UNITED REPUBLIC OF TANZANIA

Ministry of Health and Social Welfare

CMT 05103 Paediatrics and

Child Health I
NTA Level 5 Semester 1

Student Manual

August 2010
 Copyright © Ministry of Health and Social Welfare – Tanzania 2010

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
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 Table of Contents

Background and Acknowledgement ........................................................................ iv

Introduction .............................................................................................................. ix
Abbreviations .............................................................................................................x

Module Sessions
Session 1: Growth and Development in Paediatrics ..................................................1
Session 2: History Taking and Physical Examination .............................................17
Session 3: Upper Respiratory Tract .........................................................................31
Session 4: Pneumonia ..............................................................................................39
Session 5: Bronchial Asthma and Bronchiolitis ......................................................45
Session 6: Childhood Tuberculosis..........................................................................55
Session 7: Measles ...................................................................................................65
Session 8: Chickenpox and Mumps .........................................................................71
Session 9: Diarrhoeal Diseases and Rectal Prolapse ...............................................75
Session 10: Ectoparasite and Helminthic Infestation ..............................................89
Session 12: Sickle Cell Anaemia ...........................................................................101
Session 13: Malaria ................................................................................................107
Session 14: Meningitis ...........................................................................................115
Session 15: Cerebral Palsy .....................................................................................121
Session 16: Deafness, Blindness, Speech Delay and Mental Retardation.............127
Session 17: Congenital Heart Disease ...................................................................133
Session 18: Acute Rheumatic Fever and Infective Endocarditis ...........................145
Session 19: Urinary Tract Disorders ......................................................................151
Session 20: Nephrotic Syndrome and Acute Glomerulonephritis .........................159
Session 21: Disorders of the Musculoskeletal System ..........................................165
Session 22: Common Skin Conditions and Leprosy .............................................173

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
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Background and Acknowledgement
In April 2009, a planning meeting was held at Kibaha which was followed up by a Task
Force Committee meeting in June 2009 at Dodoma and developed a proposal which guided
the process of the development of standardised Clinical Assistant (CA) and Clinical Officer
(CO) training materials which were based on CA/CO curricula. The purpose of this process
was to standardize the entire curriculum with up-to-date content which would then be
provided to all Clinical Assistant and Clinical Officer Training Centres (CATCs/COTCs).
The perceived benefit was that, by standardizing the quality of content and integrating
interactive teaching methodologies, students would be able to learn more effectively and that
the assessment of students’ learning would have more uniformity and validity across all
schools.

In September 2009, MOHSW embarked on an innovative approach of developing the

standardised training materials through the Writer’s Workshop (WW) model. The model
included a series of three-week workshops in which pre-service tutors and content experts
developed training materials, guided by facilitators with expertise in instructional design and
curriculum development. The goals of WW were to develop high-quality, standardized
teaching materials and to build the capacity of tutors to develop these materials.

The new training package for CA/CO cadres includes a Facilitator Guide, Student Manual
and Practicum. There are 40 modules with approximately 600 content sessions. This product
is a result of a lengthy collaborative process, with significant input from key stakeholders and
experts of different organizations and institutions, from within and outside the country.

The MOHSW would like to thank all those involved during the process for their valuable
contribution to the development of these materials for CA /CO cadres. We would first like to
thank the U.S. Centers for Disease Control and Prevention’s Global AIDS Program
(CDC/GAP) Tanzania, and the International Training and Education Center for Health (I-
TECH) for their financial and technical support throughout the process. At CDC/GAP, we
would like to thank Ms. Suzzane McQueen and Ms. Angela Makota for their support and
guidance. At I-TECH, we would especially like to acknowledge Ms. Alyson Shumays,
Country Program Manager, Dr. Flavian Magari, Country Director, Mr. Tumaini Charles,
Deputy Country Director, and Ms. Susan Clark, Health Systems Director. The MOHSW
would also like to thank the World Health Organization (WHO) for technical and financial
support in the development process.

Particular thanks are due to those who led this important process: Dr. Bumi L.A.
Mwamasage, the Assistant Director for Allied Health Sciences Training, Dr. Mabula Ndimila
and Mr. Dennis Busuguli, Coordinators of Allied Health Sciences Training, Ministry of
Health and Social Welfare, Dr. Stella Kasindi Mwita, Programme Officer Integrated
Management of Adults and Adolescent Illnesses (IMAI), WHO Tanzania and Stella M.
Mpanda, Pre-service Programme Manager, I-TECH.

Sincere gratitude is expressed to small group facilitators: Dr. Otilia Gowele, Principal, Kilosa
COTC, Dr. Violet Kiango, Tutor, Kibaha COTC, Ms. Stephanie Smith, Ms. Stephanie
Askins, Julie Stein, Ms. Maureen Sarewitz, Mr. Golden Masika, Ms. Kanisia Ignas, Ms.
Yovitha Mrina and Mr. Nicholous Dampu, all of I-TECH, for their tireless efforts in guiding
participants and content experts through the process. A special note of thanks also goes to
CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
iv
Dr. Julius Charles and Dr. Moses Bateganya, I-TECH’s Clinical Advisors, and other Clinical
Advisors who provided input. We also thank individual content experts from different
departments of the MOHSW and other governmental and non-governmental organizations,
including EngenderHealth, Jhpiego and AIHA, for their technical guidance.

Special thanks goes to a team of I-TECH staff namely Ms. Lauren Dunnington, Ms.
Stephanie Askins, Ms. Stephanie Smith, Ms Aisling Underwood, Golden Masika, Yovitha
Mrina, Kanisia Ignas, Nicholous Dampu, Michael Stockman and Stella M. Mpanda for
finalising the editing, formatting and compilation of the modules.

Finally, we very much appreciate the contributions of the tutors and content experts
representing the CATCs/COTCs, various hospitals, universities, and other health training
institutions. Their participation in meetings and workshops, and their input in the
development of content for each of the modules have been invaluable. It is the commitment
of these busy clinicians and teachers that has made this product possible.

These participants are listed with our gratitude below:

Tutors
Ms. Magdalena M. Bulegeya – Tutor, Kilosa COTC
Mr. Pius J.Mashimba – Tutor, Kibaha Clinical Officers Training Centre (COTC)
Dr. Naushad Rattansi – Tutor, Kibaha COTC
Dr. Salla Salustian – Principal, Songea CATC
Dr. Kelly Msafiri – Principal, Sumbawanga CATC
Dr. Joseph Mapunda - Tutor, Songea CATC
Dr. Beda B. Hamis – Tutor, Mafinga COTC
Col Dr. Josiah Mekere – Principal, Lugalo Military Medical School
Mr. Charles Kahurananga – Tutor, Kigoma CATC
Dr. Ernest S. Kalimenze – Tutor, Sengerema COTC
Dr. Lucheri Efraim – Tutor, Kilosa COTC
Dr. Kevin Nyakimori – Tutor, Sumbawanga CATC
Mr. John Mpiluka – Tutor, Mvumi COTC
Mr. Gerald N. Mngóngó –Tutor, Kilosa COTC
Dr. Tito M. Shengena –Tutor, Mtwara COTC
Dr. Fadhili Lyimo – Tutor, Kilosa COTC
Dr. James William Nasson– Tutor, Kilosa COTC
Dr. Titus Mlingwa – Tutor, Kigoma CATC
Dr. Rex F. Mwakipiti – Principal, Musoma CATC
Dr. Wilson Kitinya - Principal, Masasi ( Clinical Assistants Training Centre (CATC)
Ms. Johari A. Said – Tutor, Masasi CATC
Dr. Godwin H. Katisa – Tutor, Tanga Assistant Medical Officers Training Centre (AMOTC)
Dr. Lautfred Bond Mtani – Principal, Sengerema COTC
Ms Pamela Henry Meena – Tutor, Kibaha COTC
Dr. Fidelis Amon Ruanda – Tutor, Mbeya AMOTC
Dr. Cosmas C. Chacha – Tutor, Mbeya AMOTC
Dr. Ignatus Mosten – Ag. Principal, Tanga AMOTC
Dr. Muhidini Mbata – Tutor, Mafinga COTC
Dr. Simon Haule – Ag. Principal, Kibaha COTC
Ms. Juliana Lufulenge - Tutor, Kilosa COTC
Dr. Peter Kiula – Tutor, Songea CATC
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Mr. Hassan Msemo – Tutor, Kibaha COTC
Dr. Sangare Antony –Tutor, Mbeya AMOTC

Content Experts
Ms. Emily Nyakiha – Principal, Bugando Nursing School, Mwanza
Mr. Gustav Moyo - Registrar, Tanganyika Nursesand Midwives Council, Ministry of Health
and Social Welfare (MOHSW).
Dr. Kohelet H. Winani - Reproductive and Child Health Services, MOHSW
Mr. Hussein M. Lugendo – Principal, Vector Control Training Centre (VCTC), Muheza
Dr. Elias Massau Kwesi - Public Health Specialist, Head of Unit Health Systems Research
and Survey, MOHSW
Dr. William John Muller - Pathologist, Muhimbili National Hospital (MNH)
Mr. Desire Gaspered - Computer Analyst, Institute of Finance Management (IFM), Dar es
Salaam
Mrs. Husna Rajabu - Health Education Officer, MOHSW
Mr. Zakayo Simon - Registered Nurse and Tutor, Public Health Nursing School (PHNS)
Morogoro
Dr. Ewaldo Vitus Komba - Lecturer, Department of Internal Medicine, Muhimbili University
of Health and Allied Sciences School (MUHAS)
Mrs. Asteria L.M. Ndomba - Assistant Lecturer, School of Nursing, MUHAS
Mrs. Zebina Msumi - Training Officer, Extended programme on Immunization (EPI),
MOHSW
Mr. Lister E. Matonya - Health Officer, School of Environmental Health Sciences (SEHS),
Ngudu, Mwanza.
Dr. Joyceline Kaganda - Nutritionist, Tanzania Food and Nutrition Centre (TFNC),
MOHSW.
Dr. Suleiman C. Mtani - Obstetrician and Gynecologist, Director, Mwananyamala Hospital,
Dar es salaam
Mr. Brown D. Karanja - Pharmacist, Lugalo Military Hospital
Mr. Muhsin Idd Nyanyam - Tutor, Primary Health Care Institute (PHCI), Iringa
Dr. Judith Mwende - Ophthalmologist, MNH
Dr. Paul Marealle - Orthopaedic and Traumatic Surgeon, Muhimbili Orthopedic Institute
(MOI),
Dr. Erasmus Mndeme - Psychiatrist, Mirembe Refferal Hospital
Mrs. Bridget Shirima - Nurse Tutor (Midwifery), Kilimanjoro Chrician Medical Centre
(KCMC)
Dr. Angelo Nyamtema - Tutor Tanzania Training Centre for International Health (TTCIH),
Ifakara.
Ms. Vumilia B. E. Mmari - Nurse Tutor (Reproductive Health) MNH-School of Nursing
Dr. David Kihwele - Obs/Gynae Specialist, and Consultant
Dr. Amos Mwakigonja – Pathologist and Lecturer, Department of Morbid Anatomy and
Histopathology, MUHAS
Mr. Claud J. Kumalija - Statistician and Head, Health Management Information System
(HMIS), MOHSW
Ms. Eva Muro, Lecturer and Pharmacist, Head Pharmacy Department, KCMC
Dr. Ibrahim Maduhu - Paediatrician, EPI/MOHSW
Dr. Merida Makia - Lecturer Head, Department of Surgery, MNH
Dr. Gabriel S. Mhidze - ENT Surgeon, Lugalo Military Hospital
Dr. Sira Owibingire - Lecturer, Dental School, MUHAS
Mr. Issai Seng’enge - Lecturer (Health Promotion), University of Dar es Salaam (UDSM)
CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
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Prof. Charles Kihamia - Professor, Parasitology and Entomology, MUHAS
Mr. Benard Konga - Economist, MOSHW
Dr. Martha Kisanga - Field Officer Manager, Engender Health, Dar es Salaam
Dr. Omary Salehe - Consultant Physician, Mbeya Referral Hospital
Ms Yasinta Kisisiwe - Principal Nursing Officer, Health Education Unit (HEU), MOHSW
Dr. Levina Msuya - Paediatrician and Principal, Assistant Medical Officers Training Centre
(AMOTC), Kilimanjaro Christian Medical Centre (KCMC)
Dr. Mohamed Ali - Epidemiologist, MOHSW
Mr. Fikiri Mazige - Tutor, PHCI-Iringa
Mr. Salum Ramadhani - Lecturer, Institute of Finance Management
Ms. Grace Chuwa - Regional RCH Coordinator, Coastal Region
Mr. Shija Ganai - Health Education Officer, Regional Hospital, Kigoma
Dr. Emmanuel Suluba - Assistant Lecturer, Anatomy and Histology Department, MUHAS
Mr. Mdoe Ibrahim - Tutor, KCMC Health Records Technician Training Centre
Mr. Sunny Kiluvia - Health Communication Consultant, Dar es Salaam
Dr. Nkundwe Gallen Mwakyusa - Ophthalmologist, MOHSW
Dr. Nicodemus Ezekiel Mgalula -Dentist, Principal Dental Training School, Tanga
Mrs. Violet Peter Msolwa - Registered Nurse Midwife, Programme Officer, National AIDS
Control Programme (NACP), MOHSW
Dr. Wilbert Bunini Manyilizu - Lecturer, Mzumbe University, Morogoro

Editorial Review Team

Dr. Kasanga G. Mkambu - Obstertric and Gynaecology specialist, Tanga Assistant Medical
Officers Training Centre (AMOTC)
Dr. Ronald Erasto Msangi - Principal, Bumbuli COTC
Mr. Sita M. Lusana - Tutor, Tanga Environmental Health Science Training Centre
Mr. Ignas Mwamsigala - Tutor (Entrepreneurship) RVTC Tanga
Mr. January Karungula - RN, Quality Improvement Advisor, Muhimbili National Hospital
Prof. Pauline Mella - Registered Nurse and Profesor, Hubert Kairuki Memorial University
Dr. Emmanuel A. Mnkeni – Medical Officer and Tutor, Kilosa COTC
Dr. Ronald E. Msangi - Principal, Bumbuli COTC
Mr. Dickson Mtalitinya - Pharmacist, Deputy Principal, St Luke Foundation, Kilimanjaro
School of Pharmacy
Dr. Janeth C. Njau - Paediatrician/Tutor, Kibaha COTC
Mr. Fidelis Mgohamwende - Labaratory Technologist, Programme Officer National Malaria
Control Programme (NMCP), MOHSW
Mr. Gasper P. Ngeleja - Computer Instructor, RVTC Tanga
Dr. Shubis M Kafuruki - Research Scientist, Ifakara Health Institute, Bagamoyo
Dr. Andrew Isack Lwali - Director, Tumbi Hospital

Librarians and Secretaries

Mr. Christom Aron Mwambungu - Librarian MUHAS
Ms. Juliana Rutta - Librarian MOHSW
Mr. Hussein Haruna - Librarian, MOHSW
Ms. Perpetua Yusufu - Secretary, MOHSW
Mrs. Martina G. Mturano -Secretary, MUHAS
Mrs. Mary F. Kawau - Secretary, MOHSW

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
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IT support
Mr. Isaac Urio - IT Consultant, I-TECH
Mr. Michael Fumbuka - Computer Systems Administrator – Institute of Finance and
Management (IFM), Dar es Salaam

Dr. Gilbert Mliga

Director of Human Resources Development, Ministry of Health and Social Welfare

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
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Introduction
Module Overview
This module content has been prepared to enhance learning of students of Clinical Assistant
(CA) and Clinical Officer (CO) schools.. The session contents are based on the sub-enabling
outcomes of the curricula of CA and CO. The module sub-enabling outcomes are as follows:
3.2.1. Utilize growth and development parameters in providing paediatric care.
3.2.2. Manage major childhood illnesses and diseases
3.2.4. Provide neonatal care.

Who is the Module For?

This module is intended for use primarily by students of CA and CO schools. The module’s
sessions give guidance on contents and activities of the session and provide information on
how students should follow the tutor when he/she teaches the module. It also provides
guidance and necessary information for students to read the materials on his/her own. The
sessions also include different activities which focus on increasing students’ knowledge,
skills and attitudes.

How is the Module Organized?

The module is divided into 22 sessions; each session is divided into several sections. The
following are the sections of each session:
• Session Title: The name of the session.
• Learning Objectives – Statements which indicate what the student is expected to have
learned at the end of the session.
• Session Content – All the session contents are divided into subtitles. This section
includes contents and activities with their instructions to be done during learning of the
contents.
• Key Points – Each session has a step which concludes the session contents near the end
of a session. This step summarizes the main points and ideas from the session.
• Evaluation – The last section of the session consists of short questions based on the
learning objectives to check if you understood the contents of the session. The tutor will
ask you as a class to respond to these questions; however if you read the session by
yourself try answering these questions to evaluate yourself if you understood the session.
• Handouts – Additional information which can be used in the classroom while the tutor is
teaching or later for your further learning. Handouts are used to provide extra information
related to the session topic that cannot fit into the session time. Handouts can be used by
the students to study material on their own and to reference after the session. Sometimes,
a handout will have questions or an exercise for students to answer.

How Should the Module be Used?

Students are expected to use the module in the classroom and clinical settings and during self
study. The contents of the modules are the basis for learning Paediatrics and Child Health I.
Students are therefore advised to learn all the sessions including all relevant handouts and
worksheets during class hours, clinical hours and self study time. Tutors are there to provide
guidance and to respond to all difficulty encountered by students. One module will be
assigned to 5 students and it is the responsibility of the tutor to do this assignment for easy
use and accessibility of the student manuals to students.

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 Abbreviations
ABC Airway, breathing, circulation
AFB Acid Fast Bacilli
AFP Acute Flaccid Paralysis
AIDS Acquired Immune Deficiency Syndrome
ALu Artemether Lumefantrine
AMREF African Medical Research Foundation
ANP Atrial Natriuretic Peptide
ASD Atrial Septal Defect
ASOT Antistreptolysin O Titre
BCG Bacillus Calmette Guierin
BI Bacteriological Index
BNP Brain Natriuretic Peptide
BT Blood Transfusion
CHD Congenital Heart Disease
CMV Cytomegalovirus
CNS Central Nervous System
CSF Cerebral Spinal Fluid
CT Computed Tomograph
CXR Chest X-ray
DDT Diphenyl Diethyl Tetrachloroethane
DIC Disseminated Intravascular Coagulation
DNA Deoxyribonucleic Acid
DPT Diptheria, Pertussis and Tetanus.
EBV Ebstein Barr Virus
ECHO Echocardiogram
ECG Electrocardiogram
EPI Expanded Programme for Immunization
EPTB Extra Pulmonary Tuberculosis
ESR Erythrocycte Sedimentation Rate
ETEC Enterotoxigenic Escherishia coli
FBP Full Blood Picture
FTT Failure to Thrive
Hb Haemoglobin
HIV Human Immunodeficiency Virus
KCMC Kilimanjaro Christian and Medical Centre
LBW Low birth weight
MCH Mother and Child Health
MI Morphological Index
MRI Magnetic Resonance Imaging
MUAC Mid Upper Arm Circumfernce
NGT NasoGastric Tube
OFC Occipital Frontal Circumfrence
ORS Oral Rehydration Salt
ORT Oral Rehydration Therapy
PDA Patent Ductus Arteriosus
CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
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PEM Protein Energy and Malnutrition
PPD Purified Protein Derivatives
PTB Pulmonary Tuberculosis
RBC Red Blood Cell
RH ZE Rifampiacin, Isoniazid Pyrazinamide, Ethambutol
RH Rifampiacin, Isoniazid
RPR Reactive Plasma Reagin
SLE Systemic Lupus Erythematosus
TB Tuberculosis
ToF Tetralogy of Fallot
TU Tuberculin Unit
URI Upper Respiratory Infections
UTI Urinary Tract Infection
VDRL Venereal Disease Research Laboratory
VSD Ventricular Septal Defect
WBC White Blood Cell

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CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
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 Session 1: Growth and Development in Paediatrics
Learning Objectives
By the end of this session, students are expected to be able to:
• Define the terms pediatrics, child health, child growth and child development
• Describe the two stages of growth
• Describe patterns of normal growth and development
• Explain milestone development of a child
• Interpret growth and developmental milestones

Definition of Terms
• Paediatrics: Branch of medicine which deals with children’s diseases and the care of the
children.
• Child health: Wellbeing of a child and not merely the absence of disease.
• Child growth: An increase in body size.
• Child development: The increase in the complexity of structures and of their functions
(what a child can do).
• Child growth and child development go together, but at different speeds.

Stages of Child Growth and Development

• Pre natal phase (foetus)
o During the first 3 months organs are formed
o Harmful environmental factors (infections-rubella in the mother or exposure to certain
drugs or X-rays) may interfere with development of the foetus
ƒ The child may be born with certain deformities (e.g. congenital heart diseases,
deafness, or a small head and or brain)
o During the last 6 months, the foetus increases greatly in size
ƒ This is mainly the stage in which malnutrition, anaemia or malaria in the mother
may interfere with blood supply to the foetus and interfere with foetal growth
ƒ The baby may thus be small for gestational age
• Post natal phase
o The infant
ƒ Up to 10% loss of birth weight may occur in first two weeks, but beyond neonatal
period weight loss is abnormal
ƒ Growth and development proceed rapidly in the first six months of life
ƒ Growth slows down in the second half of the year
ƒ Weight gain may vary much during infancy
ƒ Weight may be lost during acute infection
ƒ Predominantly nutrition dependent
o The child
ƒ From first years growth slows down to a regular rate, displayed in weight charts as
almost a straight line
ƒ There is often very brief weight gain
ƒ Development seems to occur in steps
ƒ The child suddenly is able to stand, walk and starting using words
ƒ Growth hormone has predominant role

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
Session 1: Growth and Development in Paediatrics 1
 o Puberty
ƒ Period of physical and sexual maturity
ƒ In girls, puberty starts between 8 and 13 years and for boys 9-13.5 years
ƒ Both growth and development undergo a rapid spurt after which slows and finally
stops
ƒ The main development in puberty is sex characteristics
ƒ In girls, the breasts start to develop, followed by axillary and pubic hair and
changes in body curves and finally menstruation
ƒ In boys the testes begin to enlarge, followed by pubic, axillary and beard hair,
enlargement of penis and muscular development

Normal Growth Pattern

• Normal growth follows a given specific pattern in terms of weight, height/length and head
circumference as follows:
o Birth weight decreases by 5 to 10% in the first 7 to 10 days
o It doubles by the age of six months, and triples by the age of nine to twelve months
and quadruples by the age of 2 years and thereafter it increases by 2 kilograms per
year
o Birth length average is 50 cm, at one year is about 75 cm and at four years it is about
100 cm
o Head circumference at birth is about 35 cm, it increases by 1cm per month and at the
age twelve months it is about 46 cm
o Arm circumference increases rapidly to about 15 cm at one year and then it increases
only slightly from one to five years
o Tooth eruption (teething) starts at about 6 months and children have twenty teeth by
the age of two to two and a half years old

Refer to Handout 1.1: Normal Values for Weight, Height/Length, Head and Arm
Circumference in Children

Assessment of Growth in Children

• Assessment of growth in children is done using different measurements
• Weight is a way of measuring growth, and is expressed in kilograms
• Length/ Height is a more accurate way of measuring growth than weight
o It is stable and not changing with conditions such as dehydration, starvation or
oedema as compared to weight
• Arm circumference is taken at the mid of the upper (MUAC)
o It increases only slightly from one to five years of age at an average of 14.5-16.5 cm
• Head circumference is taken at the greatest distance around the forehead and the back of
the head (occipito-frontal circumference, OFC)

Activity: Demonstration

Instructions
The tutor will demonstrate how to measure weight, height/length, mid upper arm
circumference (MUAC) and head circumference (OFC). Follow the demonstration carefully
and ask for clarification if you have not understood any step. After the tutor demonstration
you will work in small groups to do a return demonstration.

