
 Vaccination at 9 months has more than 95% efficacy
 Post exposure prophylaxis giving measles vaccine within 72 hours for susceptible
children older than 6 months.
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Pertussis
Tsinuel Girma
Definition Pertussis is an acute respiratory infection caused by bordetella pertussis.
Epidemiology
Pertussis occurs as sporadic and epidemic cases. Most patients are under six years
old, but any age including neonatal age groups are susceptible, since there is no
transplacental protection. Overcrowding favors the spread of the disease, because
transmission is via droplet infection. The highest infectivity is in the early stages of the
disease and the attack rate is close to 100%.
Etiology
B. pertussis and B. parapertussis are gram-positive rods which grow well on border
gengon agar (glycerin-potato-blood) media.
Pathogenesis
Transmission is through aerosol droplets at close range. Bacterias attach to ciliated
epithelium of the respiratory tract, resulting in congestion, excessive mucous production
and infiltration with lymphocytes. The lumen of the air ways especially the bronchioles
narrow, producing atelectasis and emphysema.
B. pertussis produces many toxins. Pertussis toxin (DT) plays a central role in the
pathogenesis.
The clinical manifestations are divided into three stages each lasting about two weeks:
catarrhal, paroxysmal and convalescent.
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Catarrhal stage
After the incubation period of 3 to 12 days non distinctive symptoms of low grade fever,
nasal discharge, sneezing and lacrimation are seen. This stage usually simulates
simple upper respiratory infections
Paroxysmal stage
Progressively increasing repetitive series of forceful coughs in a single expiration is the
hallmark of this stage. Children above the age of 2 years have massive inspiratory effort
(whoop) as air passes through narrowed bronchial tree. The cough is followed by
vomiting (post tussive vomiting) and profuse sweating. The intense cough and its
associated included pressure may result in hernias, rectal prolapsed, orbital edema,
ulceration of frenulum and epistaxsis which are helpful in the diagnosis. Immunized
children and adults have no distinct stages.
Convalescent stage
Severity and frequency of paroxysms decrease but cough and whoop may persist for
months.
Diagnosis
Diagnosis is confirmed by positive culture of B. pertussis on bordet – gagnon medium.
Leukocytosis due to absolute lymphocytosis greatly supports the diagnosis. An

absolute increase in neutrophils suggests a different diagnosis or secondary bacterial
infection. Chest X-rays show perihailar infiltration and variable atelectasis.
Treatment
Therapy includes:
 Limit number of paroxysms
 Clearance of airways and respiratory support if paroxysms are life threatening
 Maximizing nutrition
 Adequate rest
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Admission criteria
 Infants below 3 months of age
 Witnessed severe paroxysms
 Children with significant underlying cardiopulmonary or neuromuscular disorders
Supportive care
 Small volume frequent feeds between cough episodes when patient is at rest
 Suction airways when necessary
 Oxygen if in distress
Antibiotics
 Always indicated for suspected or confirmed cases for potential clinical benefit and
to limit spread of infection
 Standard treatment is erythromycin 40 – 50mg. kg/24h p.o. in four divided doses
for 14 days.
Prognosis
Young age (less than 2 months) and severe malnutrition are poor prognostic factors.
Complications
Complications include apnea, pneumonia (S. aureus and S.pnuemoniae), otitis media,
seizure and physical squeale of forceful coughing and the reactivation of tuberculosis.
Prevention
Primary prevention involves 3 doses of pertussis (DPT) vaccine (EPI) Secondary
prevention involves isolating the patient and treating them, vaccination and giving
erythromycin for contacts
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Rubella
Habtamu Fekadu
Definition
Rubella is a common and mild exanthematous disease associated with fever, rash and
lymphadenopathy but which can result in serious damage to infants born from infected
mothers.
Etiology
Rubella is an RNA virus of the genus rubivirus in the family Togaviridae
Epidemiology
Rubella is a widespread and highly contagious disease. It mainly affects children,
though it affects all age groups Transmission occurs mainly by respiratory droplets and
occasionally by direct close contact. Transplacental spread results in congenital rubella
syndrome (CRS).The highest risk of transmission, which is greater than 50%, and
serious damage occurs in the first trimester. The patient is infectious 1 week before and
1week after the rash.
Natural infection confers lifelong immunity. The transplacental immunity protects the
infant for 6 to 9 months.
Clinical features
The incubation period is 14 to 21 days (usually 17 days). Most infections are subclinical.
The characteristic presentations are lymphadenopathy skin rash and low-grade fever.
A tender posterior cervical, occipital, and retro-auricular lymphadenopathy appears 2

days before the onset of rash.
A discrete macular / maculopapular rash appears that starts from the face and spread
centrifugally to involve the trunk and extremity. It fades on the third day in the same
order it appeared.
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Foetal infection leads to abortion, stillbirth or congenital rubella.
Congenital Rubella Symdrome (CRS)

Congenital Rubella Symdrome (CRS) affects all organ systems. The infant presents
with IUGR, jaundice, cataract, microcephaly, congenital heart disease persistent ductus
arteriosus), purpura, hepatospleenomegally, anemia and meningoencephalitis which
manifests with convulsion and lethargy.
Late sequelae include sensorineural deafness and mental retardation .
Diagnosis
Diagnosis is mainly clinical although viral culture (nasopharynx, blood) may be used.
Treatment
Treatment is supportive and involves no specific treatment.
Prognosis
Childhood rubella has and excellent prognosis, but CRS has a poor prognosis
Prevention
Prevention is mainly through the rubella vaccine which is given in combination with
measles and mumps as MMR. It has a 90% efficacy.
Mumps
Habtamu Fekadu
Definition
Mumps is a viral illness characterized by painful swelling of salivary gland.
Etiology
Mumps is caused by a RNA virus that belongs to paramyxovirus group.
126
Epidemiology
Mumps is endemic worldwide, especially in unvaccinated and heavily populated areas
and It occurs in epidemics. Transmission occurs through airborne droplets and direct
contact of saliva. The patient is infectious two days before parotid swelling and up to
three days after the swelling subsided.
Mumps affects any age but the peak age is 5 to 9 years and 85% occur in children
under 15 yrs of age. Infants are protected by transplacentally passed antibodies.
Pathogenesis
The inhaled virus multiply in the respiratory tract and enter the blood (viremia). They
spread to many tissues (mainly salivary glands, gonads, pancreas and brain).
Clinical features
The incubation period is 14 to 24 days. 10 to 50% of cases are subclinical. Mumps
presents with:
 Painful swelling of parotid gland that rapidly grows and attains the maximum size
by 3rd day. Unilateral at onset and in 24 to 48hr becomes bilateral in most cases.
 Submandibular glands are affected in 10 – 15% of cases.
Complications
Meningoencephalitis is the most common complication. It occurs in 30% of cases.
Symptoms and signs are as any meningoencaphalitis. It carries a mortality of 2%.
Other Complications are orchitis/epididymitis, pancreatitis, oophoritis and myocarditis,
Treatment
Treatment is supportive. There is no specific treatment.
Prevention
Prevention is mainly through the mumps vaccine, which is given at the age of 15
months in combination with rubella and measles as MMR, has a 97% efficacy.
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Chickenpox
Habtamu Fekadu
Definition
Chickenpox is a highly contagious disease which is caused by varicella zoster virus and
characterized by fever, mild constitutional symptoms and centripetal skin rash
appearing on the first day of the illness.
Etiology
Chickenpox is caused by a herpes virus called varicella zoster virus (VZV) which is a
DNA, and neurotropic virus .It is the acute invasive phase of VZV whereas herpes
zoster is the reactivation form.
Epidemiology
Chickenpox is common and worldwide. The virus is transmitted mainly through airborne
droplets. Other modes of transmission are direct contact and the transplacental route
that leads to neonatal chickenpox. It is highly contagious with home contact attack rate
of 80 to 90%.
Chickenpox occurs in epidemics. The period of infectivity is 24 to 48 hours before and 3

to 7 days after the onset of rash. Infection confers lifelong immunity.
Chickenpox mostly occurs in children under 10 years of age and in most cases it is
benign, but it tends to be severe and life threatening in neonates and
immunocompromised.
Pathogenesis
The inhaled virus replicates in respiratory tract which leads to subclinical viremia which
in turn leads to secondary viremia and causes wide spread skin lesion and can involve
different organs (lung, brain etc.)
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Host immune responses limit viral replication and facilitates recovery. This VZV primary
infection establishes lifelong latent infection of sensory ganglion neurons, which when
reactivated results in herpes zoster.
Clinical features
The prodromal phase is not present in young children but it is mild in older children and
adults.there is a characteristic rash that:
 Starts as macule, becomes papule and turns into vesicle and pustules, leading to
a crust.
 Occurs in crops and all stages are present at the same time which is characteristic
of chickenpox. It is pruritic.
 Has centripetal distribution and mainly involves the trunk.
Complications
Complications include super infection of the skin lesions, encephalitis and pneumonia
Treatment
Treatment involves supportive care and acyclovir for neonates and children that are
immunocompromised.
Prognosis
The prognosis is good for healthy children but poor for neonates and those that are
immunocompromised.
Prevention
Prevention involves isolation of the patient during the infectious period, active
immunization with varicela vaccine and post exposure prophylaxis with varicella zoster
immunoglobulin (VZIG)
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Poliomyelitis
Habtamu Fekadu
Definition
Poliomyelitis is an acute viral infection caused by poliovirus.
Etiology
The poliovirus is one of the enteroviruses and there are three serotypes (1, 2, and3).
Paralysis and epidemic are often caused by type 1. Humans are the only reservoir:
there are no carriers.
Epidemiology
Poliomyelitis is eradicated from developed countries but it still occurs in developing
countries. However, the incidence is decreasing. Transmission occurs by fecal-oral
route. It is very infectious: nearly 100% of susceptible exposed children acquire the
virus. Poliovirus is excreted in stools for 6 to 8 weeks following infection.
the infected child transmits the disease for a few days before and 7 to 10 days after
symptoms appear. All unimmunized children are susceptible. It largely affects infants
and young children. Ninety percent occurs in children less than 5 years of age.
Active immunity after infection or vaccine is life long.
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Figure 18: Pathogenesis of Poliomyelitis
Ingestion of virus

invade and multiply in pharynx (tonsils) and ileum (payers patches)

Spread to adjacent lymph node  to reticulo endothelial system (RES) (primary
viremia)

Further replication in RES  release of more viruses to blood (secondary viremia)

Spread and infect the CNS through hematogenous spread and rarely along peripheral
nerves.
Primary targets are the motor neurons in the anterior horn of the spinal cord, cranial
nerve motor nuclei and vital centers in brain stem. This selective attack is characteristic
of poliomyelitis.
Clinical features
The clinical features are as follows:
 Incubation period – 7 - 20 days
 Most are asymptomatic – 90 -95%
 It has four courses:

- Inapparent (asymptomatic): in 90 to 95% of cases.
- Abortive poliomyelitis (minor illness): in 5% of cases the infection presents with
non-specific symptoms like fever, headache, sore throat and no neurologic
symptoms. Most recover in 48 to 72 hours.Sometimes this form merges with
non-paralytic poliomyelitis.
- Non paralytic poliomyelitis: in 2% of cases. This form is due to aseptic
meningitis. Besides the above symptoms, the patient manifest with severe
headache, muscle pain, tenderness, signs of meningitis and spinal rigidity which
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is thebasis for diagnosis.The symptoms and signs lasts for 1 to 2 days and most
cases the patients recover. However, it progresses to paralysis in a few
patients.
- Paralytic poliomyelitis occurs in less than 1%of cases, following non-paralytic
poliomyelitis or it may appear 4 days after symptoms of abortive poliomyelitis
subsided.
Paralysis is the hallmark of this last type, characteristically it

 is asymmetric and flaccid paralysis
 begins rapidly, progress markedly in 48 hrs.and no progress after 3 days.
 Sensory involvement is rare.
This type of infection has 4 forms: spinal, bulbar, bulbospinal and encephalitic
poliomyelitis. The first two are discussed below, since they are more common than the
later two.
Spinal poliomyelitis is the most the most common form and has the following
characteristics:
 The cervical and thoracic cords are affected
 It results in paralysis of neck, trunk, limbs or respiratory muscles, so patients
present with flaccid monoplegia, paraplegia or quadriplegia, with or without
breathing difficulty.
 Cranial nerves, sensation and autonomic nervous system are spared.
Bulbar poliomyelitis.
Bulbar poliomyelitis is rare but it is life threatening.
 It is characterized by cranial nerve motor nuclei lesion with or without vital center
involvement.
 Usually cranial nerves IX, X, and XI are affected and patients present with difficulty
of swallowing, speech, breathing etc.
 There is vital center (respiratory and circulatory) involvement.
 It manifests with shallow, irregular breathing, labile blood pressure usually
hypertension and rapid change in temperature.
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Diagnosis
History and characteristic findings are important in diagnosis. A flaccid limb paralysis or
cranial nerve palsies without sensory loss occurring during the course of an acute
febrile illness is highly suggestive of poliomyelitis. Other methods of diagnosis include:
Serology fourfold rise in antibody titer between acute illness and convalescence confirm
the diagnosis.
- Viral isolation from stool.

- CSF -increased WBC of 20-300/mm3 (largely lymphocytes), increased protein, and
normal glucose.
Differential Diagnosis
- Non paralytic poliomyelitis – Aseptic or bacterial meningitis
- Paralytic poliomyelitis Gullian Barrie Syndrome, transverse myelitis
Treatment
Treatment is supportive:
 Make the child comfortable.
 Maintain adequate fluid and dietary intake.
 Minimize skeletal deformity.
 Anticipate and treat complications.
 Maintain airway, ensure adequate ventilation
Prognosis
The prognosis for paralytic poliomyelitis depends on its type and extent. Generally,
mortality is between 2 and 20%. Most paralysis recover. However, if the paralysis
persists for 3 months or if it is extensive paralysis in the first 10 days, the patient will
remain paralyzed. The major cause of death is respiratory failure.
Prevention
Prevention includes routine EPI (OPV). The strategies for polio eradication include:
1. Strengthen routine EPI
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2. National immunization days (NID) Two doses of OPV should be given to all children
under 5 years of age annually irrespective of their immune status. This will boost
herd immunity and stop wild poliovirus spread
3. Mopping-up immunization - in high risk areas, house-to-house vaccination should be
undertaken of all children less than 5 years of age, irrespective of their immune
status.
4. Acute flaccid paralysis (AFP) surveillance- to detect and investigate all cases of AFP
in children under 15 years of age.
References
1. Robert B. The Merk manual of diagnosis and therapy; 4th edition.
2. Ghai,Gupta. Essential preventive medicine.2000.
3. Levy, Sheldon, Sulyman. Diagnosis and Management of the hospitalized child.1984.
4. Paget Stanfield, Martin Brueton etal. Disease of children in the tropics and
subtropics. 1991.
5. Fegyin, Pediatric infectious disease, 2000.
6. Behrman, Kliegman, Jenson, Nelson Text Book of Pediatrics, 16th edition, 2000.
4.2 TYPHOID FEVER
Goitom G/Yesus
Definition
Typhoid fever is a febrile systemic syndrome caused by salmonella typhi.
Epidemiology
It is endemic in most tropical countries. Humans are the only reservoir for salmonella
typhi; hence, direct or indirect contact with an infected person (sick or apparently
healthy chronic carrier) is necessary for infection.
The most common mode of transmission is ingestion of water or food that has been
contaminated with human feces.
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Pathogenesis
After ingestion, the organism invades intestinal epithelium and multiplies in the intestinal
lymph nodes. From the lymph nodes it reaches the blood stream causing transient
bacteremia. Circulating organisms reach the reticuloendothelial cells in the liver, spleen
and bone marrow where proliferation occurs and leads to bacteremia. The gall bladder
is particularly susceptible to infection and local multiplication of the organism. The large
numbers of organisms in the bladder are passed to the intestine through the bile.
Clinical Manifestation
The incubation period for typhoid fever is usually 7 to 14 days. The clinical
manifestations depend on the age of the patient.
In school age children and adolescents
Initial (first week) symptoms are fever, malaise, anorexia, myalgia, headache, and
abdominal pain. Diarrhea may be present in the early course of the disease, but later
on constipation becomes a more prominent symptom. Fever rises in step-ladder
fashion. The fever is high grade and unremitting, and may be followed by cough and
epistaxis.
In the second week there will be sustained high grade fever, fatigue, cough, and the
abdominal symptoms increase in severity. Patients appear acutely ill, disoriented and
lethargic. Delirium and stupor may also be observed. On physical examination, relative
brady-cardia, hepatomegally, splenomegally and distended abdomen with diffuse
tenderness are very common.
In about 50% of patients a reddish rash (rose spot) occurs in the lower part of the chest
and abdomen. If uncomplicated, the symptoms usually resolve in two to four weeks.
Nausea and vomiting occurring in the second week suggest a complication.
Infants and young children usually present with mild fever and malaise, which may be
misinterpreted as a viral syndrome. Diarrhea is more common in this age group than in
adults, suggesting the diagnosis of acute gastroenteritis.
135
Complications
Complications includeintestinal hemorrhage and perforation, sepsis, and pneumonia.
Diagnosis
Laboratory diagnosis involves:

Isolation of the organisms (gold standard)
 blood culture will be positive within the first few days,
 In the second and later weeks, urine and stool cultures.
Serologic tests
Widal test: diagnosis depends on demonstration of antibodies against ‘O’ and ‘H’
antigens the organism. In areas where the disease is endemic, an ‘O’ antibody titer of
1/250 or above is suggestive, but more important is a rising titer in two consecutive
tests done with in 7 to 10 days.
Another laboratory finding commonly associated is a low leukocyte count
Treatment
 Supportive
 Maintenance of appropriate fluid and electrolytes

 Surgical intervention for intestinal perforation
 Antibiotics
 Chloramphenicol 50-75 mg/Kg/24hr.PO/IV in four divided doses or,

 Ampicillin 200 mg/Kg/24hr. IV in four divided doses or,
 Amoxicillin 100 mg/Kg/24hr.PO in four divided doses
 Duration of antibiotic is 14 days
Prognosis
In developing countries mortality is higher than 10% because of the delay in diagnosis,
hospitalization and treatment.
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Prevention
Prevention involves:
 Improved sanitation
 Provision of clean water and safe waste disposal
 Hygienic food preparation practices
 Eradication of salmonella typhi from carriers
Exercise
1. Characterize the classic fever of typhoid fever.

2. What percentage of patients with typhoid fever manifest with rose spots?
3. What are the common complications of typhoid fever?
4. When do blood, urine and stool culture become positive in the clinical course of
typhoid fever?
References
1. K.C.Watson, Enteric fever, D.B JELLIFFE, J.P. STANFIELD, Diseases of children in

the subtropics and tropics, 3rd edition, 1986.
2. T.G. Cleary, Enteric fever, Behrman, Kliegman, Jenson, Nelson Text Book of
Pediatrics, 16th edition, 2000.
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4.3. TUBERCULOSIS
Goitom G/Yesus
Definition
Tuberculosis (TB) is a chronic infectious disease with diverse clinical manifestations

caused in most cases by mycobacterium tuberculosis; occasionally it can also be
caused by mycobacterium bovis or mycobacterium africanum.
Epidemiology
The main sources of infection are untreated pulmonary TP patients discharging the
bacilli. Transmission of infection occurs through the air-borne spread of droplets
containing bacilli expelled by coughing and sneezing, and inhaled by healthy persons.
People who are in frequent contact with an infectious patient are at greatest risk of
being exposed to the bacilli. In addition, consumption of raw milk containing M. bovis is
a possible way of transmission in Ethiopia.
TB affects individuals of all ages and both sexes within every socio-economic group.
However, factors making people more vulnerable to develop the disease are poverty,
malnutrition, crowded living conditions, measles, pertussis and HIV infection.
The natural history of TB is such that, in the majority of exposed people, their
immunological defense either kills all the inhaled or ingested bacilli or more often keeps
them suppressed (silent focus) causing latent M .tuberculosis infection. Under normal
circumstances, only about 10% of all individuals who are infected by the bacilli will
develop the disease throughout their lifetime (in HIV infected persons the risk is much
higher).
Pathogenesis
Primary infection occurs on the first exposure to tubercle bacilli. Infection begins with
the multiplication of the bacilli in the lungs. This is the ghon focus. Lymphatics drain the
bacilli to the hilar lymph nodes. The ghon focus and related hilar lymphadenopathy form
the primary complex. The immune response (delayed hypersensitivity reaction)
develops about 4 to 6 weeks after the primary infection. What happens next is
138
determined by the size of the infecting dose of bacilli and the strength of the immune
response. Mostly, the immune response stops the multiplication of bacilli. However, a
few dormant bacilli may persist. In a few cases the immune response is not strong
enough to prevent multiplication of bacilli and disease occurs within a few months.
In children, TB is usually primary TB. The age at which the child is infected determines
the pattern of primary disease. Up to puberty, blood-borne spread is common, resulting
in disseminated (military and extra pulmonary) disease, whereas after puberty
pulmonary spread is more common.
Post-primary TB occurs after a latent period of months or years after the primary
infection. It may occur either by reactivation or by reinfection. Reactivation occurs
mainly in response to a trigger, such as weakening of the immune system by HIV
infection, malnutrition, measles and pertussis. Post-primary TB usually affects the
lungs but can involve any part of the body. The characteristic features of post-primary
TB are: extensive lung destruction with cavitations, positive sputum smear, and upper
lobe involvement. The different types of post-primary TB are:
Pulmonary TB – involves the cavities, upper lobe infiltrates, fibrosis, progressive

pneumonia, endo-bronchial TB etc.
Extra-pulmonary TB – involves pleural effusion, lymphadenopathy (usually cervical),

central nervous system (meningitis, cerebral tuberculoma), pericarditis (effusion,
constriction) gastro-intestinal, spina, bones and joints and other less common ones.
Primary pulmonary disease
This includes the lung parenchymal focus and regional lymph nodes. About 70% of lung
foci are sub-pleural and localized pleurisy is common. All lobar segments are at equal
risk of initial infection. The hallmark of 1o PTB is the relatively large size of the regional
lymphadenitis compared with the relatively small size of the initial lung focus. In some
children progressive enlargement of the hilar lymph nodes may compress the bronchus
leading to obstruction and atelectasis. Rarely inflamed nodes attach to the
endobronchial wall causing endobronchial TB.
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The symptoms and physical findings of primary pulmonary disease in children are
surprisingly meager. Infants are more likely to manifest with signs and symptoms such
as: cough, mild dyspnea, failure to gain weight or a true failure to thrive; localized
wheezing or decreased breath sounds in those with bronchial obstruction.
Reactivation of TB
Pulmonary TB
In adults this usually represents endogenous reactivation of TB infection established

previously in the body. Pulmonary TB is uncommon in childhood but may occur in
adolescence. More patients may experience fever, anorexia, malaise, weight loss, night
sweats, productive cough and hemoptysis and chest pain than those with 1o PTB. Most
common radiographic presentation is extensive infiltrates or thick walled cavities in the
upper lobes.
The other forms of reactive tuberculosis are the extra pulmonary tuberculosis. The
signs and symptoms depend mainly on the organ(s) involved. The most common forms
are as follows:
Lympho- hematogenous (disseminated) disease
Tubercle bacilli are disseminated to distant sites, including liver, spleen, skin, and lung
apices in all TB infection. The clinical manifestation of disseminated TB depends on the
number of organisms released from the primary focus and the strength of the host
immune response.
Although the clinical picture may be acute, usually it is indolent and prolonged. Multiple
organ involvement is common. The most significant form is miliary disease which
occurs when massive bacilli are released into blood stream causing disease in 2 or
more organs. It usually complicates the primary disease within 2 to 6 month of initial
infection, and is common in infants and young children. The clinical manifestations are
protean depending on load of bacilli that disseminate and where they lodge. Patients
are usually very ill. The common findings are as follows:
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 Lesions on CXR are smaller than 2 to 3 mm in diameter initially but later coalesce to
form large lesions.
 Generalized lymphadenopathy and hepatosplenomegaly occur in 50%
 Meningitis and peritonitis occur in 20 – 40%
 Diagnosis may be difficult and high index of suspicion is required; most important
clue is resent exposure to infectious adult.
CNS disease
CNS disease is the most serious and fatal complication in children. It may arise from
metastatic focus in cerebral cortex or meninges. The brain stem is often the site of
greatest involvement (frequent dysfunction of Cranial nerves III, VI and VII.
Combinations of vasculitis, infarction, cerebral edema and hydrocephalus result in
severe damage and complicates about 0.3% of untreated TB in children. It is most
common between 6 month and 4 years of age. Clinical progression may be rapid or
gradual.
More commonly, the signs and symptoms progress slowly over several weeks and can
be divided into 3 stages:
 1st Stage lasts 1 to 2 weeks and is characterized by non specific symptoms. Focal
neurologic signs are absent but infants may show stagnation or loss of development
mile stones.
 2nd Stage: common features are lethargy, meningeal signs, seizure, hypertonicity,
vomiting, cranial nerve palsies and other focal neurologic signs. Some patients may
have signs of encephalitis: disorientation, movement disorders or speech
impairmenent.
 3rd stage is marked by coma, hemiplegia or paraplegia hypertension, decerebrate
posturing, deterioration of vital signs and even finally death
Prognosis correlates with stage of disease at the time of initiation of treatment.Stage 3

survivors have permanent disabilities
141
Diagnosis involves:
CSF analysis shows cell count is in houndred (< 500/mm3) with moderate lymphocyte
predominant, a high protein concentration (usually greater than 200mg/dl) and a low
glucose concentration.
Examination and culture of CSF is most important for diagnosis.
Complete investigation for TB is essential.
Tuberculous lymphadenitis
It is a slowly developing and painless enlargement of lymph nodes, followed by matting

and eventually drainage of pus. It is the most common form of tuberculosis in children.
Investigation involves fine needle aspiration or biopsy of lymphnode and stain and
culture for AFB and histological examination
Tuberculosis of bones and/or joints
The vertebrae are involved most of the time, and manifest classically by gibbus
deformity and kyphosis. It is usually a late manifestation.
Diagnosis of TB
Diagnosis of TB involves:
 History and physical examination
 WBC with differential ESR
 Microscopic examination of sputum or gastric aspirate
 Radiological examination (chest x-ray, x-ray of bones etc)
 Culture of organism
 Histo-pathological examination of biopsied tissues
 Tuberculin test
Children should be strongly suspected of having TB when they have contact with a
known adult case of pulmonary TB and have clinical signs and symptoms.
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Criteria for the diagnosis of tuberculosis in children
Suspected tuberculosis
An ill child with a history of contact with a confirmed case of pulmonary tuberculosis OR
Any child:
 Not regaining normal health after measles or whooping cough
 With loss of weight, cough and wheeze not responding to antibiotic therapy for
respiratory disease
 With painless swelling of the superficial lymph nodes
Probable tuberculosis
A suspected case and any of the following:

 Positive (>10 mm in diameter) induration on tuberculin testing
 Suggestive appearance on chest X-ray (e.g. unilateral hilar/ mediastinal lymph node
enlargement with or without lobar or segmental opacity, military pattern, pleural
effusion, infiltrates and cavitations)
 Suggestive histological appearance of biopsy material
Confirmed tuberculosis
 Detection by microscopy or culture of tubercle bacilli from secretions or tissues
 Identification of tubercle bacilli as mycobacterium tuberculosis by culture
Standardized Tb Case Definitions

On making the diagnosis of TB, you must also decide on the TB case definition. There
are four determinants for this: site of TB, result of sputum smear, previous TB treatment
and severity of TB.
Case definition by site and result of sputum smear for PTB

1. Smear positive case: At least 2 sputum smears positive for AFBs or 1 sputum
smear positive and CXR abnormalities consistent with TB.
2. Smear negative case: At least 2 (preferably 3) sputum smears negative for AFBs
and Chest X-ray consistent with TB.
Case definition by previous treatment
143
 New case (N): a patient who has never taken treatment for TB or has been on
anti-TB treatment for less than one month.
 Relapse(R): a patient who has been declared cured or treatment completed of
any form of TB in the past, but who reports back to the health service and is found
to be AFB smear-positive or culture positive.
 Treatment failure(F): a patient who, while still on treatment remains smear-positive
or comes again sputum smear-positive 5 months or more after starting treatment
 Return after default (D): a patient who has previously been recorded as defaulted
from treatment (completed at least one month of treatment and interrupted for at
least 2 months) and returns to the health service with smear-positive sputum.
 Transfer in (T): a patient registered for treatment in one district (woreda) and is
transferred to another.
 Chronic case (C): a patient who remains smear-positive after completing a
supervised re-treatment regimen. This is usually seen in adults and is rare in
childhood but may occur in adolescents.
 Other (O): a patient who does not easily fit into one of the above case definition
(e.g. a smear-negative PTB who returns after default)
Management
Principles of managment include:
1. Chemotherapy
2. Nutritional rehabilitation.
3. Family screening
4. Follow up
Chemotherapy
1. Drugs used for chemotherapy of tuberculosis:
 Streptomycin (S) - 1gm (vial)

 Ethambutol (E) - 400 mg
 Isoniazid (H) -100 mg, 300 mg
 Rifampicin ( R) - 150 mg, 300 mg
 Pyrazinamide (Z) - 500 mg
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2. Phases of chemotherapy
The treatment for tuberculosis has two phases:

Intensive (initial) phase: this phase consists of three or more drugs for the first 8
weeks. This has the advantage of making the patient non-infectious by rapidly reducing
the load of bacilli in the sputum and minimizing the danger of development of drug
resistance.
Continuation phase: this phase immediately follows the intensive phase and is
important to ensure that the patient is permanently cured and does not relapse after
completion of treatment. This phase at least two drugs to be taken for 6 months.
3. Drug regimens and treatment categories

In order to treat the patient with the correct drug regimen, it is important to determine
whether or not the patient has previously taken treatment for TB.
There are three different categories of treatment regimens.
Category I – Short course chemotherapy for smear- positive PTB and seriously ill
smear-negative PTB and EPTB cases
The treatment regimen for this category is:

 S (RHZ) for 2 months and then (EH) for 6 months OR
 (ERHZ) for 2 months and then (EH) for 6 months
Children who are 6 years or below get RH 150/75 mg in the continuation phase for a
total period of 4 months. Also, children older than 6 years but are seriously ill receive 4
months RH in the continuation phase.
This regimen is prescribed to:

 New smear-positive PTB patients
 New smear-negative PTB patients, who are seriously ill
 New EPTB patients, who are seriously ill
 Returns after default from DOTs, who have smear-negative PTB (case definition =
“other”)
Category II – Re-treatment regimen
The regimen for this category is:
145
 SE(RHZ) for 2 months, then E(RHZ) for 1month, and then E(RH) three times a
week for 5 months
This treatment regimen is prescribed for:

 Smear-positive relapses
 Smear-positive treatment failures
 Smear-positive return after defaults
 Smear-negative PTB patients who become smear-positive after 2 months of
treatment (case definition: other)
 Return after default from re-treatment should be given the re-treatment regimen
once again, but only once
 Relapses after re-treatment should also be given the re-treatment regimen only
once
Category III – short course chemotherapy for smear-negative PTB, EPTB and TB in
children
The treatment regimen for this category is:

 (RHZ) for 2 months and then (EH) for 6 months
This regimen is prescribed to:

 New adult patients with smear-negative PTB
 New adult patients with EPTB
 Children between 7 and 14 years old with any type of TB, who are NOT seriously
ill
Prevention
Prevention comprises:
 Adult case finding and treatment
 Chemoprophylaxis
 BCG vaccination
 Adequate nutrition
146
References
1. WHO/TB/96.2000, TB/HIV clinical manual, 1996.
2. Jeffrey R. Stark, Flor Munoz: Behrman, Kliegman, Jenson, Nelson Text Book of
3. MOH, Manual of Tb and Leprosy prevention and control programme, 2002.
4. John Crofton, Norman Horne, Fred Miller, 1992, Clinical Tuberculosis.
4.4. Tetanus (Lockjaw)

Tsinuel Girma
Definition
Tetanus is acute, spastic paralytic illness caused by tetanus toxin (tetanosparmin), a
neurotoxin produced by clostridium tetani.
Etiology
Clostridium tetani is anearobic, gram positive, spore forming motile bacteria found
worldwide in soil, dust and excreta of animals.
It lives in two forms. The spore form resists damage like boiling. The vegetative form
secretes toxin in hypoxic conditions and is killed by standard disinfections.
Epidemiology
Tetanus, particularly neonatal tetanus (tetanus neonatorum), is a major public health
problem in developing countries where it kills half a million infants each year. A
household survey in Ethiopia showed incidence rate of 4.3 per 1000 live birth and with
mortality rate of 86%. In Jimma Hospital neonatal tetanus accounted to 2.9% of
admissions.
Spores get into the body through wounds such as penetrating injuries, animal bites,
jigger and tooth extraction by local healers, otitis media and injections (quinine i.m.)
Neonates, born to unimmunized mother, will acquire it via umbilical stump due to
unhygienic cord care, and dressing with herbal medication or and applying cow dung on
the cord
147
Pathogenesis
The vegetative form produces tetanospasmin under anaerobic environment of injured
/infected site.
Neonatal tetanus manifests few days (3 to 12 days) after birth mainly with progressive
difficulty in sucking and swallowing, hunger and cry, diminished movements, stiffness to
touch and spasms. Tetanus may be localized or generalized in postnatal period.
Generalized tetanus, the most common form, manifests with spasm in different
muscles. Masseter muscle spasm (trismus) is the presenting symptom in 50% of
cases. Progressively neck rigidity, opisthotonus, laryngeal and pharyngeal spasms
appear. Continuous spasm of facial muscles result in sardonic smile (rhisus
sardonicus), pathognomonic for tetanus. Urinary retention results from sphincter spasm.
Tetanic seizures, characterized by sudden tonic first clenching arm flexion and
hyperextension of the legs in a conscious patient, may occur spontaneously or induced
by touch, sound or light.
Autonomic nervous symptom over activation leads to tachycardia, fever, labile

(fluctuating) hypertension and sweating.
Localized tetanus results in painful spasms of muscles adjacent to wound site and may
precede generalized tetanus.
Cephalic tetanus is a rare form of localized tetanus arising from wounds above the
neck. Retracted eye lids, trismus, risus sardonicus and spastic paralysis of the tongue
and pharyngeal muscle characterize it.
148
Diagnosis
Diagnosis greatly depends on clinical manifestations. No lab test is needed. Trismus
may result from dental abscess, retropharyngeal abscess, tonsillitis or parotitis.
Rabies may give trismus and seizures, but hydrophobia, clonic seizures and CSF
pleocytosis are present in rabies. Neck stiffness from meningitis may confuse.
However impaired consciousness and CSF pleocytosis are present.
Treatment
Main objectives of treatment are:
 Supportive care and proper nursing care
 Control of spasms and maintain airways
 Neutralization of toxin,
 Eradication of bacteria
 Prevention of recurrence
Eradication of bacteria
This involves surgical wound excision and debridement after administration of TAT and
antibiotics.
Excision of the umbilical sump is not recommended. Penicillin 100,000 V/kg/24 divided
into four doses should be given for 10 day to eradicate vegetative forms from wound
site. For penicillin allergic patients, erythromycin can be used.
Neutralization of toxin
Tetanus antitoxic (TAT) is used in a dose of 10,000U, half given intravascular and half
intramuscular after a skin test. High dose (50,000- 100,000 U) can be used.
Supportive care
 Patients should be cared for in a quiet dark and separate room
 Avoid unnecessary sounds and manipulations
 Feeding should be given via nasogastic tube
149
 Frequent cardiorespirator monitoring is mandatory.