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
Session 1: Growth and Development in Paediatrics 2
Normal Child Growth and Child Development
• Factors promoting growth
o Genetics-
ƒ Related to parental size, small parents tend to have small babies
o Adequate nutrition
ƒ Regulated by trophic hormones (thyroxine and growth hormone)
o Sex hormones
ƒ Pre-pubertal growth spurt.
o External factors
ƒ Illness, socio-economic status (SES)
• Factors promoting development include:
o Nutrition
ƒ Good nutrition is the basis for proper growth and development
ƒ The first six months of life are extremely important, as the brain may suffer if the
child does not get adequate nutritious food
ƒ A malnourished child is often tired or apathetic and not interested in the
environment around them
o Emotional support
ƒ For normal growth and development a child needs full emotional support
ƒ Love- A child who does not feel loved will not develop properly and will not learn
as quickly
ƒ Security-A child needs to feel safe
ƒ The love and security a child gets from his family/community helps him/her feel
friendly toward others
ƒ Acceptance as an individual-A child needs to know that his family loves him/her
for who s/he is, and they should respect the child as an individual with his/her own
likes and dislikes
ƒ Recognition-A child needs to know that his/her parents are happy and pleased
when s/he has learned something new
ƒ Wise and consistent use of authority- Children need to know what they can and
cannot do
ƒ Independence- As the child grows, he/she needs to be allowed to decide more and
more things for him/herself
o Play
ƒ Helps physical, mental and social development
ƒ If a young child does not play he/she may be ill, children have a right to play
o Language training
ƒ Adults should talk and sing with small children and encourage them to talk about
what they are thinking
ƒ Do not laugh at children when they are talking, try to understand them

Normal Milestones
• These are skills the baby and young children learn while growing
• Can be grouped into motor development, social behaviour, and language

Refer to:
Handout 1.2: Normal Developmental Milestones
Handout 1.3: Age-Weight-Height Tables

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
Session 1: Growth and Development in Paediatrics 3
Key Points
• Paediatrics and child health deal with both healthy and sick children.
• In determining growth and development, use weight, length/height, MUAC and OFC.
• Growth and development can be influenced by internal and external factors.

Evaluation
• What is pediatrics?
• What is child health?
• What is growth and development?
• What are the stages of child growth and development?
• Explain how to determine growth by weighing, measuring height/length, MUAC and
OFC of a child.

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International Student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.) Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
Session 1: Growth and Development in Paediatrics 4
 Handout 1.1: Normal Values for Weight, Height/Length,
Head and Arm Circumference in Children

Age Weight(kg) Height/length(cm) OFC (cm) MUAC (cm)

Birth 3.5 50 34
6 months 7.0 43
1 year 10 75 46 14.5
2 years 12 87 48 15
3 years 14 96 50 15.5
4 years 16 105 50 16
5 years 18 110 50 16.5

Weight
• Between 60% and 80% of standard is called underweight.
• Below 60% of standard (without oedema of feet) is called marasmus.

Height
• Below 90% of standard is called short stature.

Head circumference (OFC)

• Below normal range, abnormally small head is called microcephaly.
• Above normal range, abnormally large head is called macrocephaly.

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
Session 1: Growth and Development in Paediatrics 5
 Handout 1.2: Normal Developmental Milestones

CMT 05103 Paediatrics and Child Health I NTA Level 5 Semester 1 Student Manual
Session 1: Growth and Development in Paediatrics 6
 Handout 1.3: Age-Weight-Height Tables

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
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 Session 2: History Taking and Physical Examination
Learning Objectives
By the end of this session, students are expected to be able to:
• Describe the components of history taking in paediatrics and child health
• Describe physical examination in paediatrics
• List relevant investigations for paediatrics

History Taking
• History taking is a medical practice which collects information from the patient or patient
care taker in order to make a diagnosis and know how to approach treatment and design
appropriate scheme of management for a patient.
• In order to understand each patient, it is necessary to have his/her history taken
considering social, ethnic and cultural backgrounds.
• The doctor will not only elucidate the problems posed by disease, but also apply his or
her skill to advise patients and families on how to manage these problems.
• The initial aims of any first consultation are to understand the patient’s own perception of
their problem and start or complete the process of diagnosis.
• Appropriate skills are needed to elicit the symptoms from the patient’s description and
signs by observation and physical examination.

Components of a Good Paediatric History

Components of Good Rapport

• History taking is an important part in management of childhood diseases and illnesses.
• The child is usually brought by his/her mother or a guardian and it is important for the
health care provider to establish good rapport, in order to get a well detailed history.

History Taking
• Demographic data
o Child’s name
o Sex
o Age
o Place of residence
o Address and telephone number
o Date of taking the history/admission
ƒ Note: Report who is the informant
• Chief or main complaints
o Ask for the problem that has caused the child to be brought to the hospital
o Probe the caretaker to mention any other problems and let her/him explain, don’t
interrupt (unless critical)
o Ask the duration of each symptom and arrange the problems (symptoms) in the
chronological order
ƒ This means the symptom with the longest duration to the shortest duration
• History of presenting illness (amplification of the chief complaints)

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 o Explain in order of occurrence of the symptoms mentioned in the chief complaints
o Probe the informant to explain further how the symptoms started
o When asking the questions, look to see how the symptoms are associated with each
other or any other symptom that a patient has not reported
o When asking questions, look for complications that could have already developed but
the mother may not be aware of, write them in the history and remember them during
management/treatment
o Ask about any relieving or aggravating factors
o Ask for any treatment (including traditional treatment) given before coming to
hospital
o Ask for feeding pattern, when last was the child fed?
ƒ Children may come to hospital lethargic or with impaired consciousness only
because of hypoglycaemia
• Review of other systems
o Review the systems that have not been covered in the history of presenting illness,
this should be done systematically to avoid omissions, the systems to be reviewed are:
ƒ Cardiovascular system (CVS)
ƒ Respiratory system (RS)
ƒ Gastrointestinal system (GIT)
ƒ Genital urinary system (GUS)
ƒ Ear nose and throat (ENT)
ƒ Musculo - skeletal system (MSS)
• Past medical history
o Paediatric history
ƒ Ask for previous admissions and their reasons, diagnosis and treatment given (if
any)
ƒ History of previous diseases (if any) that are associated with the current child’s
problems or diagnosis that you are thinking about
o Antenatal history
ƒ Ask the mother (if present) for any illnesses and treatment during pregnancy, such
as malaria, syphilis, severe anaemia.
ƒ Ask the mother (if present) if she received Tetanus toxoid vaccine as per EPI
schedule
ƒ Number of previous pregnancies and their results
ƒ Serology (for HIV, VDRL), blood grouping and Hb, their results and any
medications (haematinics, IPT, PMTCT) to the mother
o Natal history
ƒ Was it a hospital or home delivery, was the pregnancy full term
ƒ Mode of delivery, (spontaneous vertex delivery (SVD), assisted breech
delivery(ASD), caesarean section , vacuum or forceps delivery)
ƒ Rupture of Membranes (timing, spontaneous or artificial, quality of the fluid -
bloody, clear, cloudy, foul-smelling)
ƒ Did the baby cry immediately after birth, or was it after some hours, was the baby
able to suck?
o Post natal history
ƒ Any diseases suffered after delivery (e.g. yellow coloration of the body, bleeding
tendency, sepsis of the cord, convulsions, etc)
• Immunization History
o Ask for the RCH card 1, look to see if the child received all the vaccines and is up to
date
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Session 2: History Taking and Physical Examination 18
 o Note: If the child is not fully immunized, then arrange for immunization before
discharge
• Dietary history
o Ask about feeding (exclusive breastfeeding/optional feeding) and complimentary
feeding (age and type of weaning foods)
o Use the normal feeding recommendations for the child’s age, and if you identify any
abnormal practice, give feeding recommendations as per guidelines
o Ask if feeding has changed during the illness
• Developmental milestones
o Ask for the child’s developmental milestones:
ƒ Gross motor (movement and posture)
ƒ Hearing and speech
ƒ Vision and manipulation
ƒ Social behaviour
o Ask specifically when the child started to do the above body functions and what the
child is able to do now
o Compare the above with the child’s age and decide if milestones are normal, delayed
or regressed
o Note: Be careful that the milestones used are based on European standards not
African, as you may encounter ambiguity

Refer to Handout 1.1: Normal Developmental Milestones from Session 1 of this

module.

• Family and social history

o Ask if the parents are alive, level of education, economic status, marital status, habits
like smoking and drinking alcohol
o If the child is an orphan, who takes care of the child, the relationship to the child and
then cover the above information about the guardian
o Gather information on the death of the parents and establish relationship with the
child’s current illness
o If the child is in school, any similar symptoms with school mates
o Ask about siblings and their well-being
o Ask about family diseases like diabetes mellitus, epilepsy, hypertensions, sickle cell,
bronchial asthma and important communicable conditions (like HIV and TB)
• Summary
o Age, sex, how many days since admission, child’s status (e.g. orphan)
o Write the chief complaints, important findings from history that will lead to diagnosis,
and also any complications developed
o Use few words, at most five lines

Physical Examination

General Examination
• Older children will usually cooperate sufficiently to be examined lying down, and routine
physical examination is no different from an adult examination
• A younger child should be examined sitting on his or her mother's lap, as any attempt to
get him or her to lie down may result in instant distress

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Session 2: History Taking and Physical Examination 19
• Always talk to children, however young; do not be afraid of looking silly if the result is a
cooperative child
• Parts of the examination that are painful or unpleasant should be left until last: if an
attempt is made to examine a child's throat at the outset, the immediate response will be
crying
• Offer the child something to play with; even a stethoscope will be a source of amusement
to a young child
• Children often find it amusing if you examine their toy first
• Sometimes a small toy clipped onto the stethoscope is interesting enough for a young
child to let you examine them without problems
• Routine examination will include the following:
o Look to see if the child is ill looking
o Look to see if the patient is dyspnoeic, listen for grunting, wheeze or stridor
o Do quick assessment of level of consciousness (AVPU)
o Look and palpate for anterior fontanelle
o Look for pallor, cyanosis, jaundice
o Examine the mucous membranes of the mouth (for ulcers or white patches-oral
thrush)
o Touch the patient and feel for temperature also at the same time put an axillary
thermometer and assess for temperature and record it
o Measure pulse rate, and decide whether it is normal or if there is tachycardia, or
bradycardia
o Count the respiratory rate and decide whether it is normal or if the child has
tachypnoeia or bradypnoea
o Measure the blood pressure (use appropriate cuff for the child)
o Look for lymph node enlargement
o Look for oedema
o Assess hydration status
o Do the anthropometric measurements
ƒ Weight
ƒ Height/length
ƒ Mid upper arm circumference (MUAC) for age
ƒ Head circumference (occipital frontal circumference)

Activity: Demonstration

Instructions
The tutor will demonstrate how to do a general examination on the real baby.

Systemic/Regional Examination
• In the paediatrics population it is advised to do regional approach instead of systemic
approach in doing physical examination
• The examination may have to be opportunistic, as each child will dictate the order of the
examination by their reactions to various procedures
• In general, start with the least threatening manoeuvres and we use the following steps:
o Inspection
o Palpation
o Percussion
o Auscultation

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Ear, Nose and Throat
• Inspection
o Discharge and lesion, ulcers, obvious deformity, if uvulectomy has been done
• Palpation
o Tenderness, Percussion (Present or none)
• Percussion (Present or none)
• Auscultation (Present or none)

Head and Neck

• Inspection
o Shape and size of the head (bossed, obvious swelling, hair pattern and texture, marks,
in newborn examine skull for plagiocephaly, cephalohematoma and caput
succedaneum)
• Palpation
o Fontanelle, if bulging or normal, sutures if are closed well or abnormal
• Lymph node enlargement, and if enlarged you should describe them by shape ,size,
texture, mobility
• Gentle percussion
o For patients with hydrocephalus for a cracked pot sound on percussion of the skull
• Auscultation (may be needed for some swellings/mass)

Chest (Thorax)
• Let the mother undress the child, to expose the chest both anteriorly and posterioly
• Avoid unnecessary exposure in newborn babies and in children with severe malnutrition,
as they are at risk of hyperthermia
• Inspection
o Look for nasal flaring
o Look at the chest for any asymmetry
o Look at the breasts and nipples, deformity, lesions, marks, scars or new growths, and
also look for visible pulsations
o Remember you had already counted breathing per minute, now see if chest moves
symmetric with each respiration, any chest in drawing
o Precordial bulging and heave
• Palpation
o Lymph nodes of the axilla
o Locate the apex beat normal is at 4th or 5th (depending on the child’s age), palpate for
thrills (palpable murmur)
o Estimate tactile vocal fremitus (older child)
• Percussion
o Lung zones following the anatomical land marks, anteriorly, axillary and posteriorly
o Normal percussion note is resonance
• Auscultation
o Auscultate for breath sounds in each zone, anterior and posterior, taking note that you
compare the two sides simultaneously
ƒ Are they vesicular, or bronchial?
o Auscultate for any added sounds such as rhonchi, crepitations/crackles, murmurs,
transmitted sounds
o Auscultate for vocal resonance (older child)
o Count heart rate, use reference range for normal values
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Session 2: History Taking and Physical Examination 21
 o Auscultate for heart sounds, and report if 1st and 2nd heart sounds are heard and
normal or you hear a 3rd heart sound (Gallop rhythm)
o Auscultate the bases of the lungs for crepitations, (suggestive of congestive heart
failure)
o Auscultate for added sounds, murmurs

Abdomen
• Inspection
o Contour, distension, symmetry, umbilicus, any obvious lesion, movement with
respiration, dilated vessels, visible peristalsis or pulsations
• Palpation
o Tenderness, succession splash, masses, liver, spleen, kidneys (bimanual palpation),
bladder (describe the texture, size, location)
• Percussion (normal percussion note is tympanic)
o Masses, fluid
• Auscultation
o Bowel sounds
• Genitalia, groins, anus
o Inspect the penis, scrotum, and female genitalia if relevant
o Rectal examination when relevant (new born gently pass rectal thermometer to verify
patency of rectum)

Extremities/Upper and Lower Limbs

• Inspection
o General examination of arms and hands, legs and feet
• Palpation
o Finger nails (clubbing or koilonychias)
o Oedema of feet
o Pulse rate, rhythm, volume and character synchronize with other peripheral pulses
(e.g. radial of the other hand, femoral and dorsalis pedis)
o Note: capillary refill (should be < 2 seconds)
o Muscles (wasting, tone)
o Joint movement, tenderness or swelling

Neurological
• Neck stiffness and Kernig’s sign
• Cranial nerves
o Optic (2)
o Occulomotor (3)
ƒ Extraoccular muscles-normal action, cause pupilary constriction and muscles of
the eye lids
o Trochlear (4)
ƒ Extraoccular muscles-ability of the eye to look downward and laterally while -the
other look down wards and medially
o Abducens (6)
ƒ Extraoccular muscles-action is to enable the eye to look laterally, and horizontally
while the other moves medially
o Trigeminal (5)
o Facial nerve (7)

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Session 2: History Taking and Physical Examination 22
 ƒ Asymmetry of face when baby cries
o Vestibulocochlea (8) - for hearing
o Glossopharyngeal nerve (9) and Vagus (10)
ƒ When baby cries look at symmetry of the uvular for cranial nerve 9 and
swallowing without nasal regurgitation for cranial nerve 10
o Accesory (11) (lift shoulders for older children)
o Hypoglossal nerve (12th cranial)
ƒ Look when the baby protrudes the tough for symmetry of the tongue
• Muscle bulkiness
o Normal or reduced
• Muscle tone
o Check by lifting the child and feel for the resistance
• Muscle power (not easy for a baby)
• Examine for obvious abnormal movements such as choreiform, tics, etc
• Coordination –
o Can be checked by watching a child playing or tying shoe laces or pointing at
something and touching without missing
• Examination of the back for spinal deformity, swelling or mass
• Primitive reflexes
o Moro reflex
o Grasp
o Stepping
o Rooting
o Sucking
o Tonic neck
o Trunk incurvation
o Crossed extension
o Parachute
o Landau

Refer to Handout 2.1: Primitive Reflexes

Diagnosis and Investigations

Note: Definitions and formulation of provisional and differential diagnosis are covered in the
Clinical Skills module and the same definitions apply to paediatrics.

Specimens Specific to Paediatrics

• Sickling test
• Gastric aspirate:
o Appearance
o For Acid Fast Bacili (AFB)
o For Gram staining
o Culture and sensitivity
Note: Specimens to be collected are covered in the Clinical Skills module

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Session 2: History Taking and Physical Examination 23
Diagnosis
• After thorough history taking and appropriate examination, in 80% of cases a diagnosis
should be reached
• The details of how to reach a final diagnosis are covered in the Clinical Skills module

Key Points
• History taking is a medical practice which collects information from the patient or patient
care taker in order to make a diagnosis and know how to approach treatment and design.
• Involvement of the child in the conversation of history taking is important, provided that
the child is old enough to understand.
• In conducting physical exams, avoid of unnecessary exposure of the neonates and
children with severe malnutrition, because of hypothermia.
• Start with the least threatening manoeuvres avoiding annoying the child before finishing
your examination.

Evaluation
• What is important to remember during history taking in paediatrics?
• List components of general physical examination in paediatrics.
• What specimens are collected in paediatrics?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th Ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th Ed.) Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd Ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd Ed.) USA: Saunders.

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Session 2: History Taking and Physical Examination 24
 Handout 2.1: Primitive Reflexes

Motor
As in any neurologic examination, evaluate general tone (normal, hypotonic, or hypertonic)
and posture (normal, opisthotonic, decorticate, or decerebrate). Newborns generally maintain
a mildly flexed position of all four extremities. Posture may be asymmetric with preference to
one side, but tone should be normal. Look carefully for any evidence of focal weakness,
unilateral or bilateral. Refer to Chapter 12 for further detail.

Reflexes
Newborns are more reflexive than at any other stage of their lives. It is not entirely clear why,
but there are some anthropologic explanations, such as primitive survival or instinctive
preparation for fright/flight. Newborn reflexes are helpful for assessing spinal function, both
sensory and motor, but may be present and normal in newborns with anencephaly and thus
are not helpful for assessing cerebral damage. There have been more than 80 newborn
reflexes described. We will illustrate some of the more commonly used ones often described
as active reflexes. Abnormalities usually present with overreaction, under reaction, or
asymmetry.

Figure 1: Reflexes

Source: Stanfield & Bwibo., 2005

Suck. The baby will suck automatically if a finger or pacifier is placed in his or her mouth

Moro. After gently lifting the baby by the arms with the head still on the mattress, release
your grip so the baby’s back falls to the underlying surface. The baby will have a double
response—first, arm abduction and elbow extension and then arm adduction, elbow flexion,
and finger curling (FIGURE 5–10).

Startle. Often confused with the Moro reflex, elicit it similarly, but the baby will flex the
arms only and have a generalized startle. Repetition will habituate this response.

Grasp. The baby will automatically grasp onto anything placed in his or her hand.

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Session 2: History Taking and Physical Examination 25
Figure 2: Moro Response

Source: Stanfield & Bwibo., 2005

Moro Response

Tonic neck: When the infant is relaxed, turn the head to one side. The infant will assume the
en garde position with the arm that would hold the sword on the same side the head faces and
the other arm flexed and held up straight

Figure 3: Examples of Common Reflexes

Source: Stanfield & Bwibo., 2005

Traction: Place fingers in the infant’s palms. As he or she grasps, lifting the baby will elicit
elbow and neck flexion. Similarly, pulling the infant to a sitting position or raising the infant
from the supine position from the shoulders also will elicit neck flexion

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Session 2: History Taking and Physical Examination 26
Figure 4: Perez Response

Source: Stanfield & Bwibo., 2005

Perez response
Hold the infant in the prone position, grasping under the abdomen. Gentle rubbing up the
spine will elicit flexion of the extremities and extension of the neck. Similarly, elicit the
Vollmer response by rubbing down the spine, which will cause flexion of the lower
extremities and extension of the back.

Galant response
Hold infant in the prone position as in the Perez response, and rub lightly along the flank. The
baby will move his or her buttocks toward the ipsilateral side. This reflex is particularly
amusing to older siblings.

Figure 5: Magnet Response

Source: Stanfield & Bwibo., 2005

Magnet response: Grasp both heels and press the thumbs on balls of infant’s feet, thus
dorsiflexing them. The baby will extend the legs

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Session 2: History Taking and Physical Examination 27
Supporting reaction: Hold the infant upright with both hands around the thorax, and then
gently place both feet on the surface. The infant will attempt to extend both legs and
straighten the trunk.

Placing response: Similar to the supporting reaction, have the infant rub the dorsum of the
foot under the edge of a bassinet or a table top.

Figure 6: Stepping Response

Source: Stanfield & Bwibo., 2005

Stepping: Hold the infant upright with both feet on the surface of a table. Move the infant
from side to side to elicit stepping movements. This is the second-best reflex for an older
sibling’s amusement

Crossed extension reflex: With the infant lying supine, straighten out one leg at the knee,
and stroke the plantar surface of that foot with your other hand. The opposite leg should first
flex and then abduct, the toes will fan, and then the leg will extend and abduct, pointing its
foot toward the foot that was stroked.

Babinski reflex: Scratching the lateral aspect of the foot will elicit dorsiflexion of the big toe
and fanning of all the others Note that this sign reverts to normal (adult sign) when
corticospinal tracts are fully myelinated around 12-24 months of age.

Ankle clonus: Abruptly press your thumb on the ball of a foot to produce sudden
dorsiflexion. Normally, there should be fewer than five beats of clonus. Also note that there
are many tests for muscle tone that are passive. Examples are the scarf sign, the heel-to-ear
maneuver, the popliteal angle, and the wrist window. They also assess tone in gestational age
assessment

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Session 2: History Taking and Physical Examination 28
Figure 7: Stepping Response

Source: Stanfield & Bwibo., 2005

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Session 2: History Taking and Physical Examination 30
 Session 3: Upper Respiratory Tract
Learning Objectives
By the end of this session, students will be able to:
• List common upper respiratory tract infections in children
• Outline presenting features of upper respiratory tract infections
• Explain the main components in examination of the upper respiratory system of children
• Describe the management of laryngotracheobronchitis, whooping cough and otitis media
in children

Common Upper Respiratory Tract Infections

• Upper respiratory diseases are many, but only a few common diseases have been selected
and discussed in this manual.