 Meticulous nursing care with attention to mouth, skin, bladder and bowel prevents
bed ulcers, infection and constipation.
 Physiotherapy
Control of spasms and airway maintenance

Diazepam (0.25 – 0.5 mg/kg, I.V) and chlorpromazine (2 -4 mg/kg, I.V) given every
three hour alternatively are still in use to control spasms. The intravenous route may be
changed and nasogastric tube used after adequate control of spasms. Two to six weeks
may be needed before tapered withdrawal of there drugs.
In selected patients tracheotomy can be done to decrease the deaths from laryngeal
spasm and ventilatory support may be needed.
Active immunization with DPT (DT) at discharge is recommended for all patients
because tetanus doesn’t result in production of toxin neutralizing antibodies that
prevents recurrence
Complications
Complications include:
 Pneumonia
 Laceration of the mouth and tongue
 Long bone fractures
 Bed sores
 Malnutrition
Prognosis
The most important factor determining outcome is quality of supportive care. The
following factors indicate unfavorable prognosis:
 Short incubation period (  1 wk)
 Short period of onset ( 3 days) - the time between appearance of trismus and
onset of generalized tetanic spasms.
 Extremes of age (e.g,neonatal tetanus)
150
 Cephalic tetanus
 Fever (if part of autonomic effect)
 Pneumonia
 Frequent spasms
Prevention
 Tetanus is completely preventable disease
 There are three major ways:
 Vaccinate all child bearing age group females with TT
 Primary vaccination of infants and children with DPT
 Proper wound management. See table 3.1.
Table 15 Tetanus prophylaxis in wound management

Prior tetanus Minor clean Other wounds
doses Wounds
DPT + TAT DPT TAT
Uncertain or Yes No Yes Yes
< 3 doses
≥3 doses No* No No” No
+ TT can be given for children >7years (Td not available in Ethiopia)

*Yes, if >10years since last dose.
“Yes, if >5 years since last dose.
References:
1. Nelson Text book of pediatrics, 16/e, W.B. Saunders, 2000
2. Disease of children in the sub tropics and tropics, A/e, Edward Arnold, 1991
151
4.5 PAEDIATRIC HIV/AIDS

Goitom G/Yesus
Definition
HIV/AIDS is an acquired immune deficiency syndrome with a fatal clinical course
caused by viral etiologic agents.
Etiology
 HIV-1 and HIV-2 come from the retroviridae family, lentivirus genus, single
stranded RNA
 HIV-2 is rare in children and is prevalent in western and southern Africa
Epidemiology
Worldwide HIV-AIDS has created an enormous challenge on the survival of humankind.
Since its recognition, the virus has infected close to 65 million individuals and over 25
million have already died due to AIDS. Currently, over 42 million people are living with
the virus, and of these more than 70% are in Sub Saharan Africa. HIV-AIDS has
caused major impact on maternal and child health and survival. Most infected children
are in developing countries. Each year around 400,000 children are newly infected.
Currently between 5 and 8 million children are infected globally. As a result of maternal
death due to AIDS, between 10 and 15 million children are orphaned.
The year 2001 estimate for HIV /AIDS infection in Ethiopia was:
 Total people living with HIV infection is around 2.2 million
 adult prevalence rate is 6.6%
 The number of children with HIV-AIDS is 200,000
 Estimated number, of death due to AIDS in 2001 is 160,000
 Estimated number. of AIDS orphans currently living is 1.2 million
Transmission
Transmission occurs via:
 vertical transmission from mother to child
 parenteral exposure to blood
152
 sexual contact
The primary route of infection in children is by vertical transmission from the mother to
the child, accounting for virtually all new cases. This may occur in the intrauterine,
intrapartum or postnatal period via breast feeding. The rate of transmission from mother
to child in sub-Saharan Africa ranges from 25 to 52%.
Risk factors that may influence rate of vertical transmission are:

 high maternal viral load
 Low maternal antenatal CD4+ count (< 29%)
 Preterm delivery (< 34 wks of gestation)
 More than 4hr interval between membrane rupture and delivery
 Low birth weight
 Second twin
Pathogenesis
In adults and adolescents, after HIV has entered the circulation intense viremia ensues,
causing flu like symptom in 50 to 70% of cases. This primary viremia results in
widespread seeding of the virus to various organs including the brain and lymphoid
tissues. HIV selectively binds to cells expressing CD4+ molecules on their surface,
primarily helper T- lymphocytes (CD4+ cells) and cells of the macrophage lineage. The
CD4+ cells migrate to the lymph nodes, where they become activated and proliferate.
This may contribute to the dramatic decrease in the number of circulating CD4+ cells
and the generalized lymphadenopathy (LAP) characteristic of Acute Retroviral
Syndrome in adolescents and adults.
Following this, there will be establishment of cellular and humeral immune response
with in 2 to 4 months, with the level of cultivable virus from blood declining markedly
and patients enter a phase characterized by lack of symptoms and a return of CD4+
cells to only moderately decreased levels. This phase is called latency period and lasts
8 to 12 years. During this seemingly quiescent period, there is a very high turnover of
virus and CD4+ cells, which gradually causes deterioration of the immune system. As
the disease progresses, the lymph nodes disrupt and free the virus to the blood,
producing high level of viremia during the later stage of the disease.
153
In young children, unlike in adolescents and adults, the latency period is short. There
are three patterns of clinical course in these younger children:
a) Rapid course of progression
 15 to 25% of new born babies present with the onset of symptoms and AIDS in the
first few months of life
 if untreated median survival is between 6 and 9 months
 such baies are mostly positive for HIV culture / PCR in the first 48 hours of life
b) Slower progression of diseases

 The majority of perinatally infected newborn (60 – 80%) show a slower progression
 the median survival time is six years
 Many patients have negative culture PCR in the first week of life
c) Long term survivors

 Less than 5% of perinatally infected children have minimal or no progression of
disease with relatively normal CD4+ counts and very low viral load for more than 8
years.
Clinical manifestations vary widely among infants, children and adolescents. Initial
symptoms may be subtle or non-specific such as lymphadenopathy, hepato-
splenomegally, failure to thrive, chronic or recurrent diarrhoea, interstitial pneumonia or
oral trash. These symptoms may be distinguishable only by their persistence. Chronic
diarrhea, wasting and severe malnutrition are predominating symptoms in African
children compared to developed countries.
Symptoms found more commonly in children than adults are recurrent bacterial
infection, chronic parotid swelling, lymphoid interstitial penumonitis (LIP), and early
onset of progressive neurological deterioration.
Opportunistic infections are generally seen with severe depression of the CD4+ count.
The most common opportunistic infections in paediatric age group are as follows:
154
Bacterial infection
More than 20% of AIDS defining illnesses in children are recurrent bacterial infection
caused primarily by encapsulated organisms such as Streptococcus pneumonae and
salmonella species. Other commonly seen pathogens are staphylococci, enterococci,
pseudomonas, H. influenza and other gram negative and gram positive bacteria. The
most common serious infections are sepsis and pneumonia, accounting for more than
50% of infections in children with HIV. The common moderate infections are otitis
media, sinusitis and skin and soft tissue infections.
Fungal infection
Most common fungal infection is oral candidacies, which involves about 20% the
oesophagus presenting with anorexia, dysphagia, vomiting and fever.
Pneumocystis carinii pneumonia (PCP)
The peak incidence is at 3 to 6 months of age. Its clinical manifestations include acute
onset of fever, tachypnea, dyspnea and marked progressive hypoxemia. Chest X-ray
findings most commonly consist of interstitial infiltrates or diffuse alveolar infiltrates.
Parasitic infection
Cryptosporidiosis, microsporidiosis, isosporiasis or giardiasis are common opportunistic

infections causing significant morbidity.
Viral infections
Herpes virus causes significant morbidity in the form of recurrent gingivo-stomatitis.

Varicella zoster may cause chicken pox and recurrent herpes zoster. Measles may
occur despite immunization and without the typical rash. Other viral infections are
disseminated CMV disease, RSV and adenovirus infections.
No organ system is spared by HIV infection. The common organs that are affected by
the disease are:
CNS
The CNS is involved in 40 to 90% of children infected perinatally. The common
manifestations are progressive encephalopathy with loss of developmental milestones,
cognitive deterioration, acquired microcephaly and motor dysfunctions.
155
Respiratory tract
Recurrent respiratory tract infections (otitis media and sinusitis) are very common.
Lymphoid interstitial pneumonitis is the most common lower respiratory tract disease,
affecting 30 to 50% of HIV infected children. It manifests with insidious onset of
tachypnea, cough, and mild to moderate hypoxemia with normal or minimal
auscultatory findings. Characteristic reticulonodular pattern is seen on chest X-ray.
Bacterial pneumonia and pulmonary and extra-pulmonary tuberculosis are also

common in HIV infected children.
Cardiovascular system
About 20% of children with HIV have some degree of cardiac involvement.
Common manifestations are gallop rhythm, tachypnea and hepatosplenomegaly, which

are clinical indicators of congestive heart failure in HIV-infected children. It is due to
cardiomyopathy, myocarditis etc.
GIT
Oral manifestations include candidiasis, ulcerative gingivitis and salivary gland disease.
Lower intestinal include persistent or recurrent diarrhea, malabsorption, abdominal pain,

dysphagia and chronic liver inflammation.
Skin
Most problems involve inflammatory or infectious disorders that are not unique to this
disease
Seborrheic dermatitis or eczema that is severe form and unresponsive to treatment is

commonly associated with HIV-AIDS And are recurrent or chronic episodes of herpes
simplex, herpes-zoster moluscum contagiosum, anogenital warts and candidial
infections.
Hematologic manifestations
Hematologic manifestations include anaemia, leucopenia, and thrombocytopenia.
Malignancy
Non-Hodgkin’s lymphoma, 1o CNS lymphoma and leiomyosarcomas are commonly
reported
156
Diagnosis
Diagnosis may involve the following:
Serologic test
In a child older than 18 month, demonstration of antibodies to HIV by ELISA and
western immunoblot test establish diagnosis. However, in infants less than 18 months
of age, ELISA can be positive due to tansplacentally passed antibodies.
Viral detection
Viral detection is very useful in young patients less than 18 month of age and may
involve:
 HIV culture
 HIV DNA or RNA by Polymerase chain reaction
WHO clinical case definition of aids in children

This detects only children with symptomatic HIV infection
Major signs include:

 Weight loss or abnormally slow growth
 Chronic diarrhea for more than 1 month
 Prolonged fever for more than 1 month
 Recurrent bacterial lower respiratory infections
Minor signs include:

 Generalized lymph adenopathy and hepato splenomegally
 Oropharyngeal candidacies
 Repeated common infections
 Generalized dermatitis
 Confirmed maternal HIV
The presence of 2 major + 2 minor suggest the diagnosis of AIDS
The Ethiopian AIDS Case Definition (revised in February 2000)
157
Major signs
1. Failure to thrive (when the weight and height for age are less than the fifth percentile
or if either one crosses two major growth percentiles.
2. Repeated (2 or more within a period of 1 year or persistent (persisting for 1 month or
more) lower respiratory tract infections (LRTI)
3. Chorinc/recurrent diarrhea for more than 1 month
4. Unexplained prolonged fever for more than 1 month
Minor signs
1. Generalized lymphadenopathy
2. Repeated or persistent common infections (Otitis media, pharyngitis,
oropharyngealcadidiasis, purulent rhinitis, sinusitis, imetigo, etc
3. Unexplained neurological disorders or developmental delay and/or microcephaly
4. Hepatosplenomegally or splenomegally
5. Extensive varicella infections or molluscum contangiosum
6. Confirmed maternal HIV infection
Fever should not be counted as a major sign in the presence of LRTI.
The purpose of this case definition is for surveillance and not for diagnosis unless ther
is laboratory evidence of HIV infection.
AIDS in a child of up to12 years of age is defined with evidence of positive HIV test in
the presence of 3 major signs alone in the absence of other known causes of
immunosuppression OR
AIDS in a child of up to12 years of age is defined without laboratory evidence of HIV
infection in the presence of:
2 major and 2 minor signs, or
3 major and 1 minor signs
In the absence of other known causes of immunosuppression.
158
Treatment
Treatment involves:
 Supportive care:
 Counselling of care-giver on the options for infant feeding (see Infant feeding
section)
 Proper feeding
 Immunization (standard)
 Growth surveillance and social support
 Early access to medical care
 Treatment of opportunistic infections
 Antiretroviral drugs (according to the national guide)
Prevention
Prevention includes:
 Prevention of HIV among parents to be
 Prevention of unwanted pregnancy in HIV infected women
 Provision of antiretroviral drugs (neverapine) to the mother and infant during
pregnancy and after delivery
 Safe delivery practice - C/S delivery may have a protective effect compared to
vaginal delivery
 Combining elective c/s delivery with perinatal administration of neverapine reduces
the transmission significantly.
 Counselling on infant feeding options.
Exercise
1. What are the modes of transmission of HIV infection?
2. Describe the 3 patterns of clinical course of HIV-AIDS in children.
3. What are the common manifestations of PCP?
4. Describe the clinical case fefinition of AIDS in children.
5. List 4 preventive measures for HIV.
159
References
1. WHO/TB/96.2000, TB/HIV clinical manual, 1996.
2. Behrman, Kliegman, Jenson, Nelson Text Book of Pediatrics, 16th edition, 2000.
4.6 Viral Hepatitis

Dula Benti & Yezna Temesgen
Definition
Viral hepatitus is an inflammation of the hepatocytes due to viral causes.
Epidemiology and Etiology

Viral hepatitus continues to be a major health problem in both developing and
developed countries. Viral hepatitis is caused by hepatotrophic viruses designated as
hepatitis A, B, C, D, E and other viruses like herpes simplex virus, cytomegalovirus,
varicella virus, HIV, rubella and others which cause hepatitis as part of their clinical
spectra. All the hepatitis viruses own RNA except the B variant, which is a DNA virus.
Hepatitis A and E do not cause chronic infection but the rest are capable of causing
chronic liver disease. The D virus is a defective virus and thus needs co-infection with
hepatitis B virus to cause infection.
Pathogenesis and pathology - see specific viral hepatitis.
Clinical features
Most are asymtomatic. Those that are symtomatic present in three forms:
Anicteric form
The symptoms are non specific. Patients present with vomiting, fever and malaise. The
diagnosis is suspected if a child has history of contact with a patient suffering from
hepatitis or if the liver enzymes (SGOT, SGPT) are elevated.
Icteric form
The patients present with fever, nausea, vomiting, abdominal discomfort, jaundice and
tender and enlarged liver.
160
Fulminant form
This is due to massive hepatic necrosis. Patients present with deep jaundice, impaired
mental status that progresses to coma, and death. The prognosis is poor.
Diagnosis
Diagnosis includes:
- Elevated liver enzymes SGOT, SGPT
- Increased serum bilirubin
- Prolonged prothrombin time, and low serum albumin occurs in severe cases
- Serology – see specific viral infections below.
Management of acute viral hepatitis.

There is no specific treatment for typical viral hepatitis. Although hospitalization may be
required for severe illness, most patients do not require hospital care.
A high calorie diet is desirable, and because many patients may experience nausea late
in the day, the major calorie intake is best tolerated in the morning. Protein intake
should be restricted.
Drugs capable of provoking adverse reactions and drugs metabolized by the liver
should be avoided.
In fulminant hepatitis, the goal of therapy is to support the patient by maintenance fluid
balance, support of circulation and respiration, control of bleeding, correction of
hypoglycemia and treatment of other complications of the comatose state in anticipation
of liver regeneration and repair
Liver transplantation is indicated in chronic hepatitis with cirrhosis and hepatocellular

carcinoma.
161
Table 16: Summary of viral hepatitis and the route of transmission.
Disease Etiology Route of transmission

Hepatitis A HAV Fecal-oral
Hepatitis B HBV Vertical(intrapartal
intrauterine), Blood
transfusion
Hepatitis C HCV Blood transfusion, sexual
exposure
Hepatitis D HDV Percutaneous
Hepatitis E HEV -oral
Hepatitis A
Etiology
Hepatitis A is a member of the picornavirus family. It can be isolated from the stools of
infected patients.
Epidemiology
The prevalence rate in developing countries reaches 100% by the age of five years.
Transmission is by person-to-person contact and spreads by the fecal-oral routes.
There is no mother to fetus transmission during pregnancy. Fecal excretion of the virus
occurs late in the course and just before the onset of symptoms. Persons with HAV are
contagious for about a week after the onset of jaundice.
Incubation may take as long as four weeks.
Pathology
There is centrilobular necrosis with increased cellularity over the portal areas. The
lobular architecture is normal. Areas of infiltration by monocytes and polymononuclear
leukocytes are also documented. With fulminant hepatitis, there is total destruction of
the parenchyma. Three months after the onset of the acute hepatitis, the liver is
162
morphologically normal. There is a rise in the level of SGPT and SGOT. The height of
elevation does not correlate with the extent of hepatocellular injury and has little use in
predicting the prognosis. A drop in the level of SGPT and a rise of bilirubin with
prolonged prothrombin time are evidences of poor prognosis.
Clinical Features
Childhood infections are usually asymptomatic in children under five or present with
mild non-specific manifestations.
Usually children will have history of contact with jaundiced individuals Most of the
symptomatic children present with abrupt onset of fever malaise, nausea, emesis,
anorexia and abdominal discomfort. Jaundice is usually subtle in young children. the
duration of illness is less than one month. After this appetite, exercise tolerance and the
feeling of well-being return. There is no chronicity and fulminant illness and recovery is
almost complete.
Diagnosis
Diagnosis involes serology: Ig M anti-hepatitis A virus antibodies are detected at the
onset of symptoms and help for diagnosis of acute infection. Thereafter raised levels of
the Ig G persists for life.
Raised levels of bilirubin, SGOT, and SGPT and prolonged prothrombin time are also
diagnostic.
Neonates:
Physiologic jaundice
Hemolytic disease of the newborn
Sepsis
Infants and older children:
Sepsis
Malaria
Relapsing
163
Prevention
Precautions like hand washing and careful handling of feces and contaminated
materials of infected children is an important step in the disease control.
Hepatitis B virus
Etiology
The hepatitis B virus is a DNA virus that belongs to the hepadna viridae. It has three
group of antigens:
 Surface antigen (hepatitis Bs antigen, HBsAG)
 Core antigens (Hepatitis Bc antigen)
 Hepatitis Be antigen.
The virus replicates in the liver, lymphocytes, spleen and other organs.
Epidemiology
The hepatitis B virus is highly prevalent in the Sub-Saharan Africa. The majority of the
infections in children are asymptomatic. The most important mode of transmission in
children is perinatal exposure to a hepatitis BsAntigen and hepatitis BeAntigen positive
mother. Both intra uterine and intrapartal routes are possible. Breast-feeding is not a
risk factor. Other risk factors like intravenous drugs, blood contacts and sexual contact
are also possible ways.
In children with chronic hepatitis B infection, HbsAg becomes positive for six or more
months and is associated with progression to chronic liver disease and hepatocellular
carcinoma. The incubation period ranges from 45 to 160 days (average 100 days).
Pathology and pathogenesis

The acute response is the same as that of hepatitis A infection. Histologic changes
persist in hepatitis with B, C, D types and may progress to chronic liver disease. Unlike
the others, injury is by immune mediated mechanisms. After infection of the
hepatocytes, viral antigens appear on the surface. (HbsAg, HbcAg). The mechanism for
chronic hepatitis is not yet known.
164
Clinical features
Children are usually asymptomatic. Symptoms are more severe with greater rate of
fulminant hepatitis than that of Hepatitis A virus
The illness is preceded by arthralgia and skin rashes, lethargy, anorexia, and malaise.
Jaundice is present in 25% of cases. Other extra hepatic manifestations are
polyarthritis, glomerulonephritis and aplastic anemia.
The common physical findings are jaundiced skin, mucous membrane and sclera,
tender hepatomegaly and splenomegally.
In the usual course of resolving HBV infection, symptoms are present for 6 to 8 weeks.
Chronic hepatitis occurs and chronic active form results in cirrhosis and hepatocellular
carcinoma.
Diagnosis
HbsAg is the first serologic marker of infection. Its rise coincides with the onset of
symptoms. HbeAg is present during the acute phase and it indicates a highly infectious
state. HbsAg level falls before the end of symptoms. Ig M anti HbcAg rises early after
infection and persists for many months before being replaced by Ig G anti HbcAg which
persists for years. Ig M anti HBcAg is not found in perinatal HBV infections.
Anti Hbc Ag is the most valuable single serologic marker of acute HBV infection
because it is present almost as early as HbsAg and continues to be present later in the
course of the disease when HbsAg has disappeared.
Only Anti HbsAg is present in persons immunized with hepatitis B vaccine. AntiHbsAg
and AntiHBcAg are detected in persons with resolved infection.
Management
Management is the same as that of the general management of viral hepatitis.
Complications
 Acute fulminant hepatitis
 Chronic hepatitis
 Cirrhosis
165
 Hepatocellular Carcinoma
Prevention
Prevention involves the immunization of neonates. More than 90% of infants who
acquire the infection perinatally will become chronic carriers. There is lesser risk of
acquiring chronic carrier state with age.
Infants born to HbsAg positive mothers should receive the vaccine at birth, in the first
month and at 6 months of age.
4.7 EPIDEMIC TYPHUS

Goitom G/Yesus
Definition:
Epidemic typhus is a louse borne febrile illness caused by rickettsia prowazekii.
Epidemiology
Typhus is characteristically seen during times of poor hygienic practices associated with
crowding, war, famine and civil conflicts. Most cases of epidemic typhus occur
sporadically but epidemics have occurred in Africa, especially in Ethiopia, Nigeria, and
Burundi.
Pathophysiology
Transmission is through human lice or head lice, which become infected by feeding on
the blood of an infected person. The rickettsia multiply in the gut of the lice and are
passed into their feces. Transmission to a susceptible human host occurs through skin
abrasions or perforations and the conjunctiva. After entry through the skin, the rickettsia
get access to blood vessels.
The incubation period is usually less than 14 days. The clinical manifestations include:
 Most patients have fever, severe headache, abdominal tenderness and pink or
erythematous rash over the trunk.
 Less common manifestations are non productive cough, photophobia, abdominal
pain, tinnitus, constipation.
166
Diagnosis
Clinical diagnosis may be impossible because there are many diseases such as
malaria, typhoid fever, meningococcemia and relapsing fever which have similar clinical
manifestations. No laboratory tests establish the diagnosis.
Treatment
Treatment includes chloramphenicole 50-100 mg/KG/24hr PO in four divided doses for

10 days, nursing care and symptomatic supportive therapy.
Exercise
1. List the factors, which lead to high prevalence of epidemic typhus?
2. What is the vector for transmission of the diseade?
References

the subtropics and tropics, 3rd edition, 1986
4.8 RELAPSING FEVER
Goitom G/Yesus
Definition
Relasping fever is an arthropod borne infection characterized by recurrent episodes of
fever and is caused by borrelia species
Epidemiology
Louse borne fever (epidemic relapsing fever)
Louse borne fever is caused by borrelia recurrentis and transmitted from person to
person by the human body louse (pediculous humanis). Human infection occurs as a
result of crushing lice during scratching, allowing infected hemolymph to enter through
167
abraded skin. Louse borne disease occurs usually in epidemics, often associated with
typhus.
Epidemics are associated with war, poverty, famine, prison setttings and poor personal
hygiene. This form of relapsing fever occurs more commonly during winter. The major
endemic focus of the disease is the high lands of Ethiopia.
Tick borne fever (endemic relapsing fever)
Tick borne fever is caused by borrelia duttoni. After ingestion of an infective meal,
spiochets invade all tissue of their arthropod hosts, including salivary glands and
reproductive tracts. Human infection occurs when saliva or feces is released by the
thick during feeding thereby permitting spirochetes to penetrate the skin and mucous
membrane.
Rodents are the principal reservoirs. Infected ticks get access to human dwellings on
the rodent host. Human contacts are unnoticed because these tics are nocturnal
feeders, have painless bite and detach immediately. Tick borne relapsing fever occurs
sporadically in many tropical and subtropical countries.
Pathogenesis
The cyclic nature of relapsing fever is explained by the ability of borrelia organisms to
continually undergo antigenic variations. Multiple variants evolve simultaneously during
the first relapse, with one type becoming predominant. During febrile episodes,
spirochetes enter the blood steam, induce development of specific antibodies, undergo
lysis and phagocytosis ending up with remission of fever. The numbers of relapses in
untreated patients depend on the number of antigenic variants of the infecting strain.
Louse borne disease has a longer incubation period, longer periods of pyrexia, fewer
relapses and longer remission periods than tick borne disease. The incubation period is
2 to 14 days. Common clinical features are:
168
Sudden onset of fever, headache, myalgia, arthralgia, nausea, and vomiting;
Additional symptoms that may occur later include: abdominal pain, cough, bleeding
manifestations (epistaxis, hemoptysis, hematuria, and hematemesis);
CNS manifestations include lethargy, stupor, meningesmus, convulsion, peripheral

neuritis, and cranial nerve palsy.
Skin manifestations may include diffuse erythematous, macular, or petechial rash;
Severe form of manifestations include: myocarditis, hepatic failure, and disseminated

intravascular coagulopathy.
The initial symptomatic period ends in a crisis in 4 to 10 days, marked by abrupt

diaphoresis, hypothermia hypotension, bradycardia, profound muscle weakness, and
prostration. This crisis is called Jarisch-Hrxheimer reaction and may occur within 1 to 2
hours of antibiotic therapy.
Diagnosis
Diagnosis involves the demonstration of spirochetes in thin or thick blood smear stained
with Giemsa or Wright stain.
Treatment
Treatment involves the following:

 Supportive
 Keep IV line opened
 Antibiotics
 Procaine penicillin 400, 000 IU IM
 Check blood film after 24 hous and, if negative, give chloramphenicole
50mg/Kg/24hr in four divided doses
 Patients should be deloused immediately after admission by shaving the head
and removing all clothing to be sprayed with insecticide or be boiled.
Prevention
Prevention involves health education on hygienic practice.
169
Exercise
1. What is the cause of relapsing febrile episodes in relapsing fever?
2. How does Jarisch-Hrxheimer manifest clinically?
References
the subtropics and tropics, 3rd edition, 1986.
4.9 MALARIA
Goitom G/Yesus
Definition
Maleria is an acute and chronic protozoan illness characterized by paroxysms of fever,
chills, sweats, fatigue, anemia and splenomegally.
Etiology
Four species of plasmodium are known to cause malaria: P. falciparum, P. malariae, P.
ovale, and P. vivax. Plasmodium species exist in variety forms and have a complex life
cycle that enables them to survive in different cellular environment in human host
(asexual phase) and anopheles mosquito (sexual phase).
Epidemiology
Malaria is of overwhelming importance in the developing world today with an estimated

300 million cases and over 1 million deaths each year. Most malarial deaths occur in
infants and young children. Malaria exists where an effective vector (anopheles
mosquito) breed in nature and where human carriers of sexual forms of the parasite are
available to these mosquitoes. The principal areas of transmissions are Africa, Asia,
and South America.
170
In Ethiopia, malaria affects 75% of the population and over five million clinical cases are
reported annually. In 2000-2001, malaria was the number one cause of outpatient
attendance, the number one cause of hospital admission and the third highest cause of
deaths in hospitals.
Malaria is transmitted to humans by anopheles mosquitoes; but it can also be

transmitted through blood transfusion and from pregnant woman to her fetus. In highly
endemic areas, P.falciparum infection of indigenous children in the first 5 years of life
causes severe and potentially fatal illness. In areas of low endemicity, however, where
the immunity of indigenous population is low, severe infection occur in all age groups
including adults.
171
Pathogenesis
The symptoms and pathology are caused by the asexual erythrocytic stage of the
malaria parasite. Four important pathologic processes have been identified in patients
with malaria: fever, anemia, immunopathologic events and tissue anoxia resulting from
cytoadherence of infected erythrocytes.
 Fever occurs when red blood cells rapture and release merozoites in to circulation.
 Anemia is caused by hemolysis, sequestration of red blood cells in the spleen and
other organs, and suppression of the bone marrow.
172
 Immunopathologic events include immune complex formation, immune suppression,

and release of inflammatory mediators such as Tumor necrosis factor which may be
responsible for many of the pathologic features of the disease.
 Cytoadherence to vascular endothelium which occurs in P. falciparum may lead to
obstruction of blood flow and capillary damage with resultant vascular leakage of
protein and fluid, edema and tissue anoxia in the brain, heart, lungs, intestine and
kidney.
The human body responds to plasmodium infection by production of partial immunity.

This averts subsequent severe form of infection, but eradication or prevention of future
infection is not achieved.
173
174
The usual incubation periods are as follows: P. falciparum, 9 to 14 days, P. vivax, 12 to
17 days, P. ovale, 16to18 days, and P. malariae, 18 to 40 days. Classic manifestation
includes febrile paroxysms alternating with periods of fatigue, but otherwise relative
wellness. Symptoms associated with febrile paroxysms include high fever, rigors,
sweats and headache, as well as myalgia, back-pain, abdominal pain, nausea,
vomiting, diarrhea, pallor and jaundice.
Paroxysms correspond with the rupture of schizonts that occurs every 48 hours with P.
vivax and P. ovale and results in daily fever spikes; and occurs every 72 hours with P.
malarae and results in alternate day or every third day fever spike. Periodicity is less
apparent with P. falciparum and mixed infections. Long-term relapse occurs in P. vivax
and P. ovale due to release of merozoits from the exo-erythrocytic source in the liver.
P. falciparum malaria is the most severe form and is associated with more intense
parasitemia. The case fatality rate reaches 30% in non-immune infants. The diagnoses
of P. falciparum malaria constitutes of medical emergency.
P. falciparum infects immature and mature RBC, whereas P. malariae infects only
mature RBC. P. falciparum is most commonly associated with serious complications
although milder or asymptomatic infection occurs in those who are partially immune.
The severe manifestations of P. falciparum malaria are as follows:

 Cerebral malaria: unarousable coma not attributable to any other causes lasting
30 minutes or more after a generalized convulsion.
 Severe anemia: a hematocrit level of less than 15%, or hemoglobin less than
5gm/dl.
 Hypoglycemia: blood glucose level of less than 40mg/dl.
 Generalized convulsion: more than 2 within 24hrs
 Renal failure: urine output less than 12ml/Kg/24 hours failing to improve after
rehydration.
 Pulmonary edema
 Shock
175
 Spontaneous bleeding (from gums, nose, intestine etc. and/or laboratory evidence
of disseminated intra vascular coagulation.
 Acidosis
 Hemoglobinuria
 Impairment of consciousness less marked than unarousable coma
 Prostration
 Jaundice
 Hyperpyrexia
 Hyperparasitemia
The commonest complications in children are cerebral malaria, convulsions, severe

anemia, and hypoglycemia.
Diagnosis
Diagnosis involves the identification of organisms on Wright or Giemsa stained smears

of peripheral blood. The thick smear is used for the detection of parasites and the thin
smear for the detection of the species of parasite.
A single negative blood smear finding does not exclude malaria, it may be necessary to
repeat the smears as frequently as every 4 to 6hours per day in order to establish a
diagnosis.
In ill patients with change of sensorium, do a lumbar puncture to rule out meningitis.
Differential diagnosis
Differential diagnosis includes viral infection such as hepatitis, sepsis, pneumonia,

meningitis, encephalitis, endocarditis, and gastroenteritis.
Treatment
Uncomplicated malaria
 First-line treatment
The first-line treatment of P. falciparum malaria is sulfadoxinr-pyrimethamine. For
the treatment of malaria caused due to P. vivax, P. mlariae or P. ovale, the first-line
drug of choice is chloroquine.
 Second-line treatment
176
If a P. falciparum positive patient returns to the laboratory with fever or history of fever
between the thrid day and fourtheenth day after treatment with sulfadoxinr-
pyrimethamine, check whether the patient has vomited the drug or had diarrhea after
treatment.
If the blood film is positive for asexual parasites and the above conditions are excluded,
give quinine orally. For details of dosages of oral quinine according to age and body
weight, see table below.
Treatment of severe P. falciparum malaria

 Prevention or early detection and treatment of convulsion, hypoglycemia, and
hyperpyrexia.
 Give prophylactic anticonvulsant - phenobarbital 5-10mg/Kg
 Start antimalarial chemotherapy with intravenous quinine (see below for dosage
and administration)
 Measure and monitor urine out put
Blood transfusion for severe anemia or symptomatic congestive heart failure.
Treatment Schedules
1a. Chloroquine
Tablets of 150 mg base or syrup 50 mg base per 5 ml.
Total dose of 25 mg base per kg over 3 days (10 mg base per kg on Days 1 and 2, and
5 mg base per kg on day 3).
Side effects include:

Dizziness, skeletal muscle weakness, mild gastrointestinal disturbances (nausea,
vomiting, abdominal discomfort and diarrhoea) and pruritus. Pruritus may be severe
but is usually over within 48-72 hours.
Contra-indications include:
 Persons with known hypersensitivity
 Persons with a history of epilepsy
 Persons suffering from psoriasis.
177
Table 17: Chloroquine treatment schedule
Weight (kg) Age (years) Day 1 Day 2 Day 3

< 4 months
5-6 Tablets ½ ¼ ¼
Syrup 5ml 5ml 2.5 ml
4-11 months
7-10 Tablets ½ ½ ½
Syrup 7.5ml 7.5 ml 5ml
1-2 years
11-14 Tablets 1 1 ½
Syrup 12.5ml 12.5ml 7.5ml
3-4 years
15-18 Tablets 1 1 1
Syrup 15ml 15ml 15ml
5-7years
19-24 Tablets 1 1/2 1 1/2 1
Syrup 20ml 20ml 15ml
25-35 8-10 years 2½ 2½ 1
36-50 11-13 years 3 3 2
50+ 14+ years 4 4 2
1b. Sulfadoxine-pyrimethamine:
Tablet containing 500mg sulfadoxine plus 25mg pyrimethamine or injection having the
same composition per 2.5 ml.
178
Table 18: Sulfadoxine-pyrimethamine treatment schedule

Weight Age Number of Intramuscular
(Kg) (Years) tablets Injection (ml)
5-6 2-3 months ¼ 0.6
7-10 4-11 months ½ 1.2
11-14 1-2 ¾ 1.8
15-18 3-4 1 2.5
19-29 5-9 1½ 3.8
30-39 10-11 2 5
40-49 12-13 2½ 6.2
50+ 14+ 3 7.5
Side effects include gastrointestinal disturbances, nausea and vomiting. Skin reactions
can occur with repeated doses ranging from a mild form to very severe, like erythema
multiforme or Stevens Johnson syndrome, which are rare but can be fatal. Patients
treated with this drug should be carefully followed-up. Other sever rarer side effects
include anemia, leucopenia and, in G6PD deficient persons, intravascular haemolysis.
Contra-indications include:
Malaria prophylaxis either alone or in combination.
Persons with a previous history of skin rash after using any form of sulfa drug.
Infants less than two months and
Persons with hepatic or renal dysfunction.
1c. Quinine
Treatment is with quinine 8 mg base/kg 3 times daily for 7 days
179
Table 19: Quinine treatment schedule
Oral (tablets)
Weight Dosage to be given daily for
Age (Years)
(Kg) 7 days
200mg salt 300 mg salt
4-6 2-4 months ¼ -
6-10 4-12 months 1/3 ¼
10-12 1-2 years ½ 1/3
12-14 2-3 years ¾ ½
14-19 3-5 years ¾ ½
20-24 5-7 years 1 ¾
25-35 8-10 years 1½ 1
36-50 11-13 years 2 1½
50+ 14+ 3 2
Side effects include dizziness, ringing in the ears, blurred vision and tremors known
collectively as “cinchonism”. At the above dosages, these symptoms are not severe
enough to stop treatment and subside spontaneously when administration of the drugs
ends. Hypoglycaemia may be caused by quinine.
There are no contra-indications to the oral administration of the drug with in the above
dosage.
1d. Primaquine
Treat with primaquine 0.25 mg base per kg daily for 14 days.
180
Table 20: Primaquine treatment schedule
Weight Age Number of tablets

(Kg) (Years) 7.5 mg 15 mg
tablet tablet
19-24 5-7 ¾ -
25-35 8-10 1 ½
36-50 11-13 1½ ¾
50+ 14+ 2 1
Side effects such as anorexia, nausea, vomiting, abdominal pain and cramps are dose
related and relatively rare at daily doses up to 0.25 mg base/kg. They may also be
accompanied by vague symptoms such as weakness and uneasiness in the chest.
Contraindications include the following:

 Pregnancy
 Children under four years
 Any condition that predisposes to granulocytopenia, including active rheumatoid
arthritis and systemic lupus erythematosus.
Intravenous Quinine administration
Dosage- start with 20mg/Kg IV over 4hrs, followed by 10mg/Kg diluted in 10ml/Kg
isotonic fluid over 4hrs repeated 8 hourly till patient can swallow, then oral tablets
10mg/Kg 8 hourly to complete 7 days or a single dose of Fancidar.
4.10 Leishmaniasis
Goitom G/Yesus
Definition
Leishmaniases are a group of zoonotic diseases caused by intracellular protozoan
parasites of the genus leishimania which are transmitted by phlebotomine sandlflies.
181
Ethiology
In Ethiopia, leishmaniasis is caused by leishmania donovani (visceral leishmaniasis two
lands), L. Ethiopia (cutaneous leishmaniasis, high lands) and occasionally L. Major and
L. tropica.
Epidemiology
An estimated 10 to 50 million people are affected worldwide in endemic tropical and
subtropical regions. Visual leishmaniasis occurs in Ethiopia mainly in arid and semiarid
lowlands below 1300 meters altitude. Endemic areas extend across the border with
neighboring countries (Sudan).
The age /sex–specific pattern indicates infants and children under the age 5, adult
above 50 and women of childbearing age to be at relatively low risk which reflects an
outdoor exposure to transmission.
Cutaneous leishmaniasis has a prevalence rate of 5.5 to 40 per 1,000 according to

surveys done in endemic areas which are situated at 14000 to 2700 meters of altitude.
Children are mainly affected with peak incidence seen at 10 – 20 years of age.
Pathogenesis
Clinical features
Classically three major forms of leishmanias are described: visceral leishmaniasis,
contaneous leishmaniasis and mucosal leishmaniasis
Visceral leishmaniasis (VL,kala– azar)

After exposure to the organism, the child may have completely asymptomatic infection
or develop mild constitutional symptoms (malaise, diarrhea), intermittent fever and
weight loss. Most children improve without therapy but one third develop active kala-
azar. In Ethiopian patients splenomegaly and fever are most common (98%), wasting
(84%) and ascites are not common.
182
Most (90%) die due to intercurrent infection (pneumonia and diarrhea), a result of the
lowered cell mediated immunity. VL is recognized as an opportunistic infection
associated with HIV. The typical hepatolplenomgally is absent but GI involvement is
prominent
Cutaneous leishmaniasis (CL)

Three forms of cutaneous leishmaniasis are described in Ethiopian patients
 Localized cuetaneous leishmaniasis (LCL)
 Non-self healing disseminated or diffuse (DCL)
 Mucocu taneous (MCL)
Localized coetaneous leishmanisis is mainly seen in children as a single lesion on

exposed skin: face, forearms. The typical lesion is a reddish plaque with irregular
border and shallow central cuter. It heals spontaneously after 8 to 10 months leaving a
hyper pigmented scar.
Diagnosis
Demonstration of the amastigotes in specimens (skin lesion, spleen bone – marrow – or
lymph node aspirates) using Giemsa stain makes definitive diagnosis. Direct
agglutination test is rapid and sensitive test. VL can have anemia, leucopenia,
thrombocytopenia, elevated hepatic transaminases and hyperglobulinemia.
Treatment
Drug therapy involves pentavalent antimony compounds. Sodium stibogluconate
20ml/kg/24 hour IV or IM for 20 to 28 days is used with cure rate of 90 to 100% (LCL),
50 to 70% (ML, and 80 to 100% (VL). Alternative treatment includes pentamidin,
ampholericin B, deroxycholate and ketoconazole.
Prevention
Preventive measures consist of community based residual insecticide spraying, control
of reservoir hosts, chemotherapy and avoidance of exposure to the nocturnal sandfly
using permethrin-impregnanted mosquito nettings.
183
4.11 SCHISTOSOMIASIS (SCHISTOSOMA)
Tsinuel Girma
Definition
Schistosomiasis is an infectious disease caused by schistosoma, flukes or trematodes
that parasitize the blood stream.
Epidemiology
Schistosoma infects more than 200 million people worldwide, primarily children and
young adults. Prevalence increases with age to a maximum at 10 to 20 years of age.
Opening of irrigation fields and heavy dependence on stream water for domestic use
increases spread. Most low lands (altitude between 1500 meters less than 2000
meters) in Ethiopia are endemic to S.mansoni. Surveys done in Ethiopia among 27,658
people showed overall prevalence of schistosoma is 25% with children predominantly
affected (up to 90% in some communities)
Etiology
Five schistosme species infect humans: S.haematobium, S. mansoni, S. japonicum, s.
intercalatum and S. mekongi. Mainly S. mansoni and s. haematobium are prevalent in
Ethiopia. Snails act as an intermediate host.
Pathogenesis
Humans are infected through contact with water contaminated with cercariae (the
infective stage of the parasite). The Cercaria penetrates the skin, migrates to lung and
finally reaches the liver.
Sexually mature adult worms from the liver migrate to their specific sites characteristic
of each species: S. mansoni to inferior mesenteric veins and S. haematobium to the
venous beds of the bladder and ureters.
184
Chronic granulomatous injury occurs at egg deposition sites: intestine (S. mansoni)
urinary bladder and ureter (S. haematobium). Cell mediated immunity plays a significant
role in tissue injury.
Symptoms occur primarily in heavily infected children.
Acute schistosomiasis (katamaya fever) occur 4 to 8 weeks after exposure mimicking a

serum sickness like syndrome manifested by fever, chills, sweating, lymphadenopathy,
hepatosplenomegally and eosinoplnia.
Children with chronic schistosoma mansoni may have bloody diarrhea and colcky
abdominal pain. The intestinal phase may pass unnoticed and the syndrome of
hepatosplenomegaly, portal hypertention, acsites and hematemesis may be the intial
presenting symptoms.
Symptomatic children with chronic schistosomiasis haematobium usually complain of

frequency, dysuria and terminal hematuria. Long standing infection results in chronic
renal failure, bacterial infection and bladder cancer.
Diagnosis
S. mansoni is diagnosed by light microscopy of stool which shows characetrstic eggs
(see tis 5.1) S. hematobium is identified from urine.
a b c
a-S. haemetobium b-S. mansoni c- S. japonicum

Figure 19: Schistosomiasis types
185
Treatment
The recommended treatment for schstosomiasis is praziquantel 40mg /kg in a single or
divided doses.
Prevention
Prfevention involves improved sanitary conditions, reducing human-water contact,
molluscicides and the treatment of infected individual help in disease control
References
1. Nelson Text of pediatrics, 16 ed, W.B. Sanders 2500
2. Disease of children in the sub tropics and tropics, A/e, Edward Arnold, 1991
3. Teklemariam, Ayele, Eyassu Habte, Gobr, and Ayche Bellehu (eds), Leishmaniasis
in Ethiopia. PP. 29 – 40 AA: Institute of Pathobiology AAU. 1982
4. Lidotjprn, B. and J. Olfasson. Kala – azar in the segen and woyto valleys Southwest
Ethiopia, Ethiop. Med. J. 1983; 21, 35 – 42
5. Ayele Teklmariam, Mekonnen Tefera, Mekonnen Muluneh et al, clinical features of

heishmanisis in Ethiopia, Ethiop. Med. J, 1988; 26: 69 – 76
6. Mengistu, Geneal, T. Laskey, Teferi Gemetchl et al cutaneous leishmaniasis in

South West Ethiopia Tras. R. Soc. Trop. Med. Hyg. 1992; 86: 149 – 153
186
CHAPTER FIVE
DISEASES OF THE RESPIRATORY SYSTEM
5.1 Upper respiratory tract infection

Habtamu Fekadu
Otitis media
Definition
Otitis media is an inflammation of the middle ear. It may be acute if symptoms for less
than 2 weeks, or chronic if symptoms for more than 2 week.
Etiology
Otitis media is casued by streptoccocus pneumonia, hemophilus influenzae and
moraxella catarrhalis
Epidemiology
Ear pain and/or discharge is one of the most common presenting symptoms to out-
patient departments in under 5 children. About one third of children will have at least
one episode of acute otitis media by 3 years of age.
Pathogenesis
The two important factors are eustachian tube dysfunction and URTI. Both lead to
obstruction of the tubes and serous fluid collection in the middle ear. If there is an
associated entry of pathogenic organisms, suppurative otitis media may follow.
Acute amifestations include otalgia, fever, ear discharge hearing loss. Infants may
present with irritability, diarrhoea, vomiting and pulling of the ear.
Diagnosis
Clinical digostic signs include>
- Ear discharge
- Visualization of tympanic membrane: red membrane, loss of normal light reflex.
187
Treatment
Treatment involves the following:
1. Antibiotics for 5 days
- Cotrimoxazole. Or
- Amoxicillin or
- Ampicillin
2. Wicking of the ear with dry cotton for discharging ear.
3. Analgesic - Acetaminophen
Complications
- Mastoiditis
- Hearing loss
- Intracranial (meningitis, brain abscess)
Acute tonsillopharyngitis
Definition
Acute tonsillopharyngitis is an Infection of the upper respiratory tract with principal
involvement of the throat and tonsils.
Etiology
Acute tonsillopharyngitis is mostly viral as parts of URTI
Group A B-hemolytic streptococcus is the most common and the most important
bacterial agent after 2 years of age.
Clinical
The clinical features of acute tonsillopharyngitis are as follows:
Viral: insidious onset
Other signs of URTI (runny nose, sneezing, coryza etc.)
Contact history with family member with URTI.
Streptococcal: is more common in children older then 2 years and peaks in children
bewteen 4 and 7 years of age. They may present with:
- Headache, abdominal pain, vomiting, high grade fever, sore throat.
188
- Diffuse redness and exudates, petechiae over the palates, and, tender cervical
lymphadenopathy.
Most strongly suggestive: - Age 5 to15 years.
- Clinical evidence of acute pharyngitis
- Absence of URTI
Complications
Complications include the following:
Suppurative: Otitis media
- Retropharyngeal and peritonsilar abscess
Non suppurative - Acute glomerulonephritis, Rheumatic fever.
Treatment
Treatment may include:
- Benzathine penicillin
- Oral penicillin
- Analgesics - paracitamol.
Nasopharyngitis (common cold)
Definition
Nasopharyngitis is a viral infection of the nasopharyngeal mucosa.
Etiology
The commonest cause of nasopharyngitis is rhinovirus. Other causes are adenovirus,
influenza, parainfluenza viruses etc
Epidemiology
Nasopharyngitis is frequent and seasonal. Person to person transmission is usually
airborne.
Clinical features
The clinical features include:
- Runny nose, often with fever, sneezing and cough.
- Sometimes accompanied by conjunctivitis.
Always check the tympanic membranes of an infant with a cold.
189
Complications
The complications of nasopharyngitis include:
 Acute otitis media
 Pneumonia
Treatment
Treatment may involve the following:
- Sooth the throat and relieve the cough with safe home remedies like tea and honey
- Nasopharyngeal drops using a syringe filled with normal saline (or drop clean water
mixed with salt using cotton), 4 to 6 times a day.
- Treat fever
- Advise the mother to return immediately if the child develops fast breathing or
difficulty of breathing or if the child becomes sicker.
- Follow up in 5 days
5.2. Acute upper airway obstruction

Tsinuel Girma
Extrathoracic (upper airway) obstruction is exacerbated during inspiration because the

pressure inside the airway becomes very negative compared to the atmospheric
pressure outside, causing the airways to collapse on inspiration. This physiologic
mechanism (stridor, the difficulty during inspiration) explains what happens in cases of
obstructions above the thoracic outlet.
Croup is a term encompassing different group of acute, mostly infectious conditions

characterized by brassy cough, inspiratory stridor, horesness of voice and different
degrees of respiratory distress secondary to laryngeal obstruction.
190
Classification
Upper airway obstruction can be classified based on mechanism (etiologic) of
obstruction.
1. Extrinsic airway compression and narrowing
Malformations/syndromes craniofacial anomalies (e.g., Pierre-Robin syndrome)
Masses
Enlarged lymph nodes
Enlarged tonsils
Trauma
Neck and chest injury
Infection
Peritonilar abscess
Retropharngeal abscess
Diphtheria
2. Intrinsic airway narrowing and/or collapse
Malformation
Larynogotracheomalacia
Larynogeal stenosis
Masses
Foreign body in the airway
Laryngeal polyps or papillomatosis
Trauma
Intubation
Burns
Neck injury
Infection
Tracheitis, bacterial
Epiglottitis
Laryngiotrachiobronchitis, viral
Other Allergic reaction: e.g., anaphylaxis, angioneourotic edema
Vocal cord paralysis
Laryngospasm
191
Laryngotrachiobronchtis (viral croup)
Epidemiology
Viral croup mainly affects children between the age of 3 months to 5 years of age.
Males are more affected than females. The rate of viral croup increases in cold season.
Fifteen percent (15%) of cases have a positive family history.
Etiology
Parainfluenza viruses account for 75% of cases. Other viruses such as adenoviruses,
respiratory synctitial viruse and measles virus can also be involved in few cases.
Rarely, mycoplasma pneumoniae and diphtetria can be isolated.
The degree of airway obstruction in children is severe compared to adults for the
following reasons:
 Small size of the airways
 Loosely attached mucous memrane
 Abundant mucous glands of the airways
 Frequent respiratory infections
The typical patient presents with a history of upper respiratory infection several days
before onset and/or other family members with common cold, low grade fever,
intermittent stridor and mild brassy cough. As the disease progresses, the patient will
have continous stridor, signs of severe respiratory distress, decreased air entry,
restlessness and lethargy. The degree of severity can be assessed and followed using
croup score (see below).
Throat examination is best deferred, since the risk of inducing laryngeal spasm is very
high.
192
Diagnosis
Diagnosis is mainly clinical. Lateral neck X-ray may show subglotic narrowing but
because of the risk of sudden laryngeal obstruction it should be done in the presence of
professionals with skills of emergency repiratory support.
Diferential Diagnosis
- Epiglotitis
- Bacterial tracehitis
- Foreign body aspiration
- Retropharygeal /peirtonsilar abscess
Treatment
Treatment includes the following:
- Supportive - Oxygen
- Intrvenous fluids
- Close monitoring
- Dexamethasone 0.5mg/kg i.m. repeat if no improvement after 4 to 6 hours.
- Racemic epinephrine
- Home -cold steam (sooth throat or reduce obstruction)
- Tracheostomy – if the distress gets worse, despite the above treatments or if there
are signs of impending respiratory failure at any time.
Complications
- Involvement of lower air ways
- Bacterial superinfection is rare
- Respiratory failure
Prognosis
Prognosis is excellent, there is usually no residual effect
193
Epiglotitis
Definition
Epiglotitis is an acute inflammatory (infectious) process involving the epiglottis and
surrounding structures.
Epidemiology
Children between the ages of 2 and 7 years are affected and the peak incidence occurs
at about 3 and a half years of age. The male to female ratio is 3:2. There is no seasonal
variation.
Etiology
H.influenzae type b cuases almost all cases of epiglotitis. Rarely streptococcus
pnuermoniae and strepococcus pyogeanes can lead to epiglotitis.
Classically epiglotitis starts suddenly with rapid progression to complete obstruction.
Patients are toxic with high grade fever, sore throat, dysphagia, tachycardia,
restlesness, drooling of saliva and stridor.
Big children hyprerextend their neck and sit leaning forward.
Throat examination, without adequate respiratory support preparation, sholud be

avoided since it causes sudden reflex laryngeal spasm.
Diagnosis
Diagnosis is mainly clinical. Blood culture and lateral neck X-Ray help for diagnosis but
they are time consuming and add little to the immediate management. Laryngoscope
shows cherry red epiglottis if it is done with proper preparation for respiratory support or
intubation.
Management
The principles of management are:
 Routine tracheostomy/nasotracheal intubation
 Oxygen
 Chloramphenicol 75 -100mg/kg /dose i.v for 7 to 20 days.
194
Foreign Body Aspiration

Tsinuel Girma
Most foreign bodies aspirated into the air ways are cleared by mucoliliary system or
cough reflex. Review of seventy nine children treated at the Ethio-Sewedish Children’s
Hospital showed a male to female ratio of 2:1 4 and a mean age 3 years. Another
review, in the same hospital showed an average of 6 cases per year: bean seeds
accounting for nearly half of aspired objects.
Aspiration is frequent in children with neurological abnormality (poor coordination of

swallowing), cleft palate, impaired consciousness and age groups of 9 months to 5
years.
The presentation varies depending on the site of blockage, degree of observation and
time of presentation after aspiration which is usually delayed. A review of cases in Black
Lion hospital showed that only 10% of cases presented within 24 hours of aspiration.
Laryngeal foreign bodies

Cough (croupy and horse) and progressive obstruction manifested by inspiratory
stridor, respiratory distress and aphonia are seen soon after aspiration. If immediate
measures are not taken obstruction aggravated by local inflammatory reaction may lead
to death.
Diagnosis
Direct Laryngoscopy confirms diagnosis and helps to remove the foreign body.
In a child suspected of laryngeal foreign body lateral and anterioposterior neck X-ray
help in the diadnosis.
Bronchial foreign bodies

Children seen shortly after aspiration will have history of choking, cough, wheeze and
blood streaked sputum. The degree of obstruction determines the type of obstruction
and presentation. If the first episode is overlooked or underestimated, latent periods of
195
days to months occur before patients develop recurrent pneumonia or intractable

wheezing (“asthma”).
There are three types of possible obstruction to the airways.

 Stop valve (complete) - there is no entry or exit of air distal to obstruction resulting
in collapse.
 Ball valve - there is only entry of air distal to obstruction resulting in emphysema
(distention).
 Bypass valve - both entry and exit of air distal to obstruction is possible.
Diagnosis
On chest X-ray (76% of cases show abnormality) opaque objects are clearly seen. If
non-radiopaque object is inhaled, indirect signs such as mediastinal shift, collapse or
overinflention are evident.
Treatment
Any child suspected of foreign body aspiration should be immediately referred to
facilities with bronchoscopy for confirmation of diagnosis and removal.
Emergency Managment of Foreign Body Aspiration

If a child is actively choking and a foreign body suspected, follow the following
procedure
In unconscious child younger than 1 year. a combination of five back blows and five
chest trust are given until successful. For those above 1 year a series of five abdominal
trusts (Heimlich maneuver) with lying or standing position is administered
Prognosis
Late presentation, delayed diagnosis and intervention as well as missed diagnosis are
major causes of prolonged morbidity and high mortality.
196
References
1. W.B Saunders Nelson Text book of pediatrics,16 eds, 2000.
2. Foreign body aspiration in children: Experience from Ethiopia
The East African Medical Journal, 73 (7): PP 459 – 62, 1996 J.U.
3. Foreign Body in the air ways in Infancy and childhood in Addis Ababa: A review of 38
case. EMJ 22 (3): PP. 135: 139, 1984.
5.3 PNEUMONIA
Goitom G/Yesus
Definition
Pneumonia is an inflammation of the parenchymal structure of the lungs, such as the
alveoli and the bronchioles.
Etiology
Bacteria, viruses and non-infectious agents result in pneumonia. The most common
causes, in developing counties, are bacterial agents especially streptococcus
pneumonia, followed by haemophilus Influenza. Staphylococcus aureus and gram
negatives (E.coli, Klebsiella, etc) are other causes in neaonates and
immunocompromized.
Epidemiology
Pneumonia is responsible for 70-80% deaths that occur due to acute respiratory
infections worldwide. In Ethiopia, pneumonia is the cause of one third of infant mortality
and one fifth of under 5 mortality.
Pneumonia is more severe in developing countries due to the high prevalence of risk
factors such as:
 Malnutrition, including Vitamin A and D deficiencies
 Overcrowding and indoor-air pollution
 Intercurrent infections such as measles, whooping cough, malaria and diarrhea
and
197
 Immune-deficient states
Severe forms of pneumonia are commonly encountered in children between the age of
6 months and 3 years.
Pathogenesis
The normal lung is sterile. Most of the agents are inhaled from the air breathed or
aspirated into the periphery of the lung from the upper air ways. After entry to the lung,
initially, a reactive oedema occur which supports proliferation of the organisms and aids
in their spread into adjacent portions of the lung. The disease may have a lobar, patchy
or diffuse distribution. The disease may be complicated in some by development of lung
abscess, collapse of the lung, and empyema
The clinical features of pneumonia resulting from most of the causative agents are
similar. The common manifestations in bacterial pneumonia are:
 In infants, initial manifestations may be mild like upper respiratory tract infection.
Cough, sudden onset of fever, and signs of respiratory distress. Respiratory
distress is manifested with rapid and difficult of breathing, nasal flaring, intercostal
retraction, chest indrawing and cyanosis.
 Other possible findings are crepitation, diminished breath sounds, bronchial
breathing and dullness on percussion.
It should be noted that fast breathing and chest indrawing are important clinical findings
in the assessment of severity of pneumonia.
 A child with cough and fast breathing (look below for cut of points of breathing) but
with out chest indrawing or difficulty of breathing is classified as having
Pneumonia.
 A child with fast breathing and chest indrawing, grunting, cyanosis or any danger
signs such as lethargy, unconsciousness or convulsion is classified as having
Severe Pneumonia.
198
Table 21: Cut off for fast breathing

The child has fast
If the child is: breathing if you count:
2 months up to 12 50 breaths per minute or
months more
12 months up to 5 40 breaths per minute or
years more
Note: The child who is exactly 12 months old has fast breathing if you count 40 breaths
per minute or more.
Diagnosis
Diagnosis is mainly reached on the basis of clinical features.
A chest X-ray may be helpful in patients who fail to respond to treatment to check for
complications such as pleural effusion, pneumatocele, atelectasis, or abscess
formation.
Treatment
 Children with severe pneumonia should be admitted for in patient care
 Supportive: include administration of oxygen nasally and hydration to replace
insensible water loss.
 Vitamin A.
 Antibiotics
 Children with pneumonia are treated at out patient level with cotrimoxazole or
amoxycillin orally for 5 days
- Advise parents to come back if there is worsening.
 Children with severe pneumonia are given:
- Intravenous antibiotics - crystallin penicillin as a first line drug
- Assess response after 48 to 72 hours, if there is no improvement or if there is
worsening, add chloramphenicole
199
Exercise
1. What are the common etiologic agents of pneumonia?
2. List risk factors which predispose children to develop severe pneumonia.
3. Describe the cut off respiratory rates for fast breathing.
4. What are the criteria for severe pneumonia?
5. Describe the treatment of severe pneumonia.
References
1. Jacob Forbes and Simone Dobson, 1997, Lower respiratory tract infection, in: Sear,
the pocket paediatrician
2. Charles G. Prober, pneumonia, Behrman, Kliegman, Jenson, Nelson Text Book of
5.4 BRONCHIOLITIS
Goitom G/Yesus
Definition
Acute bronchiolitis is a common disease of the lower respiratory tract of infants,
resulting from inflammatory obstruction of the small airways.
Aetiology and epidemiology

Acute bronchiolitis is a predominantly viral illness. About 50% of the disease is due to
respiratory syncytial virus (RSV). Other causative organisms are parainfluenza 3
viruses, mycoplasma, some adenoviruses and occasionally other viruses.
Bronchiolitis occurs most commonly in male infants between the ages of 3 to 6 months
who have not been breastfed and live in crowded conditions. The source of the viral
infection is usually a family member (older child or adult) with a minor respiratory
illness.
Pathophysiology
Acute bronchiolitis is characterized by bronchiolar obstruction due to:
200
 oedema,
 accumulation of mucus and cellular debris, and
 Invasion of the smaller bronchial radicles by virus.
The bronchiolar wall thickening affects air flow, impairing the normal exchange of gases
in the lung, which will result in hypoxemia early in the course of the disease.
Most affected infants have:
 History of exposure to older children or adults with a minor respiratory disease

within the week preceding the onset of illness. The first symptoms are a mild
upper respiratory tract infection, with serous nasal discharge and sneezing, lasting
for several days. These maybe accompanied by decreased appetite and fever.
Then there will be a gradual development of respiratory distress characterized by
wheezy cough, dyspnoea and irritability. Infants may have difficulty of sucking.
 On examination there will be tachypnea, hyper-expanded chest, severe respiratory
distress, a prolonged expiratory phase and wheezing, which is usually audible.
 Chest X-ray shows hyper-inflation of the lungs and an increased anteroposterior
diameter on lateral view.
Diagnosis
Diagnosis is mainly clinical
 Bronchial asthma
 Bacterial bronchopneumonia
 Congestive heart failure
Treatment
Treatment is supportive:
 The child should be placed in an atmosphere of cool and humidified oxygen to

relieve hypoxemia, reduce insensible water loss from tachypnea, and also relieve
the dyspnoea, cyanoses, anxiety and restlessness.
201
 Oral intake must often be supplemented or replaced by parenteral fluids.