Common Conditions
• Common cold
• Sinusitis
• Pharyngitis
• Laryngo-trachea-bronchitis (croup)
• Otitis media
• Tonsilitis
• Whooping cough

Common Presenting Features of Upper Respiratory Tract Infections

• The following are common presenting features of upper respiratory infections:
o Cough
o Difficulty breathing
o Stridor
o Tachycardia
o Runny nose/rhinorrhoea
o Fever/ High body temperature
o Mouth breathing
o Painful swallowing/refusal to feed and drooling
o Ear pain and discharge
o Headache
o Hoarseness of voice
o Cervical lymphadenitis

Main Components in the Examination of the Upper Respiratory System

• General examination
o Apart from suffering from the above features, a child with upper respiratory tract
infection may also show the following:
ƒ Toxic appearance
ƒ Cyanosis

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Session 3: Upper Respiratory Tract Infections 31
 ƒ Respiratory distress or breathlessness: signs of respiratory distress like tachypnoea
(count respiratory rate), apnoea, , nasal flaring, grunting, respiratory pattern
ƒ Red eyes
ƒ Enlarged and reddish tonsils, uvula, and pharynx
ƒ Barking cough
ƒ Swollen epiglottis, paroxysmal whoops or post-tussive vomiting
• Regional examination key points
o Inspection
ƒ Lower chest in drawing
ƒ Symmetry of the chest
ƒ Ear discharge
ƒ Tympanic Membrane appearance (if otoscope is available)
ƒ Running nose
ƒ Inspection of tonsils (red or with pus pockets)
o Palpation
ƒ Look for swelling or masses (e.g. enlarged lymph nodes)
ƒ Position of the trachea (in older children)
ƒ Apex beat /cardiac impulse
ƒ Any area of tenderness in the chest
ƒ Tactile vocal fremitus
o Percussion
ƒ Resonance
ƒ Dullness
ƒ Tenderness

Diagnosis and Investigation of the Upper Respiratory Tract Infections

Diagnosis
• History
o Breathlessness
o Cough,
o Change in voice
• Examination
o Throat
o Ears
o Nose
o Chest.
• Laboratory and imaging
o Sputum
o Blood
o Pus
o X-ray
o Laryngoscopy

Investigations
• Blood
o Full blood count
o Smear
• X-rays
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Session 3: Upper Respiratory Tract Infections 32
 o Sinuses,
o Adenoids
o Chest
• Throat/ nasal/ ear secretions or discharge (smear or culture)

Laryngotracheobronchitis

Causes
• It is predominantly caused by para influenza type 1 and 2 viruses
o Respiratory Syncytial Virus (RSV)
o Mycoplasma
o Measles
o Adenovirus

Clinical Presentation
• Age: 6 months to 3 years
• Symptoms of upper respiratory infections (common cold) lasts less than 5 days
• Cough (brassy and barking)
• Inspiratory stridor
• Respiratory distress may develop slowly or acutely
• Signs of upper airway of obstruction (drooling, stridor)
• Wheezing and productive cough may be present
• The subglottic space is a major site of obstruction which is caused by oedema resulting
from viral inflammation

Investigations
• Blood gases
• Full blood picture(FBP)
• Chest X-Ray
• Blood culture
• Serum electrolytes
• C- Reactive protein (CRP)
• Throat culture

Treatment
• Maintain airway
• Steam (a bed sheet of an infant bed makes a perfect steam tent)
• Nebulized adrenaline provides transient improvement by constricting local vessels and
reducing swelling and oedema
• Humidified oxygen
• Keep the child comfortable in a semi seated position
• Make sure the child drinks enough, if they can’t take feedings by mouth or nasogastric
tube, then IV fluids are indicated

Complications
• Pneumonia
• Ear infection
• Airway obstruction and death, although rare.
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Whooping Cough
Causes
• A prolonged, severe and distressing disease caused by Bordetella pertussis and Bordetella
parapertussis (this organism produces a milder form of the disease)
• The bacteria produce inflammation of the mucous membrane of the nose pharynx, larynx,
trachea and bronchi
• A thick stringy mucous is produced, which the child wants to get rid of by coughing
• The organism adheres to airway epithelial cells activating cytokines and stimulating
apoptosis
• This results in inflammation and cell necrosis, causing bronchitis, atelectasis and
bronchopneumonia

Three Stages of Illness

• Catarrhal stage (prodromal, preparoxysmal),
o Takes one to three weeks and is characterised by:
ƒ Rhinorrhea, conjuctival injection, lacrimation, mild cough, wheezing and low
grade fever
ƒ At this stage, diagnosis of pertussis usually is not considered because the
manifestation is similar to most non upper respiratory tract infections
• Paroxysmal stage (spasmodic cough),
o Takes two to four weeks and is characterized by:
ƒ Episodes of coughing increases in severity and frequency
ƒ Multiple coughs during expiration are followed by a sudden massive inspiration,
producing the whoop
ƒ The whoop may be absent in children younger than six month of age or in adults
ƒ Facial petecchiae and redness, venous engorgement, and cyanosis may be
prominent during the attack.
ƒ Vomiting after coughing
ƒ Paroxysms may produce anoxic encephalopathy
• Convalescent stage 2-4 weeks
o Takes two to four weeks and is characterized by:
ƒ Paroxysmal coughing and vomiting decrease in frequency and severity
ƒ Chronic cough may persist for months

Diagnosis
• Clinical findings and history are usually enough
• Pertussis is clinically suspected during the paroxysmal stage
• WBC: often leucocytosis or ‘leukemoid reaction’ (20,000-100,000/L) with absolute
lymphocytes, up to 90%
• Isolation of Bordetella pertussis from nasopharyngeal swab or nasal wash
• Chest X ray – perihilar infiltrates, atelectasis or emphysema

Complications
• Apnoea in very young infants and sudden death
• Pneumonia
• Atelectasis
• Intercurrent viral respiratory infection
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 3: Upper Respiratory Tract Infections 34
• Otitis media
• Chronic bronchiectasis
• Seizures, encephalopathy and neurologic sequelae
• Epistaxisis and sub-conjunctival bleeding
• Intracerebral bleeding
• Hypoglycaemia
• Malnutrition
• Rectal prolapse

Treatment
• Management of the disease is done by administering antibiotics and to provide supportive
therapy
o Preferred treatment is with a Macrolide antibiotic (Erythromycin, Azithromycin,
Clarithromycin) and alternatives are co-trimoxazole or chloramphenicol
o Typical beta-lactam antibiotics used for other respiratory bacterial infections
(Amoxicillin, Penicillin, Ceftriaxone) may not be NOT effective
o If treatment is started more than one week after the onset of symptoms, it is unlikely
to shorten the total duration of disease, but will decrease infectiousness
• Supportive therapy
o Oxygen may be needed for very young infants with severe attacks, especially during
the attack
o Feeding is very important.
ƒ Many small meals if the child has many paroxysmal attacks or continuous drip
feeding by nasogastric tube in severe cases
ƒ IV fluids may be needed if the child is vomiting much

Prevention
• Immunize against pertussis
• Give DPT-Hb-HiB immunization in a child not immunized
• Try to protect young infants from other coughing children
• Give erythromycin40-50 mg/kg/day in four divided doses (roughly 12.5 mg/kg every 6
hours) x 10 days to exposed infants less than 6 months

Follow Up
• The nutritional status should be carefully followed after discharge
• If the child is not recovering from pertussis within 2-3 months, send for assessment
• TB should be ruled out
• Whooping cough may be followed by habitual cough

Otitis Media
Causes
• Acute otitis media (AOM) is an infection of the middle ear with acute onset, presence of
middle ear effusion, and signs of middle ear inflammation
o Commonly caused by Pneumococcus species, Haemophilus influenzae (untypeable),
Moraxella species, rhinovirus and respiratory syncytial virus (RSV)
• Chronic suppurative otitis media involves a perforation of the tympanic membrane and
active bacterial infection within the middle ear space for several weeks or more

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 3: Upper Respiratory Tract Infections 35
 o There may be enough pus that it drains to the outside of the ear (otorrhea)

Clinical Presentation
• Children who can communicate complain of pain or discomfort in the affected ear,
however many young children are unable to communicate specific complaints
• History may reveal the following:
o Accompanying or precedent upper respiratory tract infection
o Earache
o Decreased hearing
o Fever (not required for the diagnosis)
o Otorrhea or ear discharge
o Infants may be asymptomatic or irritable
o Infants may present with pulling/tugging of the ear
o Physical
ƒ Visualization of the tympanic membrane with identification of a middle ear
effusion (MEE) and inflammatory changes is necessary to establish the diagnosis
of acute otitis media

Investigations
• No definitive laboratory tests or imaging studies exists for acute otitis media, but if there
is discharge a sample can be sent for smear and culture
• HIV screening is recommended for children with chronic recurrent suppurative otitis
media

Treatment
• For acute otitis media, children should receive antibiotics and appropriate analgesics
• Antibiotics commonly used are Gentamycin, chloramphenicol or Cirpofloxacin ear drops,
or systemic antibiotics such as Amoxyl (refer dosing for children)
• For chronic suppurative otitis media, dry ear wicking is recommended

Complications
• Hearing impairment
• Meningitis

Key Points
• Common respiratory tract diseases include the common cold, sinusitis, pharyngitis,
laryngotracheabronchitis (croup), otitis media, tonsilitis and whooping cough.
• Common presenting symptoms are cough, difficulty breathing, stridor, rhinorrhoea and
fever.
• Laryngotracheobronchitis is the upper respiratory tract disease which is caused by variety
of viruses.
• Whooping cough is very contagious disease spread by droplets from infected children.
• Immunization of all children is essential to prevent the occurrence of whooping cough in
the community.
• Complications of otitis media are meningitis and, in the long term, hearing impairment.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 3: Upper Respiratory Tract Infections 36
Evaluation
• What are the most common upper respiratory infections in children?
• What are the most common presenting features of upper respiratory infections?
• How can whooping cough be prevented in the community?
• What are the most common complications of laryngotracheobronchitis?
• How is chronic suppurative otitis media managed?
• What are the common complications of otitis media?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.) Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 3: Upper Respiratory Tract Infections 37
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 3: Upper Respiratory Tract Infections 38
 Session 4: Pneumonia
Learning Objectives
By the end of this session, students are expected to be able to:
• Define pneumonia
• Identify the clinical features of pneumonia in paediatrics
• Identify the causative organisms of pneumonia
• Formulate the diagnosis of pneumonia in paediatrics
• Identify treatment of pneumonia in paediatrics
• Identify complications of pneumonia

Definition of Terms
• Pneumonia: An infection of lower respiratory tract characterized by inflammation of the
lung parenchyma with consolidation of alveoli
• Causative organism depending on age:
o Neonates < 1 month – group B streptococci, E. Coli, Klebsiella, Chlamydia
trachomatis
o Infants
ƒ Viruses: RSV, adenovirus, measles virus
ƒ HIV and AIDS-related: Lymphoid Interstitial Pneumonitis (LIP), Pneumocystis
jiroveci Pneumonia (PCP/PJP)
ƒ Bacteria and fungi: Streptococci pneumoniae, Haemophilus influenza
o Children
ƒ Bacterial: Streptococcus pneumoniae, Hemophilus influenzae, Group A
streptococci, Mycoplasma pneumoniae
ƒ HIV and AIDS-related: Lymphoid Interstitial Pneumonitis (LIP), Pneumocystis
jiroveci Pneumonia (PCP/PJP)
ƒ Secondary pneumonia

Clinical Features of Pneumonia

• Usually following a Upper Respiratory Tract Infection (UTRI) the patient develops
worsening fever, cough or difficulty in breathing
• Tachypnea (fast breathing) is a key sign
• Tachycardia
• Fever
• Refusal to feeding
• The classic signs of consolidation might be present but they are difficult to detect in
infants, crepitations/crackles might be present
• In bacterial pneumonia, pleural inflammation causing chest or abdominal pain and an
effusion may develop

Diagnosis of Pneumonia
• Based on clinical presentation
• Chest X-ray
o Not needed if diagnosis is clear and the patient responds to treatment
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 4: Pneumonia 39
 o Needed in complications and treatment failure:
ƒ Effusion
ƒ Pneumatocele
ƒ Abscess, TB (to be considered)
• Blood
o A full blood count (FBC) not needed, but repeated ESR and Hb show the progress of
recovery
o Blood culture
o Repeated blood culture when sepsis is suspected
• Mantoux Test
o If poor response to treatment always consider Tuberculosis (TB)
o Mantoux test is not very sensitive in active pulmonary Tuberculosis (TB)
• Gastric/nasopharyngeal aspirate
o For Acid-fast bacilli stain (AFB), preferred method to diagnose TB
o One may also take this opportunity to do a Gram stain

Note: Young children are unable to produce sputum and definitive diagnosis of bacterial
infection remains difficult. The following suggest bacterial pneumonia: polymorphonuclear
leucocytosis, lobar consolidation and pleural effusion.

Activity: IMCI Part I Video Segment

Instructions
The tutor will show a short video segment entitled ‘Counting respiratory rate in a child with
cough or difficult breathing’. Take notes of key issues during the video, note down any
questions and ask for clarification during discussion.

Treatment of Pneumonia

• Treatment of pneumonia depends on severity, causative organism and age of the patient.

Refer to Handout 4.1: Classification of the Severity of Pneumonia and Treatment

Complications of Pneumonia
• Abscess formation
• Pleural involvement: pleural effusion or empyema
• Lung collapse (atelectasis)
• Pneumothorax
• Bronchiectasis
• Cardiac failure
• Septicaemia
• Meningitis

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 4: Pneumonia 40
Key Points
• Pneumonia is a disease of the lower respiratory tract which affects the lungs.
• The organisms causing pneumonia depend on the age of the child.
• The key feature of pneumonia is fast respiratory rate.
• Diagnosis of pneumonia is mainly clinical.
• Treatment depends on severity and age of the child.

Evaluation
• Define the term pneumonia.
• List the common causative organisms for pneumonia in paediatrics.
• What are the common presenting features of pneumonia in paediatrics?
• What are the complications of pneumonia?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.) Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 4: Pneumonia 41
 Handout 4.1:Classification of the Severity of Pneumonia

Signs and symptoms Classification Treatment

Manage Airway
Oxygen- use nasal prongs or nasal
catheter or a nasopharyngeal catheter
Antibiotics – benzyl penicillin
200mg/kg in 4 divided doses
Central cyanosis
Very severe Add chloramphenical 100mg/kg in 4
Severe respiratory distress
pneumonia divided doses or ampicillin 200mg/kg
Not able to drink
in 4 divided doses or Cefuroxime
Gentamicin 5mg/kg once per day
plus Ampicillin especially to children
below 6 months
Treat high fever with Paracetamol
15mg/dose
Manage Airway
Antibiotics benzyl penicillin
200mg/kg in 4 divided doses
Add chloramphenical 100mg/kg in 4
Lower chest in drawing Severe pneumonia divided doses or ampicillin 200mg/kg
in 4 divided doses or Cefuroxime

Treat high fever with Paracetamol

15mg/dose
Antibiotics amoxicillin (15 mg/kg
Fast breathing Age three times a day or cotrimoxazole
= > 60/min < 2 mo 48mg/kg or penicillin (PPF) 50,000
Pneumonia
= > 50/min 2 <12 mo I.U/kg I.M for 5 days
= > 40/min 1-5 yr Sooth the throat with safe remedy
F up in 2 days
Home care
No signs of pneumonia or
No pneumonia, Soothe throat with safe remedy
severe or very severe
cough or cold Advice the mother when to return
F up in 5 days
Any general danger sign
or chest in draining or
stridor in calm child Severe pneumonia Give first dose of an appropriate
( With or without wheeze with wheezing or antibiotic IM
after a trial of very severe disease Refer urgently to hospital
bronchodilator up to 3
cycles)

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 4: Pneumonia 42
 Give an appropriate oral antibiotic
for 5 days
Give an inhaled or oral bronchial
Fast breathing
dilator for 5 days
(With or without wheeze
Pneumonia with Soothe the throat and relieve the
after trial of
wheezing cough with a safe remedy
bronchodilator up to 3
If coughing for more than 14 day
cycles)
refer for assessment
If recurrent wheezing refer for an
assessment

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 4: Pneumonia 43
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 4: Pneumonia 44
 Session 5: Bronchial Asthma and Bronchiolitis
Learning Objectives
By the end of this session, students are expected to be able to:
• Define the terms bronchial asthma and bronchiolitis
• Describe the epidemiology of bronchial asthma and bronchiolitis
• Discuss the clinical presentation of bronchial asthma and bronchiolitis
• Describe diagnosis of bronchial asthma and bronchiolitis
• Explain the treatment of bronchial asthma and bronchiolitis
• List complications of bronchial asthma and bronchiolitis

Definition and Epidemiology of Bronchial Asthma

• Bronchial Asthma: A chronic obstructive disorder of the airways characterized by
bronchospasm and inflammation, which occur in response to a variety of stimuli
• Characterized by recurrent episodes of wheezing often associated with cough
• Symptoms may be reversible spontaneously or with treatment

Epidemiology
• Asthma is a common chronic disease, causing considerable morbidity
• Many asthma deaths could probably have been avoided
• Asthma is generally an under diagnosed and undertreated condition
• Asthma prevalence correlates well with reported allergic rhinoconjunctivitis and atopic
eczema prevalence
• Approximately 80% of asthmatics report disease onset before 6 years of age

Risk Factors, Clinical Features and Diagnosis of Asthma

• Risk factors
o Family history or coexisting atopy
o Male sex
o Parental smoking
o Hospitalized for bronchiolitis in infancy
• Triggering factors
o Allergens/irritants
o Cold weather
o Dust
o Exercise
o Stress
o Infection of the upper air way

Clinical Features
• The child becomes anxious, restless and cyanotic, prefers a half sitting position and
perspires heavily
• Tachycardia, tachypnoea, cough
• Hyperventilation of the chest
• Lower chest wall indrawing
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 45
• Prolonged expiration with audible wheeze
• As the condition becomes worst, there will be:
o Use of accessory muscles of respiration
o Reduced air intake to the lungs
o Reduced wheezing
o Inability to speak
o Tripod sitting position
o Diaphoresis
o Pulsus paradoxus

Diagnosis and Differential Diagnosis

• Diagnosis is made following compatible clinical presentation and the below
investigations
o Lung function test (spirometry or peak flow meter)
o Radiological (acute attack presents with hyper-inflated lungs)
o Arterial blood gases
o Blood and sputum eosinophils
• Differential diagnosis
o Viral bronchiolitis or other pulmonary infection
o Aspiration
o Air flow obstruction
ƒ Laryngotracheomalacia
ƒ Vascular ring,
ƒ Airway stenosis
ƒ Mediastinal mass
ƒ Foreign body
ƒ Vocal cord dysfunction
o Bronchopulmonary dysplasia, obliterative bronchiolitis
o Chronic congestive heart failure with ‘cardiac asthma’

Treatment of Bronchial Asthma

• The overall goal of therapy is to reverse the symptoms
• The secondary goal is to prevent or diminish the frequency of recurrence and to maintain
normal pulmonary functions
• The treatment of asthma in children is divided into 4 main components:
o Patient education
o Assessment and monitoring of asthma severity with objective measures of the lung
function
o Avoidance or control of asthma triggers
o Establishing a comprehensive plan of pharmacological therapy and how to manage
exacerbations

Management In-between Attacks

• All upper airway infections are to be well treated to prevent a possible attack
• Irritation by cold environment and smoke should be avoided
• Children should sleep in a dust free environment
• In persistent asthma, it may be necessary to give a child long term steroid therapy,
preferably beclomethasone dipropionate, 100 micrograms 2 to 4 times in 24 hours

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 46
Management During Attacks
• A child with the first episode of wheezing and no respiratory distress can usually be
managed at home with only supportive care, a bronchodilator is not needed
• A child with respiratory distress or has wheezing, give salbutamol by nebulizer or
metered -dose inhaler, if salbutamol is not available then give subcutaneous epinephrine
• Reassess the child after 30 minutes to determine subsequent treatment
o If the distress is still present, admit and treat the child with rapidly acting
bronchodilators and oxygen
o Give oxygen to all children who are cyanosed or if there is difficulty breathing which
interferes with talking
Refer to Handout 5.1: How to Administer Oxygen

• Short-acting, selective beta2-adrenoceptor agonists, such as salbutamol, terbutaline and

bitolterol
• Currently available long-acting beta2-adrenoceptor agonists include salmeterol,
formoterol, bambuterol, and sustained-release oral albuterol
o Tremors, the major side effect, have been greatly reduced by inhaled delivery, which
allows the drug to target the lungs specifically
• Older, less selective adrenergic agonists, such as inhaled epinephrine and ephedrine
tablets, have also been used
o Cardiac side effects occur with these agents at either similar or lesser rates to albuterol
• Anticholinergic medications, such as ipratropium bromide may be used instead
o They have no cardiac side effects and thus can be used in patients with heart disease
o They take up to an hour to achieve their full effect and are not as powerful as β2-
adrenoreceptor agonists
• Inhaled glucocorticoids are usually considered preventive medications, while oral
glucocorticoids are often used to supplement treatment of a severe attack

Refer to Handout 5.2: How to Give Rapid Acting Bronchodilators

Supportive Care
• Position
o Let the child be in the most comfortable sitting position
• Fluid
o Children with respiratory distress need maintenance IV fluids
• Feed by NGT
• Parent counselling and education
• General nursing care

Definition and Epidemiology of Bronchiolitis

• Bronchiolitis: A viral infection of the lower respiratory tract (bronchioles) that produces
obstruction of the small airways due to oedema with air trapping, resulting in respiratory
difficulty in infants
• Respiratory syncytial virus (RSV) is the major cause in > 90% of infants
• Other causes include:
o Parainfluenza virus
o Adenoviruses

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 47
 o Measles virus
o Bacteria invasion may occur

Epidemiology
• Bronchiolitis is a common illness of young children
• Approximately 50% of children have this illness during the first 2 years of life
• The infection is so severe in young infants that it occurs in epidemics

Clinical Presentation, Diagnosis and Differential Diagnosis of Bronchiolitis

Clinical Presentation
• Starts with upper respiratory infections (rhinorrhea, sneezing, cough and low grade fever)
• Wheezing that is not relieved by up to three doses of bronchodilator
• Hyperventilation of the chest, with increased resonance to percussion
• Lower chest wall indrawing
• Fine crackles or rhonchi on auscultation of the chest
• Difficulty feeding
• Nasal flaring
• Grunting in young infants
• Convulsions, lethargy or unconsciousness
• Acute symptoms last 5-6 days; recovery is complete in 10-14 days

Diagnosis
• Diagnosis is made based on the findings obtained from the history and examination, and
results of the following investigations:
o Blood gases
o Full blood picture(FBP)
o Chest X-ray (air trapping, peribronchial thickening, atelectasis, increased linear
markings)
o Nasopharyngeal swab

Differential Diagnosis
• Acute asthma, associated with viral lower respiratory infection
• Congestive heart failure
• Pneumothorax
• Pneumonia
• Inhaled foreign body
• Pertussis

Treatment and Complications of Bronchiolitis

• Ensure ABCs
• Oxygen therapy to maintain oxygen saturation at ≥ 95%
o Give oxygen 2 L/min by nasal prongs, facemask or head box (or O2 tent)
o Use humidified oxygen with nebulizer where possible
o Continuous monitoring is recommended if supplemental oxygen is required
• Fluid therapy
o Give IV fluids in the following conditions:
ƒ Moderate-to-severe or severe respiratory distress
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 48
 ƒ Tachypnoea (with RR >60/min)
ƒ Apnoeic episodes
ƒ Tiring during feeds
ƒ Generally use normal maintenance volumes, N/2 or N/4 dextrose saline
ƒ Increase fluid volumes (by up to 20%) if there is frequent fever (>38.5°C) and/or
marked increased respiratory effort
• Drugs
o Generally don’t use bronchodilators in infants less than 6 months of age
o If asthma is considered a possibility in infants aged 6 to 12 months, give a standard
start dose for bronchial asthma and observe the response (see treatment of asthma), if
responds, continue treatment as asthmatic
o Don’t use corticosteroids except: in older infants when asthma is considered a
substantial possibility, in infants with chronic neonatal lung disease, or when
condition of the patient is worsening
ƒ Generally don’t use antibiotics except in children with gross CXR changes, high
persistent fever or child is severely sick and toxic
o The following treatment modalities are not indicated
ƒ Oral antihistamines
ƒ Oral decongestants
ƒ Cool mist
ƒ Chest physiotherapy
• Feeding by NGT
• Parent counselling and education
• General nursing care
• Supportive treatment suffices in most healthy infants including humidity, fluids, and
removal of secretions
• Respiratory distress may require oxygen therapy, intravenous fluids, frequent suctioning
of secretions
• Bronchodilators and corticosteroids are used in severely distressed infants

Complications
• Apnoea
• Respiratory failure
• Atelectasis
• Otitis media
• Secondary bacterial infection
• Pneumothorax
• Pneumomediastinum

Key Points
• Asthma is a common chronic upper airway disease in children.
• The disease can be life threatening if not properly managed.
• Severe acute and life threatening asthma is associated with infections, so you should add
IV antibiotic(s) in the line of management.
• Bronchiolitis is a result of obstruction of the small airways due to oedema with air
trapping.
• Respiratory syncytial virus is the major cause of bronchiolitis in > 90% of infants.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 49
• The common presenting features of asthma and bronchiolitis are signs of URI and
wheeze.
• Treatment of severe bronchiolitis includes oxygen therapy to maintain oxygen saturation
at ≥ 95%.

Evaluation
• What do the terms bronchial asthma and bronchioliltis mean?
• What are the common clinical presentations of bronchial asthma and bronchiolitis?
• Describe diagnosis of bronchial asthma and bronchiolitis.
• How is bronchial asthma and bronchiolitis treated?
• What are the complications of bronchial asthma and bronchiolitis?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.) Cape Town, South Africa: Oxford University
Press.
• MOHSW, WHO & UNICEF (2000). IMCI: Management of the Child with a Serious
Infection or Severe Malnutrition, Guidelines for Care at the First-referral Level. Dar es
Salaam, Tanzania: Ministry of Health and Social Welfare.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 50
 Handout 5.1: How to Administer Oxygen

General Principals
Oxygen should be considered as a drug and only be given on the right indication and in the
right concentration! Especially to LBW children, where retrolental fibroplasia is a major
cause of blindness and must be avoided.

Methods of Oxygen Administration

• Low flow oxygen through a nasal catheter
o A flow of pre-warmed and humidified oxygen is passed through a nasal catheter into
the pharynx
o The catheter should be inserted several centimetres into the nose

Flow of Oxygen (litres/min) Fraction Oxygen (in %)

0.1 25%
0.2 30%
0.5 40%
1.0 50%

Figure 1: Low Flow Oxygen Through a Nasal Catheter

Source: MOHSW, 2000

• Oxygen by Mask
o If loosely fitted and covering both nose and mouth almost 100% oxygen can be given
at 5 litres/min
o Oxygen by mask at some distance is very unreliable and insufficient

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 51
Figure 2: Oxygen by Mask

Source: MOHSW, 2000

• Oxygen into a headbox

o A steadily high concentration can be achieved if oxygen is passed into a headbox kept
over the head of the baby
o The environmental oxygen concentration should be slightly above the concentration at
which the child becomes pale-cyanotic
o If arterial blood gasses are possible to measure, use this to conduct the therapy
o More oxygen (5 l/min) is consumed when given via a head box than when it is given
through a nasal catheter
o Closely monitor the child and reduce the amount of oxygen as the child gets better

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 52
 Handout 5.2: How to Give Rapid Acting Bronchodilators

Acute Asthmatic Attack

Drug Dose Indications
2 puffs in spacer regardless of
Salbutamol spray First line drug, if available
age, 3-4 times/day
For 0.10-0.15 mg/kg/dose
Salbutamol nebulization dilute with 2 ml normal saline First line drug, if available
may be given 4 hourly

Parenteral/oral
Drug Dose Remarks
0.015 mg/kg per dose
in 1:1000 (1 mg/ml) solution
Adrenaline First line drug if salbutamol for inhalation
Usually 0.2-0.4 mg SC
(Epinephrine) is not available
May be repeated after 30-60
minutes 2-3 times
Loading dose (if not pre-
treated with aminophylline):
6 mg/kg IV slowly over 10
If salbutamol and adrenaline effects are
minutes
insufficient
Aminophylline Maintenance dose:
0.9 mg/kg/h IV
Supervision of the drip must be meticulous
Aminophylline drip for 3 hrs: 2, 7
mg/kg in 5% dextrose 20 ml/kg.
Speed 2 drops/kg/min
Addition for severe cases only
5mg/kg/dose IV
Hydrocortisone No effect in bronchiolitis
May be repeated every 6 h for 1-
or Effect after several hours only
2 days
Prednisolone If you can stop within 1 week no tapering
1-2 mg/kg/day orally for 7days
off needed
Refer to information on ARI- In case of fever, clear infectious component
Antibiotics
Pneumonia or bronchopneumonia

Long Term Treatment Of Asthma

0.3 mg/kg/d in 3 doses orally as maintenance. If available,
Salbutamol
salbutamol for inhalation is even better. See above.

If Not Enough Response: ADD Corticosteroids for a Short Period

1 - 2 mg/kg/d once daily oral dose 1 - 3 weeks, to avoid side
Prednisolone effect. Withdraw gradually (several weeks) if given more than
1 week. If given for less than one week, OK to stop abruptly.
Inhaled steroid twice daily for 3 months, then evaluate. Rinse
Budesonide or similar mouth after spraying to prevent oral thrush. If available,
introduce it early in the treatment plan.
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 53
If Still Not Enough Response: ADD
1- 2 yr. age: 16 mg/kg/d in 3 doses orally
3- 6 yr. age: 13 mg/kg/d in 3 doses orally
Theophylline
7 -12 yr. age: 10 mg/kg/d in 3 doses orally
older: 8 mg/kg/d

Note: Ephedrine is a much less effective drug than those above.

Dose 3 mg/kg/day in 3 doses orally.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 5: Bronchial Asthma and Bronchiolitis 54
 Session 6: Childhood Tuberculosis
Learning Objectives
By the end of this session, students are expected to be able to:
• Describe childhood tuberculosis
• Explain the presenting features of childhood tuberculosis
• Use the score chart to diagnose childhood tuberculosis
• Explain the treatment of childhood tuberculosis
• Name the complications of childhood tuberculosis
• Explain the prevention of childhood tuberculosis

Overview
• Tuberculosis (TB) is a granulomatous inflammatory condition, and is the most common
cause of infection-related death worldwide
• In 1993, the World Health Organization (WHO) declared TB to be a global public health
emergency
• Mycobacterium tuberculosis is the most common cause of TB in both adults and children
o Other rare causes are Mycobacterium bovis and Mycobacterium africanum
o The proportion of both paediatric and adults TB cases caused by M. bovis is very low
and is generally associated with close contact with cattle
• TB equally affects children of both genders, but an increased risk of mortality exists at the
extremes of age
o Young children and especially newborns are at a high life risk when they are exposed
to a contagious source
• In about 95 % of cases, TB is an airborne disease
• Development of the disease depends much on the competence of the immune system to
resist multiplication of the organisms
o The immune competence depends on age, nutritional status, coexisting infections like
HIV/AIDS, measles, and whooping cough
• TB most commonly attacks the lungs (as pulmonary TB), but can also affect the CNS,
lymphatic system, circulatory system, the GUS, bones, joints and even the skin
• Internationally, according to the WHO, more than 8 million new cases of TB occur each
year
• The incidence and prevalence of paediatric TB worldwide varies according to the burden
of the disease in different countries
• It has been estimated that 3.1 million children under 15 years of age are infected with TB
worldwide
• According to the WHO, children with TB represent 10 % to 20 % of all TB cases
o The majority of these cases occur in low-income countries where the prevalence of
HIV and AIDS is high
• The WHO states over 250,000 children develop TB annually and 100,000 children will
continue to die each year from TB

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 55
Clinical Features
• Chronic cough for 14 days or more
• Positive history of TB contact (especially with a positive sputum smear)
• Suspected HIV or AIDS
• Prolonged fever
• Failure to thrive
• Cases of malnutrition, failing to respond to adequate nutritional, and anti-infective
treatment
• Failure to return to health after infections, particularly after measles, whooping cough or
streptococcal infection

Localizing Signs and Symptoms

• Chronic cough, respiratory wheezing and wasting
• Febrile illness with pleural pain and effusion
• Pneumonia not improving in spite of adequate treatment
• Chronic swelling of lymph nodes with or without drainage
• Abdominal swelling with ascites
• Signs of heart failure with pericardial effusion
• Chronic painful swelling in a weight-bearing joint
• Refusal to bend, stiff painful back, spinal deformity and paraplegia may indicate TB spine
(Pott’s disease)
• Unexplained change of temperament, irritability, fever, vomiting, headache, convulsions,
meningeal signs, cranial nerve involvement and finally paralysis and coma-may indicate
TB meningitis
• Signs of space occupying intracranial tumour
• Painless haematuria or sterile pyuria

Disseminated TB
• Although the usual site of tuberculosis is the lungs, other organs can be involved
(disseminated TB)
• This develops in small number of infected people whose immune systems do not
successfully contain the primary infection into the primary focus
• Disseminated disease can occur within weeks after the primary infection, or may lie
dormant for years before causing illness
• Infants, the elderly, those infected with HIV and those who take immune-suppressing
medications are at higher risk for the disease worsening, because of their weaker immune
systems
• In disseminated disease, organs and tissues affected can include:
o Bones and joints
o Bronchus
o Cervical lymph nodes
o Eye
o Larynx (voice box)
o Lining of the abdominal cavity (peritoneum)
o Lining of the brain and spinal cord (meninges)
o Lining of the heart (pericardium)
o Organs of the male or female urinary and reproductive systems

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 56
 o Skin
o Small bowel
o Stomach

Tuberculous Adenitis
• TB lymphadenitis (TB adenitis) is the inflammation and/or enlargement of a lymph node
in response to local, or generalized TB infections
• Tuberculous adenitis may affect a single node or a localized group of nodes (regional
adenopathy) and may be unilateral or bilateral
• Tuberculous adenitis presents as painless swelling of the lymph nodes most commonly at
cervical and supraclavicular sites
• Lymph nodes are usually discrete in early disease but later become matted together
• May be inflamed and have a fistulous tract draining caseous material
• Systemic symptoms are usually limited to HIV-infected patients, and concomitant lung
disease may or may not be present
• The diagnosis is established by fine-needle aspiration or surgical biopsy
• Acid fast bacilli (AFB) are seen in up to 50% of cases
• Cultures are positive in 70-80%

Tuberculous Arthritis
• Chronic arthritis caused by extra pulmonary TB
• Presents with the following specific features in addition to the above general features:
o Limping
o Non-tender swollen joint

Tuberculous Osteomyelitis
• This refers to infection of the bone by M. tuberculosis
• Involves mainly the thoracic and lumbar vertebrae (known as Pott's disease) followed by
knee and hip
• Clinically, there may be extensive necrosis and bony destruction with compressed
fractures (with kyphosis) and extension to soft tissues, including psoas "cold" abscess

Tuberculous (TB) meningitis

• Occurs when tuberculosis bacteria (M. tuberculosis ) invade the membranes and fluid
surrounding the brain and spinal cord
• The infection usually begins elsewhere in the body, usually in the lungs, and then travels
through the bloodstream to the meninges where small abscesses (called microtubercles)
are formed and when these abscesses burst, TB meningitis results
• Fever and headache are the cardinal features
• Confusion is a late feature and coma bears a poor prognosis
• Meningism is absent in a fifth of patients with TB meningitis. Patients may also have
focal neurological deficits
• In areas where TB prevalence is high, TB meningitis is most common in children aged 0 -
4 years, and in areas where TB prevalence is low, most cases of TB meningitis are in
adults

Refer to Handout 6.1: Score Chart for Diagnosis of Tuberculosis in Children

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 57
Important Points to Remember
• A history of a positive TB contact is a very positive marker
• Only 15% of TB children have a positive smear, so a negative smear does not exclude
pulmonary TB (PTB)
• There are no typical radiological features for PTB

Tuberculin Test
• The Mantoux test is performed by intradermal injection of 5 TU = 0.1 ml 1:2.000 diluted
OT or 0.1 ml PPD (strength 0.0001 mg per dose) with a special Mantoux syringe
• Read after 72 hours depending on the solution used
• Measure the diameter of the induration
o Less than 10 mm: negative
o 10 mm or more: positive (if the child did not receive BCG vaccine)
o At least 15mm: positive (if the child did receive BCG vaccine)
• A negative test does not exclude tuberculosis infection or disease:
o If the test is performed before the hypersensitivity has developed (may take 10 weeks
after infection)
o If the child is anergic after measles, in severe malnutrition, during steroid or cytotoxic
drug therapy or in miliary tuberculosis or HIV/AIDS
o An unequivocal (6-10 mm) reaction may occur in atypical mycobacterial infections
and within 3 years after BCG.
• Note: Prior BCG vaccination is not a good reason to omit a Mantoux test if TB is
suspected
• Gastric aspirate/ Sputum
o Smear for AFB
o Culture for Mycobacterium
• X-ray
o Serial X-ray of lungs (if not too expensive) is more helpful than only one
examination, primary focus may be difficult to see
o Common X-ray findings: enlarged lymph nodes, effusion, cavitation, consolidation,
atelectasis, calcification, miliary "snowstorm" appearance
o X-ray of abdomen may show calcified lymph nodes in abdominal TB

Other examinations
• Blood- FBP and ESR
• Urine in selected cases
• CSF in selected cases (low sugar plus lymphocytosis in meningitis)
• Biopsy of lymph node, synovial, bone-marrow, pleura
• Ophthalmoscopy- choroidal tubercles often present in miliary TB
• Ascitic tap for suspected abdominal TB with ascitis
• X-ray of the spine for spinal TB, collapsed intervertebral discs

Treatment
• Give a full course of treatment to all confirmed or highly suspected cases
• When there is doubt (e.g. when the child is highly suspected or a child fails to respond to
other likely diagnoses)
• Follow National guidelines for treatment of TB as shown below
• Precaution: Avoid streptomycin in children as the injections are painful and there is a
risk for irreversible damage to the auditory nerve

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 58
 Refer to Handout 6.2: Drugs Used to Treat TB

TB Treatment Categories

Figure 1: TB Treatment Categories

New sputum smear, positive PTB and severe
Category 1
forms of EPTB
Relapse, treatment failure and sputum smear
Category II
positive return after default
New Sputum smear negative and EPTB (less
Category III
severe)
Category IV Chronic cases

• Less severe extra-pulmonary TB: lymph node, bone (other than spine), unilateral
pleural effusion, peripheral joint and adrenal gland.
• Severe extra-pulmonary TB: meningitis, miliary, pericarditis, bilateral or extensive
unilateral effusion, spinal, intestinal and genito-urinary tract
• Most children diagnosed to have tuberculosis are treated as category III

Figure 2: Dose-bodyweight Relation for Patient Treated with Category III Regimen
ADULT
CHILD
Duration of Pre-treatment
Drugs Pre-treatment weight
Treatment weight
5-10 kg 11-20 kg 21-30 kg 31-50 kg >50 kg
2 months
RHZE
intensive phase, ½ tablet 1 tablet 2 tablet 3 tablet 4 tablet
150/75/4
daily observed
00/275
4 months
continuation
phase, daily
RH
observed ½ tablet 1 tablet 2 tablet 3 tablet 4 tablet
150/75
OR
EH
6 months ¼ tablet ½ tablet 1 tablet 2 tablet 2 tablet
400/150
continuation,
monthly supply,
self administered
Source: MOHSW, 2006.

Note: The 2RHZE/4RH regimen requires daily observed treatment by a health worker or by
treatment supporter throughout the 6 months duration.

Complications of Tuberculosis
• Pleurisy with or without pleural effusion
• Pneumothorax
• Empyema

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 59
• Respiratory failure
• Right ventricular failure
• Fungal colonization of the cavities (e.g Aspergilloma)
• Blood borne dissemination

Prevention
• Early detection and treatment of all TB cases as soon as possible
• Making sure that all patients are compliant with their treatment
• Contact tracing by investigating all family members and other close contacts
• Isolating all sputum – positive open TB cases as far as possible
• Avoiding overcrowding and improving housing conditions
• Separation and isolation of suspected TB cases in hospital (TB infection control)
• Isoniazid preventive therapy for children exposed to TB
• Child spacing advices to mothers who have active TB
• Drink only pasteurized or properly boiled milk
• Ensuring BCG immunization is done to all under five year olds
o BCG is contraindicated for children with symptomatic HIV disease or AIDS
• Improving nutritional status of all families and communities
• Giving education to the community on how the disease is spread

Key Points
• Childhood TB infection is widespread, but development of disease depends much on the
immune status of the child.
• Immunization by BCG is essential to prevent severe form of the disease and disease
progression but BCG vaccination does not prevent pulmonary TB in older children and
adults
• Severe forms of the disease are seen in children with HIV/AIDS and malnutrition.
• Tuberculous adenitis is the most common form of extra pulmonary TB.

Evaluation
• What is the name of the organism causing tuberculosis?
• What are the common presenting features of childhood tuberculosis?
• How is childhood tuberculosis diagnosed?
• What are the common complications of childhood tuberculosis?
• What are the preventive measures of childhood tuberculosis?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.) Cape Town, South Africa: Oxford University
Press.
• NTLP. (2006). Tuberculosis Manual. (5th ed.) Dar es Salaam, Tanzania: Ministry of
Health and Social Welfare/National Tuberculosis and Leprosy Programme.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 60
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai M. et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 61
 Handout 6.1: Score Chart for Diagnosis of Tuberculosis in
Children
SCORE IF SIGN OR SYMPTOM IS PRESENT
Total
0 1 2 3 4
Score
GENERAL FEATURES
Duration of Less than More than 4
2-4 weeks
illness 2 weeks weeks
Failure to
Weight No weight Weight
thrive or
gain gain loss
weight loss
Reported Proven Smear+ Proven
TB contact None
not proven /EP Smear+
Tuberculin
Positive
test
Not improved
Malnutrition
after 4 weeks
Chronic
No response
infant Recurrent
to antibiotics
disease
LOCAL FEATURES
TB suggestive
feature like
Chest x-ray infiltration,
cavity or hilar
lymph nodes
Lymph Cervical, sub-
nodes mandibular
Swelling of Suggestive
bone or feature on X-
joint ray
Without With
Ascitis abdominal abdominal
mass mass
Chronic
Meningitis
C.N.S. signs
Angle
X-ray
deformity of
feature
the spine
TOTAL SCORE
MOHSW, 2006.

Note: A score of 9 or more indicates a high likelihood of tuberculosis

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 62
 Handout 6.2: Drugs Used to Treat TB

Drug Dose: Side Effects:

Isoniazid (H) Prophylactic: 5mg/kg
Good penetration into Curative: 10-(15 in severe
Neuropathy, rarely seen.
all tissues. cases) mg/kg/d, max 300-
Add Pyridoxine 2 mg/kg to
(R150 mg/H 100mg (500 severe inf.) mg, in one
malnourished children.
combination: oral dose. When given twice
Rimactazid) weekly 20-25 mg/kg/dose.
Streptomycin (S)
Damage to 8th cranial nerve (rare):
Is replaced by other
discontinue drug. Rash, fever:
drugs.
20-(30) mg/kg/d max 1 g reduce dose.
Can still be used in
One IM dose. Because of a general policy to
meningitis, miliary
discourage IM drugs in TB: not in
and bone TB during
general Tanzanian policy.
admission.
Hepatotoxicity rarely in children.
Rifampicin (R) 10-15 mg/kg/d max 600 mg
More common in combination with
Good penetration to one oral dose before
INH usually within the first 3
CNS. breakfast.
months of therapy.
Expensive. When given twice weekly
Leucopoenia, thrombocytopenia.
10-15 mg/kg/dose.
Body fluid may turn orange or red.
Hepatitis.
30 mg/kg/d, one oral dose,
Pyrazinamide (Z) Gastrointestinal reactions.
max 2 g.
Flu-like symptoms.
25 mg/kg/d for 8 weeks; then Retrobulbar neuritis, blurring
15 mg/kg/d (maintenance vision: in that case stop drug.
Ethambutol (E)
dose). Difficult to assess in preschool
Max dose 1 g, one oral dose. children.
MOHSW, 2006

Note: Steroid therapy given additional to anti-TB treatment is beneficial in TB meningitis,

pleural TB with large effusion and TB pericarditis. Dosage: 1-2mg/kg per day.
Although steroids are immune-suppressants they can be used in HIV positive patients as the
benefit outweighs the risk.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 63
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 6: Childhood Tuberculosis 64
 Session 7: Measles
Learning Objectives
By the end of this session, students are expected to be able to:
• Define measles
• Explain the pathogenesis of measles
• Describe the clinical presentation of measles
• Discuss the complications of measles
• Explain the management of measles
• Outline the preventive measures for measles

Definition and Pathogenesis

• This is an acute and highly contagious infection caused by measles virus
• The measles virus is a RNA virus
• Transmission occurs through airborne, respiratory secretions or close contact with
respiratory droplets from infected individuals
• The virus enters the body through the mucous membranes of the nasopharynx and
conjunctiva
• They may multiply, giving local reactions
• The viruses are then carried around in the bloodstream, finally reaching the skin (rash)
• Decreased immunity leads to increased susceptibility to complications from viruses
damaging the epithelial layer of the skin, digestive tract, respiratory tract, ears, eyes and
even the brain
• Secondary bacterial infections can occur

Clinical Presentation
• Incubation period takes 8-12 days from exposure to the onset of symptoms and 14 days
from exposure to the onset of rash
• The illness starts as a severe cold with high fever, cough, watery red eyes and nasal
discharge
• Prodromal phase takes 3 days, and it is characterised by cough, coryza, conjunctivitis
• Koplik spots are white spots, sand grain dot-sized in a red back ground on the mucous
membrane of the mouth, especially the inside the lips and cheeks opposite the lower
molars.
o These are pathognomonic for measles
• Rash phase
o Maculopapular rash appears on the 4th day
ƒ It dark red, slightly raised and irregular starts from the face, neck, and then
spreads all over the body
o The rash is difficult to see on a dark skin
ƒ Desquamation and depigmentation of the skin usually follows
o The rash phase is accompanied by high fever