Antibiotics should be given if there are secondary bacterial infections like bacterial
pneumonia.
Exercise
1. What is the common chest x-ray finding in bronchiolitis?
References
5.6 Bronchial Athma

Tsinuel Girma
Definition
Bronchial asthma is a diffuse obstructive lung disease with hyper reactivity of the
airways and reversibility of air flow obstruction spontaneously or with treatment.
Epidemiology
Worldwide 100 to 200 million cases of asthma are seen yearly accounting for 40,000 to
50,000 deaths. Bronchial asthma was reported in 2.8% of school children in Addis
Ababa while 18.2% had at least one episode of wheezing in the last 12 months. It is
rare in rural setting. Increasing industrialization and urbanization is associated with high
incidence of asthma.
Children are more affected than adults, but a study in Jimma demonstrated a lower rate
in children. Before puberty, the ration of males o females with asthma is 2:1 but later it
occurs equaly. Most children (85%) will have their first symptoms before 5 years of age.
Children with severe chronic asthma and steroid dependence have high (95%) chance
of becoming adult asthmatics.
202
Risk factors include:

 Allergy (inherited) like eczema, urticaria or hay fever
 Polygenic inheritance
If one parent has asthma, there is a 25% risk of asthma in their child. If both parents are
affected there is a 50% chance.
 LBW
 Poverty, frequent respiratory infections
Etiology
There is no well defined single etiologic agent. Multiple factors interplay to disturb the
mechanisms that maintains the balance between contraction and relaxation of bronchial
smooth muscle.
Autonomic, immunologic, endocrine, infectous and psychosocial factors interplay.
Pathophysiology
The airway inflammation results from different chemical mediators.
Mediators are released from local mast cells through:
i. IgE mediated specific allergens
ii. Non specific stimulation
Mediators and their effects

Early phase (10 to 30 minutes)
- preformed mast cells products (histamine, leukotreins, etc)
- these mediators produce bronchoconstriction, excessive mucus production and
mucosal edema
Late phase (after 6 hours)

- Local mucosal infiltration with eosinophils, lymphocytes and neutrohpils.
- There will be synthesis of mediators from prostaglandins
- Mediators result in worsening of the obstruction and hyperresponsivness
The airway obsturcition and hpoxia is more pronounced in children for the following
reasons:
203
 Small size of airways

 Abundant mucous glands
 Soft and easily deformable rib cage
 Poor collateral ventilation of alveoli
Diagnosis
Before initiation of any form of treatment the following information is needed:
a) Establishing the diagnosis
b) Identify the triggering factors
c) Asses degree of severity
Establishing the diagnosis

Classic symptoms of asthma are recurrent acute or insidious onset of cough and
wheezing typically worse at night and triggered by upper respiratory infections. Patients
may show spontaneous improvement or rapid response to therapy. Patients may have
family history of asthma.
Findings on physical examination depend on severity and presence of acute attack

during examination. Patients will have varying degree of respiratory distress and
wheeze.
Few patients may have atypical presentation such as:

 Persistent cough with no wheezes
 Wheezing with no cough
 Isolated tachypnoea with no wheezes
Assess degree of severity

Establishing the severity of asthma by grading will help in selecting treatment plans
and have objective parameters during followup.There is little experience and evidence
based practice with regard to this in Ethiopia. One method of grading is shown in table
22.
204
Table 22: Evaluation of severity of an asthma attack

(From the international Consensus)
Sign Mild Moderate Severe Imminent arrest
Breathlessness On walking, can On talking, On lying down

lie down prefers to sit
sit up
Speaking Phrases Words Cannot speak
Parts of
Levelof May be phrases Always Sleepy or
consciousness agitated Agitated Confused
Usually
agitated
Breathing rate Increased Increased Increased
Accessory No usually usually Paradoxical
muscle use movement
Wheezing Moderate strong Very strong absent
End of expiration
Pulse rate Increased Increased Increased Bradycardia
The presence of several parameters in the table, but not necessarily all, indicates the
general classification of the exacerbation.
Identifying triggering factors
The list of triggering factors is long but some common cause is:
 Viral upper respiratory infection mainly due to RSV and para influenza viruses.
 Tobacco smoke exposure
 Change in climate
 Exercise
 Drugs (e.g. ASA)
 Chemicals (e.g. malthion insecticides)
205
It is very common to get a child with respiratory complaint and wheeze. Many conditions
can have overlapping symptoms with asthma, but frequently seen are:
 Infectious – pneumonia, bronchiolitis
 Congestive heart failure
 Foreign body aspiration
 Tuberculosis
Diagnosis
Diagnosis of asthma is mainly clinical with limited information obtained from
investigation.
Microscopic examination of sputum shows eosinophilia. Chest X-ray is not routinely

done unless there is suspicion of associated pneumonia or complication like atelectasis.
Therapuetic trials are occurring with bronchodilators.
Management
The management is divided in two phases with different objectives:
 Management of acute exacerbations or attacks.
 Daily or long term management
Management of acte athma (attack)

Attacks are intermittent spells of severe symptoms of asthma caused by airflow
obstruction.
Objectives of treatment are to:

 prevent death from severe airway obstruction
 restore best level of activity and optimal lug function
 prevent relapse by treatment of inflammation
 Principles of treatment
 First determine severity of attack (see table below)
 Give best treatment available
206
 close follow –up of the response to the emergency drugs
Mild to moderate attack of asthma

Epinephrine 0.01 ml per kg sc of the 1:1000 (1mg/ml) ampoule, given at intervals of 20
minutes for 2-3 times relieves the bronchospasm rapidly in the majority of the cases.
The disadvantage is its short duration of action and its effect on the heart (tachycardia
etc).
If the patient shows complete response, long acting beta adrenergic is given.
Salbutamole is recommended in a dose of 0.1mg/kg divided in to three doses.
Prescribing low dose of prednisolone for 5-7 days helps for rapid resolution of
inflammation and reduce relapse.
Admission criteria
Admit a child if there is:
 no response or incomplete response to adrenaline
 status asthmatics (progressive respiratory distress despite administration of the
usually effective drugs (sympathomimetics)
 severe attack on presentation
 Risk of death from asthma is high in those with:

Recent emergency admission
Use of steroids
Steroid dependent asthma
Sudden onset of severe obstruction
Unreliable family for follow up
Principles of treatment consists of:

1) Oxygen through nasal prongs
2) Aminophyline 4mg/kg i.v slowly over 20 minute every 6hours
3) Hydrocortisone 4-6mg/kg i.v every 6 hourly for 48-72 hours
4) Start salbutamole when patient starts to take po properly
5) Treat and prevent dehydration which may result from respiratory loss
207
Long term management

Objectives of treatment include:
 To reduce or avoid acute attacks
 To reduce limitation of activity
 Minimal or no use of bronchodilators
Principles of treatment (depends on the degree of severity)

 avoid allergens
 use bronchodilators according to the need
 give anti-inflammatory therapy in selected cases
Essential drugs in Ethiopia are:

 Salbutamol 0.1mg /kg /day three times daily.
 Prednisolone 2mg/kg/24 hours
References
1. Nelson text book of pediatrics ,16 eds,W.B Saunders, 2000
2. Prevalence of wheeze and asthma and relation to atopy in urban and rural
Ethiopia.Yemanebirhan H.,Bekele Z,Venn A,Parry E,Britton J. Lancet vol,350,No
9071,pp 85-90.1997.
3. Prevalence of wheeze and asthma related symptoms among school children in
Addis Ababa, Ethiopia.Melaku K, and Berhane Y.Ethiop. Med.J.37 (4) 247-54, 1999
Oct.
208
CHAPTER SIX
DISEASES OF THE CARDIOVASCULAR SYSTEM
6.1 Approach to an infant or child with congenital heart disease

Habtamu Fekadu
Objectives
By the end of this topic, the reader should be able to:
 Describe the magnitude and type of congenital heart disease

 Recite the commonest types of congenital heart disease
 Describe the common manifestations
 Know how to approach systematically a child suspected of having congenital heart
disease
 Describe the principle of management
General Considerations
Congenital heart disease (CHD) occurs in approximately 8 of 1,000 live births. In 10-
15% of cases there are associated congenital abnormalities.
They are classified as:

1 Acyanotic - there is no cyanosis
e.g. ventricular septal defect, persistent ductus arteriosus and coarctation of aorta
2. Cyanotic- which present with cyanosis
e.g. tetralogy of fallot and transposition of great arteries,
Ventricular septal defect is the commonest of all CHD and tetralogy of fallot is the most
common cyanotic CHD.
The causes of most congenital heart disease is unknown. For most, it is multifactorial,
whereby genetic predisposition, chromosomal abnormalities and environmental or
maternal conditions play a role.
209
The mode of inheritance is polygenic.

Genetic predisposition – the risk of recurrence is 2-6% (the general risk is 0.8%) if a
parent or a sibling is affected.
Chromosomal abnormalities – 50% of children with down’s syndrome have CHD.
Environmental or maternal conditions- maternal diabetes, rubella drugs (lithium,
ethanol)
Clinical Presentation
The manifestations and age of onset varies depending on the type of heart defects.
Most are asymptomatic at birth and the majority start to be symptomatic in the first 1 or
2 years of life. Newborns present either with shock, which usually occurs within the first
two weeks of life, or respiratory distress or cyanosis or the combination of these
symptoms and signs.
Infants and children present with symptoms of congestive heart failure, such as
tachypnea, tachycardia, chest retractions, nasal flaring and wheezing. The heart failure
is usually present during the first weeks of life (2 to 4 months) as the pulmonary
vascular resistance falls after birth or it may be triggered later by an intercurrent
infection.
Other symptoms are feeding difficulty (become dyspneic or sweating excessively while
sucking), irritability, failure to thrive and recurrent pneumonia. Those with cyanotic CHD
present with cyanosis, cyanoyic spells, squating and clubbing with long standing
cyanotic CHD. Older children will have exercise intolerance.
Evaluation of an Infant or Child with Congenital Heart Disease
If an infant or child develops the above symptoms and signs, the following diagnostic
approach for the diagnosis of CHD helps to narrow the differential diagnosis. Perform a
full cardiovascular examination, in particular evaluate for the femoral pulse (for
coarctation of the aorta), character of the heart sounds, the type of murmur, cyanosis,
oxygen saturation, chest x-ray (to see whether the pulmonary blood flow is increased,
normal or decreased and the cardiac size and shape) and electrocardiography.
210
Once CHD is suspected:
Step one – Determine whether it is cyanotic or acyanotic by looking at the tongue and if
possible oxygen saturation using pulse oximetry.
Step two - Identify clinical findings such as respiratory distess, shock, pulse (normal,
decreased in legs or decreased in all limbs), second heart sound (single or splitted) or
murmur (harsh loud systolic or continuous and the location of the murmur).
- Do chest x-ray to asses cardiac size and shape and whether the pulmonary
vascular markings are increased, normal or decreased.
Step three – Based on the above findings, try to identify the most likely diagnosis and
differential diagnosis. The final diagnosis is made by echocardiography and cardiac
catheterization.
Step four – Start management. These patients are best managed at hospital level so
refer the patient as early as possible.).
Therapeutic measures
 Position the patient with the head and trunk elevated if the child is in distress or
breathless.
 Give oxygen if the patient is hypoxic, cyanotic or in distress.
 If the child is in heart failure, start digoxin and diuretic (furosemide).
 Refer the patient as early as possible for better diagnosis and management.
 Bed rest, and salt restriction
References
1. Nelson Behrman, Kliegman, Text Book of pediatrics; 2000.
2. Jordan, Scott. Heart disease in pediatrics.1989.
3. Levy, Sheldon, Sulyman. Diagnosis and Management of the hospitalized child.
1984.
211
6.2 Rheumatic fever

Habtamu Fekadu
Objectives
By the end of this topic, the reader sould be able to:
 Know the magnitude and risk factors for rheumatic fever.
 Descibe the pathogenesis of rheumatic fever.
 Describe the major mode of presentation and cosequences.
 Know the principle of treatment and prevention of rheumatic fever.
Definition
Rheumatic fever is a non suppurative acute inflammatory complication of group A
streptococcal pharyngeal infections, characterized mainly by carditis, arthritis and
chorea appearing alone or in combination, with resdual chronic heart disease as
possible sequel of the carditis.
Epidemiology
In the early1960, acute rheumatic fever and its major complication, rheumatic valvular
heart disease, were frequent worldwide. Nowadays it almost disappeared in the
western world, however it is still prevalent in developing countries.
Climate (high temperature), poverty, crowding, poor housing conditions and inadequate
health services are the major risk factor for the frequent occurrence of acute rheumatic
fever in developing countries (Shaper 1972). It is frequent in children aged between 5
and 15 years because they are susceptible to Group A streptococcal pharyngitis.
Approximately 20% of all sore throats are due to Group A streptococcal and only few
(0.5 to 3%) develop acute rheumatic fever. The risk depends on the host factors (age,
genetic predisposition and carriers), if untreated, and the streptococcal strain (M type).
Streptococcal skin infection does not result in acute rheumatic fever.
Pathogenesis
The exact pathogenesis remains unexplained but the most accepted is an abnormal
immune response to some still unidentified component of Group A streptococci. The
212
antibodies produced against the streptococci antigen cross react and cause
immunologic damage to the heart valves, muscle and pericardium (pancarditis), joint
synovium (arthritis), nervous tissue (sydneham chorea), skin (erythema marginatum)
and subcutaneous tissue (subcutaneous nodule).
The latent period, i.e. the duration between sore throat and acute rheumatic fever, is
usually 1 to 3 weeks.
Clinical presentation
Symptoms develop after 1 to 5 weeks following streptococcal pharyngitis.
There is no single specific manifestation rather carditis, arthritis, sydneham chorea,

erythema marginatum and subcutaneous nodule appear alone or in various
combination. The onset is insidious.
1. Carditis – occurs in 40 to 80% of patients

- It presents with fever, dyspnea and cough and the main signs are tachycardia,
mitral regurgitation murmur and cardiac enlargment. In severe cases there are
signs of heart failure
- Aortic regurgitation may occur with the mitral regurgitation
- Other signs are arrhythmia and pericarditis
2. Athritis – is the commonest manifestation

- It is migratory and involves several larger joints (knee, ankle, elbow and wrist)
- the affected joint is swollen,red warm and exquisitely tender. These signs
disappear within 24 hours if antiinflamatory drug is given.
- It may resolve completely without any residual sequel.
3. Sydneham chorea – is purposeless jerky, repetitive movements particularly involving

the hands and face.
- Early manifestations are emotional liability (easily induced crying and inattention)
and deterioration in handwriting.
- Occurs at the same time or following other features. It usually occurs several
months after the sore throat.
4. Erythema marginatum – is a serpiginious rash over the chest and trunk
- It disappears in hours or days.
213
5. Subcutaneous nodule – is small painless nodules which occur more frequently on the
extensor surface of large joints (elbow, wrist and knee) and spine.
Other minor manifestations are fever and arthralgia.
Laboratory Findings
Laboratory findings may include:
- Increased acute phase reactants – elevated ESR and C-reactive protein
- CXR – may show cardiomegaly
- Evidence of preceding streptococcal infection
- elevated antistreptolysin O antibody (ASO) titer
- throat culture
- Other tests - ECG, Echocardiography
Diagnosis
No single clinical feature or test is diagnostic of acute rheumatic fever.So the modified
Jones criteria which consist of 5 major and 4 minor plus evidence of preceeding
streptococcal infection is used for diagnosis.
Table 23 - Modified Jones criteria
Major criteria Minor criteria

- Carditis - Fever
- migratory polyarthritis - Arthralgia
- Erythema marginatum -↑ESR or C-reactive protein
- chorea - Prolonged PR interval
- subcutaneous nodule
Plus
Evidence of preceding streptococcal infection
(↑antistreptolysin O antibody(ASO) titer, throat culture)
To diagnose acute rheumatic fever the following should be present:
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- - 2 major or 1 major and 1 minor criterion, plus evidence of preceding

streptococcal infection
- Chorea, plus evidence of preceding streptococcal infection
Clinical course
- Except for carditis, all manifestations subside without residual effect.
- The long term outcome depends on the severity of carditis. Patients with severe
carditis are usually left with residual chronic rheumatic heart disease which is
worsened by rheumatic recurrence.
Treatment
Treatment involves:
1) Bed rest – for patients with heart failure.
2) Treatment with of Group A streptococcal pharyngitis.
- 10 days course of amoxicillin or a single i.m. injection of benzathine penicillin.
3) Anti-inflammatory drugs – to control the clinical features
- Arthritis – aspirn 100 mg/kg/day in 4-6 divided doses
- Carditis without heart failure - aspirn 100 mg/kg/day in 4-6 divided doses for 4
weeks.
- Carditis with heart failure
- Predinsolone 2 mg/kg/day for 2 to 4 weeks depending on patient response and
aspirin during tapering of predinsolone and continued for 3 to 4 weeks.
- Digoxin and diuretic for the heart failure.
- The best parameters to follow response are symptoms of heat failure, heart
rate, ESR and ,C-reactive protein
4) Chorea –most recover without treatment
- Chlorpromazine and phenobarbital are helpful.
Prevention
Prevention involves the following:
1. Primary prevention: Early (within 1 week) treatment of streptococcal pharyngitis to
prevent an initial attack of acute rheumatic fever.
215
- 10 days course of amoxicillin or single i.m. injection of Benzathine penicillin.

2. Secondary prevention:
- Prevent recurrences so as to reduce the damage to heart valves and the risk of
chronic rheumatic heart disease.
- Indicated for children who have had acute rheumatic fever or have rheumatic
heart disease.
- Monthly single i.m. benzathine penicillinor daily oral penicillin
References
1. Nelson Behrman, Kliegman, Text Book of pediatrics; 2000.
2. Jordan, Scott. Heart disease in pediatrics.1989.
3. Levy, Sheldon, Sulyman. Diagnosis and Management of the hospitalized child. 1984.
4. avery
6.3 INFECTIVE ENDOCARDITES

Tsinuel Girma
Definition
Infective endocarditis is an infectious disease, mostly bacterial, involving the
endocardium (including the valves) or intima.
Etiology
The common causes include :
Streptococcus viridans
Staphylococcus aureus
Enterococcus
- Culture negative (10% of cases)
Pathophysiology
Infective endocarditis most often occurs as a complication of underlying congenital or
rheumatic heart disease but can occur with no cardiac malformation. Rheumatic
216
valvular heart diseases, primarily mitral and aortic, represent common lesions in
Ethiopia.
Preceding dental, urinary or intestinal procedures are identified in one third of the
patients as a source of contamination of the blood and as a result the endocardium.
Vegetation is found at the site of endocardial or intimal erosion that results from high
velocity blood flow. Thus children with cardiac defects like VSD, PDA and left-sided
valvular lesions are at high risk of infective endocarditis.
The onset of symptoms can be acute and severe, with high intermittent fever and
prostration or insidious with isolated prolonged fever. Commonly, it varies within a
range between the two forms.
Early symptoms are nonspecific and consist of low grade fever, chills, fatigue, arthalgia,
headache, splenomegally, clubbing and petechial rashes. Many of the basic
dermatologic manifestations develop in untreated patients. These are Osler nodes
(tender pea sized Intradermal nodules in the pads of the fingers), Janeway lesions
(painless small erythematous or hemorrhagic lesions on palms and soles) and bleeding
beneath the nails (splinter hemorrhages).
Thre should be a high index of suspicion in the evaluation of a febrile child with
underlying heart disease.
Diagnosis
The gold standard for diagnosis is appropriately collected blood culture. Take 3 to 5
separate samples even during afebrile periods. In patients with no prior antibiotic
treatment, culture identifies etiologic agents in 90% of cases. Additional information can
be obtained from echocardiography, raised ESR, leukocytosis, mild normoctytic
anemia, and microscopic hematuria (may have RBC casts) or a manifestation of
immune complex glomerulonephritis.
The following diseases have to be considered:
 Recurrence of rheumatic fever
 Malaria
217
 Tuberculosis
Treatment
Any patient with diagnositic possibility of infective endocarditis should be treated in a
hospital.
Medical management should provide both specific treatment of the infection and
supportive treatment for congestive heart failure.
Initial empiric antibiotic should be effective for both Gram-positive and Gram negative
organism combine cloxacillin (100 mg /kg per 24 hours), ampicillin (300 mg/kg per 24
hr, IV) and gentamicine (3 to 4 mg / kg per 24 hours IV). Adjustment of drugs can be
done depending on blood culture results. Therapy should continue for 4 to 6 weeks
(except gentamicin for 2 weeks).
Prevention
The prevention of infective endocarditic involves appropriate treatment of infection in
high risk children, proper general dental care and oral hygiene and antimicrobial
prophylaxis. Oral amoxicillin can be given 1 hour before dental procedures and surgery
of the upper respiratory tract. Intramuscular or IV ampicillin plus gentamicin is
recommended before surgery of the genitourinary and gastrointestinal system.
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CHAPTER SEVEN
DISEASE OF THE GASTROINTESTINAL SYSTEM
Dula Benti and Yezna
Objectives
By the end of the chapter, the student is expected to:
 Describe introductory concepts about diarrheal disease and portal hypertension

 Explain the epidemiology of the above diseases
 Identify the etiologic factors of these diseases
 Describe the pathology and pathogenesis of the mentioned diseases
 Explain the diagnostic modalities and clinical features of these diseases
 Describe the treatment, complications, prevention and prognosis of the above-
mentioned diseases.
Introduction
Digestive system disorder comprises a range of both acquired and congenital disorders.
Digestive system disorders are manifested by vomiting, disphagia, diarrhea, anorexia,
constipation, abdominal pain, abdominal distension or mass, jaundice, GI hemorrhage,
etc. Many of these symptoms are common to disorders of several parts of the
gastrointestinal tract as well as extra intestinal diseases. For this reason, disorders of
organs outside the gastrointestinal tract should be considered in the differential
diagnosis. In this short review, only few diseases of the digestive system are discussed.
7.1 Diarrheal disease

Definition
Diarrhea is defined as passage of three or more loose or watery stools per 24 hours or
increase in stool frequency or liquidity that is considered abnormal by the mother.
There are three clinical types of diarrhea
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1. Acute watery - A diarrheal episode that begins acutely and lasts for less than
fourteen days with passage of watery stools without blood.
2. Dysentry – This is diarrhea with blood in the stool.
3. Persistent diarrhea - This is a diarrheal episode that starts acutely and lasts for
fourteen days or longer.
Acute Diarrheal Disease
Epidemiology
An estimated 500 million children in the developing world suffer from diarrhea three or
four times a year. One out of every twenty children born into the developing world dies
before reaching the age of five from dehydration resulting from diarrhea. Diarrheal
disease cause about 30% of infant deaths in developing countries and contribute a lot
to the high prevalence of malnutrition. Dehydration from diarrhea is one of the five
leading causes of death in children under five years.
Acute watery diarrheal episodes are the commonest form, accounting for 80 to 82% of
the cases. Children of 6 to 11 months of age are the most commonly affected, a time
that coincides with initiation of complementary feeding. Highest mortality of diarrheal
disease is encountered among infants.
Risk factors for diarrhea include the following:

Behavioral:
 Improper infant and young child feeding (suboptimal breast feeding, using feeding
bottles, eating food hours after cooking it etc.)
 Drinking contaminated water
 Not washing hands
 Not disposing of feces safely
Host factors:
 Malnutrition - malnurished children have frequent episodes of diarrhea and each
episode is more severe and long lasting
 Measles – recent measles predisposes to diarrhea
 Immunosuppression – like HIV/AIDS
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Etiology
The commonest cause of acute watery diarreah is rota virus and others are escherichia
coli, vibrio cholerae, giardia lamblia, cryptosporidiu, etc
The commonest cause of dysentry is shigella and others are campylobacter jejuni,
entero invasive E.coli, entamoeba histolytica etc.
The transmission is usually through the fecal-oral route-by ingestion of fecally

contaminated water or food or direct contact with infected feces.
Pathophysiology
Microbial agents cause diarrhea by any one of the following mechanisms:
 Villous damage and epithelial cell destruction e.g rota virus
 Mucosal adhesion e.g giardia lamblia
 Mucosal invasion e.g shigella, entamoeba histolytica
 Release of toxins e.g vibrio cholerae, ETEC
Two mechanisms of watery diarrhea have been identified.
1. Secretary diarrhea
Secretary diarrhea occurs when there is increased secretion of fluid and electrolytes
(sodium, chloride) due to the microbial toxins in the small intestine beyond the
absorptive capacity of the bowel. This results in a net fluid and electrolytes, e.g vibrio
cholerae, enterotoxigenic E.coli (ETEC)
2. Osmotic diarrhea
If there is intake of non-absorbable solute which is isotonic, there will be diarrhea with
no dehydration. If there if intake of non-absorbable solute which is hypertonic, water
and salts are lost from the extra cellular fluid which results in more diarrhea with
hypernatremic dehydration.
Complications
The commonest complications that are expected in patients with acute watery diarrhea
are:
 Dehydration and hypovolemic shock
 Electrolyte imbalance, most importantly hypokalemia, hyponatremia
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 Base deficit acidosis

 Hypoglycemia
 Malnutrition
Dehydration is the main cause of death from acute diarrhea. It is associated with loss
of body fluid and electrolytes mainly sodium through the diarrheal stools.
Table24: Assessment and classification of dehydration
Clinical signs Degree of dehydration

Two of the following signs:
 Lethargy or unconsciousness
 Sunken eyes Severe
 Not able to drink or drinking poorly Dehydration
 Skin pinch goes back very slowly
(takes >2 sec)
Two of the following signs:
 Restless, Irritable
 Sunken eyes Some
Dehydration
 Drinks eagerly, thirsty
 Skin pinch goes back y slowly (takes
<2 sec)
No enough signs to classify as some or No
Severe dehydration ehydration
Other important signs of dehydration or hypovolemia are rapid and feeble /absent
pulse, low blood pressure, cool and moist extremities, depressed fontanel, decreased
urine out put.
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Degree of Dehydration The fluid deficit

No dehydration 0 to 4%of total body weight
Some dehydration 5-10% of total body weight
Severe dehydration 10% of total body weight
Electrolyte and acid-base abnormalities include:

Hypokalemia due to loss of K+ in diarrheic stools.
Hyponatremia due to loss of K+ in diarrheic stools..
Acidosis due to loss of bicabonate in diarrheic stools.
Diarrhea results in malnutrition due to reduced intake and absorption, and increased
requirement associated with diarrhea.
Investigation
Because most acute watery diarrhea is caused by viruses, there is no need to do stool
examination. Do stool microscopy only for dysentery.
Management of acute diarrhea

The principles of treatment focus on:
 Giving extra fluids to replace the lost fluid and electrolytes. The amount and how
to give depends on the degree of dehydration.
 Continuous feeding
 Antibiotics/ Anti-protozoal – see the indications below
 Advise the mother when to return
Composition of ORS solution

It more or less goes in conjunction with the diarrheal losses:
Composition mmol/lt Essential features

Na+ 90 replaces lost Na+
K+ 20 prevents hypokalemia
Citrate/Hco3 10/30 correct acidosis
Glucose 111 facilitates Na absorption
Osmolality 310 Isotonia
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Treat dehydration as follows:

No dehydration Treatment plan A
Some dehydration Treatment plan B
Severe dehdration Treatment plan C
See Annex at the end of these lecture notes for treatment plans A, B and C
Antibiotics in acute diarrhea

Antibiotics are given only in patients with bloody diarrhea and suspected cholera with
severe dehydration. They have no practical value for others because they are
ineffective for the pathogens rota virus, and most of the time the etiologic pathogen is
not known. Otherwise determination of the specific etiologic agents in the laboratory is
impractical.
Antibacterial or antiparsitic therapy

Anti microbial agents should not be used routinely. The indications are:
1. Dysentery - oral antibiotics for 5 days should be given.
2. The first line drugs is cotrimoxazole.
3. The second line drug is nalidixic acid
4. If cholera is suspected,
 Cotrimoxazole or erithromycin are the first line drug in younger children.
Tetracycline is the drug of choice for children older than 8 years.
5. Anti-protozoals are considered if trophozoites or cyst of giardia, or trophozoite of E.
histolytica are seen in stool microscopy.
Persistent Diarrhea
Definition
Persistent diarrhea is a diarrheal episode that starts acutely and lasts for fourteen days
or longer.
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Etiology
About 10% of acute diarrheal episodes become persistent. There is no single microbial
cause although shigella, salmonella and enteroaggregative escherchia coli, giardia
lamblia and cryptosporidium (in immunocompromized children) play a role.
Persistent diarrhea can lead to death through negative effects on nutrition status.
Several studies have shown that children with persistent diarrhea are more likely to die
than children with diarrhea of shorter duration. A strong relationship exists among
persistent diarrhea, malnutrition and mortality
Risk factors include:

 Malnutrition
 Recent introduction of animal milk or formula
 Young age less than 18 months of age
 Immunological impairment eg. AIDS
 Recent diarrhea
Nutritional Impact
Persistent diarrhea is a nutritional disease. It usually occurs in malnourished children
and is itself an important cause of weight loss and severe malnutrition. Such effects are
seen due to decreased absorption of nutrients especially fat, lactose and poor intake
and also giving of dilute, low energy foods in patients with persistent diarrhea.
Management
First check the level of dehydration and treat accordingly. Usually, treatment with ORS
would suffice in children with persistent diarrhea. Only few patients need intravenous
rehydration. Then check for blood in the stool. If so, treat for shigellosis. Do stool
microscopy and if trophozoite of giardia or entamoeba are found, treat accordingly. If
there is still no response, stool culture and sensitivity should be done to look for other
bacterial causes of bloody diarrhea.
Nutritional therapy
The most important aspect of treatment for persistent diarrhea is proper feeding.
Goals of treatment include:
 To reduce the amount of animal milk (or lactose) in the diet temporarily
225
 To provide a sufficient intake of energy, protein, vitamins and minerals to improve

nutritional status
 To avoid giving foods or drinks that may aggravate the diarrhea as animal milk or
lactose
 To ensure that the child’s food intake is adequate to correct malnutrition
For children older than six months the goals are as follows:
 Continue breast feeding
 Give only half of the usual amount of animal milk or give it as a fermented form,
yoghurt (for the lactose intolerance)
 Ensure a diet of full energy food. About six times per day, give thick cereal with
vegetable oil, vegetable, chicken or fish. Avoid diluted foods. Supplement the
dietwith folate, vitamin B12, Zinc and Iron.
 If diarrhea stops after five days, give the same amount of food for one more week.
Re-introduce the usual animal milk over days to full-strength diet.
 Give an extra meal each day for at least one month
Prevention of diarrhea
The presention of diarrhea involves:
Interrupting the spread of infection
- Give only breast milk for the first 6 months
- Do not use feeding bottles
- Prepare and store food safely
- Use clean water for drinking
- Wash hands when soiled
- Dispose of feces safely
Strengthening host defenses

- Exclusive breast feeding till 6 months and continue breast
- feed at least for two years
- Start complementary feeds at age of 6 months
- Give balanced diet in adeguate amount
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- Immunize against measles
7.2 Portal hypertension
Definition
An increase in portal venous pressure to greater than 10 to 12 mm Hg.
Causes of Portal Hypertension

Portal hypertension results from the obstruction of portal blood flow anywhere along the
course of portal venous system. It is due to prehepatic, intrahepatic or posthepatiic
obstruction to the flow of portal blood. In children most important causes are
extrahepatic.
Extra hepatic portal hypertension may be caused by:

 Umbilical infection in neonates
 Intraabdominal infection in older children
o Acute appendicitis
o Primary peritonitis
 Umblical cathetrization during the neonatal period
Intra hepatic portal hypertension may be caused by:

 Hepatocellular disease
o Acute and chronic viral hepatitis
o Congenital hepatic fibrosis
o Hepatotoxity
 Cirrhosis
 Schistosomiasis
 Biliary tract disease
 Extra hepatic biliary atresia
Post sinusoidal obstruction may be caused by:

 Budd-chiari syndrome
Idiopathic portal hypertension is another form.
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Pathophysiology
The primary hemodynamic abnormality is increased resistance to portal blood flow,
which results in the development of collateral for porto systemic shunts. Complications
occur due to the development of a remarkable collateral circulation. Collaterals in the
esophagus, stomach and anorectal region are prone to rupture and bleed under
increased pressure.
Clinical features
Bleeding from esophageal varices (hematemesis and melena), with bouts of life
threatening hemorrhage is the commonest form of presentation.
Jaundice, stigmata of cirrhosis, ascitis, encephalopathy, caput medusa (dilated veins

around the umbilicus), splenomegaly (with hypersplenism) may occur.
If no clinical or biochemical features of liver disease are seen and liver size is normal,
portal vein obstruction is the most likely cause. If enlarged, hard liver with normal
hepatic function is seen, congenital hepatic fibrosis is more likely.
Diagnosis
Diagnosis may involve:
Ultrasound with doppler
- To delineate the size and architecture of the liver
- To check for patency of the portal vein
- To show the direction of flow within the portal system.
Endoscopy
- Most reliable for detecting esophageal varices.
- Stool examination for detection of ova of parasites.
Treatment
Treatment comprises two components:
 Emergency treatment of life threatening hemorrhage
 Prophylaxis for initial or subsequent bleeding
228
Emergency treatment may include:

 Fluid resuscitation: crystalloids followed by packed RBC
 Vitamin K, infusion of platelets or fresh frozen plasma for correction of coagulopathy
 NG tube to document and monitor ongoing bleeding in the stomach.
 Cimetidine or ranitidine to decrease the risk of bleeding from gastric erosions.
 Pharmacological treatment to decrease portal pressure with asopressin which act by
increasing splanchinic vascular tone thus decreasing portal blood flow or others
 Endoscopic sclerosis of esophageal varices.
 Sangstaken blakemore tube is inserted to stop bleeding by mechanically
compressing esophageal and gastric varices.
 Surgical - portocaval shunt
Prognosis
Portal hypertension secondary to intrahepatic disease has a poor prognosis. In portal
vein obstruction, episodes of bleeding become less frequent and less severe with age
as a collateral circulation develops.
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CHAPTER EIGHT
HEMATOLOGICAL DISEASES
Assfawossen Bekel
8.1 Anemia
Objectives
By the end of this course the students are expected to:
 To be able to define anemia
 To recite the common nutritional causes of anemia
 To know the classification of the anemias
 To describe the approach to the anemic child
 To mention the clinical manifestations of childhood anemia
 To describe the treatment of the nutritional anemias
Definition
Anemia is defined as reduction of the RBC volume or hemoglobin (Hb) concentration
below the range of normal values in healthy persons (see table below)
General considerations
 Anemia is a relatively common problem. Finding the underlying cause is equally

important since anemia is not a specific diagnostic entity.
 Although a reduction in the amount of Hb reduces the oxygen carrying capacity of
the blood, few clinical disturbances occur until the Hb. level falls below 7-8 g/dl
 Physiologic adjustment to anemia include:-
1. Increase in cardiac output
2. Increase 02 extraction by tissues
3. Shunting of blood flow to vital organs and tissues
4. Increase in RBC 2,3 DPG concentration
230
There are different classification methods but a useful classification of the anemia
divides them based on the RBC morphology: microcytic, macrocytic or normocytic and
based on colour normochromic or hypochromic.
Approach to the child with anemia

Even though anemia in childhood has many causes, the correct diagnosis can usually
be established with relatively little laboratory cost. Frequently careful history and
physical examination (Hx and P/E) suggest the cause.
History (HX):
 Dietary habit, growth and development, symptoms of chronic illnesses,
malabsorption, blood loss.
 Hx of jaundice or family Hx of anemia, gallbladder disease, splenomegally or
splenectomy
 Age and ethnic background
 History of malarial attack
 History of bleeding disorder.
Physical examination (P/E):

 Anthropometry: Poor growth leading to chronic disease and/ or hypothyroidism
 Congenital anomalies leading to Fanconi’s anemia, Diamond-Blackfan syndrome
 Look for pallor in the mucus memmbrane, nail beds, and palm.
 Petechiae and purpura
 Lymphadenopathy and hepatosplenomegally
 Evidence of chronic or recurrent infections
Laboratory studies
The initial laboratory evaluation of the anemic child generally consists of CBC with
differential, platelet count, peripheral morphology, stool exam, blood film and
reticulocyte count.
The following algorithm shows how this limited laboratory information together with
undertaking a history and physical exam may lead to a specific diagnosis or focus
additional investigations to a limited diagnostic category.
231
Table 25: Mean and ranges of normal hematologic values in infancy and childhood
Hemoglobin (g/dl) Hematocrit Reticulocte NCV Leukocytes Neutrophils Lymphocytes Eosinophils

(%) (%) (fl) ( WBC/mm3) (%) (%) (%)
Age Mean Range Mean ange Mean Lowest Mean Range Mean Mean Mean
range
Cord 16.8 13.7 -20.1 55 45- 65 5 110 18,000 (9-30x103) 61 (40-80) 32 2
b/d 16.5 13.0 -20.0 50 42-66 1 12,000 (5-21x103) 40 63 3
2week 12 9.5-14.5 36 31-41 1 12,000 6-18x103) 30 48 2
3 mo’s 12 10.5 -14.0 37 33-42 1 70.74 10,000 (6-15x103) 45 48 2
6mo-6yr 13 11.0 -16.0 38 34-40 1 76-80 8,000 (4.5-13.5x103) 55 38 2
7-12yr
adult
female 14 12-16 42 37-47 1.6 80 55 (35-70) 35 3
male 16 14-18 47 42-52 80 7,500 (5-10x103)
Fl = femtoliters; MCV = mean corpuscular volumes

WBC = white blood cells
Iron Deficiency Anemia
Introduction and epidemiology

- Iron deficiency anemia is the most common Hematologic disease of infancy and
childhood.
The body of newborn infant contains about 0.5gm of Iron, whereas the adult content is
5gm. To make up for this discrepancy together with the normal loss of iron by shedding
of cells, an average of 1mg of iron must be absorbed each day during the first 15 yrs of
life. Absorption is only 10% and takes place in the duodenum. A diet containing 10 mg
of iron/day is necessary for optimal nutrition.
Those who are at greatest risk include:

Children 6-24 months
Adolescents (especially females)
Special risk groups: low birth weight and premature
232
Etiology
Anemia results from a decreased iron store which may be casued by low birth weight
and unusual perinatal hemorrhage. It results in increased requirements (children 6-
24/12, adolescents).
It may be caused by blood loss (especially in older children).
Clinical manifestations Mild iron deficiency is usually asymptomatic
With moderate to severe anemia, findings include:

 Pallor, fatigue irritability, anorexia, pica
 Tachycardia, cardiac dilatation and systolic murmurs
 Adverse effects on behavior and cognition (decreases IQ)
Laboratory findings
In progressive iron deficiency, a sequence of biochemical and hematological events
occur as follows:
 Hemossiderin  ferritin  serum iron  TIBC and
% Saturation
Hb, microcytosis, hypochromia  FEP 
Poikilocytosis and RDW
 The bone marrow is hypercellular with erythroid hyperplasia

 Hemossiderin can’t be demonstrated in marrow specimens by Prussian blue
staining.
 Reticuloyte count is usually normal but may be elevated
 Hypochromic, microcytic anemias
* Lead poisoning  coarse basophilic stippling of the RBCs
 Serum lead level
 Anemia of chronic illnesses
233
Treatment
- The regular response of iron deficiency anemia to adequate amount of iron is an
important diagnostic and therapeutic feature. Oral administration of simple ferrous
salts (sulfate, gluconate, fumarate) provides inexpensive and satisfactory therapy.
- Treatment may also include:
 6mg/kg/day of elemental iron in 3 divided doses for 2-3 months.
 treatment of underlying causes
 blood transfusion is indicated only when the anemia is severe (< 4 gm/dl) or
when the patient has decompensated
 Reticlocytosis begins within 48-72 hrs and peaks at 5-7 days.
Prevention
Prevention involves the following:
 Prevention and treatment of infestation (deworming) by intestinal parasites
 Supplemental iron for young children above 6 months and LBW babies
 Prevention of low birth weight and prematurity
 Prevention and treatment of causes of chronic blood loss
8.2 Megaloblastic Anemias

Megaloblastic anemia is a macrocytic anemia caused by deficiencies of vitamin B 12,
folic acid (FA) or both.

- The RBCs at every stage of development are larger than normal and have an open,
finely dispersed unclear chromatin and an asynchrony between maturation of the
nucleus and cytoplasm.
- Both FA and vitamin B12 are cofactors required in the synthesis of nucleoproteins
Etiology
Megaloblastic anemia is caused by
 Inadequate dietary intake (vitamin B12, FA)
 Malabsorption (vitamin B12, FA)
 Increased requirements (growth, hemolysis)
 Inborn errors of metabolism – vitamin- B12
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 Rarely, deficiency of intrinsic factor – Vitamin B12
Clinical manifestions include:
 the usual clinical features of anemia- pallor, fatigue, etc.
 Mild jaundice due to ineffective erythropoiesis
 Smooth and cherry red tongue
 Hemorrhage due to thrombocytopenia- in advanced cases
 Peripheral neuropathy, ataxia (esp. in B12 def.)
Laboratory Findings
Laboratory findings include:
 Macrocytosis with aniso- and poikilo-cytosis on peripheral smear
 Large neutorphils with hyper segmented nuclei
 Neutropena and thrombocytopenia- in advanced cases
 Bone marrow exam  Erythroid hyperplasia with erythroid and myeloid
precursors.
 In RBCs and serum levels of B12 and FA level
 Schilling test (B12)
Differential diagnosis is as follows:
 Hemolytic Anemias
 Bone marrow failure syndromes (e.g. Fanconi’s anemia )
 Liver disease, Hypothyroidism, etc
Treatment
Treatment involves administering:
 Folic Acid- orally /parenterally: 1-5 mg/ 24hr, for 3-4 wks
 Vitamin B12 – preferably parenterally
235
Questions
1. List the risk groups for iron deficiency anemia in children.
2. Discuss the approach to the anemic child
3. Dscuss the treatment of iron deficiency anemia
4. Describe the laboratory finding of a child with megaloblastic anemia
References
1. Nelson text book of pediatrics, 16th edition, 2000
2. William W.Hay, et al, Current pediatric diagnosis and treatment, 15th edition, 2001
3. A.V.Hottbrand, et al, Essential hematology, 4th edition, 2001
8.2 Bleeding Disorders
Objectives
By the end of this course, the students are expected:
 To describe the haemostatic mechanisms
 To describe the approach to the bleeding child
 To recite the laboratory studies in a bleeding child
 To be able to list the important causes /mechanism of bleeding disorders
 To discuss about the primary abnormalities in hemophilia, clinical presentation
and management.
 To describe the clinical presentations, and underling problems in ITP.
236
General Considerations
When blood vessels are injured, the clotting process maintains vascular integrity or
causes blood flow to cease through injured vessel.
If clotting is impaired hemorrhage occurs; if it is excessive thrombosis and its

complication occur. Once clotting is initiated, anticoagulants must confine the clotting
process to the site of injury only. The clot must then be physiologically lysed to re-
establish blood vessel patency.
The classic haemostatic mechanism includes:

 The vascular response
 Platelet adhesion and aggregation
 Clot formation and stabilization
 Limitation of clotting to the site of injury by regulatory anticoagulants
 Re-establishment of vascular patency through fibrinolysis and vascular healing.
The vascular endothelium is the primary barrier against hemorrhage; when small
vessels are transected it undergoes vasoconstriction to limit the local hemorrhage.
Platelets are also essential for the control of hemorrhage from small blood vessels.
More extensive injury (involvement of large blood vessels) requires the participation and
co-ordination of the full haemostatic process to provide a firm, stable, fibrin clot.
Generally bleeding disorders may occur as a result of:

 Qualitative or quantitative abnormalities of platelets
 Qualitative or quantitative abnormalities in plasma coagulation factors
 Vascular abnormalities
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Procoagnlant Anticoagnlants
Kallikrein
Vll Vll
Fxll xlla TFPI
Hnwk
Prekalikrein FX1 x1a P-C/S
PL
FIX 1xa Ca++ AT-III
VIIIa P-C/S
vwf FVIII
Fx Xa
PL AT-III
Ca++
Protarombin (full) Thrombin (lla)
Fibrinogen (1) Fibrin

F XIII
Clot
Figure 20: The clotting cascade with sequential activation and amplification of clot
formation
Terms:
HMWK = high molecular weight Kininogen
PL= Phospholipid
Ca++= calcium
TF= tissue factors
TFPI= tissue factor pathway inhibitor
P-C/S= protein C and S
AT- III= antithrombin III
Approach to the Bleeding Child

The clinical history (Hx) provides the most useful information:
History
 Site /sites of bleeding
 Severity and duration of hemorrhage
 The age of symptom onset
 Was the bleeding spontaneous or after trauma?
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 Was there a previous personal or family history of similar problems? Family

pedigree.
 Do symptoms correlate with the degree of injury/ trauma?
 History of drug intake.
 Are there lumps with bruising for which there is minimal trauma?
 Was there increased bleeding during surgery or dental procedures?
 History of delayed/slow wound healing
 Menstrual history in post pubertal females
Physical Examination
 Should focus on whether symptoms are primarily associated with the mucous
membrane or skin (mucocutaneous bleeding) or the muscle or joints (deep
bleeding)
 Look for petechiae, ecchymoses, hematomas, hemarthroses mucous membrane
bleeding.
 Hepatosplenomegally
 Search for evidence of underlying disease
Laboratory tests
Laboratory tests may involve:
 Screening tests: platelet count, bleeding time (BT), PT, PTT
 If screening tests are norma,l do thrombin time,
 If screening tests are abnormal, factor assay depending on the clinical findings
In a patient with an abnormal bleeding history and a positive family history, normal
screening tests should not preclude further laboratory evaluation
Bleeding time
- Assesses the function of platelets and blood vessels
- The normal range is between 4 and 8 minutes
Platelet count
- The normal platelet count is between 150 to 450 x 106/L
- Thrombocytopenia < 150,000/mm3
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- Patients with platelet count > 50,000/m3 rarely have very significant clinical
bleeding
PTT (Partial thromboplastin time)

- Measures the intrinsic pathway
- Normal ranges vary between laboratories
PT (Prothrombin time)
- Measures the extrinsic pathway
- In most laboratories, the normal of ranges between 10 and 13 sec
Thrombin time (TT)

- Measures the final step of the clotting cascade in which fibrinogen is converted to
fibrin
- Normal TT varies between labs but is usually b/n 11 and 15 sec.
Idiopathic Thrombocytopenia Purpura (ITP)

Definition
Idiopathic thrombocytopenia purpura is a primary quantitative platelet disorder
characterized by an autoimmune destruction and clearance from the circulation.
Acute Idiopathic thrombocytopenia purpura (ITP)
Etiology and pathogenesis

One to four weeks following exposure to common viral infections, a small number of
children develop an antibody directed against the platelet surface following which
antibody coated platelets are recognized by the fc receptors on the splenic
macrophages, ingested and destroyed. A preceding history of viral illness is described
in 5 to 65% of cases (e.g. EBV infection)
The classic presentation of ITP is that of an apparently healthy 1 to 4 year old child who
has a sudden onset of generalized petechiae and purpura. Often there is bleeding from
the gums and mucous membrane. It may be the initial presentation of SLE, HIV
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infection, rarely, lymphoma. A physical examination is normal except for petechiae and
purpura. Seventy to eighty percent of cases have spontaneous resolution. Less than
one percent develops intracranial hemorrhage. Ten to 20% develop chronic ITP.
Laboratory findings
Except for thrombocytopenia, other blood tests are normal.
A bone marrow examination, when done, reveals normal granulocytic and erythrocyte
series with characteristically normal or increase no of megakaryocytes
Treatment
Most children don’t require treatment. At the present time, there is no consensus
regarding the management of acute ITP. Therapy doesn’t appear to affect the natural
history of the disease but appears to be capable of inducing a more rapid rise in platelet
count.
Initial treatment options include: -

 Prednisone
Indications: - 1. Patients with significant bleeding
(I.e. hematuria, hematochezia, epistaxis)
2. Platelet count <10,000/mm3

Dose:1- 4 mg/kg/day for 2-3 weeks or until platelet count is >10,000/mm3
 Intravenous immune globulin (IVIG)
 Intravenous Anti- D therapy
Platelet transfusion is not indicated in ITP unless life threatening hemorrhages occur.
Prognosis
70-80% will have spontaneous resolution within 6 months time. 10-20% will develop
chronic ITP. Less than 1% develops intracranial hemorrhage.
Chronic ITP
Chronoc ITP is characterized by:
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 Persistent thrombocytopenia for more than 6months following acute ITP. Features
associated with the development of chronic ITP include: female sex, age of less
than 1year, and more insidious onset of ITP.
 Careful evaluation for associated problems should be done (e.g. SLE, HIV, etc)
 Splenectomy is one of the treatment options after careful consideration.
Questions
1. Discuss the difference in clinical presentation between ITP and hemophilia
2. Discuss the approach to the the bleeding child
Hemophilia A (factor VII deficiency) and Hemophilia B (factor IX deficiency)
General considerations
 Hemophilia A and hemophilia B are the most common and serious congenital
coagulation factor deficiencies that result in severe inherited bleeding disorder.
 Hemophilia has been known since biblical times when Talmudic writings permitted
the avoidance of circumcision when there was a repeated history of death from
circumcision bleeding in male siblings.
 The symptoms of hemophilia A and B are virtually identical.
Genetics and classification

Hemophilia occurs in 1 out of 5000 males, with 85% having factor VIII deficiency and 10
to 15% having factor IX deficiency. The disease occurs predominantly in males and is
inherited in an X-linked recessive manner.
Hemophilia is classified into three levels, based on level of clotting factors:

1. Mild - more than 5% (5u/dl) of factorVIII is present in the blood
2. Moderate - 1 to 5% (1-5u/dl)
3. Severe - less than 1 % (< 1u/dl)
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Pathophysiology
 Factor VIII and IX participate in a complex required for activation of factor X.
 In hemophilia A/B, clot formation is delayed and not robust.
 The clot that is formed may be friable and re-bleeding occurs during physiological
lyses of clots or with minimal trauma.
Neither factor VIII nor factor IX crosses the placenta, thus bleeding symptoms may be
present from birth or occur in the fetus but they usually go unnoticed in the newborn. It
is only when the child begins to crawl and walk that mobility causes the initiation of the
symptoms which include:
 Easy bruising, intramuscular hematomas and hemarthroses
 Persistence of bleeding from minor traumatic lacerations of the mouth
 The commonest presentation of hemophilia is hemarthroses, which may be induced
by minor trauma but often occurs spontaneously.
 Uncontrolled bleeding during circumcision.
 Life threatening bleeding in the hemophilic patient is caused by bleeding in to vital
structures (CNS and upper air way) or by exsanguinations (external, GI or iliopsoas
hemorrhage)
Treatment
Treatment involves:
 Prevention of trauma
 Psychosocial support (families and child)
 Avoid Aspirin and other NSAIDs
 Replacement therapy (blood, plasma, cryoprecipitate)
 Desmopressin (DDAVP) for mild hemophilia A
Complications
 Chronic joint destruction
 Risk of transfusion- transmitted infections
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References
3 A.V.Hottbrand, et al, Essential hematology, 4th edition, 2001
8.3 Leukemia
Objectives
By the end of this course the student is expected:
 To describe the primary abnormality in leukemia
 To know the epidemiology of leukemia
 To discuss the common clinical manifestations and investigation
 To list the principles of management
 To enumerate the prognostic factors
Definition
The leukemias are a group of malignant diseases arising from the bone marrow in
which genetic abnormality in a hematopoietic cell give rise to a clonal proliferation of
cells of the lymphoid and myelogenous series resulting in disruption of normal marrow
function and ultimately in marrow failure.
Epidemiology
Leukemia is the most common childhood malignancy accounting for more than one-
third of pediatric malignancies.
- ALL– 77% ; AML- 11%; CML <5%
- The peak age for ALL is 4 year with 85% of the patients diagnosed between 2 and
10 years.
Etiology
The precise cause of leukemia remains unknown. Both genetic and environmental
factors like drugs, ionizing radiations, viruses, etc, appear to be involved in the
development of the disease.
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Acute lymphoblastic leukemia (ALL)

Acute lymphoblastic leukemia (ALL) accounts for 77% of the leukemias
Classification
Classification is based on:
 Morphologic appearance of the blasts – L1, L2, L3
 Immunophenotype - B - Progenitor
- T - Progenitor
Clinical manifestations are related to decreased bone marrow production of red blood
cells, white blood cells and platelets because of leukemic infiltration of the bone
marrow.-Include:
 pallor, petechiae, purpura, fever, bone and joint pain
 Hepatosplenomegaly and lymphadenopathy
 Fever (mostly due to infection) is a common clinical presentation
 Rarely, signs suggestive of increased intracranial pressure secondary to leukemic
infiltration of the meninges.
Laboratory findings and diagnosis

Laboratory findings and diagnosis involve the following:
 Single or panytopenias (anemia, thrombocytopenia and neutropenia) occurs in
99% of the cases.
 Most patients with ALL present with a total WBC count of<10,000/mm3.
 Immature lymphocytes (blasts) in the peripheral blood.
 The diagnosis of ALL is strongly suggested by peripheral blood findings suggestive
of bone marrow failure and it is confirmed by bone marrow examination.
 Other important studies include chest x-ray (mediastinal mass), CSF- analysis,
and renal function test and serum uric acid level.
Differential diagnosis includes:
 Infectious mononucleosis
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 Aplastic anemia, and myelofibrosis

 Malaria
 Disseminated tuberculosis
 HIV infection
Treatment
Treatment includes:
Supportive treatment:
- Transfusion with blood products
- Nutritional support
- Treatment of infections, when present
Drug therapy
For patients with average/ standard risk groups i.e. those with favorable prognosis (age
between 1 and 10 years, initial WBC count more than100,000/mm and L1 and L2
morphology)
 Induction remission: 4 to 6 weeks
(Vincristine, prednisone and L-asparaginase)
 CNS- prophylaxis and/or therapy: 4 to 6 weeks
(Intrathecal methotrexate)
 Maintenance treatment – for up to 2 to 3 years. (Mercaptopurine, methotrexate
and intermittent dose of prednisone and vincristine)
Remission is defined by less than 5% of blasts in the bone marrow and return of
neutrophils and platelet count to near normal levels after 4 to 5 weeks of treatment, is
98%.
The long term survival is more than 80% after 5 years.
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Prognosis
Poor prognostic factors include:
 Age less than 1year and more than 10 years
 Initial WBC count of more than 100,000/mm3
 L3 morphology
 clinical CNS leukemia at diagnosis
 Mediastinal mass
 T- cell immunophenotype
 Certain chromosomal translocations (e.g. t(9,22), t (4;11)
 Relatively slower remission
Relapse
- 10% relapse after completion of treatment in the subsequent 4 years. Bone marrow
is the commonest site of relapse; other common sites include the CNS and testes
but any site can be affected with relapse.
Exercise
1. Describe the clinical presentation of a child with ALL.
2. Discuss the laboratory workup and diagnosis of ALL.
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8.4 LYMPHOMA
Objectives
By the end of this course the student is expected:
 To describe the epidemiology and pathology of the lymphomas

 To be able to list the important clinical manifestations
 To recite the diagnostic laboratory work up
 To briefly mention the treatment modalities and prognosis
Definition and general consideration

The term lymphoma refers to malignant proliferation of lymphoid cells, usually in
association with and arising from lymphoid tissues (i.e. lymph nodes, thymus and
spleen). They are the third most common cancers in children.
There are two major categories of lymphoma: Hodgkin’s and non- Hodgkin’s lymphoma
Hodgkin’s Disease (HD)

Epidemiology
The epidemiology of Hodgkin’s disease is as follows:
 Arises in lymphoid tissues
 Accounts for 5% of cancers in children < 15 years
 Three epidemiological forms occur :
- Childhood form (< 14 yrs old)
- Young adult form (15-34 yrs old)
- Older Adult form (55-74 yrs old)
There is a 4:1 male predominance in the first decade and the frequency is equal during
adolescence when the majority of the cases occur.
Etiology
The exact cause of Hodgkin’s disease remains unknown.
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- Genetic predisposition, viral infections especially ebsteinbarrvirus, pre-existing

immunodeficiency, etc are the associated risk factors in the development of the
disease
Pathology
The Reed-Sternberg cell, a large (15 to 45 microm in diameter) cell with multiple or
multilobulated nuclei is considered the hall mark of Hodgkin’s disease.
Four histological types are present

 Lymphocyte predominant (10 to 20% of cases) it has the most favorable outcome.
 Nodular sclerosing (40 to 60% of cases)
 Mixed cellularity (20 to 40% of cases)
 Lymphocyte depleted (5to 10% of cases) it has least favorable outcome
Spread occurs via:– lymphatic system to adjacent lymph nodes
Hematogenous: - liver, spleen, bone,
Various degrees of immune impairment (especially in cell mediated immunity) are seen
in Hodgkin’s disease.
Clinical Manifestation
Clinical manifestations include the following:
 Painless, firm, cervical or supraclavicular adenopathy is the most common
presenting sign.
 The growth rate of lymph nodes is variable and involved nodes may wax and wane
for weeks or months
 Inguinal and axillary sites- uncommon but still possible
 Anterior mediastinal mass is often present (50%)
 Rarely, hepatosplenomegally
 Sometimes patients might present with airway obstruction, pleural/pericardial
effusion, hepatic dysfunction or bone marrow infiltration (pancytopenia) and rarely
with nephrotic syndrome
 Systemic symptoms include fever, drenching night sweat, weight loss (B-
symptoms).
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Diagnosis
 Diagnosis involves undertaking a history and physical exam to investigate:

 Persistent, painless, unexplained, rubbery adenopathy unassociated with an
obvious underlying inflammatory or infectious process.
 Lymph node biopsy
 Staging – 4 stages (I-IV) according to Ann Arbor staging system
 Studies necessary for clinical staging of HD include CBC, ESR, LFT, chest and
abdominal CT, CXR and/or BM-biopsy
Differentail diagnoses include leukemia, tuberculosis and HIV infection
Treatment
The treatement is largely determined by disease stage, the patient’s age at diagnosis,
the presence or absence of B- symptoms and the presence of bulky nodal disease. It
may involvechemotherapy and radiotherapy
Prognosis
Cure rates are 90% in the early stage and 60-70% in the advanced stage
Poor prognostic factors include advanced stages, B- symptoms, failure to achieve

remission and early relapse.
Non- Hodgkin Lymphoma (NHL)

Epidemiology
In children, as opposed to adults, NHL is a high grade, rapidly growing and diffuse
neoplasm.
It results from malignant clonal proliferation of lymphocytes of T- or B-, or indeterminate

cell origin.
A special type of lymphoma, Burkitt's lymphoma, was first described in 1958 as "a
sarcoma involving the jaws in African children". It is most frequent in equatorial Africa
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where it accounts to 50% of childhood cancers. There is a strong epidemiologic

association between Epstein Barr virus and Burkitt's lymphoma. Unlike HD, the
incidence of NHL increases throughout life
Etiology, pathology and pathogenesis

EBV infection has a major role in the pathogenesis of the disease even though the
actual mechanism remains unknown.
Pre- existing immunodeficiency (congenital/acquired) also predisposes to the

development of the disease
Three histological subtypes exist:

 Lymphoblastic (usually of T- cell origin)
 Large cell (LCL, of T-, or B-, or indeterminate cell origin)
 Small non-cleaved cell lymphoma (SNCCL, Burkitt’s and non-Burkitt’s subtypes, B-
cell origin)
Clinical manifestations are as follows:
 The presenting signs and symptoms vary with the disease site and extent which in
turn correlate with histolgic subtype
 Lymphadenopathy, mediastinal mass, pleural effusion, ascites hepatosplenomegally
 Cough, dyspnea, swelling of the face
 Abdominal pain, abdominal distension, vomiting, constipation
 Burkitt's lymphoma presents with large jaw and/or abdominal mass with /without
CNS involvement
Laboratory findings
- Features of tumor lyses syndrome (increased serum uric acid, K and phosphorous)
- Increased LDH
Diagnosis
Is made after biopsy with histology, immunophenotyping and cytogenetic studies
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- Leukemia
- Tuberculosis
- HIV infection
Treatment and prognosis

 Chemotherapy
 About 90% of patients with limited stage NHL are cured with current
chemotherapeutic regimens.
Questions
1. Mention the difference in clinical presentation between childhood Hodgkin's and
non-Hodgkin's lymphoma
2. Discuss the risk factors and clinical presentation of Burkitt's lymphoma.
References
1. Nelson text book of pediatrics,16th edition, 2000
2. William W.Hay, et al, Current pediatric diagnosis and treatment ,15th edition, 2001
3. Philip Lanzkowsky, pediatric oncology, 1983
4. A.V.Hottbrand, et al, Essential hematology, 4th edition, 2001
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CHAPTER NINE
DISEASES OF THE RENAL SYSTEM
Mekete and wogene
Objectives
At the end of this chapter students should:
 Understand the diagnosis and management of urinary tract infection and
differentiate upper UTI from cystitis.
 Identify common causes of acute glomerulonephritis and understand its diagnosis
and management.
 Understand the diagnosis and management of nephrotic syndrome
 Understand pathophysiology and common causes of ARF (Acute Renal Failure).
 Understand the diagnosis ARF and its complications.
 Understand principles of management of ARF and its complications.
9.1 Introduction
Anatomy
The kidneys lie in the retroperitoneal space slightly above the level of the umbilicus.
The kidney has an outer layer, the cortex, which contains the glomeruli, proximal and
distal tubules, and collecting ducts, and an inner layer, the medulla, which contains the
straight portions of the tubules, the loops of Henle, the vasa recta and the terminal
collecting ducts.
The blood supply to each kidney usually consists of a main renal artery that arises from
the aorta; multiple renal arteries may occur. Each kidney consists of approximately 1
million nephrons (glomeruli and associated tubules). The glomerular network of
specialized capillaries serves as the filtering mechanism of the kidney.
Glomerular filtration
As the blood passes through the glomerular capillaries, the plasma is filtered through
the glomerular capillary walls. The ultra filtrate is cell free and it contains all the
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substances in the plasma (electrolytes, glucose, urea, creatinin, phosphate and low
molecular weight proteins) except proteins having a molecular weight of 68,000 or more
such as albumin and globulins.
The glomerular filtration rate (GFR) may be estimated by measurement of serum

creatinin level. Creatinin is a product of muscle metabolism. Its production is relatively
constant, and its excretion is primarily through glomerular filtration, although tubular
secretion may become important in renal insufficiency. In contrast to the concentration
of blood urea nitrogen, which is affected by state of hydration and nitrogen balance, the
serum creatinin level is primarily influenced by the level of glomerular function.
However, the serum creatinin level does not rise above normal until the GFR falls by 30
to 40%.
9.2. Urinary Tract Infection (UTI) in Children

Definition
UTI refers to a group of conditions in which there is growth of bacteria within the urinary
tract.
Etiology and epidemiology

Approximately 3.5% of girls and 1% of boys develop UTI. During the first year of life, the
male: female ratio is 2.8-5.4: 1.This ratio becomes 1: 10 beyond the age of 1to 2years
of age. In girls the first UTI usually occurs by the age of 5yr, peaks during infancy and
toilet training. In boys most UTIs occur during the first year of life.
The etiologic agents in UTI are mainly colonic bacteria. E.coli, klebsiella, and proteus
are among the commonest causes. E.coli causes 75-90% of UTIs in females.
Pathogenesis
Nearly all UTIs (except in neonates) are ascending infections, the origin being the
colon. The bacteria arise from the fecal flora, colonize the perineum and enter the
bladder via the urethra. In uncircumcised boys, the bacteria arise from the flora beneath
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the prepuce. In some cases, the bacteria ascend to the kidney to cause pyelonephritis.
In rare cases, renal infection may occur by hematogenous spread. UTI in neonates,
however, is mostly hematogenous in origin.
The pathogenesis of UTI is based in part on the presence of bacterial pili and fimbriae
on the bacterial surface. Host risk factors for developing UTI include female sex,
uncircumcised male, toilet training, constipation, urethral instrumentation, anatomic
abnormalities, neuropathic bladder, pinworm infestation and others.
Classification of UTI There are three forms of UTI: pyelonephritis, cystitis and
asymptomatic bacteriuria.
Asymptomatic bacteriuria: This is a benign condition characterized by presence of

positive urine culture without any manifestations of infection and occurs almost
exclusively in females.
Cystitis: Cystitis indicates involvement of the urinary bladder Cystitis does not result in
renal injury.
Pyelonephritis: Refers to involvement of renal parenchyma and it may result in renal

injury called pyelonephritic renal scarring. When there is no parenchymal involvement,
the condition is termed pyelitis.
Newborns with UTI may present with fever hypothermia, poor feeding, failure to thrive
or sepsis. Infants may have malodorous urine, irritability and poor feeding.
Symptoms of cystitis in older children include dysuria, urgency, frequency, suprapubic

pain, incontinence and malodorous urine. Isolated cystitis does not cause fever.
Pyelonephritis presents with any or all of the following: abdominal or flank pain,
malaise, fever, nausea, vomiting, and occasionally diarrhea. Patients may appear toxic.
255
Diagnosis
Although culture of properly collected urine is mandatory for confirmation of UTI, it may
be suspected based on patients’ presentation and urinalysis.
256
Table 26: Urine Culture Interpretation in UTI
Method of collection Quantitative culture:UTI present

Urine by Suprapubic Any number of bacteria
Puncture
Catheterization Growth of urinary pathogens in any number(the
exception is up to 2-3x10³*CFU/ml of
coagulase negative staphylococcus)
Midstream clean- Febrile infants or children usually have ≥
void 50x10³ CFU/ml of a single urinary pathogen,
but infection may be present with counts from
10x10³ CFU/ml.
Midstream clean- Symptomatic patients usually have ≥ 105
void CFU/ml of a single urinary tract pathogen.
Midstream clean- Asymptomatic patients: at least two specimens
void on different days with ≥ 105 CFU/ml of the
same organism.
*CFU = Colony Forming Units
Urinalysis
Urinalysis should be done from the same specimen and pyuria (>5 WBC/HPF) suggests
infection, although infection can occur in the absence of pyuria. Pyuria can be present
without UTI. Microscopic hematuria is common in acute cystitis. WBC casts in the urine
suggest renal involvement.
Other Investigations
With acute renal infection, leukocytosis, neutrophilia, and elevated ESR and C-reactive
protein are common.
Repeated UTI needs further investigation to exclude possible structural abnormalities.
Methods of urine collection include:
257
 For toilet trained children

Midstream clean catch sample
Catheterization
*Suprapubic puncture
 In infants
Catheterization
Application of adhesive, sealed, sterile collection bag
*Suprapubic puncture
*Bacteriologic results are more reliable, but the procedure should only be considered in
a specialized pediatric setting.
Treatment
Acute cystitis should be treated with a 3 to 5 day course of therapy with one of the
following antibiotics:
 Trimethoprim - Sulfamethoxazole (6-12mg TMP and 30-60mg SMX /kg/24hr)
 Nitrofurantoin- 5-7 mg/kg/24hr in 3 to 4 divided doses
 Amoxicillin - 50 mg/kg/24 hrs
Pyelonephritis is treated by a 14 days course of either

 Ceftriaxone (50-75mg/kg/24hr), or
 Ampicilline (100mg/kg/24hr) and gentamycin
(3 - 5 mg/kg/24hr)
Prognosis
Prognosis is excellent with lower UTI but is guarded with pyelonephritis.
9.3 Acute Glomerulonephritis (AGN)

Glomerulonephritis may have an acute or chronic presentation. Primary renal diseases
presenting as acute GN include PSGN, IgA nephropathy, membranopliferative GN and
idiopathic rapidly progressive GN. AGN can also occur in the course of various
systemic illnesses.
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There are five major clinical presentations of GN: acute nephritic syndrome, nephrotic
syndrome, rapidly progressive GN, asymptomatic abnormalities of the urinary sediment
(hematuria, proteinuria) and chronic GN. Acute nephritic syndrome is characterized by
the abrupt onset of hematuria, with RBC casts or dysmorphic RBCs and proteinuria
(usually non-nephrotic range), temporally associated with impairment of renal function.
Acute Poststreptococcal Glomerulonephritis (APSGN)
Definition.
APSGN is a classic example of nephritic syndrome, which is characterized by sudden
onset of gross hematuria, edema, hypertension, proteinuria and renal insufficiency.
Etiology and Epidemiology

PSGN is the commonest cause of postinfectious GN. The condition follows infection of
the throat or the skin with nephritogenic strains of group A Beta-hemolytic streptococci.
During cold weather, PSGN commonly follows streptococcal pharyngitis whereas during
warm weather the GN generally follows pyoderma. Although epidemics have been
described, the condition is most commonly sporadic. It is most common in children
aged between 5 and 12 years of age.
Pathogenesis of PSGN
The pathogenetic mechanisms leading to renal damage are generally not well
understood. Although the exact mechanisms of immune complex formation are not
clear, evidences such as depression in serum C3 level and morphologic studies
suggest immune complex mediated glomerular injury.
Typical patients with acute PSGN develop an acute nephritic syndrome 1 to 2 weeks
after an antecedent streptococcal pharyngitis or 3-6 weeks after streptococcal
pyoderma.
The severity of renal involvement varies from asymptomatic microscopic hematuria to
acute renal failure. Patients commonly have nonspecific symptoms such as malaise,
lethargy, abdominal or flank pain and fever.
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Edema mainly develops from salt and water retention. Hypertension is seen in 60% of
cases. In severe cases, patients may develop encephalopathy and/or congestive heart
failure from sever hypertension and acute renal failure.
Nephrotic syndrome may develop in 10 to 20% of cases.
Laboratory findings
Urinalysis demonstrates hematuria, usually with RBC casts, proteinuria of ++ and less,
and polymorphonuclear cells.
The level of complement factor C3 is usually reduced.
Renal function test (blood urea nitrogen and serum creatinin level) may be normal or
elevated.
Confirmation of the diagnosis requires clear evidence of invasive streptococcal

infection. A positive throat culture may support the diagnosis or may simply represent a
carrier state. On the other hand, a rising antibody titre to streptococcal antigen (s)
confirms a recent streptococcal infection. The ASO (anti-sreptolysin O) titre is
commonly elevated after a pharyngeal infection but rarely rises after pyoderma. The
best antibody titre to document cutaneous infections is anti-DNAase B titre.
Renal biopsy should be considered only in selected cases.