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 7: Measles 65
Complications of Measles
• Complications are common and often cause death, especially in malnourished children
• Complications are also more common in immunosuppressed children (HIV, leukaemia)
• The common complications of measles are:
o Otitis media (common in infants)
o Bronchopneumonia
o Gastrointestinal symptoms/ viral gastroenteritis
o Myocarditis
o Activation of latent tuberculosis
o Keratitis
o Malnutrition
o Xerophthalmia
o Croup (laryngotracheobronchitis)
o Mouth ulcers
o Deep or extensive mouth ulcer (concrum oris)
o Encephalitis/ Encephalopathy (rare)
o Subacute sclerosing pan encephalitis is late neurologic complication of slow measles
infection, occurring years after the acute illness

Diagnosis of Measles
• History of fever, nasal discharge and red eyes
• Examination- koplik spots usually pathognomonic but are not always present at the time
of the most pronounced rash
• Chest X-ray in bronchopneumonia, if there is failure of treatment suspect TB
• In case of complicated measles the following can be seen:
o Diarrhoea (including dysentery and persistent diarrhoea)
o Pneumonia
o Stridor
o Mouth ulcers
o Ear infection and severe eye infection (which may lead to corneal ulceration and
blindness)
o Encephalitis

Management of Measles
• Admit to hospital for proper treatment if the child has:
o General danger signs such as lethargy, inability to drink, convulsions
o Malnutrition
o Bronchopneumonia, severe or very severe
o Laryngotracheobronchitis
o Dehydration, vomiting for more than 24 hours
o Xerophthalmia
o Other factors, such as anaemia
o Neutropenia below 1000/mm3 is a sign of serious condition
• Supportive care
o For fever give antipyretics if temperature >38.5oC
• Nutrition
o The most important part, especially in malnourished children
o Nasogastric tube may be needed
o Vitamin A should be given to all children with measles

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 7: Measles 66
 ƒ Vitamin A improves outcome in malnourished children
ƒ Dose: 100,000 I.U < 6 months, up to 200,000 I.U for children > 1 year
o Breastfeeding should be encouraged especially during illness
• Fluid
o Rehydrate dehydrated children
o Check daily for signs of dehydration in case of high fever and hyperventilation
o Increase the amount of maintenance fluid
• Antibiotics
o Treat all bacterial complications with antibiotics
• Treat pneumonia
o In early stages the cause is virus, later bacteria super infection
o Pneumonia is sometimes very severe
o Penicillin plus Gentamycin may then be tried
o Oxygen may be needed
• Treat otitis media
• Care of the mouth
o Clean the child's mouth with clean water 4 times a day
o Apply gentian violet (GV) 0.25% (½ strength GV paint) to sores
• Treatment of Laryngotracheobronchitis
o Maintain airway
o Steam, a bed sheet of an infant bed makes a perfect steam tent
o Nebulized adrenaline provides transient improvement by constricting local vessels
and reducing swelling and oedema
o Humidified oxygen
o Make sure the child drinks enough if can’t take small feedings by mouth or
nasogastric tube, IV fluids are indicated
o Decrease of mucosal swelling
ƒ Prednisolone 2mg/kg/day or hydrocortisone 100 mg IM (might be advantageous)
o Antibiotics (if bacterial infection is suspected)
ƒ Amoxyllin 15mg/kg/dose 8 hourly or chloramphenicol
• Care of eyes and skin
o Daily washing and inspection
o Secondary bacterial infection may require antibiotic eye ointment
• Treatment of encephalopathy
o Refer to hospital

Prevention of Measles
• Measles vaccine is highly effective, providing protection for roughly 95% of children
after a single dose
• Immunize against measles at 9 months, give simultaneously Vitamin A 100,000 IU
• Do not postpone immunization because of moderate intercurrent illness
• In case of measles contact immunize non-immunized children above 6 months on
admission (if 6-9 months on admission: make sure revaccination takes place at 9 months)
• Attend reproductive and child health (RCH) clinic for growth monitoring
• Ensure good nutrition, including vitamin A rich food
• Five days before and after the rash the child is still infectious
• Because respiratory transmission is very efficient, active cases of measles should be
isolated where possible, especially from immunocompromised individuals

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 7: Measles 67
 Refer to Handout 7.1: Immunization Schedule for Tanzania

Key Points
• Measles is highly a contagious disease.
• Measles needs to be treated aggressively as it can have fatal complications.
• Immunization of children is essential to prevent them from getting the disease.

Evaluation
• What is the causative agent for measles?
• How is measles spread in the community?
• What are clinical features of the disease?
• What are the treatment options for measles?
• What are the common complications of the disease?
• How can measles be prevented in the community?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.) Cape Town, South Africa: Oxford University
Press.
• MOHSW (2008). DTP-HepB-Hib: Expanded Programme on Immunization. Dar es
Salaam, Tanzania: Ministry of Health and Social Welfare.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 7: Measles 68
 Handout 7.1: Immunization Schedule For Tanzania

EPI IMMUNIZATION SCHEDULE

ANTIGEN DISEASE AGE DOSAGE SITE

BCG Tubercul At birth 0.05 ml Right

osis shoulder

1 year + 0.1 ml Right

shoulder

MOHSW, 2008

EPI IMMUNIZATION SCHEDULE

ANTIGEN DISEASE AGE DOSAG SITE
E
OPV 0 Polio At birth (0-14 2 drops Mouth
days)

OPV1 Polio 4 weeks after 2 drops Mouth

0 dose
OPV2 Polio 8 weeks after 2 drops Mouth
1 dose
OPV3 Polio 12 weeks after 2 drops Mouth
2 doses
6
MOHSW, 2008

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 7: Measles 69
 EPI IMMUNIZATION SCHEDULE - B
ANTIGEN DISEASE AGE DOSAGE SITE

DTP-HepB-Hib Diphtheria, 4 weeks 0.5 ml Left thigh

1st dose Tetanus,
Pertussis,
Hepatitis B
Haemophillus
Influenzae B
DTP-HepB-Hib Diphtheria, 8 weeks 0.5 ml Left thigh
2nd dose Tetanus,
Pertussis,
Hepatitis B,
Haemophillus
Influenzae B

DTP-HepB-Hib Diphtheria, 12 weeks 0.5 ml Left thigh

3rd dose Tetanus,
Pertussis,
Hepatitis B,
Haemophillus
Influenzae B
MOHSW, 2008

EPI IMMUNIZATION SCHEDULE

ANTIGEN DISEASE AGE DOSAGE SITE

Measles Measles 9 0.5 ml Right

months thigh

MOHSW, 2008

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 7: Measles 70
 Session 8: Chickenpox and Mumps
Learning Objectives
By the end of this session, students are expected to be able to:
• Name the causative agents for chickenpox and mumps
• Describe the clinical presentation of chickenpox and mumps
• Explain the diagnosis and treatment of chickenpox and mumps
• Describe the complications of chickenpox and mumps
• Explain the prevention of chickenpox and mumps

Overview of Chickenpox
• Chickenpox: A viral childhood disease caused by varicella zoster
• The virus infects susceptible individuals by the conjunctivae or respiratory tract and
replicates in the nasopharynx and upper respiratory tract
• It disseminates by a primary viremia and infects regional lymph nodes, the liver, the
spleen and other organs
• A secondary viremia follows, resulting in a cutaneous infection with the typical vesicular
rash
• Chickenpox almost never occurs twice in the same individual
o After primary infection chickenpox remains dormant in host nerve cells and may
reactivate in the form of ‘shingles’ or ‘zoster’ with age or immunocompromised state

Epidemiology
• Varicella is a highly contagious infection of childhood
• The peak age is 5-10 years, but the disease can occur at any age
• Transmission is by direct contact, droplet and air
• The incubation period is 14 to 16 days (11 to 20 days)

Clinical Features of Chickenpox

Activity: Group Discussion

Instructions
You will work in small groups to think back to a time when you had chickenpox or knew a
child with chickenpox. Create two lists, one on the features observed with chickenpox and
the other on how it was treated. Record your answers. One group will present their
responses and others will share in discussion.

• Prodromal symptoms
o Fever, malaise and anorexia may proceed the rash by 1 day
• Rash
o Small red papules that rapidly progress to non umbilicated oval vesicles or an
erythematous base
o The fluid progresses from clear to cloudy, and the vesicles ulcerate, crust and heal

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 8: Chickenpox and Mumps 71
 o A new crop appears for 3-4 days beginning on the trunk, the head, the face, and less
commonly, the extremities
o There may be 100-300 lesions, with all forms of lesions being present at the same
time
o Pruritus is almost universal
o Lesions may be present on all mucus membranes
o Systemic signs and fever
• Reactivation
o After primary infection, varicella zoster virus remains dormant in the dorsal root
ganglion and can reactivate with stress, old age, or immunocompromised state
o Reactivation zoster or ‘shingles’ occurs in specific a dermatomal distribution
• Congenital varicella
o Varicella in pregnant woman may lead into foetal varicella infection, characterized by
low birth weight, cortical atrophy, seizures, mental retardation, chorioretinitis,
cataracts, microcephaly, intracranial calcifications, and diagnostic cicatricial scarring
of the body or extremities

Diagnosis and Treatment of Chickenpox

Diagnosis
• History of fever and typical rash
• Examination of typical vesicular rash

Treatment
• Symptomatic therapy including non-aspirin antipyretic, cool bath and careful hygiene
• Intravenous acyclovir in immunocompromised patients
• Oral acyclovir (20 mg/kg/dose qid) for 5 days shorten the duration of illness in children
who are not immunocompromised if given within 24 hours of the first cutaneous lesion

Complications and Prevention of Chickenpox

Complications
• Although chickenpox is generally a mild disease, complications can arise
• Infection by varicella zoster virus is a more severe disease for neonates, adults, and
immunocompromised individuals
• HIV-infected children frequently have a prolonged course and may have recurrent
episodes of varicella zoster infection or reactivation ‘shingles’
• Secondary infection of skin lesions by streptococci or staphylococci is common
o Infection may be mild or life threatening (e.g. toxic shock or necrotizing fasciitis)
• Thrombocytopeania and hemorrhagic lesions or bleeding
• Pneumonia
• Myocarditis
• Pericarditis
• Orchitis
• Hepatitis
• Ulcerative gastritis
• Glomerulonephritis
• Arthritis

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• Reyes syndrome may be preceded by varicella, therefore avoid aspirin
• Neurologic complications: post-infectious encephalitis, cerebellar ataxia, nystagmus and
tremor, Guillain-Barré syndrome, transverse myelitis, cranial nerve palsies, optic neuritis,
and hypothalamic syndrome

Prevention
• A single dose of a live attenuated varicella vaccine recommended in healthy children ages
1-12 years
• The vaccine is not part of the EPI in Tanzania
• When available, human varicella zoster immunoglobulin should be given to
immunocompromised patients, neonates and pregnant women who have had significant
contact with chickenpox but have no antibodies to varicella zoster virus

Overview and Clinical Features of Mumps

• Mumps: An infection caused by RNA virus of the family paramyxovirus
• Transmission is by droplet spread and the incubation period is 2-3 weeks

Clinical Features
• Fever, malaise, parotitis
• Pain and swelling of the parotid gland may be unilateral at first and then bilateral
• The swelling may be easier to see than to feel
• The swelling is between the angle of the mandible and sternomastoid muscle, extending
beneath the ear lobe which is pushed upwards and outwards
• The swelling usually subsides within 7-10 days, but patients are infectious from a few
days before the swelling is seen up to 3 days after the enlargement subsides
• CNS manifestations are seen and are a possible causes of aseptic meningitis
• Orchitis can be seen, especially in older children and young adults

Diagnosis, Differential Diagnosis and Treatment of Mumps

• Diagnosis is based on the presenting features (signs and symptoms) as stated above
• Differential diagnosis
o Malnutrition can present with enlarged parotid and cervical lymph nodes, but there is
no fever associated with it
o Extrapulmonary TB may also present with enlarged cervical lymph nodes
o HIV infected children may also present with enlarged parotid gland(s)
• Treatment
o No specific treatment is available except for supportive treatment
• Prevention
o Live attenuated vaccine to children (when to give depends on country but ranges from
9-15 months), but is not part of Tanzania EPI

Complications of Mumps
• Pancreatitis
• Meningoencephalitis
• Epididymo-orchitis or oophritis
o Can lead to infertility later in life though not common

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Rare Complications
• Nephritis
• Myocarditis
• Mastitis
• Deafness
• Arthritis
• Thrombocytopenia
• Thyroiditis
• Occular manifestations

Key Points
• Chickenpox is a highly contagious disease transmitted by droplet or airborne route.
• Chickenpox is a fairly mild disease but severe complications can occur especially in
immunocompromised and newborn children
• Mumps is a self limiting viral disease which affects many children.
• In few children with complicated mumps, infertility can be a long term consequence.

Evaluation
• What are the organisms that cause chickenpox and mumps?
• How are chicken pox and mumps spread?
• What are clinical features of both diseases?
• How are chickenpox and mumps treated?
• What are the common complications of the diseases?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.) Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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 Session 9: Diarrhoeal Diseases and Rectal Prolapse
Learning Objectives
By the end of this session, students will be able to:
• Explain the pathophysiological mechanisms of diarrhoea in children
• Explain management of diarrhoea and dysentery in children
• Describe the classification of diarrhoea and dysentery in children
• Explain complications of diarrhoeal diseases in children
• List causes of rectal prolapse

Overview of Diarrhoeal Diseases

• Diarrhoea: The passage of three or more loose or watery stools in 24 hours
• Dysentery: An acute diarrhoeal disease characterized by bloody stool, fever vomiting and
abdominal cramps
• Non-specific defence mechanisms
o Acts against all potential pathogens
o This defence depends on:
ƒ Integrity of the lining of the gut, the secretions, saliva, mucus and acid from the
stomach
ƒ Motility of the intestines which limits the colonization and evacuates irritating
agents
ƒ Normal bowel flora which inhibit the multiplication of pathogens
• Specific immunological mechanisms
o The mechanisms are both cellular and humoral
o Secretory IgA is excreted from the mucosa to neutralize specific pathogens in the
lumen, and is protected from degradation by the digestive enzymes
o The infant’s gut is colonized shortly after birth by Lactobacillus bifidus, together with
the associated acidic medium, it discourages the growth of pathogenic organisms

Aetiology of Diarrhoea
• Viruses
o Rotavirus
ƒ The most important cause of diarrhoea in small children
o The Norwalk agent
o Adenoviruses
o Many others
• Bacteria
o Many bacteria can cause diarrhoea
o Bacillary dysentery is caused by non-motile Gram-Negative bacilli of Shigella
species, this is known as shigellosis
o The Shigella species causing this include:
ƒ Shigella sonnei
ƒ Shigella dysenteriae (causes outbreaks)
ƒ Shigella boydii
ƒ Shigella flexneri

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• Parasites
o The protozoans (e.g. Entamoeba histolytica) and some encountered in children with
HIV or AIDS (e.g. Giardia lamblia, Cryptosporidium)
o Amoebic dysentery is bloody diarrhoea caused by Entamoeba histolytica
o Helminths (e.g. Strongyloides stercoralis, Trichuris trichiura)
• Parenteral diarrhoea
o Not associated with bowel infection, but is an alimentary response to infection
elsewhere in the body, (e.g. malaria, otitis media, UTI)

Pathophysiology of Diarrhoeal Diseases

• Impaired absorption
o Maldigestion (e.g. lactase deficiency)
o Increased osmotic load in lumen
o Damage to the absorptive surface
o Inadequate mucosal enterocyte replication (e.g. Protein Energy Malnutrition (PEM))
• Invasion
o Local tissue damage and leakage (e.g. Shigella and E. Histolytica)
o Local stimulation and systemic spread (e.g. salmonella food poisoning)
o Abnormal colonization (e.g. large bowel organisms in small bowel)
• Toxigenic secretory diarrhoea:
o V. cholerae and enterotoxigenic E. coli (ETEC) cause diarrhoea by toxic stimulation
of cell excretion
o Bacteria produce enterotoxins that pass through the cell wall and stimulate enzymatic
reactions in the cell, which result in excessive secretion into the bowel
• Mucosal invasion with limited spread and local inflammation
o Affects infants between six months and three years of age
o Incubation period is one to three days with a short duration of illness it is
characterized by watery stools, which may be preceded by vomiting and fever
o The Rotavirus particles invade and destroy patches of enterocytes on the surface of
the small bowel
o In salmonella food poisoning, the bacteria penetrate the epithelial cell and spread as
far as the mucosal lining
• Mucosal invasion with local damage to cells and villi
o Shigella attack epithelial cells, cause micro ulcers which enlarge to wide areas of
inflammation and discharge
• Lactase insufficiency (intolerance)
o Any form of mucosal damage may impair enzyme production and absorption of the
bowel
o If infants feed on milk, lactose (milk sugar) is digested into glucose and galactose and
absorbed, when there is lactase insufficiency, the lactose is not broken down
o The colonic bacteria reduce the lactate by fermentation into lactic acid, short-chain
fatty acids and gas

Transmission, Management and Complications of Diarrhoeal Diseases

Transmission
• Diarrhoeal diseases are transmitted by the faecal oral route
• Persistent diarrhoea is common in:

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 o Immunocompromised patients (e.g. HIV infected patients) as the body has no
resistance
o Malnutrition cases
o People living in overcrowded conditions where water supply is poor
o Areas where faecal and refuse disposal is poor
• Humans are the only reservoir for bacillary dysentery outbreaks and during infection
people may be asymptomatic carriers for up to 3 months
• Shigella species multiply in food stuffs

Management
• Evaluation (assessment of dehydration status and classification degree of dehydration)
o Severe dehydration includes two of the following signs:
ƒ Lethargic or unconscious, sunken eyes, not able to drink or drinking poorly and
skin pinch goes back very slowly
o Some dehydration includes two of the following signs:
ƒ Restless, irritable, sunken eyes, drinks eagerly, thirsty, skin pinch goes back slow
o No dehydration
ƒ Not enough signs to classify as some or severe dehydration
• Rehydration using oral rehydration therapy (ORT)
• Zinc
• Nutrition
• Medication

Dysentry
• The incubation period is 1-4 days
• In undernourished child the result is fulminating and fatal disease
• Typical case:
o Sudden onset with fever, colicky abdominal pains and diarrhoea
o After a few motions, diarrhoea stops and dysenteric syndrome occurs, characterized
by abdominal cramps (colicky pains) and tenesmus
o Passage of bloody mucoid stools
o There may be associated vomiting
o Toxaemias due to serotoxin secreted by bacilli
o Fever, rapid pulse
o Convulsions may occur
o Dehydration is dangerous
o There may be oliguria, muscle cramps, and shock
o Rectal prolapse may occur in infants
• Stool
o Macroscopically appear dark red (bloody) with a lot of mucus
o Microscopy shows numerous white blood cells and red blood cells
o Macrophages are confused with trophozoites of E. histolytica
o Culture
• Blood
o Leucocytosis 15,000 per mm
• Urine for protein, red blood cells or casts
• Other tests: abdominal ultrasound, creatinine, urea and electrolytes
o These can be done at hospital level

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Session 9: Diarrhoeal Diseases and Rectal Prolapse 77
 Refer to:
• Handout 9.1: Assessment of Diarrhoea
• Handout 9.2: Assess, Classify and Identify Treatment
• Handout 9.3: Treatment Plan for Diarrhoea

Activity: Case Study

Instructions
Read the scenario below and then answer the questions.

Case Scenario
A 10 month old child presents to your clinic with a history of diarrhoea for 8 days, there is no
blood in the stool and upon examination the child is alert, has sunken eyes, is drinking
eagerly and the skin pinch goes back very slowly.

Question
Identify where the patient falls on the chart in Handout 9.2: Assess, Classify and Identify
Treatment and then use Handout 9.3: Treatment Plan for Diarrhoea to determine how to
treat the child.
Note: start at the top of the chart in Handout 9.2 and rule out the first row before moving to
the second.

• Complications
o Dehydration
o Fluid and electrolyte imbalance
o Renal insufficiency
o Hypoglycaemia
o Malnutrition
o Anaemia

Relationship Between Malnutrition and Diarrhoea

• Diarrhoea can precipitate clinical malnutrition, and especially if repeated may contribute
to severity of the problem
• Malnourished children suffer longer and more severe attacks of diarrhoea than children
with normal nutritional status

Ways Diarrhoea and Infections Contribute to Malnutrition

• Decreasing nutrient intake
o Anorexia
o Withholding of food
o Food substituted by dilute alternatives
• Decreased nutrient uptake by the gut
o Reduced enzymes required for digestion and absorption
o Impaired absorption from damaged bowel
o Intestinal hurry and decreased transit time
• Tissue degradation
o Cell destruction by organisms
o Tissue mobilization for nutrients

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 o Leakage of nutrients through damaged surfaces
• Increased metabolic rate
o Pyrexia
o Increased protein turnover for repair

Ways Severe Malnutrition Affects Infections

• Severe malnutrition is associated with infections that are more severe, prolonged and
frequent
• Impaired immunity
o Cell-mediated immunity depressed
o Humoral immunity sometimes depressed
o Interaction in the systems impaired
• Damaged protective barriers
o Dermatosis with cracks in the skin so pathogens can invade
o Compromised intestinal integrity
• Impaired alimentary secretions
o Gastric acid is decreased, the killing of the pathogens is less effective
o Decreased secretions of various non-specific defence factors in saliva, mucus and
other alimentary secretions
o Pancreatic juice is deficient
o Bile volume is reduced
• Poor tissue repair
o This results in prolonged illness and opportunities for repeated infections

Prevention and Control of Diarrhoea

• Infant feeding is protective against diarrhoeal disease
o Exclusively breastfeeding for first 6 months
o Continue breastfeeding until at least 2 years of age
o Improve weaning practices
• Environmental improvement to stop the faecal oral contamination cycle
o Hygienic practices when preparing food
o Provision of safe drinking water
o Hand washing with soap and water after defecation, cleaning baby’s bottom, and
before eating, feeding a child or preparing food
o Proper disposal of faeces in a latrine
• Immunization against diseases (e.g. measles)
• Promotion and use of oral rehydration therapy (ORT)
• Early diagnosis and treatment of infected person

Rectal Prolapse
• Rectal prolapse is the protrusion of a few or all layers of the rectal mucous membrane
through the anus with or without bleeding
o Most commonly a benign self limiting condition
o Common in children between 1 and 5 years
o Smooth red round mass coming out of the anus
• Causes (Consider rectal prolapse as a presenting sign of an underlying condition)
o Prolonged diarrhoea
o Infestation with Trichuris trichiura
o Malnutrition

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 o Poor muscle tone and weakened anal sphincter
o Whooping cough (pertussis)
o Straining due to constipation
• Differential diagnosis
o Rectal polyp
o Intussusceptions of the rectum
• Management
o Reduce with gentle constant pressure
o Firm strapping across buttocks to maintain the reduction
o Correct underlying cause of diarrhoea and malnutrition
o Treat helminthic infections
• Complications
o Recurrent prolapse
o Bleeding
o Strangulation with gangrene
o For complicated rectal prolapse cover the prolapse with clean moist cloth then refer to
hospital

Key Points
• Diarrhoea is defined as the passage of three or more loose or watery stools in 24 hours.
• Diarrhoea can occur due to a variety of causes, but in our setting most are viral in origin.
• In the management of diarrhoea, it is necessary to assess the degree of dehydration and
treat according to the right plan.
• All children with diarrhoea should be given Zinc supplementation for 10-14 days.
• Dysentery is an acute diarrhoeal disease characterized by bloody stool, fever vomiting
and abdominal cramps.
• Dysentery must be treated aggressively to prevent deadly complications like renal failure.