Complications
Complications of acute PSGN are those of acute renal failure and include hypertension,
heart failure, encephalopathy, hyperkalemia and metabolic acidosis.
Treatment
There is no specific therapy for APSGN. The management is directed towards treating
complications of ARF.
Although there is no evidence that antibiotics change the course of the illness, a 10
days treatment with systemic penicillin is generally recommended.
Prevention
Early systemic antibiotic therapy for streptococcal throat or skin infection does not
eliminate the risk of GN. Family members of patients with AGN should be cultured for
group A Beta- hemolytic streptococci and treated if culture positive.
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Course and Prognosis

The acute phase generally resolves within 6-8 weeks.
Urinary protein excretion and hypertension usually normalize by 4-6 weeks after onset;
however, microscopic hematuria may persist for 1-2 year after initial presentation.
Complete recovery occurs in more than 95 % of children with APSGN and recurrences
are extremely rare
9.4 Nephrotic Syndrome

Definition
This is a syndrome characterized by heavy proteinuria (>40mg/m²/hr),
hypoalbuminemia (< 2.5g/dl), edema and hyperlipidemia.
Etiology
Nephrotic syndrome may occur as a result of any form of glomerular disease and may
be associated with a variety of extra renal conditions.
Approximately 90% of children with this condition have some form of the idiopathic
nephrotic syndrome. In the remaining 10%, the syndrome is secondary to some form of
glomerulonephritis. Other possible causes include tumors (lymphoma, leukemia),
infections (hepatitis B, malaria, etc), drugs (isoniazaid), systemic disease (systemic
lupus erythematous, juvenile rheumatoid arthitis, diabetes) and congenital nephrotic
syndrome.
Idiopathic Nephrotic Syndrome (minimal change disease)

Idiopathic nephrotic syndrome accounts for approximately 90% of nephrosis in
childhood. It occurs in three morphologic patterns: minimal change disease (85%),
focal segmental glomerulosclerosis (10%) and mesangeal proliferative (5%).
Etiology and Epidemiology
The cause is unknown
It is primarily a pediatric problem, being 15 times more common in children than in

adults.
Incidence of nephrotic syndrome is 2-3/100,000 children/year
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The condition most commonly occurs between the ages of 2 and 8 years of age but it is
reported as early as 6 months and throughout adulthood. Male to female ratio is
approximately 2:1
Pathophysiology
Nephrotic syndrome results from alterations in the selective permeability of the

glomerular basement membrane. The protein loss is generally more thanb 2g in 24
hours (normalloss would be less than 150mg in 24 hours). The protein lost is primarily
composed of albumin resulting in hypoalbuminemia. Edema appears when serum
albumin falls below 2.5 g/dl, however, the mechanism of edema formation in nephrotic
syndrome is incompletely understood.
The serum level of almost all lipids is increased in nephrotic syndrome as a result of
increases in lipoprotein synthesis and low levels of lipoprotein lipase.
Attacks may follow URTI
It usually presents with pitting edema, initially noted in periorbital area and in the lower
extremities. The edema becomes generalized with time.
Some children present with hypotension secondary to significant shift of fluid from
intravascular to third space and they may rarer develop renal failure
With massive pleural effusion and ascites, patients may develop dyspnoea.
Unlike nephritic syndrome, gross hematuria and hypertension are uncommon.
Diagnosis
Urinalysis reveals proteinuria (+3or +4 on dipstick).
Serum albumin level is generally < 2.5g /24 hr.
The serum cholesterol and triglyceride levels are generally high
C3 level is often normal
 Renal biopsy is generally not indicated for children between 1 and 8 years of age,
however, it is indicated in children with features that make minimal change disease
less likely. These are:
262
- hematuria
- hypertension
- renal insufficiency
- hypocomplementemia
- age <1yr or >8yr
Complications
Infection is the major complication of nephrosis. Contributing factors include

hypogammaglobulinemia, decreased bactericidal activity of leukocytes and edema fluid
acting as a culture medium.
The commonest infectious complication in nephrotic syndrome for unknown reasons is

spontaneous bacterial peritonitis. S.pneumoniae is the commonest cause of
spontaneous bacterial peritonitis in these patients. Other infections include pneumonia,
cellulitis, sepsis, and UTI.
Patients with nephrosis also exhibit increased tendency for arterial and venous
thrombosis (2-5%).
Treatment
General measures
- Children with mild to moderate edema can be managed as outpatienst.
Salt should be restricted (until the edema resolves)
Diuretics can be used cautiously to reduce the edema. In mild cases, chlorothiazide or
spironolactone can be used but in severe cases with respiratory distress secondary to
massive pleural effusion and ascites or severe scrotal edema frusemide (P.O, or IV with
poor response to P.O treatment) can be administered with careful monitoring of renal
function and serum electrolytes.
Steroids
More than 95% of children with minimal change disease, ~50% with mesangeal
proliferation and ~20% with FSGS respond to steroids.
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In children with presumed minimal change disease prednisolone should be

administered in a dose of 60mg/m2/24hr or, 1-2mg/kg/24hr (maximum 80 mg/d) in 3 to
4 divided dose for 4 to 6 weeks. Eighty to ninety percent of patients respond to steroid
therapy with the median time to remission of 10 days. Remission is defined by
proteinuria of trace or negative for 3 consecutive days.
After the initial 4 to 6 week course, the prednisolone dose should be tapered to 40
mg/m²/d and given every other day as a single morning dose. The alternate-day dose is
continued for the next 2 to 3 months and discontinued without tapering the dose.
Patients with proteinuria of 2+ or more after 8 weeks of steroid treatment are said to
have steroid resistant nephrosis.
Relapses (3-4+ proteinuria plus edema), should be treated with prednisolone daily in
divided dose as above until they enter remission. The prednisolone dose is then
changed to alternate-day dosing and tapered over 1 to 2 months.
Patients who relapse while on alternate-day treatment or within 28 days of stopping

prednisolone are termed steroid dependent. Patients who responded well to steroid
therapy but relapse 4 or more times in 12 months period are termed frequent relapsers.
Cytotoxic drugs
Cytotoxic agents such as cyclophosphamide can be considered in frequently relapsing
nephrotic syndrome or if patients suffer severe corticosteroid toxicity. They may also
help in some steroid resistant cases.
Prognosis
Most children with steroid responsive nephrotic syndrome have repeated relapses until
the end of second decade of life when the disease resolves spontaneously.
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9.5 Acute Renal Failure (ARF)
Definition
Acute renal failure (ARF) is a clinical syndrome in which a sudden deterioration in renal
function results in inability of the kidneys to maintain fluid and electrolyte homeostasis.
Etiology
Causes of ARF are conventionally classified as prerenal, intrinsic renal and postrenal
a) Prerenal causes
- Hemorrhage
- Dehydration
- Sepsis
- Cardiac failure and others
b) Intrinsic renal causes
- Glomerulonephritis, such as PSGN, and rapidly progressive GN.
- Acute tubular necrosis (ATN)
- Hemolytic uremic syndrome
- Acute interstitial nephritis
c) Post renal causes
- Posterior urethral valve
- Urolithiasis
Pathogenesis
Prerenal causes of ARF produce decreased renal perfusion via decrease in the total or
effective circulating blood volume. The result of decreased perfusion is decrease in
GFR and cortical blood flow. There is no evidence of renal damage. If the underlying
cause of the renal hypoperfusion is reversed promptly, renal function returns to normal.
If hypoperfusion persists, intrinsic renal parenchymal damage may develop.
Intrinsic renal causes lead to ARF through different mechanisms, some of which are not
well understood. There is evidence of renal parenchymal damage. Acute tubular
necrosis occurs most often in critically ill infants and children who have been exposed
to nephrotoxic and/or ischemic insults. The typical pathologic process of ATN is tubular
cell necrosis.
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For postrenal causes to result in renal failure, the obstruction should be bilateral if both
kidneys are functioning or it should be complete obstruction of a single functioning
kidney. In general, relief of the obstruction results in recovery of renal function except in
patients with associated renal dysplasia or prolonged urinary tract obstruction.
In ARF, signs and symptoms may predominantly be that of the precipitating disease,
and hence findings related to common cause should be looked for.
Clinical findings related to the renal failure include pallor, decreased urine output,
edema, hypertension, vomiting and lethargy.
Renal failure may be oliguric (urine output <0.5 ml/Kg/hour <400 ml /m2) or non–oliguric
(as in aminoglycoside nephrotoxicity).
Diagnosis
The diagnosis of ARF is established by detecting elevated bun (blood urea nitrogen)
and creatinin levels. Considerable information however can be obtained from urinalysis
in addition to clinical findings:
 Presence of hematuria, proteinuria and RBCs or granular casts on urinalysis
suggests intrinsic ARF, in particular glomerular disease.
 The presence of WBCs and WBC casts with low-grade hematuria and proteinuria,
suggests tubulointerstital disease. Urinary eosinophils may be present in children
with drug induced tubulointerstital nephritis.
Urinary indices (specific gravity, osmolality, urine Na) may be useful in differentiating
prerenal ARF from intrinsic ARF.
Other Laboratory investigations can be done to detect the underlying cause.
Complications
266
Metabolic
 Hyponatremia
 Hyperkalemia
 Hypocalcemia, hyperphosphatemia
 Hypermagnesemia
 Hyperuricamia
Metabolic acidosis
Cardiovascular
 Pulmonary edema
 CHF
 Hypertension
 Arrhythmias
 Pericarditis
Neurologic
 Coma
 Seizures
Hematologic
 Anemia
 Coagulopathies & bleeding diathesis
Treatment
Initial measures
Patients with ARF should be admitted to a hospital for careful monitoring.
Determination of the intrvascular volume (hydration) status is of critical importance

when initially evaluating a patient with ARF. If there is no evidence of volume overload
or cardiac failure, intravascular volume should be expanded by IV administration of
isotonic saline, 20 ml/kg over 30 minutes. Severe hypovolemia may require additional
fluid boluses. After volume resuscitation, hypovolemic patients generally void within 2
hours. Failure to pass urine suggests the presence of intrinsic or postrenal ARF.
267
Diuretic therapy should be considered only after the adequacy of circulating blood
volume has been established. Furosemide can be administered as a single IV dose of 2
tp 4 mg/kg. If there is no urine even after catheterization, diuretics should be
discontinued and fluid restriction becomes essential.
Specific complications of ARF
Fluid overload (CHF, hypertension, pulmonary edema)

treatment with salt and water restriction
- Diuretics - Furosemide
- Beta blockers and vasodilators can also be considered for treatment of hypertension
in addition to the above measures
Hyperkalemia (serum K >6mEq/L)
- yperkalemia may lead to cardiac arrhythmia, cardiac arrest, and death.
- reat with- K- restriction or sodium polystyrene sulphonate
- When it is >7mEq/L, it requires emergency measures:
- Regular insulin with glucose (50%)
- Calcium gluconate
- NaHC03
Acidosis
Acidosis is rarely severe
Treat with bicarbonate in severe acidosis
(PH < 7.15 or serum bicarbonate <8mEq/L).
Hypocalcaemia
- Treat with lower serum phosphorus by giving phosphate-binding antacids, this
increases the serum calcium level.
- - If tetany develops, administration of IV Ca carbonate is needed.
Hyponatremia
Treat with fluid restriction.
- ypertonic saline (3%) for symptomatic cases or when serum Na is <120mEq/L
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Seizures
Treatment involves controling attacks using diazepam
- Treat underlying cause: electrolyte abnormalities
Fluid and caloric management

Patients with relatively normal intravascular volume should be restricted to an amount
of fluid equal to insensible loses (400ml/m²/24hr) plus urine output only.
 In general, glucose-containing fluids (10-30%) without electrolytes are used as
maintenance fluids.
 Moderate protein restriction (to avoid accumulation of nitrogenous wastes) and
increasing caloric intake are generally recommended.
Treat underlying causes
 Peritoneal dialysis
 Dialysis may be considered for severe complications not responding to conservative
measures
Exercise
1. A 7 year old male child presented with history of urinary frequency, dysuria and
suprapubic pain of 3 days duration. There is no history of fever. Urinalysis revealed
11 WBCs and 6RBCs per HPF.
a) What is the most likely diagnosis?
b) How do you confirm the diagnosis?
2. Discuss clinical and laboratory features that differentiate nephrotic syndrome from
nephritic syndrome.
3. Outline the management of a patient with idiopathic nephrotic syndrome.
4. List 5 complications of ARF.
269
References
1. Nelson Textbook of pediatrics 17 th edition, 2004
2. Robert w. Schrier. Renal and electrolyte disorders 4th edition, 1992.
3. William W. Hay, Jr. Anthony R. Hayward, Myron J. Levin, Judith M. Sondheimer.
Current pediatric diagnosis & treatment, 15 th edition, 2001
4. Cecil, Essentials of medicine 5th edition.
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CHAPTER TEN
DISEASES OF THE NERVOUS SYSTEM
Solomon Amsalu
10.1 Bacterial Meningitis

Objectives
By the end of this section, readers should be able to:
 Describe the causes of bacterial meningitis in children
 Discuss the clinical manifestations of meningitis
 Discuss the diagnostic methods in meningitis
 Discuss the management of meningitis
Introduction
Bacterial meningitis indicates inflammation of the meninges as a result of bacterial
infection.
Bacterial meningitis is one of the most potentially serious infections in infants and older
children.
The possibility of bacterial meningitis should be considered in all febrile infants with
altered mental status or evidence of other neurologic dysfunction.
Etiology
 The first 2 months of life – group B streptococcus, gram negative enteric bacilli and
listeria monocytogenes. Occasionally – Hemophilus influenzae (both type b and
non-typable strains) and other pathogens found in older patients.
 2 months to12 years of age – Hemophilus influenzae type b, Streptococcus
pneumoniae and Neisseria meningitides
 In children more than 12 years old – neisseria meningitides and streptococcus
pneumoniae
Alterations in host defenses due to anatomic defects or immune deficits increase the
risk of meningitis from less common pathogens such as pseudomonas aeruginosa,
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staphylococcus aureus, Staphylococcus epidermidis, salmonella and listeria

monocytogenes.
Epidemology
The risk is greatest among infants 1 - 12 months of age. 95% of cases occur between 1
months and 5 years of age.
The major risk factor is lack of immunity to specific pathogens associated with young
age.
The mode of transmission is probably person-to-person contact through respiratory

tract secretions or droplets.
H. influenzae type b
 Most commonly occurs between 2 months and 2 years of age.

 Peak incidence occurs in infants 6 to 9 months of age.
 Otitis media, HIV infection and CSF leaks increase the risk of H. influenzae
meningitis.
Streptococcus pneumoniae
 The risk is greater among blacks than whites, especially among blacks with sickle
cell anemia.
 Other risk factors include otitis media, sinusitis, pneumonia, CSF ottorrhea, or
rhinorrhea and splenectomy
Neisseria meningitides
 Epidemics are usually caused by group A and C.
 In the absence of epidemic most infections are due to group B.
Pathology
The brain is hyperemic, edematous and contains exudate in the subarachnoid space.
Thrombosis may occur in meningeal veins or venous sinuses. Destructive changes can
take place in the cortex. Inflammation of spinal nerves and roots produces meningeal
signs, and inflammation of cranial nerves produce cranial neuropathy.
Increased intracranial pressure is due to

 Cell death (cytotoxic brain edema)
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 Cytokine induced increased capillary vascular permeability (vasogenic cerebral

edema) and,
 Increased hydrostatic pressure (interstitial cerebral edema) following obstructed
reabsorption of CSF in the arachinoid villus or obstruction of the flow of fluid with in
or exiting from the ventricles.
Hydrocephalus is uncommon after the neonatal period. It often takes the form of
communicating hydrocephalus. Less often obstructive hydrocephalus develops.
Pathogenesis
Bacterial meningitis is usually the result of bacteremia from an upper respiratory

infection.
Invasion by direct extension is less common but may occur from purulent infections of
the paranasal sinuses, mastoids, or rarely from abscesses contiguous to the meninges.
Bacteria may also gain entry to the CNS through penetrating wounds, lumbar puncture,
neurosurgical procedures or midline dermal sinus tracts.
The mode of onset has two predominant presentations:
 Sudden onset with rapidly progressive manifestations of shock, purpura, DIC and
reduced level of consciousness is a dramatic and often fatal presentation of
meningococcal sepsis with meningitis; it may evolve to death with in 24 hours.
 Subacute presentation - more often, meningitis due to H. influenzae type b and
pneumococcus (and some cases of meningococcal meningitis) is preceded by
several days of upper respiratory tract or gastrointestinal symptoms.
The signs and symptoms of meningitis are related to:

 Non specific findings associated with a systemic infection or
 Manifestations of meningeal irritation like nuchal rigidity, back pain, Kerning sign and
Brudzinski sign. In young infants these signs may not be evident.
Increased ICP is suggested by headache, emesis, bulging fontanel or diathesis of the

sutures, oculomotor or abducens nerve paralysis, stupor, coma or signs of herniation.
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Focal neurologic sign may be due to vascular occlusion or abscess formation. It is most
commonly seen in patients with pneumococcal meningitis.
Seizures that occur on presentation or with in the first 4 days of onset are usually of no
prognostic significance. Seizures that persist after the fourth day of illness and those
that are difficult to treat are associated with poor prognosis.
Diagnosis
The diagnosis of acute pyogenic meningitis is confirmed by CSF analysis, which
reveals microorganisms on Gram stain and culture, a neutrophilic pleocytosis, elevated
protein and reduced glucose concentrations.
Lumbar puncture (LP) should be performed when bacterial meningitis is suspected.
Contraindications for an immediate LP include

 Evidence of increased intracranial pressure
 Severe cardiopulmonary compromise
 Infection of the skin overlying the site of LP
If an LP is delayed, an immediate imperical therapy should be initiated. The CSF may

appear turbid. The cell count is usually greatly elevated (>1000/mm3) and reveals a
neutrophilic predominance. CSF protein is elevated usually >100mg/dl and glucose is
decreased (<40 mg/dl or two third of the blood glucose.
Gram’s stain reveals an organism in 70% of cases.
Blood culture may reveal the responsible bacteria in 80 -90% of cases.
A latex particle agglutination test is used to detect bacterial antigen in the CSF.
Treatment
Antibiotic therapy
Prompt treatment of bacterial meningitis with an appropriate antibiotic is essential. The
initial selection always should be made before definitive cultures are available.
Ampicillin and chloramphenicol are effective for initial treatment of bacterial meningitis
in infants and children.
Once an organism is isolated and antimicrobial susceptibility is determined,

antimicrobial therapy can be modified.
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Suggested antibiotics and duration of therapy

 H. influenzae type b: chloramphenicol 100 mg/kg/d for 7 - 10 days.
 S. pneumoniae: aqueous penicillin G 300,000 IU/kg/d for 10 - 14 days.
 N. meningitidis: aqueous penicillin G 300,000 IU/kg/d for 5 - 7 days.
If no etiologic agent is identified the initial antibiotic therapy should be continued for 10
to 14 days.
Gram-negative bacillary meningitis (E. coli and P. aeruginosa) should be treated for
three weeks. Initial therapy might include combination of ampicillin and gentamycin or
ceftiaxone.
Corticosteroids
Rapid killing of bacteria in the CSF effectively sterilizes the meningeal infection but
releases toxic cell products after cell lysis that precipitates the cytokine mediated
inflammatory response.
The use of intravenous dexamethasone 0.15 mg/kg/dose every 6 hours for 2 days is
indicated for children greater than 6 weeks of age. Use of corticosteroids is associated
with less fever, lower CSF protein and lactate levels and a reduction on permanent
auditory nerve damage. Most experience with dexamethasone treatment has been with
H. influenzae type b infection.
Corticosteriods appear to have maximum benefit if given just before antibiotics and
should be administered within 1 to 2 hr of antibiotics.
Supportive care
 Supportive care involves: Vital sign monitoring and neurologic assessment should
be made frequently during the 1st 72 hrs.
 Intravenous fluid administration should be restricted to one half to two thirds of
maintenance, until it can be established that increased ICP and SIADH is not
present.
 Shock must be treated aggressively to prevent brain and other organ system
dysfunction.
Increased ICP should be treated with:
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 Endotracheal intubation and hyperventilation (in order to maintain Pco2

approximately 25 mmHg).
 Intravenous furosemide and mannitol osmotherapy may reduce ICP.
 Immediate therapy for seizures includes intravenous diazepam.
Serum glucose, calcium and sodium level should be monitored.
After immediate management of seizure, patients should receive phenytoin (15 - 20
mg/kg loading dose, 5 mg/kg/d maintenance).
Complications
Neurologic complications include seizures, increased ICP, cranial nerve palsies, brain
abscess, hydrocephalus,stroke, herniation and subdural effusion.
Syndrome of inappropriate secretion of antidiuretic hormone may exacerbate cerebral

edema or produce hyponatremic seizures.
Prognosis
With appropriate therapy mortality is 1 to 8%. The highest mortality rates are observed
with pneumococcal meningitis. Severe neurodevelopmental sequelae may occur in 10
to 20 % of patients.
Poor prognostic factors include:

 Age under 6 months
 More than 106 colony forming units of bacteria /ml of CSF
 Seizure occurring more than 4 days into therapy
 Coma or focal neurologic signs on presentation
Sensorineural hearing loss is the most common sequelae of bacterial meningitis. Other
common sequelae include mental retardation, seizures, and delay in the acquisition of
language and visual impairment.
Prevention
N. meningitides
Chemoprophylaxis is recommended for all close contacts with rifampin 10 mg/kg/dose
every 12 hr (maximum dose of 600 mg) for 2 days.
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Meningococcal quadrivalent vaccine against groups A, C, Y and W135 is recommended

for high-risk children older than two years and during epidemics.
Hemophilus influenzae type b

Chemoprophylaxis should be given for all household contacts with rifampin 20 mg/kg/24
hours (maximum dose of 600 mg) given once each day for 4 days.
Vaccination with H. influenzae type b vaccine is recommended
Streptococcus pneumoniae
No chemoprophylaxis or vaccination is required for normal hosts, as secondary cases
rarely occur.
Polyvalent pneumococal vaccine is recommended for cases with asplenia, splenectomy

and nephrotic syndrome.
10.2 Aseptic Meningitis
Aseptic meningitis is an inflammatory process of the meninges. It is a relatively

common occurrence and is caused by a large number of different etiologic factors.
The CSF is characterized by mild mononuclear predominance, normal or slightly

elevated protein and the absence of microorganism on Gram stain and on routine
culture.
CSF glucose is usually normal but may be decreased in certain viral infections like
mumps.
In the majority of instances, the illness is self-limited; however, with some etiologies the
resulting disease may be severe, protracted, recurrent and progressive and lead to
disability and death.
Viruses are the cause of most cases of aseptic meningitis. Enteroviruses account for
approximately 85% of all cases of aseptic meningitis.
Other etiologies include mycobacterium tuberculosis, fungi, protozoa, parasites and

malignancy.
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Hospitalization is usually necessary because of the possibility of treatable bacterial

disease and the frequent need of fluid therapy for dehydration.
Treatment is symptomatic.
EXERCISE
1. What are the leading etiologies of meningitis in children?
2. What findings on CSF are suggestive of bacterial meningitis?
3. How do you treat acute bacterial meningitis in the absence of culture?
10.3 Coma
Solomon Amsalu
Objectives
By the end of this section the reader should be ble to:
 Discuss main causes of coma
 Discuss the approach to a comatose patient
Levels of impaired consciousness

Levels of impaired consciousness include:
Lethargy. A state of decreased responsiveness to stimuli.
Obtundation: A state of much more decreased responsiveness to stimuli.
Stupor: Abnormal response to a given stimuli.
Coma: A state of unconsciousness from which the child can not be aroused by stimuli
The conscious state is maintained by the central reticular formation, which extends from
the medulla oblongata through the pons, midbrain and dorsal hypothalamus to the
reticular nuclei of the thalamus. These interconnected nuclei act as an alerting system
that keeps the cerebral cortex in a state of wakefulness when incoming stimuli are
received.
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Disturbances of arousal and awareness may be the result of structural lesions, diffuse
encephalopathies and status epilepticus (Table 27).
Table 27 Causes of coma

Structural Intracranial mass lesions
Metabolic Anoxic- ischemic coma
Hypoglycemia
Hyperglycemia
Hyponatremia
Hepatic dysfunction
Renal failure
Toxins Lead
Sedative and hypnotic drugs
Trauma Head injuries
Infection Meningitis, encephalitis, severe
generalized infection
Non convulsive status epilepticus
Assessment of impaired consciousness
A modification of the Glasgow coma scale (Table 27) is a useful tool for the grading of
the degree of coma and the severity of the insult in infants and in children.
A coma score of less than five is associated with a grave prognosis, while a score five
to eight may indicate a better prognosis in the child than in the adult.
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Table 28: Glasgow coma scale

Eye opening
Spontaneous 4
To Voice 3
To pain 1
None
Verbal response
Older Children Infants & young children
Oriented 5 Appropriate words; smiles fixes, and follows 5
Confused 4 Consolable crying 4
Inappropriate 3 Persistently irritable 3
Incomprehensible 2 Restless, agitated 2
None 1 None 1
Motor response
Obeys 6
Localizes pain 5
With draws 4
Flexion 3
Extension 2
None 1
Proper evaluation of the comatose patient involves obtaining a history, performing a

rapid directed physical and neurological examination and obtaining certain laboratory
studies, while the patient's airway and vital signs are protected. An attempt is made to
delineate the cause of coma in the hope of finding a treatable process.
ABCs
Before obtaining a history and physical examination make sure that the patients airway,
breathing and circulation (ABCs) are stable.
History
Ask for history of:
 Head trauma
 Ingestion of certain house hold product and drugs in toxic amounts
 Medical illnesses like seizure disorder, diabetes, chronic renal disease, chronic liver
disease, cardiac disease or recent febrile illness.
280
Physical examination
 Do meticulous physical examination
 Observe for signs of trauma and posture of the patient
 Presence of seizures, signs of liver disease and stiff neck.
Localization
1- Motor response to pain
 Decorticate posturing (arm flexion with leg extension). Implies hemisphere or
diencephalon dysfunction. May be caused by destructive lesions or metabolic
derangement.
 Decerebrate posturing (extension of legs and arms) implies dysfunction of
midbrain or upper pons on a structural or metabolic basis.
2- Respiratory pattern
 Cheyne - Stokes respiration (a crescendo-decrescendo breathing pattern with
apneic pauses in between) implies bilateral hemisphere dysfunction or
diencephalic lesion with an intact brain stem.
 Central neurologic hyperventilation (rapid deep breathing) usually indicates
damage between midbrain and pons.
 Apneustic breathing consists of a prolonged inspiration followed by an expiratory
pause and is usually a sign of pontine lesion.
 Ataxic (irregular or agonal) breathing in usually a pre-terminal event signifying
disruption of medullary centers.
 Coma with hyperventilation frequently signifies a metabolic derangement
3- Examination of pupils
 Reactive pupils in a comatose patient without other responses suggest a metabolic
cause.
 Damage to the midbrain usually produces mid dilated pupils that do not react to
light but may fluctuate in size.
 Pontine damage produces pin point pupils that react to bright light when viewed
with a magnifying glass.
 A unilaterally fixed, dilated pupil is seen with damage to the third nerve (table 3).
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Table 29: Rostral caudal progression of coma
Area involved Level of Pupils Muscle tone Respiration

consciousness
1. Diencephalon Agitation Responds to Some purposeful Yawning and
(thalamus/hypo lethargy light briskly Movement in sighing
thalamus Obtundation response to pain; Cheyne
combative Stokes
Movement,
Decorticate
2- Midbrain Stupor  coma Mid-position Decerebrate Neurogenic
fixed hyperventilation.
3- Pons Coma Pin point Decerebrate Apneustic
4- Medulla Coma Mid position Flaccid Ataxic
fixed
Laboratory Studies
Laboratory Investigations should be individualized but must address structural,
infectious, and metabolic causes of coma. Investigations include:
 Blood: Complete blood count, blood film, serum electrolytes, calcium,
phosphorus, glucose, creatinine, ammonium level, liver function studies and a
toxic screen.
 CSF: Must be analyzed if meningitis or encephalitis is suspected.
 Urine: Glucose, ketones and further studies as indicated
 EEG: May be indicated if seizures are suspected etiology of coma
 Skull X-ray
 CT or MRI - If mass lesions are suspected
Treatment
 Establish a clear airway. Begin bag and mask resuscitation if patient is not
breathing spontaneously
 Check carotid pulse, if it is absent, carry out external cardiac massage.
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 Cannulate vein for administration of parenteral fluids, blood and drugs as

indicated.
 Control seizures, Phenytoin is least likely to cloud consciousness.
 Remember that lack of oxygen and glucose for brain metabolism can lead to
permanent damage; Use these whenever it is necessary.
 Identify the specific cause of coma and correct the problem in a safe and
controlled fashion.
Exercise
1. What are the main causes of coma in the pediatric patient?
2. What are the initial steps to be taken in a comatose patient?
3. How are the motor response, respiratory pattern and pupillary examination helpful in
neuro-localization?
10.4 Seizure Disorders
Objectives
By the end of this section the reader should be able to:
 Describe how to approach a child with seizure
 Describe the different types of seizure disorders
 Discuss treatment of seizure disorders
Definitions
A seizure is a sudden involuntary disturbance of brain function manifested by
impairment or loss of consciousness, abnormal motor activity, behavioral abnormalities,
sensory disturbances or autonomic dysfunction.
Epilepsy is recurrent seizure unrelated to fever or an acute cerebral insult.
Prevalence
Seizures are common in pediatric age group (3-5%).
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Epilepsy occurs in 0.5 - 1 % of the population. In 60% of cases epilepsy begins in

childhood.
Classification of seizures
Partial seizures
- simple partial (consciousness retained)
- motor - sensory
- autonomic - psychic
- complex partial ( consciousness impaired)
- simple partial, followed by impaired consciousness
- consciousness impaired at onset
- partial seizure with secondary generalization
Generalized seizures
- absences
- generalized tonic clonic
- tonic
- clonic
- myoclonic
- atonic
- infantile spasms
Unclassified seizures
Approach to a child with seizure

The diagnosis of seizure/epilepsy is difficult because of the wide variety of clincal
features, the intermittency of symptoms and their similarity to other disorders. Therefore
the correct diagnosis involves three steps:
1. Differentiate between seizure and non seizure disorders.
2. Determine the type of seizure.
3. Identify the cause of seizure.
Forst establish whether the child has seizure or not by taking history from the
eyewitness and if possible by EEG. Take the following history:
- Is it the first or recurrent seizure.
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- Aura – automayism ,epigastric pain, etc. The aura of seizure is very short.
- During the seizure
- the type of movement, duration, associated loss of consciousness, associated
symtoms and whether it can be stimulated or stopped with strain
- After the seizure stops
- Postictal headache, confussion, sleep
- Focal neurologic deficit (Todd’s pralysis)
Pseudoseizures (or hysterical seizure) tend to occur in public where the patient can
gain attention, injuries are rare, and the description of the seizures are often bizarre.
Once you have decided this a siezure, determine the type of the seizure based on the
description of the seizure from the history and if possible using EEG. See the
classification above for the type of the seizures.
3.Identify the cause of the seizure using:

- History
Hx of birth injury,
Perinatal Hx–for asphyxia, jaundice, meningitis
Hx of encephalitis, meningitis
Hx of head injury
Hx of drug intake
Hx of metabolic or systemic diseases
Family Hx of seizure or neuroligic diseases
- Physical examination
- congenital malfomation
- focal neurologic deficit (hemiplegia, monoplegia
- Signs of systemic diseases
- Investigations – based on Hx and physical findings, selectand do the following
tests.
- complete blood count
- VDRL
285
- Biochemical tests (blood glucose, serum calcium, electrolytes, etc)

- EEG
- Neuroradiological – skull x-ray,CT
After the above assessment, one decides on the type and cause of the seizure, and
plan treatment.
Partial Seizures
Simple partial seizures (SPS)

- Motor activity is the most common symptom of SPS
- Characterized by asynchronous clonic or tonic movements
- Tends to involve the face, neck and extremities
- Automatism do not occur
- Some patients have aura
- Duration - 10 to 20 seconds
- No postictal phenomenon
Complex partial seizures (CPS)

- An aura is present in approximately one third of the children
- Automatism occur in 50 to 75% of cases
- Automatism consists of confused, repetitive, purposeless behavior during which
the patient has limited awareness of his actions and no memory of the event
following the seizures.
- The average duration of CPS is 1 to 2 minutes.
Generalized Seizures
Absence seizures
Simple (typical) absence (pititmal) seizures Characterized by sudden cessation of motor
activity with a blank facial expression
- More common in females
- Rare before the age of 5 years
- Never associated with aura
- Rarely persist longer than 30 seconds
- Not associated with postictal state
- Frequently associated with automatism
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- Hyperventilation for 3 to 4 minutes routinely produces an absence seizure.

- Electroencephalogram /EEG/shows typical 3/sec. spike and generalized wave
discharge
Complex (atypical) absence seizure

- Has associated motor component
- Frequency of seizures per day is usually less than simple absence
Generalized tonic clonic seizures

- Common
- Patients suddenly lose consciousness, eyes roll back, entire body musculature
undergoes tonic contractions, and they become cyanotic in association with
apnea. The clonic phase of the seizure is heralded by rhythmic clonic contractions
alternating with relaxation of all muscle groups.
- Loss of spincter control is common
- Postictally, it is followed by 30 minute to 2 hour deep sleep
Myoclonic Epilepsy
- Characterized by repetitive seizures consisting of brief, often symmetric muscular
contraction with loss of body tone. It may cause a forward fall resulting in facial
injury.
Febrile seizures
 They are the most common seizure disorder in childhood
 Incidence approaches 3 to 4 % in young children
 They occur between 9 months and 5 years of age
 The peak age of onset 14 to18 months
 They usually develop when the core temperature reaches 390c or more
 Seizure type is generalized tonic clonic of few seconds to 10 minutes duration
Atypical febrile seizure

 Seizure persisting for more than 15 minutes
 Repeated convulsions for several hours or days
 Focal seizure
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Risk factors for development of epilepsy

 Positive family history of epilepsy
 Onset before 9 mo of age
 Atypical febrile seizure
 Delayed developmental milestones
 Abnormal neurologic findings
Risk of epilepsy
 With several risk factors - 9%
 No risk factor - 1%
Treatment
Treatment involves:
- Control fever
- Oral diazepam reduces risk of recurrence and it should be give at the onset of each
febrile illness (usually for 2-3 days).
Investigation
- Complete blood count
- Fasting blood sugar, serum calcium, magnesium and serum electrolytes
(phosphorus, sodium and potassium)
- Skull X ray
- EEG
Treatment of seizure /eplilepsy

First afebrile convulsion with negative family history and Normal examination & EEG:
- 70 % of them will not have another convulsion
- Anticonvulsant is not recommended
If it is recurrent seizure, begin anticonvulsant therapy.

Start with a single drug, increase the dose until seizure control is achieved or
undesirable side effects develop.
A single anticonvulsant is adequate in most children.
288
Table 30: Drug of choices for aseisure
Type of seizure Drug of choice

Partial Carbamazepine
Absence Ethosuximide,
clonazepam
Grandmal Phenytoin, phenobarbital
Myoclonic Clonazepam,sodium
valporate
When to stop anticonvulsant

Two seizure free years for a patient with no risk factors
Risk factors for recurrence

- Age more than 12 years at onset
- Neurologic dysfunction
- History of prior neonatal seizures
- Numerous seizures before control is achieved
Chance of recurrence with no risk factor is approximately

20 to 25%.
Drug withdrawal should be gradual over a period of 3 to 6 months.
Neonatal seizures
Generalized tonic clonic convulsions do not occur in the first month of life because
arborization of axons and dendritic processes as well as myelination is incomplete in
the neonatal brain.
Types
- Focal seizures
Consists of rhythmic twitching of muscle groups particularly extremities and face. It is
often associated with localized structural lesion, infections and subarachnoid
hemorrhage.
- Multifocal clonic seizures

Many muscle groups are involved
289
- Tonic seizures
Characterized by rigid posturing of the extremities and trunk
- Myoclonic seizures
Brief focal or generalized jerks of extremities
- Subtle seizures
Consist of chewing motion, excessive salivation, apnea and pedaling movements.
EEG Classification
Clinical seizures with a consistent EEG event
- Focal clonic
- Focal tonic
- Some myoclonic seizures
Likely to reposed to anticonvulsant
Clinical seizures with inconsistent EEG event

- Generalized tonic seizure
- Subtle seizure
- Some myoclonic seizures
May not respond to anticonvulsant
Electrical seizures with absent clinical seizure

- May be seen in comatose infants.
Etiology
The most common cause is hypoxic ischemic encephalopathy.
Other causes include metabolic, infectious, traumatic, structural and hemorrhagic

disorders.
Investigation
Investigation is geared to the etiology and may involve blood glucose and serum
electrolytes or a lumbar puncture
Treatment
Treat the cause
Administer glucose and oxygen.
290
Administer anticonvulsant
- Phenobarbitone – loading dose of 20mg/kg iv and maintainance 4 to 6 mg/kg.If no
response, repeat 10mg/kg.
- Phenytoin- loading dose of 20mg/kg and maintainance dose of 4 to 6 mg/kg.
- Cacium gluconate – if it is difficult to control with above treatment especially for
infants who are asphyxiated, preterms, amd infants of diabetic mothers
Prognosis
The prognosis depends on the primary cause of the disorder
Status Epilepticus
Status epilepticus is a continuous convulsion lasting longer than 30 minutes, or the
occurrence of serial convulsions between which there is no return of consciousness.
Generalized tonic clonic seizures predominate.
Etiology
There are 3 major subtypes
1. Prolonged febrile seizures is the most common cause
2. Idiopathic status epileptics
No underlying CNS lesion
Cause - sudden withdrawal of anticonvulsants
-non-compliant patients
3. Symptomatic status epilepticus
- Underlying neurologic disorder or a metabolic abnormality
- Higher mortality rate
Treatment
General measures
- Check airway, breathing and circulation
- Give oxygen (facemask)
- Insert naso-gastric tube
- Open iv line and draw blood for CBC, electrolytes, glucose and creatinine
- If there is hypoglycemia give intravenous glucose (5 ml/kg of 10 % dextrose)
291
Anticonvulsants
- Diazepam 0.1 - 0.3 mg/kg iv (2 mg/min) followed by
- phenytoin 15-30 mg/kg iv (1 mg/kg/min)
(Alternate Phenobarbital 15 - 20 mg/kg iv during 10-30 minutes)
If seizures are controlled continue with maintenance dose of phenytoin or

phenobarbital.
If the seizure doesn't stop with in 30 minutes treat with paraldehyde iv infusion or
general anesthesia
Exercise
1. What is the difference between convulsion and epilepsy?
2. How do you clinically distinguish between absence and generalized tonic clonic
seizure?
3. How do you manage a child in status epilepticus?
292
CHAPTER ELEVEN
POISONING
Assfawossen
Objectives
By the end of this course the student is expected to:
 Describe the epidemiology of poisoning in children
 Recite the principles of management
 Discuss the clinical presentation and management of common pediatric
poisonings.
Definition
A poison is any substance that can harm or cause death when taken in to the body or
absorbed.
Epidemiology and general considerations

- Poisoning in children below 5 years of age accounts for 50% of all cases. Almost all
these exposures are unintentional. More than 90% occur at home and most involve
only a single substance.
- Ingestion is the most common route (76%), with dermal, ophthalmic, and inhalation
each occurring in about 6% of cases.
- About 60% involve non drug products, most commonly cosmetics, personal care
products, cleansing substances, plants, foreign bodies and hydrocarbons.
- More than 75% of pediatrics poisoning exposures can be managed without direct
medical intervention, because either the product involved is not inherently very toxic
or the quantity of the material involved is not sufficient to produce significant toxic
effects.
- Poisoning exposures in children 6-12 years of age are much less common (4%).
Toxic exposures in adolescents are primarily intentional (suicide/abuse) or
occupational.
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Approach to the management of the poisoned child

I. History should include: -
Description of toxins
- Product names, ingredients and concentrations
Magnitude of exposure
- Amount ingested and/or length of contact time
Time of exposure
Progression of symptoms
Medical history
- Underlying diseases and/or concurrent drug intake can increase the susceptibility
for toxic effects.
Criteria for hospital admission

 Exposure to caustic/corrosive substances
 Exposure to an amount sufficient to anticipate manifestation
 Exposure to a substance that causes delayed symptomatology or prolonged ones
dose e.g slow release preparations, amanita phalloydes mushrooms, methanol,
ethylene glycol.
 When symptoms are already present
 Suspicion of chemical mal-treatment of children or intentional overdose
NB: A history of significant toxic exposure usually requires observation for at least 6
hours.
Initial medical care

- Initial attention should focus on life support, rapid assessment and resuscitation
(e.g. treatment of shock, seizures and dysrrhythmias)
Physical examination
A brief physical exam including v/s, pupilary size and reaction to light, mental status etc.
should also be done pending complete exam after resuscitation and stabilization of the
patient.
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Definitive care
1. Preventing absorption
Dermal and ocular
- Flush the affected area with tepid water
- Soap and water can be used for dermal exposures
Inhaled toxin
- Move the patient away to fresh air and/or give O2
GIT decontamination
NB: most liquid toxins are almost completely absorbed with in 30 minutes of ingestion
and most solid forms within 1 to 2 hours. GI-decontamination beyond this time is
unlikely to be of value.
I. Emesis
The only emetic routinely used is syrup of ipecac. The onset of vomiting is usually 20 to
30 minutes after dosing with vomiting occurring in 90 to 95% of patients.It removes only
one-third of stomach contents
Contra indications include: -

 Loss of protective air way reflexes of coma/convulsion
 Ingestion of caustics/corrosive
 Ingestion of petroleum distillates and hydrocarbons
 Ingestion of substances likely to produce abrupt depression of consciousness or
early onset of seizure
 Prior significant vomiting/hematemesis
 Children les then 6 months old.
ii. Gastric lavage

Although used for many years, objective data do not document its efficacy particularly in
children. It is time consuming and even under the best of circumstances removes only a
fraction of gastric contents. It Should only be used in older children and only in selected
situations. The contraindications are almost similar to emesis
iii. Activated charcoal (AC)
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Its use has increased dramatically over the past two decades as data demonstrating its
efficacy has accumulated. AC is specially prepared to have a large adsorptive surface
area. Many but not all toxins are adsorbed on its surface some of which include: heavy
metals, iron, cyanide, hydrocarbons, alcohols, caustics and corrosives.
The usual dose is 10 to 30g for a child and 30 to 100 g for adolescent and adults.
iv. Cathartics
Cathartics are commonly used in conjunction with activated charcoal to hasten the
clearance of AC toxin complex although no evidence shows that this is of value.
Commonly used cathartics include: sorbitol, MgSo4, etc
v. Whole bowel irrigation (WBI)

- Whole bowel irrigation involves instilling large volumes of a polyethylene glycol
electrolyte solution in the stomach to cleanse the entire GIT. It should be used with
caution in young children because of the risk of fluid and electrolyte imbalance.
Enhancing elimination
- Enhancing elimination is useful for only few toxins
a) Diuresis and/or iron trapping
 Alkalinization of urine
Increases excretion of weak acids e.g. salicylates, phenobarbitone
 Acidifying urine
Increases excretion of weak bases e.g. amphetamine
b) Dialysis
Hemo-/peritoneal-dialysis for selected agents
II. Laboratory Evaluation

- Includes at least toxicological screening and determination of blood levels
11.1 Organophosphates (OPs)
OPs are insecticides most commonly used at home or in the environment for
eradicating insects. Most pediatric poisonings are accidental e.g. include –
malathion,parathion, fenthion
296
Mechanism of action and pathophysiology

OP insecticides bind to and phosphorylate carboxylic esterase enzymes, including RBC
cholinesterase (acetyl cholinesterase or true cholinesterase) plasma cholinesterase
(pseudocholinestrase) and neurotoxicesterase (CNS).
The phosphorylation is time dependent and relatively irreversible; the process renders
the enzymes incapable of degrading the neurotransmitter. Excessive Acctylcholine
(Ach) accumulates in the neuro-effector junctions in the skeletal muscles system, in the
autonomic and CNS produces first stimulatory and then inhibitory effects on
neurotransmission.
The sign and symptoms of a particular OP poisoning depend on the balance between
stimulation of muscarinic and nicotinic receptors. Mixed clinical syndrome is common.
1. Stimulation of the muscarinic receptors produces a constellation of sign and
symptoms that are best remembered with the mnemonic: DUMBELS
Defecation
Urination
Miosis
Bradycardia, bronchorrhea, bronchospasm
Emesis
Lacrimation
Salivation
2. Stimulation of the nicotinic receptors causes release of epinephrine and nor

epinephrine producing a clinical picture best remembered by the mnemonic:
MATCH
Muscle weakness and fasciculation
Adrenal medulla activity increase
Tachycardia
Cramping of skeletal muscle
Hypertension
297
Typically the patient presents anxious and diaphoretic with tachycardia, miosis,
excessive salivation, copious vomiting and profusely watery diarrhea by systems, the
signs include the following:-
- HEENT: salivation, lacrimation, miosis, blurred vision
- Respiratory system: dyspnea, tachypnea, bronchorrhea, bronchospasm, and
pulmonary edema
- CVS:tachycardia,bradycardia,hypotension, arrhythmias, conduction block
- GIT: nausea, vomiting, diarrhea, abdominal cramps
- Neurologic: anxiety, tremulousness, ataxia, muscle fasciculation,slurred speech,
seizures, choreoathetosis, diminished level of consciousness with confusion and
rarely coma in severe cases.
Diagnosis
Diagnosis can be made using four criteria:
i) Appropriate history of exposure to an insecticide
ii) Sign and symptom of excessive muscarinic and nicotinic stimulation
iii) Depressed plasma and RBC cholinesterase
iv) Response to atropine and pralidoxime therapy
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Management
1. General measures
General supportive care should be provided including fluid and electrolyte replacement
and intubation and artificial ventilation when necessary.
2. GI – decontamination
- Activated charcoal
- Gastric lavage
3. Dermal decontamination
Removal of clothes, washing with soap and water
4. Antidote administration
a. Atropine is a competitive antagonist of Ach. Give 0.01 mg/kg IV every 15’ until
signs of atropinization occur(mydriasis,decreased secretion,tachycardia)
b. Pralidoxime chloride (2 PAM) chemically breaks the bond between the
organophosphate and the enzyme. Iteverses both muscarinic and nicotinic effects
of OP-poisoning. It hould be administered in all cases of known/suspected OP-
poisonings. 25 – 50 mg/kg IV should be given over 30-60 minutes time. it can be
repeated in 1hr and then every 8-12 hrs until improvement is noted
11.2 Carbamate insecticides
Carbamate insecticides produce similar but mild form of toxicity to that of OP-
poisonings.
Two important differences distinguish carbamates from OP-poisonings:
i) Carbamate toxicity is typically short lived. Spontaneous hydrolysis of the
carbamylated acetyl cholinesterase complex regenerates enzymatic activity, usually
within 24 hrs.
ii) Little or no CNS toxicity occurs because of inability of carbamates insecticides to
cross the blood brain barrier.
299
Treatment
Some as OP-poisonings except that pralidoxime is not recommended in carbamates
poisonings.
11.3 Hydrocarbons
Hydrocarbons include a wide array of chemical substances containing hydrogen and

carbon atoms only and found in thousands of commercial products. Lighter fluid, paint
thinners and removers, some furniture polishes, cleaning agents, solvents, various
automotive products and ordinary fuels are common examples.
Pathophysiology
Hydrocarbons can be absorbed after ingestion, inhalation or dermal contact. Most
cases involve accidental imbibing by young children. Abuse by inhalation also occurs in
adolescents.
The most important toxic effects of hydrocarbons is aspiration pneumonitis. Aspiration

occurs at the time of ingestion when changing and gassing occurs but can also be
secondary to vomiting that commonly occurs after ingestion.
Small amounts (less than 1ml) of compounds with low viscosity such as mineral spirits,
naphtha, kerosene, gasoline and lamp oil spread rapidly across surfaces and cover
large areas of the longs when aspirated and cause significant injury.
Pneumonitis doesn’t result from dermal absorption of ingestion without aspiration. Other
less common toxic effects of hydrocarbons include hepatotoxicity, renal toxicity,
dysrhythmias and sudden death. Chronic abuse of volatile hydrocarbons can also lead
to cerebral atrophy, neuropsychological changes and peripheral neuropathy.
Clinical and laboratory manifestation

Manifestations include
- Transient, mild CNS depression
- Coughing, mild to severe respiratory distress
- Fever and leukocytosis. The fever can stay for as long as 10 days
- Abnormality on CXR
300
Treatment
 Treatment is supportive and involves oxygen, intubations and mechanical ventilation
when indicated. Antibiotics are not indicated routinely
11.4 Acetaminophen
Acetaminophen is the most widely used analgesic and antipyretic commonly available
at home. Acetaminophen toxicity results from the formation of a highly reactive
intermediate metabolite, N-acetyl p-benzoquinonemine (NAPQI) which in large amount
causes hepatocellular necrosis and damage. The acute toxic dose in children less than
12 years of age is about 200mg/kg clinical and laboratory manifestation.
If untreated, patients who have acutely overdosed pass through four stages of toxicities.
301
Table 31: Stages of N-acetyl p-benzoquinonemine toxicity
Time after
Stage ingestion Characteristics
I. ½ - 24 hr Anorexia, nausea, vomiting,
malaise, pallor, diaphoresis.
II. 24 - 48 hr Resolution of above; RUQ
abdominal pain and
tenderness; elevated
bilirubin, PT, hepatic
enzymes; oliguria.
III. 72 - 96 hr Peak liver function
abnormalities; anorexia,
nausea, vomiting, malaise
may reappear.
IV. 4 day – 2 wk Resolution of hepatic
dysfunction or complete
liver failure.
- Plasma level should be measured after 4 hours of ingestion and level plotted on
monogram to determine whether antidote treatment is indicated.
- LFT including enzymes, bilirubin and PT should be followed daily
RUQ - right upper quadrant

PT - prothrombin time
Treatment
Treat with:
- Antidote – N – acetylcysteine (NAC)
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11.5 Salicylates
The incidence of salicylate poisoning has declined, particularly in young children, as the
use of alternative antipyretics has increased.
Pathophysiology
Salicylates directly or indirectly affect most organ systems by:
1. Uncoupling oxidative phosphorylation
2. Inhibiting Krebs cycle enzymes
3. Inhibiting amino acid synthesis
4. Decreasing platelet adhesiveness
5. Increasing pulmonary capillary permeability
Stimulation of respiratory center  Hyperventilation  Respiratory alkalosis

compensatory alkaluria  urinary excretion of both K-& Na- Hco3
 Serum K  exchange of H- for k+ in the renal tubules  “paradoxical aciduria”
Clinical and laboratory manifestations

Chronic toxicity lrads to signs and symptoms that mimic flu or other febrile illness.
Acute toxicity is manifested by::

- Nausea and vomiting 20 to gastric irritation
- Dehydration and metabolic acidosis eventually develop
- CNS changes such as agitation, restlessness and confusion are important signs of
serious toxicity
- Coma may develop 20 to cerebral edema
- Pulmonary edema or hemorrhage may develop in more severe cases
- Hyperglycemia or hypoglycemia, particularly in infants
- Hepatotoxcity occurs both from chronic exposure and acute over dosage/toxicity.
Laboratory investigations
- Serial serum salicylate levels and urine PH and volume should be monitored
- Other plasma PH, glucose, K+, other electrolytes, clotting studies and liver
function test
303
Treatment
- Rehydration and correction of electrolyte abnormalities
- Alkalinization of urine using iv Hco3
- Hemodialysis in severe cases
304
11.6 Co-Poisoning (co)

Co:- is a tasteless and colorless gas produced by incomplete combustion of carbon
compounds. It binds to Hb, displacing 02, with an affinity for Hb about 250 x that of 02. It
impairs the ability of Hb to release 02 to tissues. Itbinds to cytochrome oxidase in
tissues, impeding 02 utilization
Clinical presentation
The clinical presentation of co-poisoning is only approximately correlated to the
measured carboxy-Hb level. Early symptoms are usually misdiagnosed as flu-like
illnesses. Signs and symptoms include:
 Levels of 10-20%: headache, dyspnea on exertion and weakness predominate
 Levels of 20 -30%: severe headache and nausea may appear
 Levels of 30-40%: severe headache, nausea, vomiting and impaired judgment
 Levels of 50-60%: confusion, syncope, seizures and coma predominate
 Levels of more than 60-70%: coma, seizure, cardio respiratory depression, death
Laboratory analysis
- Determination of carboxy-Hb. level in blood and expired air
- chest x-ray (30% of patients have an abnormal finding);
- EKG
Treatment
- General supportive care
- 100% 02 by mask
- Hyper baric 02 therapy
Prognosis
- 10% develop long term neuropsychiatric complications
Exercise
1. Discuss the management principles of poisoning.
2. Mention the clinical manifestation of a child with CO poisoning
3. Describe the management principles of a child with op-poisoning
305
References
3. Peter Vicelli, Hand book of medical toxicology, 1993
306
ANNEX
Annex 1
Treatment plan A: Treat diarrhea at home
Counsel the mother on the 3 rules of home treatment:
Give extra fluid, continue feeding, when to return
1. GIVE EXTRA FLUID (as much as the child will take)
Tell the mother to breastfeed frequently and for longer at each feed.
 If the child is exclusively breastfed, give ORS or clean water in addition to
breast milk.
 If the child is not exclusively breastfed, give one or more of the following:
ORS solution, food-based fluids (such as soup, rice water, and yoghurt
drinks), or clean water.
It is especially important to give ORS at home when:
- The child has been treated with plan B or plan C during this visit.
– The child cannot return to a clinic if the diarrhea gets worse.
TEACH THE MOTHER HOW TO MIX AND GIVE ORS. GIVE THE MOTHER
TWO PACKETS OF ORS TO USE AT HOME.
SHOW THE MOTHER HOW MUCH FLUID TO GIVE IN ADDITION TO THE
USUAL FLUID INTAKE.
Up to 2 years50 to 100 ml after each loose stool
2 years or more 100 to 200 ml after each loose stool
Tell the mother to:
 Give frequent small sips from cup.
 If the child vomits, wait 10 minutes. Then continue, but more slowly.
 Continue giving extra fluid until the diarrhea stops.
} SEE MOTHER’S CARD
307
2. Treatment plan B: Treat some dehydration with ORS

Give in clinic recommended amount of ORS over 4-hour period
DETERMINE AMOUNT OF ORS TO GIVE DURING FIRST 4 HOURS.
Age* Up to 4 4 months 12month 2 years

months up to 12 up to 2 up to 5
months years years
Weight < 6 kg 6 -< 10 kg 10 -<12kg 12 - 19kg
Amount in ml 200-400 400-700 700-900 900-1400
*Use the child’s age only when you do not know the weight. The approximate
amount of ORS required (in ml) can also be calculated by multiplying the child’s
weight (in kg) by 75.
 If the child wants more ORS than shown, give more.
 For infants under 6 months who are not breastfed, also give 100-200 ml clean
water during this period.
SHOW THE MOTHER HOW TO GIVE ORS SOLUTION.
 Give frequent small sips from a cup.
 If the child vomits, wait 10 minutes. Then continue, but more slowly.
 Continue breastfeeding whenever the child wants.
AFTER 4 HOURS:
 Reassess the child and classify the child for dehydration.
 Select the appropriate plan to continue treatment.
 Begin feeding the child in clinic.
IF THE MOTHER MUST LEAVE BEFORE COMPLETING TREATMENT:
 Show her how to prepare ORS solution at home.
 Show her how much ORS to give to finish 4-hour treatment at home.
 Give her enough ORS packets to complete rehydration. Also give her 2 packets
as recommended in plan A.
308
Treatment plan C: treat severe dehydration quickly

FOLLOW THE ARROWS. IF THE ANSWER IS “YES”, GO ACROSS. IF “NO”,
GO DOWN.
 Start IV fluid immediately. If the child can drink, give ORS by mouth while the drip is
set up. Give 100 ml ringer’s lactate solution (or, if not available normal saline),
divided as follows.
Age First give 30 Then give 70

Can you give ml/kg in: ml/kg in:
intravenous (IV) Yes Infants (under 12 1 hour* 5 hours
fluid immediately?
months)
Children (12 30 minutes* 21/2 hours
No months up to 5
years)
*
Repeat once if radial pulse is still very weak or not detectable.
 Reassess the child every 1-2 hours. If hydration status is not improving, give
the IV drip more rapidly.
 Also give ORS (about 5 ml/kg/hour) as soon as the child can drink: usually
after 3-4 hours (infants) or 1-2 hour (children).
 Reassess an infant after 6 hours and a child after 3 hours. Classify
dehydration. Then choose the appropriate plan (A, B or C) to continue
treatment.
Is IV treatment
Yes
available  Refer urgently to hospital for IV treatment.
nearby? (with in
30 minutes)?
 If the child can drink, provide the mother with ORS solution and show her
No
how to give frequent sips during the trip.
Are you trained to

 Start rehydration by tube (or mouth) with ORS solution: give 20 ml/kg/hour
use a nasogastric
(NG) tube for for 6 hours (total 120 ml/kg).
rehdration?
 Reassess the child every 1-2 hours:
No
Yes
- If there is repeated vomiting or increasing abdominal distension, give the
Can the child drink?
No fluids more slowly.
Refer URGENTLY - If hydration is not improving after 3 hours, send the child for IV therapy.
to hospital for IV or
NG treatment  After 6 hours, reassess the child. Classify dehydration. Then choose the
appropriate plan (A, B or C) to continue treatment.
309
NOTE: If possible, observe the child for atleast 6 hours after rehydration to be
sure the mother can maintain hydration giving the child ORS solution by mouth.
Drug Supplied Dose Comments

Section 1
Anesthetics
Atropine Vial: 0.1 mg/ Preoprative: 0.01 mg/kg i.v., Well absorbed. May be given
mL, i.m., p.o. Maximum dose 0.4 any route including via
0.4 mg/mL, mg. endotracheal tube. Overdose-
0.6 mg/mL CPR bradycardia: 0.05 agitation, urinary retention,
mg/kg every 2-5 minutes. photophobia, tachycardia.
Diazepam Tablet: 2 mg, Sedation: 0.1-0.3 mg/kg i.v. Irritating to veins. Do not mix
5 mg, 10 mg 0.5-0.8 mg/kg p.o. with other intravenous drugs.
Ampoule: 10 Status epilepticus: 0.3 mg/kg Respiratory depression in high
mg/2 mL i.v. doses. In status epilepticsu,
Liquid: 1 0.5 mg/kg p.r. follow with a long-acting drug
mg/mL such as phenobarbiotone.
Lidocaine Vial: Arrhythmias: 1 mg/kg load, In high dose, associated with
1% (10 20-50 μg/kg per minute seizures, hypotension, heart
mg/mL), infusion. Therapeutic range block. Beware exceeding
4.5-21 μmol/L. maximum dose when infiltrating
Local infiltration: Maximum a large area.
doses: 7 mg/kg (with
adrenaline), 4.5 mg/kg
(without adrenaline).
Oxygen 1-5 L/min by nasal prongs or Neonats: prologed high doses
mask. associated with retineal
changes. Keep O2 saturateion
<95% in permature infants.
Chance of suppression of
hypoxic drive very rare in
children.
310
Section 2
Antirheumatic
and analgesic
drugs
Acetysalicylic acid Chewable: 80 Antipyretic: 10-15 mg/kg per Bleeding risk, particularly with
mg Tablet: dose P.O. every 4-6 hours. platelet and coagulation
325 mg, 650 Maximum dose 60-80 mg/kg disorders. Severe poisoning in
mg per 24 hour. Antirheumatic: overdose. Monitor levels when
suppository: 60-100 mg/kg per 24 hour : 6 using high dose. Therapeutic
150 mg, 650 hourly. range 1.5-2.0 mmol/L.
mg
Ibuprofen Tablet: 200 Antipyretic: 20 mg/kg per 24 Gastritis, platelet dysfuncion,
mg, 300 mg, hour - 8 hourly p.o. decreased renal funciton in
400 mg, 600 Antirheumatic: small children.
mg 20-35 mg/kg per 24 hour - 8
hourly p.o.
Morphine Tablet: 100 10-20 mg/kg per dose p.o. or Severe liver toxicity in
Paracetamol mg, 500 mg p.r. every 4-6 hours. overdose, particularly if mixed
Suppository: Maximum 90 mg/kg per 24 h. with alcohol. Do not exceed
100 mg maximum daily dose.
Syrup: 125
mg/mL
Section 3
Antiallergics
Chlorpheniramine Tablet: 4 mg 0.35 mg/kg per 24 hour - 4 Sedating, hypotension if i.v.
Liquid: 0.5 doese, p.o., i.v. or i.m. given quickly, Movement
mg/mL disorder with cumulative, high
Ampoule: 10 doses. Many alternative drugs.
mg/ml
Adrenalin Tablet; 10 Physiological replacement: 4 mg hydrocortisone is
Hydrocortisone mg, 20 mg 14-20 mg/m2 per 24 hour - 3 equivalent to 1 mg prednisone.
311
Ampoule: 100 doese p.o. Topical: Hypertension,

mg, 250 mg, Apply 2-3 times daily immunosuppression, electrolyte
500 mg sparingly. abnormalities in prolonged use.
Cream; 0.55, Anti-inflammatory: 0.8-4.0 significant absorption may
1.0% mg/kg per 24 hour - 4 doses occur with topical use on a raw
Ophthalmic: i.v. or p.o. skin.
2.5%
Suppository:
10 mg, 25 mg
Prednisone Tablet: 1 mg, Physiologic replacement: Prednisolone better for hepatic
5 mg, 50 mg 4-5 mg/m2 per 24 hour - 2 disease since not metabolized
Liquid: 2 doses p.o. in liver. usual steroid side
mg/mL, 5 Anti-inflammatory: 0.5-2.0 effects in chronic use.
mg/mL mg/kg per 24 hour - 2 doses
p.o.
Wean to alternate day doses
if possible for long-term
treatmetn.
Section 4 poison
antidoes
Activated Powder 1-2 g/kg in water or sorbitol Do not give with emetic or will
charcoal given p.o. absorb the drug. If giveing by
nasogastric tube in comatose
child, ensure nasogastric tube
is definitely in the stomach and
not lung.
Naloxone Ampoule: 0.4 0.05-0.1 mg/kg per dose. Half life only 1-2 hours. Repeat
mg/mL, 1.0 Maximum 2 mg/dose. Repeast doses will be required before
mg/mL 3-5 minutes until effect original narcotic overdose has
achieved. If no response after
worn off.
3 doses, sedation probably not
312
due to narcotic overdose.