Evaluation
• What are the common causes of diarrhoeal diseases in our setting?
• What are the clinical features of severe diarrhoea?
• How is severe diarrhoea treated?
• How can diarrhoea be prevented in the community?
• What is the treatment of dysentery?
• For complicated rectal prolapse, what should be done?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• MOHSW, WHO, UNICEF. (2007). Integrated Management of Childhood Illness:
Facilitator Guide. Dar es Salaam, Tanzania: Ministry of Health and Social Welfare.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 9: Diarrhoeal Diseases and Rectal Prolapse 80
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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Session 9: Diarrhoeal Diseases and Rectal Prolapse 81
 Handout 9.1: Assessment of Diarrhoea

Check for General Danger Signs

ASK LOOK
• Is the child able to drink or breastfeed? • See if the child is lethargic or
• Is the child vomiting everything? unconscious
• Has the child had convulsions? • See if the child is convulsing now.
• Does the child have diarrhoea?

IF YES, ASK LOOK AND FEEL

• For how long? • Look at the child’s general condition
• Is the blood in the stools • Is the child:
o Lethargic or unconscious?
o Restless and irritable?
• Look for sunken eyes
• Offer the child fluid.
• Is the child:
o Not able to drink or drinking poorly?
o Drinking eagerly, thirsty?
• Pinch the skin on the abdomen
o Does it go back slowly?
o Very slowly (longer than 2
seconds)?

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 Handout 9.2: Evaluation-Assessment and Classification for
Diarrhoea

Two of the following signs:

• Lethargic or unconscious -If child has no other severe
• Sunken eyes classification
SEVERE
• Not able to drink or -Give fluid for severe dehydration
DEHYDRATION
drinking poorly (Plan C)
• Skin pinch goes back very
slowly
Two of the following signs: -Give fluid and food for some
• Restless, irritable dehydration (Plan B)
SOME
• Sunken eyes -Advise mother when to return
DEHYDRATION
• Drinks eagerly, thirsty immediately
• Skin pinch goes back slow -Follow-up in 5 days if not improving
-Give fluid and food to treat diarrhoea
Not enough signs to classify at home (Plan A)
NO
as some or severe -Advise mother when to return
DEHYDRATION
dehydration immediately
-Follow-up in 5 days if not improving

If diarrhoea 14 days or more:

-Treat dehydration before referral
SEVERE
unless the child has another severe
• Dehydration present PERSISTENT
classification
DIARRHOEA
-Refer to hospital
-Advise mother on feeding a child
PERSISTENT
• No dehydration who has persistent diarrhoea
DIARRHOEA
-Follow-up in 5 days

If blood in stools:
-Treat for 5 days with oral antibiotic
o First line drug for shigellosis is Or
Erythromycin 12.5 mg/kg/day
divided into 4 equal doses for a
period of 5 days or
o Cotrimoxazlole (Trimethoprim-
sulfamethoxazole)-8/40 mg/kg bid
• Blood in stools DYSENTERY
× 5 days

-Treatment for dehydration depends

on the degree of dehydration (refer to
treatment plan for dehydration)

-Follow-up in 2 days

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 Handout 9.3:Treatment plan for Diarrhoea

Source: MOHSW, 2007.

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Additional Information on Zinc Supplementation (20 mg tablet) (Rule 2)

• Prescribe zinc supplementation for children with no or some dehydration

• Give zinc supplementation to all children with diarrhoea for 10 to 14 days
• Zinc should be given as soon as the child can eat

Why Zinc?
• Zinc decreases the length and severity of diarrhoea
• Zinc is important for the child’s immune system and helps to fight off new episodes of
diarrhoea in the following 2 to 3 months
• Zinc improves appetite and growth

Additional Information on When to Return to the Clinic (Rule 4)

• Passes many stools
• Is very thirsty
• Has sunken eyes
• Seems not to be getting better
• Has a fever
• Does not eat or drink normally
• Has blood in stools
• A child with blood in the stools
o Treat for dehydration and Shigella infection
o Prescribe antibiotic effective against Shigella
o Manage dehydration

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Source: MOHSW, 2007.

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Source: MOHSW, 2007.

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CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
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 Session 10: Ectoparasite and Helminthic Infestation
Learning Objectives
By the end of this session, students are expected to be able to:
• List four common ectoparasites affecting children
• Explain the clinical features of common ectoparasites in children
• Describe the treatment and prevention of common ectoparasites for children
• Discuss common helminthic infestations in children
• Explain common presenting features of each helminthic infestation in children
• List investigations and treatment for each helminthic infestation in children

Ectoparasites and Helminthic Infestations in Children

• Ectoparasites
o Louse
o Jiggers
o Tumbu fly
o Scabies
o Fleas
• Helminthics
o Ascaris
o Threadworm
o Tapeworm
o Schistosoma

Louse Infestation (Pediculosis)

• Infestation of the scalp, hairy parts of the body, or clothing with adult lice (blood sucking
parasites) and their larvae or eggs
• Types of lice
o Head louse - Pediculus humanis capitis
o Body louse - Pediculus humanis corporis
o Pubic louse - Phthrus pubis.
• Clinical features
o Severe itching
o Secondary bacterial infection of the scalp
o Spreads onto the neck and scapular region
o Lymphadenopathy
o The lice lay eggs (nits) that are firmly attached to the hair
o Eggs appear as grey-white specks
o When sucking blood, body lice causes small, red, slightly prominent itching skin
lesions
o Lice live and lay eggs in the clothing
• Treatment
o Shave the head
o Gamma benzene hexachloride (Lindane) 1% or benzyl benzoate emulsion (BBE)
6.25-12.5%. Lindane not recommended for children < 2 yrs
o Wash hair the following day and comb with special nit comb

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 o Treat secondary infection with topical antibiotic ointment and systemic penicillin
• Prevention
o Health education , cleanliness
o Launder clothes, caps, hats to destroy nits and lice
o Case finding and treatment
o Look for lice in other members of the family

Jiggers
• The intracutaneous infestation of human skin by the female sand flea known as Tunga
penetrans, also called ‘Tungiasis’
• Clinical features are covered in the Communicable Diseases Module, but specifically in
children:
o The pregnant female of Tunga penetrans attaches itself to the skin of the toe or foot,
burrows into the dermis and grows rapidly to discharge eggs if not removed
• Treatment
o Clean infected areas properly
o The jigger should be prised out carefully and destroyed, or remove the intact flea with
a sterile needle or scalpel
o The wound should be treated with antiseptics (may need to be covered with antiseptic
gauze) and systemic antibiotics may be necessary
o A course of tetanus toxoid should be given
• Prevention
o Affected areas of the soil may need to be burnt to kill the fleas
o Daily inspection of the interdigital clefts, roots of the nails, and soles of the feet
should detect fresh burrowing female jiggers and thus removed
o Children should be put on foot enveloping shoes to prevent attacks

Tumbu Fly Infestation (Myiasis)

• Tumbu fly (Cordylobia anthropophagi, also called mango fly) is a causative agent for
myiasis
• Types
o Obligatory myiasis
ƒ Caused by larva of this parasite, which invade living tissues
o Facultative myiasis
ƒ Caused by larva which invade the dying/decaying tissue, like necrotic wounds
o Accidental or intestinal myiasis
ƒ Caused by eggs of parasite, which are ingested accidentally and hatch in the gut
• Spread
o Eggs are laid in the soil which has been contaminated by the sweets or urine of the
infected animals like human and the rat (the normal host) or can be laid in damp
clothing or bed linens
o They hatch in two days and the larva forms contact the skin of the human and cause
formation of a furuncle-like swelling
• Management
o Put petroleum jelly on the furuncle, larva will try to come out and then squeeze and
pull it out
• Prevention
o Iron clothes, especially those left to dry over grass

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Scabies
• The highly contagious disease scabies is caused by the itch mite, Sarcoptes scabiei which
is transmitted by close personal contact
• Children from the same family, house or school tend to present at the same time
• The life cycle is in the Communicable Disease Module
• Clinical features are covered in the Communicable Disease Module
• Diagnose by identification of the mite in blunt scrapings from broken papules or vesicles,
examined on a slide using a low power microscope
• Complications include secondary bacterial infection leading to pyoderma, cellulitis and
even septicaemia
• Treatment
o All children and other affected members of the family should be treated together to
prevent reinfection
o In children below 5 years old Benzyl Benzoate Emulsion (BBE) 6.25% strength
should be used, and in older children 12.5% strength
o This procedure should be repeated on two or three consecutive days
o Sulphur ointment (cream containing precipitated sulphur 6-10%) applied once daily
for 7 days can be used
o Lindane 1% applied to the whole body; wash after 6 hours
o Permethrin (5%) can be used in children.
ƒ It is less irritant and more effective than BBE, but is more expensive
o Antihistamines to relive itching and antibiotics for bacterial super infection (refer
dose for children)
o Further details of treatment not specific to children can be found in the
Communicable Disease Module, Ectoparasite Infestation Session 4

Note: Infestation by human flea (Pullex Irritans) is covered in the Communicable Disease
Module

Hookworms (Necator americanus or Ancylostoma duodenale)

• Small round worms that live in the upper part of the small intestine
• They suck blood and protein from their host.
o N. Americanus sucks 0.03 ml of blood per day
o A. Duodenale sucks 0.2 ml of blood per day

• Transmission
o Through unbroken skin (barefoot walking)
o Source of infection is faecal contamination
o Ingestion of larvae
• Clinical features
o Usually asymptomatic in light infections
o Itching at site of skin penetration
o GI symptoms: worms attach to and suck blood from mucosa of small intestine leading
to iron-deficiency anaemia, peptic ulcer-like symptoms in heavy infections
o Diagnosis
ƒ Stool exam for eggs
ƒ Mild eosinophilia
ƒ Low Haemoglobin (Hb) level

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• Treatment
o Mebendazole 500 mg per oral (PO) as a single dose or Albendazole 400 mg PO as a
single dose
o If there is anaemia (Hb<10g/dl), give ferrous sulphate 6mg/kg/day of elemental iron

Ascaris lumbricoides (Roundworm)

• Large worms (about 30 cm long) living in the small intestine
• Transmission
o Ingestion of eggs
o Source of infection is faecal contamination of soil and vegetables, particularly in
regions using human faeces as fertilizer
• Clinical features
o Asymptomatic in many
o Adult worms live in small intestine and may exit through the nose or mouth of
infected person
o Occasionally may cause obstruction of pancreatic or bile duct, appendix, or small
intestine
o During larva migration in the lungs, dry cough, fever, transient pulmonary infiltrates
(Loffler's syndrome) and/or eosinophilia may occur
o Children may develop malnutrition due to protein loss
• Diagnosis
o Stool examination for eggs
o Dead adult worms in faeces or vomitus
o Eosinophilia during migration phase, none during adult phase
• Treatment and prevention
o Mebendazole 500 mg PO as a single dose or albendazole 400 mg PO as a single dose.

Enterobius vermicularis (Pinworm or Threadworm)

• Transmission
o Humans are the only host
o Adult worms live in caecum and migrate at night to perianal skin to deposit eggs
o Self-inoculation by faecal contaminated hand-to-mouth, person to person contact,
autoinfection
• Clinical features
o Asymptomatic carrier state
o Severe nocturnal perianal itching
o Occasionally vaginitis
• Diagnosis
o Sticky tape test (5 to 7 tests required to rule out infection)
o Examination of perianal area at night may reveal adult worms seen with naked eye
• Treatment
o Mebendazole 500mg PO as a single dose or albendazole 400mg PO as a single dose
o Personal hygiene
ƒ Clean underwear
ƒ Pajamas to sleep
ƒ Bathe in morning and wash hands after defecation
o Treat all members of family simultaneously
ƒ Reinfection common

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Tapeworms
• Flat worms that live in the small intestine
• There are of two types, Taenia solium and Taenia saginata
• Transmission is by ingestion of cestode eggs or undercooked meat containing larvae

Taenia solium (Pork Tapeworm)

• Clinical features
o Ingestion of larval cestode in pork leads to intestinal adult tapeworm infection
o Usually asymptomatic
o Ingestion of eggs (results in cysticercosis)
o Eggs hatch within the small intestine and larvae travel to subcutaneous tissue, muscle,
CNS, and/or the eye, where they eventually form cysts to which the host responds
with an inflammatory response as they die (after 4-5 years)
o Can develop blindness or neurological manifestations
o Neurocysticercosis is most frequent
o Headache, seizures, focal neurologic deficits, hydrocephalus

Taenia saginata (beef tapeworm)

• Clinical features
o Can grow to 25 meters in length in the small bowel
o Usually asymptomatic
o Occasionally develop abdominal discomfort, weight loss, and diarrhoea, segments
(proglottids) can crawl out of anus
• Diagnosis of tapeworm infestation
o Examine stool for eggs or gravid proglottids
• Treatment of tapeworm infestation
o Albendazole 400 mg PO as a single dose or praziquantel 40 mg/kg PO as a single
dose

Schistosoma mansoni
• Found in the tropics and the cause of schistosomiasis
• Transmission
o Acquired when larvae, released from snail, penetrate unbroken skin
o During exposure in slow-moving infested fresh water
o Adult worms live in terminal venules of bowel passing eggs into stool
o Eggs must reach freshwater to hatch; schistosomiasis cannot multiply in humans
o No person-to-person transmission because snail intermediate host is required
• Clinical features
o Pruritic skin rash at site of penetration (cercarial dermatitis)
o Acute schistosomiasis (Katayama fever) at time of egg deposition (4-8 weeks after
infection)
o Fever, hives, headache, weight loss, cough, abdominal pain, diarrhoea and blood
stained stool (lasts up to 3 months)
• Diagnosis
o Examine stool for ova (eggs)
o Rectal biopsy
• Treatment
o Praziquantel 40mg/kg/day
• Complications

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 o Caused by granulomatous response and fibrosis secondary to egg deposition by adult
worms in the veins surrounding the intestine (worms in mesenteric vein, eggs in portal
tracts of liver and bowel)
o Heavy infections: intestinal polyps, portal and pulmonary hypertension

Key Points
• Ectoparasites affecting humans are many but only a few are of importance.
• Hygiene is extremely important in the prevention ectoparasites
• In immunocompromised children, scabies can be severe and life threatening.
• Helminthic infestations are fairly common in children.
• Helminthic infestations can cause anaemia and malnutrition.
• Treat all members of the family even if only one child has helminthic infestation.

Evaluation
• What are the common complications of scabies?
• Why are antihistamines used in management of ectoparisites?
• What are the common helminthic infestations of public health importance?
• How is Taenia solium transmitted?
• How is schistostomiasis treated?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Cook, G. et al.(2003) Manson’s Tropical Diseases. (21st Ed.) London: Saunders.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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Session 10: Ectoparasites and Helminthic Infestations 94
 Session 11: Anaemia
Learning Objectives
By the end of this session, students are expected to be able to:
• Define the term anaemia
• List the types and causes of anaemia in children
• Describe clinical features of anaemia
• Describe the management of anaemia
• Describe the prevention of anaemia

Definition, Causes, Clinical Features and Investigations of Anaemia

• Anaemia: Low haemoglobin (Hb) concentration in the blood below the reference range
for age and sex
• It literally describes the circumstance where there is a lack of haem
• Haem is the oxygen carrying molecule which contains iron and it is attached to the
proteineous molecule called globin

Figure 1: Reference Range for Anaemia

Age Hb Concentration (g/dL)
Cord Blood 13.5-20.5
1st Day 15.0-20.5
6Mon-6Yrs 11.0-14.5
6-14Yrs 12.0-15.5

Causes of Anaemia
• In most cases the cause has many factors and results from:
o Inadequate intake, such as in nutritional deficiency
o Impaired absorption (e.g. disorders of gastrointestinal tract, or following gut surgery)
o Increased loss (acute or chronic blood loss) (e.g. from bleeding, hookworm
infestation)
o Marrow failure (uncommon but serious) may be inherited but is more commonly
acquired

Clinical Features
• Non-specific
o Symptoms depend on how rapidly the anaemia develops
o In chronic, slow blood loss, the body adapts to the increasing anaemia, and patients
can often tolerate extremely low concentrations of Hb (e.g. 7 g/dL) with remarkably
few symptoms
o Increasing lethargy or tiredness
o Difficulty in breathing or breathlessness (in older children)
o More unusual symptoms are headache, faintness
o Pallor (palms), pallor of conjunctiva may mislead you if the child had been crying
o Tachycardia, systolic flow murmur and cardiac failure occur with severe anaemia

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 o Respiratory distress in severe anaemia, and even features of cerebral hypoxia such as
convulsions may be seen

Note: For the last two points, prompt action should be taken

Investigations
• Full blood count and blood film examination
• Blood smear and/or rapid antibody test for malaria (especially if with fever)
• Additional investigations will depend on the cause

Types of Anaemia

Iron Deficiency Anaemia (IDA)

• A condition where the iron available to the body has been reduced
• Iron deficiency is the most common cause of anaemia worldwide and is frequently seen in
general practice
• Caused by defective synthesis of Hb, resulting in red blood cells that are smaller than
normal (microcytic) with reduced amounts of Hb (hypochromic)
• Inadequate supply of iron is caused by:
o Inadequate dietary intake of iron-containing foods
o Impaired or decreased absorption
o Acute or chronic blood loss such as in hookworm infestation
o Increased demand during growth

• Clinical features (in addition to the above non-specific features)

o Several skin, nail, and other epithelial changes may be seen in chronic IDA
ƒ Atrophy of skin occurs in about a third of patients
ƒ Rarely, nail changes such as koilonychia (spoon shaped nails) which may result in
brittle, flattened nails
ƒ Angular stomatitis, in which painful cracks appear at the angle of the mouth,
sometimes accompanied by glossitis
ƒ These changes are likely due to a reduction in the iron-containing enzymes in the
epithelium and gastrointestinal tract
• Investigations in IDA (in addition to the above investigations)
o Haematinic assay or iron panel (serum ferritin, serum iron, total iron binding capacity
(TIBC), transferrin) if available
o Stool for ova
o Urea and electrolytes, liver function tests if suspect renal or liver problems (at hospital
level)
o Fibreoptic and/or barium studies of GIT (done at hospital level if indicated)

Haemolytic Anaemia
• Anaemia due to hemolysis (increased destruction) of red blood cells
• The haemolysis could be intravascular or extravascular
• Causes:
o Inherited
ƒ Membrane abnormalities: hereditary spherocytosis and hereditary elliptocytosis
ƒ Haemoglobinopathies: thalasemias and haemoglobin S,C,D
ƒ Red cell enzyme defects: glucose-6-phoshate dehydrogenase deficiency

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 o Acquired
ƒ Immune: autoimmune (warm or cold), alloimmune (e.g. haemolytic transfusion
reactions, haemolytic disease of the newborn) or drug induced
ƒ Non-immune: mechanical (artificial cardiac prosthesis e.g. valves,
microangiopathic haemolytic anaemia) paroxysmal nocturnal haemoglobinuria
(PNH) or secondary to systemic disease (renal or liver failure)
o Miscellaneous
ƒ Infections (e.g. malaria)
ƒ Drugs and chemicals
ƒ Burns
ƒ Hypersplenism
• Clinical features
o Jaundice
o Other features as above (for overall anaemia)
• Investigations (in addition to the above investigations)
o Elevated serum bilirubin (unconjugated or indirect), reticulocytosis
o Excess urinary urobilinogen
o Possibly evidence of abnormal cells (e.g. sickle cells)
o Blood grouping, Rhesus factor, direct antiglobulin (Coombs’) test (at hospital level)

Megaloblastic Anaemia (also known as macrocytic anaemia)

• A type of anaemia in which red cells appear large
• Causes
o Folic acid or Vitamin B12 deficiency in the diet
o Poor absorption or utilization of these nutrients
o Increase loss of these nutrients due to infections
• Clinical features and investigations same as stated above for overall anaemia

Treatment of Anaemia
Figure 2: Medication Information for Anaemia
Medicine Dose Note
5 mg/kg/day elemental Fe, in 1-2
divided doses (if possible) orally for
Give with fruits between meals for
3 mo
better absorption
Ferrous sulphate
Occasionally may need to continue
Do not give in kwashiorkor or in
up to 6 months but reduce dose to 2-3
severe infections in the acute phase
mg/kg elemental iron OD

5mg/day all ages

(megaloblastic or with IDA: 3 mo
After attacks of malaria and SCA
Folic acid
Haemoglobinopathy: lifelong crisis

To be used in haemolytic conditions

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Session 11: Anaemia 97
Blood Transfusion (BT)
• Should be given on strict, lifesaving indications
• Serious risks include infection (HIV, Viral hepatitis) or allergic reaction to blood
• Indicated if Hb < 4 g/dl, if there are signs of cardiac failure, respiratory distress or brain
anoxia
• Give 10 ml/kg packed red cells (if unavailable 20 ml/kg whole blood)
• Blood transfusion (if not for acute blood loss) to be given in not less than 4 and not more
than 5 hours
• In cardiac failure Furosemide 1mg/kg IV should be given before the BT to avoid acute
volume overload and pulmonary oedema
• General considerations for BT (WHO)
o Acute blood loss, when 20% to30% of the total blood volume has been lost and
bleeding is continuing
o Severe anaemia
o Septic shock (if IV fluids are insufficient to maintain adequate circulation and in
addition to antibiotic therapy)
o To provide plasma and platelets for clotting factors, if specific blood components are
not available
o Exchange BT in neonates with severe jaundice (at hospital level)
o BT is not given at dispensary or health centre level
o Refer the patient to a hospital with a donor
o Children with haemolytic anaemia should be referred to hospital for proper
management

Prevention of Anaemia
• Promote breastfeeding and mixed complementary foods containing meat or fish, dark
green leafy vegetables (cooked for a short time) and fruits
o Prolonged use of cow's milk will lead to iron deficiency anaemia
• Avoid tea during meals as it interferes with iron absorption
• Growth monitoring and immunization are essential
• Proper hygiene and sanitation (e.g. use of latrines to prevent infections and infestations)
• Identify and treat helminthic infections
• Use insecticide treated mosquito nets to prevent malaria
• Give folic acid (age 4 weeks to 6 months) and iron (age 6 weeks to 6 months) to
premature low birth weight infants and to twins

Key Points
• Anaemia is defined as low haemoglobin (Hb) concentration in the blood below the
reference range for age and sex.
• The causes of anaemia in children have many factors.
• In treatment of anaemia it is important to give a combination of both ferrous sulphate and
folic acid because in most cases it is not easy to identify the type of anaemia.
• Blood transfusion can be life-saving for children in need.
• Breastfeeding and a diet full of meat or fish, dark green leafy vegetables and fruits can
help prevent anaemia in children.