Section 5
Anticonvulsants
Clonazepam Tablet: 0.5 Initially, 0.01-0.05 mg/kg per Increase gradually. Do not
mg, 2 mg 24 hour - 3 doses p.o. stop suddenly, Drowsiness
Increase at weekly intervals common, also slurred speech,
to maximum 3 mg/kg per 24 ataxia and salivation.
hour.
Diazepam Capsul: 250 20-30 mg/kg per 24 hour - 1- Nausea, gastritis. Rare bone
Ethosuximide mg 2 doses p.o. Increase dose marrow depression and
Liquid: 50 slowly at 4-7 day intervals. hepatitis. Therapeutic rang
mg/mL Maximum dose 1500 mg/24 280-700 μmol/L.
h.
Phenobarbital Tablet: 15 Status epilepticus: After Respiratory depression,
mg, 30 mg, control with diazepam, load hypotension.
60 mg, 100 with 18 mg/kg by slow i.v. Therapeutic range 65-170
mg infusion. Maximum dose, if μmol/L.
Liquid: 5 seizures continue, 30 mg/kg.
mg/mL Chronic dose: 5 mg/kg per
Ampoule: 30 day - 2 doses p.o. but needs
mg/mL, adjusting with age.
120 mg/mL
Phenytoin Tablet: 50 mg Status epilepticus: After Therapeutic range 40-80
; capsule: conrol, load with 18 mg/kg by μmol/L.
100 mg; slow i.v. infusion. Risk of hypotension is
Suspension: Maintenance: 5-10 mg/kg appreciable if given by fast
6 mg/m, 25 per 24 hour - 2 doses p.o. infusion. Chronic effects
mg/mL Absorption very variable in include hirsutism, gum
Ampoule: 50 children. hyperplasia, rash, ataxia.
mg/mL Suspension very variably
absorbed.
313
Valproic acid Capsule: 125 intially, 10 mg/ kg per 24 Therapeutic range 350-700
mg, 250 mg, hour - 3 doses p.o. μmol/L.,
500 mg Increase 5-10 mg/kg weekly Valproic acid may affect levels
Liquid: 50 to maximum range 30-60 of other anticonvulsants if
mg/mL mg/kg per 24 hour. added.
Gastritis, tremor, rare hepatitis.
Section 6.1.1.
Intestinal
anthelminthics
Albendazole Tablet: 400 Hydatidosis or cysticercossi: Occasionally diarrhea,
mg, 200 mg 15 mg/kg per day - 2 doses abdominal pain, migration of
p.o. for 28 days. Maximum Ascaris through mouth.
400 mg b.i.d.
Hookworm or ascariasis: 400
mg once p.o.
Levamisole Tablet: 150 Hookworm or Ascaris: 2.5 Low toxicity, low cost.
mg, 50 mg mg/kg once p.o.
Mebendazole Tablet: 100 Hookworm, Ascaris, Occasional diarrhea and
mg Trichuris: abdominal pain.
Suspension : 100 mg b.i.d x 3 days p.o. for
20 mg/mL all ages over 2 years.
Niclosamide Tablet: 500 Tapeworms: <2 yer: 500 mg Minor side effects. Drug not
mg oce p.o. absorbed.
2-6 yr: 1 g
> 6 yr: 2 g
Praziquantel Tablet: S.mansoni: 40 mg/kg per Frequently headache,
150 mg, 600 day - 2 doses. dizziness.
mg s.japonicum: 60 mg/kg per Occasionally abdominal pain,
day - 3 doses. fever, sweating, rash, Severe
Cysticercosis: 50 mg/kg per headache associated with
314
day - 3 doses for 2-4 weeks. treatmetn of

Tapeworms: 20 mg/kg p.o. neurocysticercosis.
once.
Flukes: 75 mg/kg per day - 3
doses p.o. for 1 day.
Pyrantel pamoate Tablet: 250 Hookworm or ascariasis: Occasional abdominal pain,
mg 11 mg/kg once p.o. headache, rash, fever.
Suspension: maximum 1 g.
50 mg/mL
Section 6.1.2
Antifilarials
Diethylcarbamazi Tablet: 100 Filariasis, pulmonary Drug effects include headache,
ne mg, 50 mg eosinophilia: nausea, vomiting, fever, rare
6 mg/kg per day - 3 doses encephalopathy. Rapid killing
for 21 days. of large filarial loads associated
Start with 0.5 mg/kg on day 1 with fever and allergiv reactions
and increase to full dose that may be severe.
over 4-5 days as tolerated.
Invermectin Tablet: 6 mg, O.Volvulus: Occasional Mazzotti reactions
3 mg 150 μg/kg p.o. once. Repeat due to reaction to death of
every 6-12 months. microfilariae with fever, facial
swelling, joint pain.
Section 6.2
Antibacterials
Amoxicillin Capsule: 500 40 mg/kg per 24 hour - 3 Absorbed as ampicillin.
mg, 250 mg doses p.o. Achieves better serum levels
Tablet: 250 than oral ampicillin, Side
mg, 125 mg effects as for ampicillin.
Suspension:
50 mg/ mL
Ampicillin Powder: 125 Severe infections: Amoxicillin preferred for oral
315
mg, 250 mg, 200-400 mg/kg per 24 hour - therapy

500 mg, 1 g, 4 doses i.v. Except when treating diarrhea
2g Maximum 2 g. Repeated 6 caused by shigella or
Capsule: 500 hourly. Salmonella. Rashes common,
mg, 250 mg particularly with EBV infection.
Suspension:
50 mg/mL
Amoxicillin and Tablet: 500 40 mg/kg per 24 hour - 3 Calvulinic acid extends
clavulinic acid mg, 250 mg doses p.o. coverage to include beta-
suspension: lactamase producing H.
125 mg/mL. influenzae and E. Coli. Main
250 mg/mL side effect is gastrointestinal
upset and diarrhea.
Benzyle penicillin Powder: Sever infections: For injection only. Well
1mIU, 5 mIU, 200000 u/kg per 24 hour - 3 tolerated. Rare sensitivity
10 mIU doses i.v. reactions and serum sickness.
Cefotaxime Powder: 500 100-200 mg/kg per 24 hour - Rare sensitivity reactions and
mg, 1 g, 2g 3 doses i.v. serum sickness.
Chloramphenicol Capsule: 250 50 - 75 mg/kg per 24 hour - 4 Oral route well absorbed. Dose
mg doses i.v. or p.o. related and idiosyncratic bone
Suspension: marrow depression.
50 mg/mL
Powder: 1 g
Eye drops:
1%
Cloxacillin Capsule:500 100-200 mg/kg per 24 hour-4 Oral form bitter. Long-term,
mg.250 mg doses i.v. high dose therapy associated
Suspension: with urinary cast formatiion.
25 mg/mL
Powder: 500
mg, 1 g, 2 g
316
Doxycycline Tablet: 250 Oral: 30-40 mg/kg 24 hour - Well absorbed by oral route.
Erythromycia mg 3 doses p.o. Intravenous form is very
Capsule: 250 Intravenous: 20-50 mg/kg irritating
mg per 24 hour - 4 doses i.v. and needs diluting and slow
Suspension: infusion.
50 mg/mL Gastrointestinal upset with oral
Powder: 500 form.
mg, 1g Do not give i.m.
Eye ointment:
0.5%
Gentamicin Vial: 20 mg, 7.5 mg/kg per 24 hour - 3 Ototoxic and nephrotoxic in
80 mg doses i.v. or i.m. high doses.
Eye ointment:
0.3%
Metronidazole Tablet: 250 C. difficile: 20 mg/kg per 24 Frequently nausea, headache
mg hour 4 doses i.v. or p.o. and metallic taste. Occasional
Suspension: Amebiasis: 35-50 mg/kg per "antabuse" effect with alcohol.
50 mg/mL 24 hour - 3 doses p.o. x 10
Vial: 500 mg days.
in 100 ML Giardiasis: 15 mg/kg per 24
hour - 3 doses for 5 days.
Intravenous: 30 mg/kg per
24 hour 3-4 doses
Sulfamethoxazole Tablet: 400 PCP. Toxoplasmosis: 80 Only use i.v. form if p.o. not
/trimethopirim mg/80 mg, mg/16 mg SMX/TMP per tolerated
200 mg/40 kg/24 hour - 3 or 4 doses
mg p.o. or i.v. 2-3 weeks>
Suspension: Prophylaxix: 40 mg/8mg
40 mg/8 mg SMX/TMP per kg - 2 doses
per mL p.o. 3 d/wk.
317
Vial: 80
mg/16 mg per
mL
Rifampin Capsule: 300 Leprosy: >35 kg: 600 mg Discolors body fluids. May
mg, 150 mg supervised monthly cause liver impairment in long-
20-35 kg: 450 mg supervised term use. Reduce dose if liver
monthly disease. See "leprosy."
12-20Kg: 300 mg supervised
monthly
< 12 kg: 150 mg supervised
monthly
Tuberculosis: 10 mg/kg daily
unsupervised
15 mg/kg: 3 d/wk supervised
Meningitis prophylaxis: 10
mg/kg per 24 hour - 2 doses
p.o. for 4 days. Maximum
600 mg/d.
Section 6.2.4
Antituberculosis
Ethambutol Tablet: 100 Tuberculosis: Optic neuritis, red/green color
mg, 400 mg 15 mg/kg daily unsupervised blindness, peripheral neuritis.
p.o. Reserved for use in children old
30 mg/kg 3 d/wk supervised. enough for eye testing. See
"Tuberculosis."
Isoniazid Tablet: 300 Tuberculosis: Hepatitis rare in children.
mg, 100 mg 5-10 mg/kg 9maximum 300 Peripheral neuropathy,
mg) P.O. daily unsupervised. prevented with pyriodoxine
15 mg/kg p.o. 3 d/wk daily, also rare in children.
supervised 9maximum 600 Occasional hypersensitivity
mg). reactions.
318
See"Tuberculosis."
Pyrazinamide Tablet: 500 Tuberculosis: 35 mg/kg p.o. Hepatitis, Jaundice,
mg daily unsupervised. hyperuricemia, diabetes.
50 mg/kg p.o.
3 d/wk supervised.
Rifampin See section 6.2.3. See
"tuberculosis."
Streptomycin Powder: 500 Tuberculosis: Ototoxic and nephrotoxic. See
mg, 1 g 15-20 mg/kg per 24 hour - 2 "Tuberculosis." Also drug of
doses i.m. Maximum 1 g/d. choice for brucellosis in
conjunciton with doxycycline.
Griseofulvin Tablet: 250 15 mg/kg per 24 hour once No effect given topically. Well
mg, 125 mg p.o. Treatment course 4-6 tolerated. Take with food-
Suspension: weeks. absorption improved.
25 mg/mL
Ketoconazole Tablet: 200 5-10 mg/kg per 24 hour p.o. - Risk of hepatitis in courses
mg 2 doses. longer thtn 14 days. Interferes
Suspension: with hepatic metabolism of
20 mg/mL several other drugs.
Nystatin Suspension: Apply cream liberally to Not absorbed when given p.o.
100 000 u/mL affected area.
Cream: 100 Suspension:
000 u/g 200 000 u/dose p.o. 4 times
daily.
Sodium Bottle: 20 mg/kg Sb base i.m. or i.v. Numerous side effects. If
Stibogluconate contains for 3-4 weeks giving i.v., use slow infusion or
equivalent of risk of thrombosis. ECG
100 mg changes and conduction
Sb/mL
319
Chloroquine Tablet: 100 Treatment: Doses calculated as

mg, 150 mg 10 mg/kg base one then 5 chloroquine base.
(Chloroquine mg/kg base at 6, 24 and 48 Not for prophylaxis if epilepsy.
base) hours. P. falciparum resistance
Syrup: 10 Prophylaxis: widespread.
mg/mL 5 mg/kg base (maximum 300 Corneal opacities and retinal
(chloroquine mg base) once weekly. damage in chronic high dose,
base) dermatoses, see "Malaria." do
not givewith halofantrine.
Mefloquine Tablet: 250 Malaria prophylaxis Do not give with, or after,
mg treatment: halofantrine; risk of severe
25 mg/kg (maximum 1.5 g) - arrhythmias. GI effects and a
1 or 2 doses. range of neuropsychiatric
15-19 kg: 1/4 tab weekly problems from insomnia to rare
20-30 kg: 1/2 tab weekly convulsions and psychosis.
31-45 kg: 3/4 tab weekly Not for use in patients with
>45 kg: 1 tab weekly epilepsy.
Primaquine Tablet: 15 0.3 mg/kg base per day for Hemolysis in patients with G-
mg. 7.5 mg 14 days. 6PD. Calculated as active
base. Only for eradiation of
P.vivax and P.ovale.
Occasional
methemoglobinemia.
Quinine salts Table: 300 Oral: Not for prophylaxis, only
mg, 200 mg 25 mg/kg per 24 hour - 3 treatment. Side effects
(sulfate) doses p.o. for up to 7 days in common at usual dose
Ampoule: 300 partially resistant areas. If cinchonism (tinnitus, headache,
mg/mL quinine resistance nausea, visual disturbance).
(dihydrochlori suspected, follow by: Monitor glucose: hypoglycemia
de) doxycycline, clindamycin or common.
320
fransidar. Arrhythmias, especially if given

Dihydrochloride: by fast i.v. push. See 'Malaria
20 mg/kg loading dose in 5% "Do not give with halofantrine.
dextrose over 4 hours, then
10 mg/kg over 2-4 hours.
Reapeat 8 hourly until oral
therapy can be started.
Section 10
Antianemia
Folic Acid Tablet: 1 mg, Deficiency: 0.5 - 1.0 mg/kg per Will not prevent neurologic
5 mg 24 hour p.o. abnormalities due to vitamin
Vial: 5 mg/mL Maintenance: B12 deficiency.
<1 yr: 30-45 μg/24 h
1-3 yr: 100 μg/24 h
4-6 yr: 200 μg/24 h
2-10 yr: 300 μg/24 h
> 10 yr: 400 μg/24 h
Iron Gluconate, Deficiency: 3-6 mg(Fe)/kg Calculated dose depends on
Tablet: 300 per 24 hour - 2 or 3 doses iron base. Liquid may stain
mg (35 mg p.o. teeth. Absorption decreased
Fe) Prophylaxis: 1-2 mg (Fe)/kg by tetracycline and antacides.
Syrup: 60 per 24 hour - 1-2 doses Give with meals to decrease
mg/mL (7 mg p.o. (maximum 15 mg/24 h gastrointestinal upset. Very
Fe), Sulfate fe). toxic in overdose.
Tablet: 300
mg (60 mg
Fe)
Syrup: 30
mg/mL (6 mg
Fe)
Drops: 125
321
mg/mL (25
mg Fe)
Vitamin K1 Ampoule: 1 Neonatal prophylaxis: 0.5- Intravenous dose rarely
mg/0.5 mL, 1.0 mg.i.m., S.C. or i.v. associated with allergic
10 mg/mL Sever liver disease: 5 mg/24 reactions. The risk is less with
h i.v. or i.m. vitamin K1 compared to other
Deficiency: 1-2 mg/dose i.v. vitamin K preparations.
2-5 mg/dose p.o.
Section 11
Plasma and
substitutes
Dextran 70 500 mL bags Resuscitate with a maximum Several starch and gel based
of 6% o 20 mL/kg. plasma substitutes exist.
solution Dextran 70 is as effective as
fresh plasma for resuscitation
of severe shock in burns and
sepsis. rare allergic reactions.
Section 12
Cardiovascular
Captopril Tablet: 6.25 Children: Start 0.6 mg/kg per Start with small test dose and
mg, 12 mg, 24 hour - 3 doses p.o. observe for hypotension.
25 mg, 50 Increase to effect. Maximum
mg, 100 mg 150 mg/d.
Digoxin Tablet: 62.5 Digitalizing dose: Well absorbed orally.
μg, 125 μg, Give as 1/2, 1/4, 1/4 Intravenous dose is 75% of p.o.
250 μg separated by 8 hours. dose. Do not give i.m. Reduce
Syrup: 50 μg/ < 2 yr: 40 μg/kg load - 3 dose in renal failure.
mL doses p.o. Toxicity is enhanced by
Ampoule: 50 > 2 yr: 30 μg/kg load - 3 hypokalemia.
μg/mL, doses p.o. High doses - visual
250 μg/mL Maintenance dose: disturbances, arrhythmias.
322
Start 12 hours after loading

dose completed.
<2 yr: 10-15 μg/kg per 24
hour - 2 doses p.o.
>2 yr: 5-10 μg/kg per 24 hour
- 2 doses p.o.
Adrenalin Ampoule: Anaphylaxis: Use 1/1000 Preferably give infusion via

1/1000 (1 strength given s.c. 0.01 central line. Absorbed
mg/mL) mL/kg per dose (maximum intraosseously or via
1/10000 (0.1 0.3 mL). repeat every 10 endotracheal bolus.
mg/mL) minutes. Hypertension, arrhythmias,
CPR: Use 1/10000 strength. nervousness, headache.
give i.v. 0.1 mL/kg per dose.
Repeat every 3-5 minutes.
Inotrope: Mix 0.3 mg
adrenalin/kg in 50 mL D5W.
1mL/h = 0.1 μg/kg per
minute. Dose range 0.1-0.5
μg/kg per minute.
Hydralazine Tablet: 10 Acute hypertension: 0.1-0.5 Oral dose may take 3-4 days
mg, 25 mg, mg/kg per dose i.m. or i.v. 4- for full effect. Intravenous dose
50 mg 6 hourly. should be given slowly. High
Powder: 20 Chronic: 0.75-3.5 mg/kg per dose associated with lupus-like
mg/mL 24 h-3-4 doses. Start low syndrome.
and increase as needed.
Methyldopa Tablet: 125 Acute hypertension: 5-10 Positive Coombs test common.
mg, 250 mg mg/kg per dose 4-6 hourly. fever, liver dysfunciton and
Vial: 50 Maximum 65 mg/kg per 24 h. hemolysis.
mg/mL Chronic: 10 mg/kg per 24 h-
3-4 doses. Increase every 2
323
days as needed to maximum

65 mg/kg per 24 hour.
Nystatine Rinse: 1% Head lice: Avoid contact with eyes and
Permethrin Skin cream: Apply rinse after raw skin.
5% shampooing. Cover scalp Care required for treating
Tube: 30 g then washoff afer 10 children <2 yrs because of risk
minutes. of absorption, Stinging and
Scabies: < 2 yr: 1/4-1/8 tube rash, May requrie second
2-5 yr: 1/4 tube treatment in 1 week.
5-12yr: 1/2 tube Prolonged itching may occure
>12 yr: 1 tube despite successful treatment.
Massage cream on skin from
head to foot. Wash off after
12 hours.
Silver sulfadiazine Cream: 1%, Once daily burn treatment- If large areas covered, three
Jar 500 g less frequent for other may be significant sulfonamide
Tube; 30 g wounds. and silver absorption.
Section 14
Diagnostic
agents
Section 15
Disinfectants
Chlorhexidine Solution: 5% Apply liberally, topically. Not for irrigating body cavities.
for dilution Avoid eyes. Occasional
sensitivity.
Povidone/Iodine Solution: 10% Apply undiluted topically as a Absorption throught large

surgical scrub. wounds may be associated
with acidosis, electrolyte
abnormaliteis and high iodine
levels. Contraindicated in
324
premature infants.
Section 16
Diuretics
Furosemide Tablet: 20 Oral: 3-6 mg/kg per 24 hour Hypokalemia, alkalosis,
mg, 40 mg 3-4 doses p.o. dehydration, hyperuricemia.
Liquid: 10 Intravenous: 0.5-1.0 mg/kg Ototoxicity in high dose.
mg/mL per dose i.v.
Ampoule: 10 Infusion: 0.1-1.0 mg/kg per
mg/mL hour. Maximum dose 6
mg/kg.
Hydrochlorothiazi Tablet: 25 1-2 mg/kg per 24 hour - 2 Monitor electrolytes in
de mg, 50 mg p.o. Maximum 100 mg/d. prolonged dose.
Spironolactone Tablet: 25 1-4 mg/kg per 24 hour - 2-4 Possible K+ retensiton. Beware
mg, 100 mg doses p.o. if using potassium
supplementaiton.
cantraindicated in renal failue.
Section 17
Gastrointestinal
Aluminum Tablet: 500 Adult: 1-2 tabs, 4 times daily. Aluminium accumulation does
hydroxide mg Child: Up to 5 mL 3 times not occur if renal fuction
Liquid: 4% daily. normal.
Constipation.
Cimetidine Tablet: 200 Oral: 20-40 mg/kg per 24 Diarrhea, rash, gynecomastia,
mg, 300 mg hour - 4 doses before meals. dizziness. May increase serum
Liquid: 60 Intravenous: 20-40 mg/kg levels of phenytoin and
mg/mL per 24 hour - 4 doses. theophylline.
Ampoule: 150
mg/mL
Magnesium Liquid: 5.5% Child: 5 mL 4 times daily. Laxative.
hydroxide
Metoclopramide Tablet: 5 mg, GE reflus: 0.1 mg/kg per Cisapride has fewer side
325
10 mg dose before meals. effects as a motility agent.

Liquid: 1 Maximum 0.5 mg/kg per 24 Chronic tardive dyskinesia
mg/mL hour. seen with long-term use.
Ampoule: 5 Antiemetic: 1-2 mg/kg per
mg/mL dose 4-6 hourly. Maximum
10 mg/kg per 24 hour. Give
with diphenhydramine, 1
mg/kg per dose to prevent
dystonia.
Section 18 Vial: 40 u/mL, Given in mixture with soluble Several preparations but all
Hormones 100 u/mL insulin. May be mixed in one longer acting (onset 1-2 hours,
Intermediate syringe. Ratio is usually: 2/3 peak >4 hours). Local
insulin dose intermediae and 1/3 reactions, fat hypertrophy and
soluble. hypoglycemia in overdose. Not
for use in infusion.
Soluble insulin Vial: 40 u/mL Varies but starts 0.25 u/kg Several preparations but all
per 24 hour. short acting (onset 30-60
usually final dose 0.75-1.0 minuts, peak 2-4 hours). Local
u/kg per 24 hour s.c. reactions, fat hypertrophy and
Infusion: 0.1 u/kg per hour hypoglycemia in overdose.
for treatmetn of DKA.
Chloramphenicol Drops: 0.5% Apply 4 times a day. Stinging sensation. Very rare
eye drops Ointment: aplastic response.
1.0%
Gentamicin eye Drops: 0.3% Apply 4 times a day. well tolerated.
drops Ointment:
0.3%
Section 25 Vial: 25 Load: 6 g/kg i.v. over 20 theophylline in stabilized form
Antiasthma mg/mL minutes. Reduce dose by 50% for intravenous use. Ony give
Aminophylline if child taking oral theophylline. i.v. since irritating. Numerous
Infusion: 0.5-1.0 mg/kg per
side effects.
326
hour. Check level if available. Keep

55-110 μmol/L. Required
infusion dose depends on
many variables including age.
Arrhythmias, seizures,
gastrointestinal upset.
device-may be made easily
with a plastic cup or bottle.
with practice, may be used by
children of 1-2 years of age.
Adrenalin Ampoule: For acute asthmatics with Nebulized adrenalin is a stong
1/1000 (1 very poor air entry. bronchodilator. Its alpha
mg/mL) Subcutaneous: 1/1000 effects may improve air entry in
1/10 000 (0.1 strength. Give 0.01 mL/kg children <1 year of age who do
mg/mL) per dose (maximum 0.3 mL). not respond to salbutamol. In
Repeat every 10 minutes. emergency, nebulized
Intravenous: Ony in dire sdrenalin may be given safely if
emergency. Use 1/10 000 monitored carefully. Aerosol
strength. Give 0.1 mL/kg per treatmetn is often of some
dose (maximum 1 mL). value in small children with
Dilute and give slowly. bronchiolitis.
Nebulizer: Dilute 1 mL of
1/1000 to 4 mL with saline.
May give continously initially
until controlled. Monitor
closely. Also for bronchiolitis.
Salbutamol Tablet: 2 mg, Acue: Nebulized salbutamol Oral form of little use in wheezy
4 mg may be given continously in children. Systemic effects-
Syrup: 2 emergency. Cut back to 2-4 tremor, hyperactivity common.
mg/5 mL hourly when controlled. Chronic abuse and overdose
Inhaler: 100 Exercise asthma: 1 associated with sever side
327
μg inhalation 20 minuts before effects -arrhythmias, increased

Nebulizer: 2.5 sport. risk of fatal attacks. Should be
mg 5.0 mg Give with spacing device. used with an anti-inflammatory
Chronic: 1 puff twice a day to in most cases.
be given before anti-
inflammatory medication.
Section 27 Tablet: 100 Scurvy: 100-200 mg/24 h Diarrhea with very large doses.
Vitamins and mg, 250 mg, p.o. at least 2 weeks.
minerals 500 mg Maintenance: 35-45 mg/24
Ascorbic acid hour p.o.
(Vitamin C)
Glucose 5%, 10%: Hypoglycemia: (25%, 50%) Follow acute treatmetn for
500 mL, 1000 0.5 -1.0 mL/kg i.v. hypoglycemia with
mL Maintenance: (5%, 10%) For maintenance glucose. Do not
25%, 50%: maintenacy fluid use glucose solutions alone for
25 mL requirements, use 10%in fluid managemtn or risk of
neonates. Add Na+ (20 serious electrolyte
mEq/L) and K (15 mEq/L) abnormalities.
per liter to avoid electrolyte Numerous premixed glucose
abnormalitis. and electrolyte solutions exist.
Iodine oil: 480 Single treatmetn of 1mL, Not for long-term treatmetn or
mg/mL capsule p.o. provides risk of serious side effects.
Capsule: 200 sufficient iodine for many Iodine deficiency better treated
mg months. with mass dietary
supplemntation programs.
Nicotinamide Tablet: 50 mg Pellagra: 50 mg b.i.d.p.o for Nutritional rehabilitation
1 week necessary after initial
treatment.
Pyridoxine Tablet: 25 Deficiency: 50 mg/24h - 2 Chronic treatment with high
(Vitamin B6) mg, 100 mg doses. doses can cause a neuropathy
Ampoule: 100 Isoniazid neurophathy (>2 g/24 h).
328
mg/mL prophylaxis: Pyridoxine is widespread.

1-2 mg/kg per 24 h p.o Deficiency indicates sever
seizures: 50 mg i.v. single malnutriton. Isoniazid
dose under EEG monitoring, neuropathy is rare in children.
then 200 mg/24 h for 2
weeks.
Retinol Tablet: 10 Malnutrition: 200 000 units Dangerous in overdose. Not
(Vitamin A) 000 U p.o. if evidence of for high dose chronic treatment.
Capsule: 200 keratomalacia. Repeat in 2 Birth defects associated with
000U days. high maternal doses.
Oil: 100 000 Maintenance: 200 000 unit Do not exceed 10 000 units
u/mL capsules 6 monthly to daily in women of reproductive
Ampoule: 50 children in high risk areas. age. Single dose treatment
000 u/mL Diarrhea, measles: 200 000 improves outcome in diarrhea
units on admission. and measles.
Riboflavin Tablet: 5 mg maintenance: Isolated deficiency rare-usually

(vitamin B2) 1-2 mg/24 h. part of global malnutriton.
usually forms part of
amultivitamin prepariton.
Sodium chloride 0.9%: 500 0.9%: 10-30 mL/kg may be Hypernatremia, fluid overload
mL, 1000 mL given safely for fluid in overdose. Do not attempt to
3%: 10mL resuscitation. Larger replace Na+ deficit rapidly.
vials volumes may be necessary
but require close monitoring.
3%: Each mL contains 0.5
mEq na+. Give in boluses of
2-5 mL/kg for symptomatic
hyponatremia. Replace
slowly.
Thiamin Tablet: 50mg, Beriberi: 1 mg/kg per 24 hour Rare allergic reactions to
329
(Vitamin B1) 25 mg p.o. or i.v. intravenous form.

Ampoule: 100 Maintenance: 1-2 mg/24 h.
mg/mL
330

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PAEDIATRICS AND CHILD HEALTH

Health Science students

Health Science students

Tsinuel Girma (MD), Habtamu Fekadu (MD), Goitom G/Yesus (MD),

Chapter Two: Neonatology .......................... .....................................................78

Chapter Three: Shock.................................. ...................................................115

Chapter Six: Diseases of the cardiovascular system .......................................209

Chapter Seven: Diseases of the gastrointestinal system .................................219

Chapter Eight: Hematological diseases....... ...................................................230

Chapter Nine: Diseases of the renal system ...................................................253

Chapter Ten: Diseases of the nervous system ................................................271

Annex ........................................................... ...................................................307

ABC Airway, breathing and circulation

1.1. CHILD HEALTH IN ETHIOPIA

Integrated Management of Childhood Illnesses. (IMCI), Ministry of Health, Ethiopia.

Demographic and Health Survey. 2000.

The expanded programme on immunization (EPI), launched in Ethiopia in 1980 is

Vaccination is the administration of any vaccine or toxoid for prevention of disease.

Immunization is the process of inducing immunity artificially.

It can be active or passive

 Active immunization involves stimulating the immune system to produce antibodies

 Passive immunization provides temporary protection through the administration of

Determinants of the Immune response

Biologic nature of immunizing agents

Table 1 The main antigenic preparations

Type of antigen Vaccine example

*Live attenuated vaccine (diminished virulence retaining desired antigens)

Vaccines for routine (EPI) use in children

Table 2: Recommended Storage Temperature of EPI

Type of vaccine Storage temperature

Injection safety procedures in immunization

Factors that contribute to unsafe injection are:

Guidelines on injection safety include:

 Use of AD syringes preferably

 Children 6-11months -100, 000iu

Table 3 - Administrations of Vaccines

Side effects of vaccines

OPV: Paralytic polio from vaccine strain poliovirus

DPT: The major side effect is from the pertussis component

Major side effects include (per 100,000 vaccinations):

Contraindication and precautions

Contraindications: there are circumstances in which a vaccine, either first dose or

The contraindications for specific vaccines include:

The following precautions are necessary:

The following are not contraindications

 Well controlled epilepsy

Vaccines in special circumstances

Measles target population

Measles outbreak Yes

No Vaccinate all children*

Vit. A if not provided in the

Nelson. Text Book of Pediatrics. 16th Ed. W.B. Saunders. 2000

Manual for routine EPI, MOH, Ethiopia, 2003 (draft)

1.3. GROWTH AND DEVELOPMENT

An understanding of the normative pattern of physical growth and the emergency of

Understanding of how biological and environmental forces interact to shape

Understanding of how parents conceptualize development facilitates guidance and

Factors Affecting growth

Neural control of growth