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Session 11: Anaemia 98
Evaluation
• What is anaemia?
• What are the common causes of anaemia?
• How is anaemia diagnosed?
• How is anaemia treated?
• How is anaemia prevented?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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Session 11: Anaemia 99
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Session 11: Anaemia 100
 Session 12: Sickle Cell Anaemia
Learning Objectives
By the end of this session, students are expected to be able to:
• Define sickle cell anaemia
• Explain the characteristics of red blood cells with abnormal haemoglobin
• Describe the clinical presentation of sickle cell anaemia
• Explain the management of a child with sickle cell anaemia

Definition of Terms
• Sickle cell disease (SCD): Denotes all genotypes that contain at least 1 sickle gene, in
which haemoglobin (Hb) S makes up at least half of the Hb present
o In addition to homozygotic HbSS (sickle cell anaemia [SCA]) in which only HbS is
produced, at least 5 other major genotypes are linked to the disease, including:
ƒ HbS– β0 thalassemia- almost indistinguishable from SCA phenotypically
ƒ HbSC disease with intermediate clinical severity
ƒ HbS/hereditary persistence of foetal Hb (S/HPHP) - mild form or symptom free
ƒ HbS/HbE syndrome - rare and generally mild clinical course
ƒ Other rare combinations
ƒ SCA is the most severe and most common form
• Sickle cell anaemia: Originates from inheritance of one copy of the sickle cell gene from
each parent, who may either be heterozygous (Hb AS) or homozygous (Hb SS)
• Sickle cell trait: When one has normal adult Hb A and an abnormal Hb S (i.e.
heterozygous [HbAS])
o These children are asymptomatic
• HbS is a result of the substitution of valine for glutamic acid in position 6 of the beta (ß)
chain of Hb

Note: HbAS offers some protection against falciparum malaria. The infestation of the malaria
plasmodium is halted by the sickling of the cell which it infests.

Characteristics of Red Blood Cells with Abnormal Haemoglobin (HbSS)

• Red blood cells (RBC) are abnormal and have short life span of 8 to 20 days
• Under low oxygen tension (that is when deoxygenated)
o Cells become elliptic (thus the name sickle cell), rigid, sticky and fragile
o Cells clump together and occlude small blood capillaries

Clinical Features of Sickle Cell Anaemia

• Although a diagnosis of the disease can be made at birth, clinical abnormalities usually do
not occur before 6 months
• By the end of childhood, functional asplenia due to repeated sickling of red cells and
ultimately infarction of splenic tissue results in susceptibility to overwhelming infection
with encapsulated organisms such as Streptococcus pneumoniae and Haemophilus
influenzae
• The risk is decreased but still significant even in the vaccinated population

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 12: Sickle Cell Anaemia 101
• Subsequently, other organs are damaged
• Typical manifestations include recurrent pain and progressive infarction

Figure 1: Age and Features of Sickle Cell Anaemia

Age Features

0-4 months • No features (due to presence of fetal Hb)

• Pallor
• Dactylitis (hand and foot syndrome)
o Severely painful symmetrical swelling of the hands and feet
>4 months-1 caused by infarctions of the small bones
year o May be the initial manifestation, is most common in those < 2
years
• Jaundice
• Recurrent infections
• Splenomegaly
• Pallor
• Jaundice
2-5 years • Recurrent infections
• Hepatosplenomegaly
• Recurrent infections
• Pallor
• Jaundice
• Bossing of the skull
>5 years
• Long thin extremities
• Autosplenectomy
• Adolescents may have delayed puberty

Sickle Cell Crises

• Vaso-occlusive (thrombotic) or painful crisis
o The most common form of crisis
o Caused by occlusion of the small blood vessel and restrict blood flow to organs
o This results into ischaemia, pain and organ damage
o Pain in the limbs and joints and tenderness
o Hydration and analgesics are the mainstay of therapy
o If IV fluids needed, give isotonic sodium chloride solution
• Sequestration crisis
o Also called ‘acute or splenic sequestration crisis’
o A medical emergency
o Is specific form of acute hypersplenism in young children
o A large amount of blood is trapped in the spleen causing a sudden fall in Hb
o Children develop painful, rapid and massive splenic enlargement with consumption of
large volumes of erythrocytes
o They present with marked pallor, shock or sudden weakness, dyspnea, and left-sided
abdominal pain in addition to the splenomegaly
o Death due to hypovolemic shock occur rapidly
o Treatment consists of IV fluids and erythrocyte (packed red blood cell) transfusions
o To prevent recurrences, splenectomy may be indicated

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 12: Sickle Cell Anaemia 102
 o In most patients with SCA, the spleen eventually involutes and sequestration is no
longer a problem
• Acute chest syndrome
o Common cause of morbidity and mortality
o Triggered by painful crises, respiratory infection or surgery
o This condition is characterized by:
ƒ Difficulty breathing
ƒ Tachycardia, tachypnea and hypoxemia are common
ƒ Patients present with a new infiltrate on chest X-ray, often with chest pain and
fever
o Treatment includes oxygen therapy, IV antibiotics, and analgesics
o Simple transfusion administered early may halt progressive respiratory deterioration
• Haemolytic crisis
o Acute accelerated drop in Hb level
o The RBC breaks down at a faster rate
• Aplastic crisis
o Associated with Parvovirus B19 infection
o Depression of the RBC precursors in the bone marrow
o Presents with pallor, tachycardia and fatigue
o Inadequate production of RBC can be life threatening when the RBC life span is short

Hypersplenism
• Hypersplenism is a clinical syndrome in which cytopenias result when splenic function
becomes excessive as the spleen enlarges
• This has been attributed to the following four possible mechanisms
o Excessive splenic phagocytic activity
o Splenic production of antibodies that results in the destruction of hematopoietic cells
o Over activity of splenic function
o Splenic sequestration
• If results in recurrent severe anaemia necessitating repeated blood transfusion,
splenectomy may be indicated (refer to hospital)

Complications and Management

• Avascular necrosis of head of femur
• Autosplenectomy due to repeated infarcts
• Osteomyelitis by salmonella
• Acute papillary necrosis causing haematuria
• Prone to infections due to low immunity
• Chronic ulcers (legs)
• Priapism may occur at any age but more common after puberty
• Cerebral infarction
o Presenting complaint depends on the nature of the event and includes gait disturbance,
aphasia, altered level of consciousness, hemiparesis or hemiplegia or seizures
• Blindness from retinal detachment
• Gallstones (cholelithiasis) because of chronic haemolysis
Management
• Investigations
o Hb range typically 6-8 g/dl
o Sickling test (may be negative if transfused within last 3 months)

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Session 12: Sickle Cell Anaemia 103
 o Hb electrophoresis (done at hospital level)
o Full blood picture (FBP) may apart from anaemia, indicate macrocytosis
(megaloblasts or reticulocytes), total white blood cells (WBC) may be high
(leucocytosis)
o In hypersplenism, anaemia, reduced levels of WBC’s and platelets may be seen
o Reticulocytosis (high number of immature RBC’s)

Treatment
• No specific treatment, but the following help to alleviate symptoms
o Prophylaxis with folic acid 5mg daily, and chloroquine 5 mg/kg weekly to prevent
malaria
o Do not give iron as there are plenty of iron stores coming from the destruction of the
Haem group that may actually lead to iron overload
o When a child has malaria, treat with Artemether/Lumefantrine (ALu) or Quinine if
they have severe malaria
o Growth monitoring, immunization and proper nutrition
o Treat other infections vigorously
• For sickle cell crises
o Sickle cell crises are precipitated by fever, dehydration, infection, hypoxia or surgery
o Give analgesics (e.g. paracetamol)
o IV fluids , normal saline or ringer’s lactate
o Treat infections vigorously (give pre-referral antimalaria and antibiotics,( i.e. inj.
quinine 10 mg/kg IM and inj. chloramphenical 25 mg/kg IM respectively)
o Keep warm, and refer to hospital

Key Points
• Sickle cell anaemia originates from inheritance of one copy of the sickle cell gene from
each parent, who may either be heterozygous (Hb AS) or homozygous (Hb SS).
• HbS is a result of the substitution of valine for glutamic acid in position 6 of the beta (ß)
chain.
• Children with sickle cell anaemia need weekly chloroquine and daily folic acid.
• Iron is not needed because the stores are plenty following destruction of the Haem group
of the Hb molecule.

Evaluation
• What is sickle cell anaemia?
• What are common presenting features of sickle cell anaemia?
• W hat are the common sickle cell crises?
• What are the complications of sickle cell anaemia

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 12: Sickle Cell Anaemia 104
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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Session 12: Sickle Cell Anaemia 105
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 12: Sickle Cell Anaemia 106
 Session 13: Malaria
Learning Objectives
By the end of this session, students are expected to be able to:
• Define malaria and how it is transmitted
• Describe the pathogenesis of malaria
• Outline the clinical presentation of malaria
• Explain the diagnosis and treatment of malaria
• Describe the prevention and control of malaria

Overview of Malaria
• Malaria: A parasitic acute and chronic protozoan infection caused by a parasite
plasmodium, which infects Red Blood Cells (RBCs)
• History shows malaria has infected humans since the beginning of mankind
• Although a worldwide problem, malaria predominantly occurs in tropical and sub-tropical
areas
• It remains the most common public health problem in Tanzania.
o It is the number one cause of morbidity and mortality especially in children below
five years of age
• The 4 Plasmodium species known to cause malaria include Plasmodium falciparum (P.
falciparum), Plasmodium vivax, Plasmodium ovale and Plasmodium malariae
• P. falciparum infections (constitutes >90% of the cases in Tanzania) causes severe forms
of malaria than the other species
• In P.vivax and P.ovale, some exo-erythrocytic forms remain as dormant forms called
hypnozoites.
o This helps them survive in temperate countries
o They can get re-activated once in 3-6 months to cause relapses
• In P.falciparum and P.malariae infections, relapses from the liver do not occur but the
blood infection may remain chronic and if untreated, may remain for years
• Is acquired from the bite of an infected female anopheles mosquito, but can be
transmitted through blood transfusion, use of contaminated needles and mother to child
transmission during pregnancy
• The incidence of malaria in the community is measured by means of 2 indices, the
parasite rate (Blood Sliderandom selection in the population) and splenic rate (enlarged
spleen in school children)
• The life cycle is covered in Parasitology and Communicable Diseases Modules

Pathogenesis of Malaria
• Rupture of infected erythrocytes containing the schizont results in fever and merozoite
release.
• Merozoites enter new RBCs, and the process is repeated, resulting in increase in parasite
burden
• Outcome of the infection depends on host immunity
o Individuals with immunity can spontaneously clear the parasites
o In those without immunity, the parasites continue to expand the infection

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 13: Malaria 107
 o P falciparum infection can result in death
• Infected RBCs rupture, causing haemolytic anemia and pigment deposition in
reticuloendothelial cells
• Activation or stimulation of organs of reticuloendothelia system results in hepatomegaly
and/or splenomegaly
• The infected RBCs may also sludge and stick in organs, interfering with circulation and
inducing pneumonia, encephalitis, or enteritis
• Antibody production seems to be correlated with clearance of the erythrocyte (but not the
hepatic) stage of parasites
• In P. falciparum infection
o Available RBCs numbers are higher as RBCs of all ages are infected and the
parasitized RBCs escape from destruction by sequestration
o The parasite has better skills for attack and can enter most RBCs hence
hyperparasitemia (heavy parasitemia)
o The malaria is characterised by development of sticky knobs on surface of red cells,
adhesion of red cells to the endothelial cells of post-capillary venules and adherence
of parasitized red cells to uninfected cells
o Adherence and sequestration result in poor tissue function, organ dysfunction,
anaerobic glycolysis in tissues and lactic acidosis
ƒ This contributes to placental dysfunction and suppression of erythropoiesis
o Cytokines and a high burden of parasites contribute to end-organ disease, and it
specifically involves the central nervous system (CNS), lungs, and kidneys
o Adherence results in sequestration of the parasite in small post-capillary vessels, and
for this reason, only early forms are observed in the peripheral blood, before the
sequestration properly develops (an important diagnostic clue that the patient is
infected with P falciparum)
o Sequestration of parasites may contribute to mental-status changes and coma,
observed exclusively in P falciparum infection
o Hypoglycemia, severe anaemia and multiorgan dysfunction are also contributed by
hypoxia
ƒ These manifestations may be observed in young children and pregnant women
• Sickle cell trait and glucose-6 phosphate dehydrogenase (G6PD) deficiency are associated
with some protection against severe malaria

Clinical Features of Malaria

• Malaria is most severe in children lacking antibodies and is milder in children having
survived initial attacks
• The illness is characterized by nonspecific prodrome prior to the onset of sudden high
fevers and chills
.
Uncomplicated Malaria
• Malaria attacks are very common in young children in endemic areas
• Fever is the most common feature
• Onset of symptoms may resemble a flu-like illness
• Children may present with a cough and/or vomiting and diarrhoea
• In infants early symptoms vary and may be difficult to recognize.
o They may be limited to refusal to feed/poor appetite and restlessness
• Older children may complain of body malaise, headache, joint pains, body ache, poor
appetite and body weakness

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• Older children, that have reached semi-immunity, may have asymptomatic infection
• Pallor and an enlarged spleen are less common in older children, but are more common in
children < 5 years
• Hepatomegaly also seen
• An uncomplicated malaria attack can become severe malaria

Severe Malaria in Children

• Cerebral malaria
o Mainly in children < 5 years old
o Convulsion lasting 30 minutes or more
o Convulsions begin onset of neurological disease
o Deterioration can be within hours
o May have fever, headache, vomiting and/or drowsiness
o Hypoglycaemia is a major risk
o 10% of survivors get severe neurological sequelae (hemiparesis, epilepsy, blindness)
• Convulsions
o Repetitive abnormal muscular movements
o May be the first sign of cerebral malaria but about 5% of all children get febrile
convulsions when they have fever regardless of the cause
• Impaired consciousness
o Altered level of consciousness
o Acute confused state
o Coma (indicates worse prognosis)
• Change of behaviour
o Hallucinations
o Delusions
o Agitation
• Severe malaria anaemia
o Hb < 7 g/dl or hematocrit < 21%
o Peak age 1-2 years old, during malaria attack rapid deterioration
o Probably caused by longstanding low grade parasitaemia
• Hyperparasitaemia
o > 5000 asexual parasites per 200 WBC (> 20,000 asexual parasites per μL)
• Respiratory distress
o May be a primary lung problem due to pulmonary edema
o May be a compensatory hyperventilation due to lactic acidosis
o Indicates worse prognosis
• Hypoglycaemia
o Blood glucose <2.5 mmol/L
o An emergency, therefore must be detected and treated
• Prostration/extreme weakness
o Generalised weakness such that the child is unable to stand or sit up without support
• Circulatory collapse/shock
o Combination of malaria with gram negative septicaemia
o ‘Algid malaria’ with severe hypotension and shock
o Low systolic BP (<50 mm Hg in children using paediatric cuff) should be measured
regularly and septicaemia treated/ruled out
• Vomiting everything
o Throwing up after every feed/drink (including breast milk and water)

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• Inability to drink or breast feed
o Not able to swallow
• Acute renal failure
o Oliguria (urine output < 0.3 ml/kg/hr in children)
• Jaundice
o Yellow colouration of mucus membranes
o Results from hepatic dysfunction, haemolysis
• Haemoglobinuria
o From massive intravascular haemolysis
o Dark brown or positive Hb on dipstick urine
• Bleeding tendency/Disseminated Intravascular Coagulation (DIC)
o Rare
o Bleeding from venepuncture sites or spontaneous haemorrhage

Diagnosis and Treatment of Malaria

• The goal of appropriate diagnosis and treatment is to reduce morbidity, mortality and
socio-economic losses

Investigations
• Blood smear (thick or thin smear if species identification required)
o Positive blood films, thick and thin
o A single negative blood slide does not rule out malaria
o Repeat at least twice in case of high suspicion of malaria
• Rapid diagnostic tests (paracheck) are qualitative techniques based on detection of
malaria parasite antigens
• Blood glucose
• Haemglobin/ haematocrit
• Other investigations if indicated (e.g. chest x-ray in respiratory distress)

Treatment
• In serious disease (e.g. suspicion about cerebral malaria and in severe malaria) treatment
should be given even when blood slides are negative
• Uncomplicated malaria
o First line Æ artemether(20mg)-lumefantrine(120mg) (ALu)
o The dose of ALu is 1.5/12 mg/kg body weight twice a day for three days
o The dosing schedule for ALu (strength 20/120 mg) is reported in Handout 13.1
o Contraindications
ƒ Children <5kg body weight
ƒ Lactating mothers with child below 5 kg of body weight
ƒ First trimester of pregnancy
o Second line Æ Quinine 10 mg/kg/dose orally 8 hourly for 7 to 10 days is indicated
for:
ƒ Treatment of uncomplicated malaria where ALu is contraindicated
ƒ Treatment of uncomplicated malaria where ALu has failed

Refer to Handout 13.1: Dosage Schedule of ALu

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• Severe malaria
o Quinine is the drug of choice
ƒ Dose: 10 mg/kg/dose of quinine in 10 mls/kg of 5% dextrose / DNS
ƒ Infused over 4 hours and repeated every 8 hours
ƒ Watch for hypoglycaemia or arrhythmia during therapy with Quinine
ƒ It is given intravenously until the child is able to take orally (mostly 3 days),
duration 7 days
ƒ Or full dose of ALu after incomplete dose of quinine
ƒ Oral quinine maintenance doses should be 7 mg/kg body weight in patients with
impaired renal function
ƒ Non-response to quinine therapy- Artemether 3.2 mg/kg (loading dose) I.M
followed by 1.6 mg/kg I.M daily for 6 days
• Neonatal malaria
o Considered severe, thus refer immediately to hospital for admission
o Can be congenital or acquired, most of these young infants have weight < 5 kg
o Broad spectrum antibiotic
o Parenteral quinine 10mg/kg 8 to 12 hourly till the baby is able to breast-feed, then oral
quinine is given to complete 7 day treatment
o If the neonate is not able to breast feed, give 10% glucose IV 60ml/kg/24 hours
o Give blood transfusion if HB is <10g/dl

Refer to Handout 13.2: Supportive Therapy

Prevention, Control and Follow-up

• Prompt and effective treatment with Artemisia-based combination therapies
• Mosquito bite avoidance especially during the night using mosquito coils, mosquito
meshing, insecticide treated nets (permethrin insect repellents, long clothing)
• Vector control, indoor spraying, eliminate mosquito breeding sites
• Antimalarial chemoprophylaxis for
o Patients with sickle cell anaemia
ƒ Chloroquine 5 mg base/kg weekly
o Non-immune travellers
ƒ Mefloquin 5mg/kg weekly, proguanil 3mg/kg daily, malarone
(proguanil/atovaquin) daily, doxycyclline 100mg daily (> 12yrs)
o Hyper reactive malaria splenomegaly (refer to appropriate health level)
• Drug prophylaxis of malaria should only be used by visitors, not for indigenous
population, except for pregnant women (IPT) and children with sickle cell anaemia
• Children with cerebral malaria should be followed up after 4 weeks

Key Points
• Malaria is a serious protozoal infection which causes serious morbidity and mortality in
children.
• Malaria has to be treated aggressively because it can cause severe disease and may result
in death.
• Preventive measures for malaria include avoidance of mosquito bites, chemoprophylaxis
and vector control.

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Evaluation
• What is malaria?
• Describe the pathogenesis of malaria.
• List the clinical presentation of uncomplicated malaria.
• How can you treat severe malaria?
• What are the preventive measures for malaria?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• NMCP. (2006). National Guidelines for Malaria Diagnosis and Treatment. Dar es
Salaam, Tanzania: Ministry of Health and Social Welfare/National Malaria Control
Programme.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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 Handout 13.1: Dosage Schedule of ALU

Dosage schedule of ALu

Colour
Kg dose 1st 2rd 3rd 4th 5th 6th
hours 0 8 24 36 48 60
Code
Age tabs tabs tabs tabs tabs tabs Coarte
m
5 up to 3mo 1 1 1 1 1 1 yellow
15 up to
3yrs
15 up 3yrs 2 2 2 2 2 2 blue
to 25 up to
8yrs
25 up 8yrs 3 3 3 3 3 3 red
to 35 up to
12yrs
35 and 12yrs 4 4 4 4 4 4 green
above and
above
Source: MOHSW, 2006.

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 Handout 13.2: Supportive Therapy

Exclude meningitis. Don't give

corticosteroids, mannitol, or heparin. With
COMA effective antimalarial treatment recovery
within 2-3 days. Restrict fluid to
maintenance. Monitor urine output.
Avoid warm clothing.
HYPERPYREXIA
Paracetamol 15 mg/kg/dose orally.
Diazepam rectally or paraldehyde or
Phenobarbitone. See chapter 5 on
CONVULSIONS Convulsions. If post convulsive drowsiness
persists > 1h, Cerebral malaria is most
likely.
May be caused by haemolysis; give blood
transfusion (on strict indications, life saving).
SEVERE ANAEMIA See chapter 12 on Anaemia. Treat anaemia
patients with fever as malaria, even when
blood slide is negative.
Strict fluid balance if urinary output is less
than 0,5 ml/kg/h. Peritoneal dialysis may be
ACUTE RENAL FAILURE
necessary in anuria. See chapter 47 on
Paediatric Procedures.
BLEEDING DISORDERS & DIC Vitamin K injection. Fresh whole blood.
IV Dextrose 5% 10 ml/kg, 10% 5 ml/kg,
25% 2 ml/kg, Thereafter change
HYPOGLYCAEMIA
Quinine/dextrose 5% IV to Quinine/dextrose
10%. Oral feeds.
GRAM NEG. SEPTICAEMIA Antibiotics: see 14.8 treatment septicaemia.

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 Session 14: Meningitis
Learning Objectives
By the end of this session, students are expected to be able to:
• Define meningitis
• Explain the causes of meningitis
• List the types of meningitis
• Describe the clinical features and complications of meningitis
• Explain the treatment and follow up care of a child with meningitis

Overview of Meningitis
• Meningitis: The inflammation of the meninges
• Meninges are the membranes that cover the brain and spinal cord, namely dura mater, pia
mater and arachnoid mater

Causes of Meningitis

Figure 1: Causes of Meningitis

Cause Age

Group B Streptococcus spp First month mainly

E. Coli, Proteus spp First month mainly

Klebsiella spp, Listeria monocytogenes First month mainly

Haemophilus influenzae Mainly 1 month to 4 yr. age (up to 12 yr.)

Mainly 1 month to 4 yr. age, but may occur
Streptococcus pneumoniae
later, also in adults
Neisseria meningitidis Mainly 1 month to adulthood
Mainly after penetrating head injury and VP-
Staphylococcus spp
Shunt
Mycobacterium tuberculosis See notes on TB

Note: In the case of immunosuppressed children fungal infections may cause of meningitis

Types of Meningitis
• Purulent (bacterial) meningitis
• Tuberculosis meningitis
• Viral/aseptic meningitis

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Purulent (bacterial) Meningitis
• A serious disease caused by Neisseria meningitidis (meningococcus), Streptococcus
pneumoniae (pneumococcus), or other bacteria
• Unless adequate Rx is given death or permanent complications may occur
• Pathology
o Pia and arachnoid layers are congested and inflated with inflammatory cells
o A thin layer of pus forms, this may cause obstruction to the free flow of CSF leading
to the hydrocephalous
o The CSF pressure rises rapidly, protein content increases, and cellular reaction which
varies in the type and severity according to the nature of inflammation and causative
organism
• Signs and symptoms
o Infants 0 to 3 months
ƒ Initial signs are indistinguishable from those of neonatal sepsis and may include
fever, cyanosis, vomiting, a high pitched cry, drowsiness, inability to suck and
convulsions
ƒ Neurological manifestations may follow, including bulging fontanelle, seizures,
lethargy, and neck stiffness
o Children more than 3 months
ƒ History of vomiting or inability to drink or breastfeed, headache or pain in back of
neck, convulsions, irritability, recent head injury
ƒ Stiff neck, and/or bulging fontanelle, positive Kernig or Brudzinski sign
ƒ Fever
ƒ Repeated convulsions
ƒ Lethargy or irritability
ƒ Petechial rash or purpura
ƒ Evidence of head trauma suggesting possibility of a recent skull fracture
ƒ Unequal pupils
ƒ Rigid posture or posturing
ƒ Focal paralysis in any of the limbs or trunk
o In severe disease
ƒ There is internal bleeding especially on adrenal glands which control blood
pressure and blood electrolytes
ƒ Child may collapse and die before the meningitis is suspected

Diagnosis and Complications of Bacterial Meningitis

Diagnosis
• Lumbar puncture and examination of CSF (CSF is cloudy in purulent meningitis)
• CSF
o Protein level and CSF glucose level investigation
o Even without functioning laboratory, a lumbar puncture may reveal diagnosis, turbid
CSF in a clean tube
o Cells, protein, sugar, Gram stain and, in suspected cases, examination for acid-fast-
bacteria (TB)
o Cell-count result should be known within ½-1 hour
• A random blood glucose should be obtained just before the lumbar puncture in order to
compare blood and CSF glucose
• Culture and sensitivity test if possible (hospital level)

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• Four reasons for delaying lumbar puncture
o Cardio respiratory compromise
o Signs of increased intracranial pressure (e.g., retinal changes, unequal pupils or focal
neurological signs)
o Local infection/defects
o Bleeding disorders

Complications
• Complications may occur from a few days to a few weeks after onset

Figure 2: Complications of Bacterial Meningitis

Complication Clinical Presentation

Hearing loss Evaluate latest on discharge

Subdural effusion Deep tendon reflexes

Hydrocephalus Head circumference increasing, before fontanelle is closed

Brain abscess Focal neurological signs, impaired consciousness, WBC high

Paresis, ataxia Observation, neural, examination

Vision impairment Evaluate during hospital stay and on discharge

Note: If fever/other signs are still ongoing after 3 to 4 days of treatment, check whether
treatment is adequate or consider subdural effusion and other focus of infection (bone, joint,
ears).

Treatment of Bacterial Meningitis

General Care
• Monitoring vital signs hourly during first days
• If mother is breastfeeding she should express breast milk
• Normal food should be given as soon as the child can suck and eat without risk of
aspiration
• Head circumference (HC) should be measured on arrival and twice a week

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Antibiotics

Figure 3: Antibiotics for the Treatment of Bacterial Meningitis

Antibiotic Dose

Penicillin G 300 to 400.000 U kg/d in 4 doses preferably IV (or IM)

Ampicillin 200 to 300 mg/kg/d in 4 doses IV

Chloramphenicol 100 mg/kg/d in 4 doses IV (IM during referral)

Cefotaxime 200 mg/kg/d IM,IV in 3 to 4 doses

Ceftriaxone 100 mg/kg/d IM,IV in 1 dose

Ceftazidime especially for
150 mg/kg/d IV in 3 doses
Pseudomonas meningitis

Duration of Treatment
• Pneumococci 10 to 14 days
• Haemophilus 10 days
• Meningococcus 7 days
• Unknown cause 14 days
• Gram negatives organisms 3 weeks
• Always at least 7 days IV, thereafter in select cases consider oral treatment if child is
well, provided complete adherence to therapy can be guaranteed

Combination of Antibiotics
• Unknown cause
o Ampicillin + Chloramphenicol (treatment of first choice)
o Penicillin G + Chloramphenicol
o Cephalosporin (3rd generation only)
• Haemophilus influenza: Ampicillin + Chloramphenicol
• Pneumococci: Penicillin G + Chloramphenicol, in case of therapeutic failure add
Rifampicin 20 mg/kg/d in 2 doses orally or switch to 3rd generation Cephalosporins
• Meningococci: Penicillin G, 7 days only
• Tuberculosis: (See notes on Tuberculosis)

Fluid
• IV fluid may be needed during the first days
• Give the daily maintenance, but not more!
• Monitor carefully for signs of fluid overload
• If serum sodium is below 135 mmol/l reduce fluid intake to 80% of maintenance, if below
125mmol/l keep the vein open (at hospital level)
• Give maintenance via NG-tube or orally as soon as it is safe (no risk of aspiration)

Treatment of Convulsions
• Rectal diazepam or paraldehyde until convulsions have stopped

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Treatment of Cerebral Oedema
• Most importantly, elevate the head about 30 degrees
• Treat for hypoglycaemia and fever accordingly

Follow Up
• Important to do out-patient follow up to exclude complications (e.g. hydrocephalus)
• Measure head circumference to see if hydrocephalus develops
• Community based rehabilitation can help, if permanent sequelae

Tuberculosis and Viral Meningitis

Tuberculosis Meningitis
• Onset is gradual, and presentation includes:
o Headache
o Drowsiness
o Possible constipation
o Vomiting and loss of appetite
• Later, neck stiffness and positive Kernig’s signs are present and child is drowsier
• Finally, becomes spastic, has convulsions and dies in coma unless treatment has been
given
• CSF is clear or slightly cloudy
• CSF microscopy shows increased cells, normally lymphocytes
• CSF glucose is low and the protein is moderately raised
• Mantoux test may be positive

Viral or Aseptic Meningitis

• Less severe than purulent meningitis
• Lumbar puncture shows the CSF is almost clear
• CSF microscopy shows more cells, mainly lymphocytes
• CSF glucose is normal
• Treatment is with fluids and observation

Key Points
• Meningitis is a serious infection affecting the meninges of the brain.
• There are different types of meningitis, including purulent (bacterial) meningitis,
tuberculosis meningitis and viral/aseptic meningitis.
• Management of this disease should be very aggressive to prevent possible serious
consequences and death.
• In the children who happen to develop permanent complications, community based
rehabilitation is essential.

Evaluation
• What is meningitis?
• How does meningitis get transmitted in the community?
• How is a child with meningitis diagnosed?
• How is meningitis treated?

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References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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 Session 15: Cerebral Palsy
Learning Objectives
By the end of the session, students are expected to be able to:
• Define cerebral palsy
• Discuss the causes and clinical presentation of cerebral palsy
• Describe diagnosis, management and follow up of a child with cerebral palsy

Overview of Cerebral Palsy

• Cerebral palsy: A permanent non-progressive disorder of movement, tone and posture
resulting from damage to, or lesions of, an immature brain
• Such a lesion is static and non-progressive, but the symptoms may change according to
the age of the child

Causes
• Prenatal
o Hereditary
o Malformation of the brain
o Rubella
o Syphilis
o Toxoplasmosis herpes
o Excess radiation
o Prematurity
o Asphyxia
• Perinatal (Birth to 7th day)
o Asphyxia
o Intracranial bleeding
o Anoxia caused by placenta praevia
o Abruptio placenta
o Jaundice and infections
• Postnatal (8th day to 2 years)
o In a child earlier considered healthy; meningitis, encephalopathies (e.g. pertussis,
cerebral malaria, trauma)
• Unknown Origin
o Normal pre-, peri- and post natal history and a birth weight above 2500 gm

Clinical Features of Cerebral Palsy

Early Signs
• Feeding difficulties, inability to suck or swallow
• Failure to fix gaze when feeding, delayed smiling
• Abnormality of muscle tone, usually hypotonic, floppiness
• Behaviour abnormalities, irritability, lack of interest, sleep disturbances
• Delayed milestones

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Clinical Distribution of Motor Involvement
• Monoplegia
o Only one limb involved in motor movement
• Paraplegia
o Only legs involved in motor movement
• Hemiplegic
o Paresis of one side of the body
• Diplegia
o Spastic paresis, more in legs than arms
• Quadriplegia
o Severe paresis of both legs and arms

Nature of Motor Dysfunction

• Spasticity
o Hypertonic muscles, increased reflexes, paresis tendency to contractures
• Dyskinesia
o Impairment of voluntary movement
ƒ Dystonia with change in muscle tone between high tonus when disturbed or upset
and low tonus in rest, no contractures
ƒ Hyperkinesia with too many movements, involuntary and abnormal postures of
two different kinds
ƒ Athetosis-Slow twisting movements of hands and arms
ƒ Chorea- Rapid jerky movements, mainly of proximal parts of arms and legs
ƒ Neonatal reflexes persist
• Choreoathetosis
o Ataxia
ƒ Difficulties with co-ordination of movements, balance, tremor, low muscle tonus
ƒ Flaccidity during infancy

Additional Dysfunctions
• Mental retardation (more severe in proportion to number of limbs involved)
• Many children with strange pattern of movement have normal intelligence
• Speech disorders
• Difficulties in chewing, swallowing
• Drooling
• Hearing impairment, common in kernicterus and athetosis
• Strabismus, refractive errors and blindness
• Epilepsy, increased risk in spastic cerebral palsy
• Orthopaedic problems (e.g. dislocation of the hip, tightness of Achilles tendon, scoliosis)
• Growth retardation, partly because of feeding problems, vomiting, neglect
• Behaviour problems, learning disorders, disturbance of perception, attention deficit

Diagnosis, Management and Follow Up

Diagnosis
• Mainly clinical
• Teamwork with physiotherapist/occupational therapist is advisable

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Rehabilitation
• There is no treatment for cerebral palsy since it is neither an active nor a progressive
lesion
• The focus is on rehabilitation
• Parental counselling
o There is no cure for cerebral palsy but the parents should learn how to help the child
to live as rich a life as possible, including close relations to other people
o Build on what the child can do, don't focus only on what cannot be done
o A good cooperation with a community health worker skilled in community based
rehabilitation is essential
• Rehabilitation may involve several disciplines
o Physiotherapy to improve motor function
o Occupational therapy to improve activities of daily living
o Speech therapy to improve speech and communication
o Community or social worker to improve social interaction, education of family and
community
o Doctor to diagnose, coordinate and set objectives of treatment

• Surgery
o Mainly to prevent deformities, release contractures, improve function and facilitate
the care of the child

Drugs

Figure 1: Anticonvulsive Drugs

Drug Dose: Remarks:
Diazepam 0.25-0.5 (max!) mg/kg at 5mg/minute Immediate onset
slowly IV until the convulsion stops
May cause severe respiratory
Age ½ yr. to 2 yr.: max 5 mg depression
2 yr. to 10 yr.: max 10 mg
10 years and older: max 15 mg Avoid IM administration; this
is slower than rectal
May be repeated after 10 minutes, unless administration
the child has apnoea.

Or rectally
Age below 3 yr.: 5 mg, older: 10 mg
Phenytoin 15 mg/kg IV in normal saline diluted 1:10 Onset after 20-40 minutes
over 20 minutes

Not faster than 1 mg/kg/min.

Maintenance after 6 hours: 4 to 8

mg/kg/day in 2 doses (the older the child
the lower the dose/kg)

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
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Phenobarbital Loading dose: 10-15 mg/kg If additional Diazepam must be
given, it should be done with
IV not faster than 1 mg/kg/min great care

After 6 h: 5 mg/kg/d in 1-2 doses

Follow Up

• Goal is a life-style for the child and family which is personally satisfying and attracts
respect from others
o Ideally a community based rehabilitation (CBR) programme should assist the parents
in their care of the child
o Community resources and awareness should be mobilized
o Parents need support and encouragement not to give up hope and continue to invest
time to do exercises even though progress might be slow

Activity: Case Study

Instructions
Read the scenario below and answer the question which follows.

Scenario:
John, aged 18 months, is brought to the dispensary by his mother who reports that the child
has feeding difficulties, inability to suck and has rapid jerky movements, mainly of proximal
parts of arms and legs. You conduct a physical examination and discover that John has signs
of cerebral palsy.

Question
How would you manage the patient? Remember to consider both rehabilitation and follow
up of the child and the parents.

Key Points
• Cerebral palsy is a permanent, non-progressive disorder of movement, tone and posture
resulting from damage to or lesions of the immature brain.
• Clinical features of cerebral palsy include spasticity, muscle weakness, poor coordination,
involuntary movements, and ataxia.
• There is no treatment for cerebral palsy since it is neither an active nor a progressive
lesion, instead the focus should be on rehabilitation.

Evaluation
• What is cerebral palsy?
• What are the causes of cerebral palsy?
• How do you manage cerebral palsy?

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Session 15: Cerebral Palsy 124
References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 15: Cerebral Palsy 125
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 15: Cerebral Palsy 126
 Session 16: Deafness, Blindness, Speech Delay and
Mental Retardation
Learning Objectives
By the end of this session, students are expected to be able to:
• Describe the causes of deafness, blindness and speech delay
• Describe the diagnosis of deafness, blindness and speech delay
• Describe the treatment of deafness, blindness and speech delay
• Describe the causes, classification and management of mental retardation

Deafness
• Intact hearing is a fundamental requirement for the development of language and speech
in infancy since speech develops as a mimic of sounds heard
• Hearing impairment or hearing loss at an early age may lead to profound speech delay
and distortion of quality of the speech
• Hearing loss may be conductive or sensorineural
• Causes of deafness
o Conductive loss
ƒ Middle ear diseases such as otitis media with effusion
ƒ Malformations of the middle ear structures
o Sensorineural hearing loss
ƒ Intrautrine infection with rubella or cytomegalovirus
ƒ Acquired infections such as meningitis and severe malaria
ƒ Perinatal complications such as birth asphyxia and kernicterus
ƒ Ototoxic drugs such as aminoglycosides
ƒ Tumours and the medicines given for their treatment
o Genetic inheritance (deafness may be dominant or recessive)
• Diagnosis
o History
o Examination
o Audiological assessment
• Treatment
o Treatment of hearing impairment may be medical or surgical
o Refer children with hearing loss to a specialist

Blindness
• Blindness: A corrected visual acuity in the better eye of less than 3/60, and severe visual
impairment as a corrected acuity in the better eye of less than 6/60
• Types
o Partial visual loss
o Legal blindness
• Causes
o Most common are due to
ƒ Vitamin A deficiency
ƒ Corneal scarring from measles
ƒ Use of harmful traditional eye remedies

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 ƒ Ophthalmia neonatorum (infectious conjunctivitis)
ƒ Cataracts (common congenital)
ƒ Retinopathy of prematurity
ƒ Excessive oxygen therapy in newborns
o Others
ƒ Optic atrophy
ƒ Retinal degeneration
ƒ Retinoblastoma
ƒ Congenital glaucoma
ƒ Hereditary
• Diagnosis
o Some causes can be identified at birth (congenital cataracts, glaucoma)
o Commonly made when the child is between 4 and 8 months old
o Parental suspicions of unusual behaviour
o Eye examination
• Treatment
o Refer for assessment

Speech Delay
• Speech: The motor act of communicating by articulating verbal expressions
• Language: The knowledge of a symbol system used for interpersonal communication
• A child is considered to have speech delay if the child's speech development is
significantly below the norm for children of the same age
• A child with speech delay has speech development that is typical of a normally
developing child of a younger chronologic age
• The speech-delayed child's skills are acquired in a normal sequence, but at a slower-than-
normal rate
• Causes of speech delay
o May be a symptom of many disorders including:
ƒ Hearing impairment
ƒ Maturation delay (developmental language delay)-late talkers, common in boys
ƒ Mental retardation (common cause)
ƒ Expressive language disorder
ƒ Cerebral palsy
ƒ Autism
o Environmental factors/psychosocial deprivation (e.g. malnutrition, child neglect)
o Global delay, the most common cause (all milestones delayed)
o Familial
• Differential Diagnosis
o Stammering dysarthria due to mechanical problems
o Neuromuscular problems
• Diagnosis
o Delay of normal speech or no more speech
o Normal speech requires
ƒ Adequate hearing
ƒ Cognitive development
ƒ Coordinated sound production
• Treatment
o Refer to ear, nose and throat (ENT) specialist and speech therapist

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
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Mental Retardation
• Mental Retardation: A specific developmental disorder in which a child has
significantly sub average intellectual functioning with an intelligence quotient (IQ) of
approximately 70 or below
• Intelligence is the ability to learn and understand
• A mentally retarded child demonstrates global language delay and also has delayed
auditory comprehension and delayed use of gestures
• Causes
o In approximately 30-40% of the cases the cause cannot be determined
o Before birth (during pregnancy)
ƒ Intrauterine infections like German measles (Rubella) and syphilis
ƒ Poor maternal nutrition
ƒ Placental insufficiency
ƒ Hypoxia
ƒ Maternal medication, alcohol use and use of herbs
ƒ Hereditary (one or both parents may be of low intelligence)
ƒ Chromosomal defects such as Down’s syndrome
o During and after delivery
ƒ Hypoxia
ƒ Complicated or difficult labour
ƒ Asphyxia or deformed head, this may interfere with the normal brain development
and function
o After delivery
ƒ Infections of the brain such as meningitis may interfere with normal brain
development
ƒ Kernicterus (very high bilirubin levels due to blood group incompatibility)
ƒ Hypothyroidism
ƒ Trauma to the CNS
ƒ Metabolic disorders
ƒ A child’s brain needs stimulation to function properly
ƒ Deprived or neglected child (his/her intelligence may suffer and this may not be
reversed)
• Classification of Mental Retardation
o Mild retardation (IQ 55-70)
ƒ These children have normal language ability and social behaviour
ƒ They can go to school but will perform poorly
o Moderate retardation (IQ 40-55)
ƒ Most of these children can talk
ƒ All of them learn to communicate
ƒ Most learn to care for themselves with supervision
o Severe Mental Retardation (IQ 25-40)
ƒ Development of this child is generally slow
ƒ Many can be trained to look after themselves under supervision
ƒ Can communicate in simple ways
o Profound Retardation (IQ 20-25)
ƒ A few of these children learn to care for themselves completely
ƒ Some achieve simple speech, unsocial behaviour
• Treatment
o The general approach is educational rather than medical

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 o The health worker is responsible for early detection of mental retardation
o Additional personnel involved include:
ƒ Psychiatrists or psychiatric clinical officers
ƒ Physiotherapists
ƒ Occupational therapists
ƒ Speech therapists
ƒ Clinical psychologists
• A child with mental retardation may have or develop other problems such as a physical
disability, epilepsy or behaviour disorder
• Caring for a mentally retarded child may involve several activities
o Occupational therapy programmes in areas of self-help, such as toileting and feeding
o Initiate activities of daily living like cooking, sweeping and washing
o Provision of opportunity for vocational/income generating activities such as tailoring,
mat making or brick making
o Help them learn to make use of leisure time such as games, storytelling or singing
o Exercises that stimulate physical development such as exercise to help the child to sit,
stand and walk
o Refer to a speech therapist to assist the child with language and speech
o Counsel and explain to the caregiver about the outcome of the child’s condition
o Encourage the community to form self-help parent groups that can help in supervising
treatment programmes as prescribed in hospital such as occupational, physiotherapy,
speech therapy and drug therapy
o Encourage establishment of regular habits like eating and sleeping
o Encourage integration of the child in family activities
o Encourage parents to enrol children to school
o Educate community about medical conditions that aggravate mental retardation such
as malaria, diarrhoea and vomiting
o Stress early diagnosis and prompt and thorough treatment
• Prevention
o Genetic counselling
ƒ Explain to the couples the possibility of having a similar child if they have one
mentally retarded child
ƒ Discourage women from giving birth before 20 years of age and after 35 years
ƒ If possible ensure early detection of foetal abnormalities where therapeutic
prevention might be an option
o Prenatal care
ƒ Advise pregnant women to have a balanced diet
ƒ Avoid alcohol and cigarettes
ƒ Obtain proper immunization
ƒ Check VDRL and HIV
o Intranatal prevention
ƒ Encourage mothers to attend antenatal visits
ƒ Delivery in hospitals or maternity centres to be assisted by skilled personnel
o Postnatal prevention
ƒ Advise parents to protect children from communicable diseases such as malaria
and diarrhoea

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Activity: Case Study

Instructions
Read the scenario below and answer the questions.

Scenario
Anna, a 4 year old child, is brought to the clinic by her parents because she has the speech
ability of a 1 year old child, delayed use of gestures and unsocial behaviour. Her mother had
a difficult labour, and Anna suffered from meningitis as a result of otitis media with effusion
at 3 months of age. On examination Anna shows significant intellectual functioning.

Questions
1. What are Anna’s problems?
2. What are the causes of those problems?
3. What is the treatment approach?
4. Outline the care plan for Anna

Key Points
• Normal hearing is a fundamental requirement for the development of speech in infancy.
• The most common cause of severe visual impairment is retinopathy of prematurity,
followed by congenital cataracts.
• Normal speech requires adequate hearing, cognitive development and coordinated sound
production.
• Mental retardation is a specific developmental disorder in which the chid has significantly
sub average intellectual functioning with an intelligence quotient (IQ) of approximately
70 or below.

Evaluation
• What are the causes of deafness?
• Explain the different types of blindness
• What are the causes of speech delay?
• What is the management of mental retardation?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 16: Deafness, Blindness, Speech Delay and Mental Retardation 132
 Session 17: Congenital Heart Disease
Learning Objectives
By the end of this session, students are expected to be able to:
• Describe the causes of congenital heart disease (CHD)
• Classify congenital heart diseases
• Describe common acyanotic and cyanotic congenital heart diseases
• Describe the treatment of CHD
• Explain the causes of heart failure
• Describe the clinical features and treatment of heart failure

Overview of Congenital Heart Disease (CHD)

• Idiopathic in 85 to 90% of cases
• Caused by an interaction between environmental factors and genetic predisposition
• Known teratogenic agents include maternal alcohol ingestion, phenytoin use during
pregnancy, and/or exposure to rubella in the first trimester
• Single gene abnormalities (e.g. Marfan’s syndrome)
• Congenital heart abnormalities may be found in children with chromosomal aberrations
(e.g. 40% chance in trisomy 21, Down’s syndrome)
• A positive family history of CHD may be found in at least 10% of first degree relatives
• Congenital heart malformations occur in at least 7 per 1000 live births

Figure 1: Types and Percentage of Congenital Heart Abnormalities

Name of Abnormality Percentage of all CHD

Ventricular septal defect (VSD) 38%

Patent ductus arteriosus (PDA) 20%

Coarctation of the aorta 10%

Tetralogy of Fallot (ToF) 6%

Aortic stenosis(AS) 4%

Atrial septal defect (ASD) 3%

Isolated pulmonic stenosis 3%

Note: The above congenital heart abnormalities account for more than 80% of all CHD

Classification of Congenital Cardiac Anomalies

Acyanotic
• Left-to-right shunts
o Atrial Septal Defect

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 o Ventricular Septal Defect
o Patent Ductus Arteriosus
o AV Canal Defects
• Without shunts
o Coarctation of aorta

Cyanotic
• The 5 Ts
o Tetralogy of Fallot (ToF)
o Transposition of the Great Arteries (TGA)
o Truncus Arteriosus
o Tricuspid Atresia
o Total Anomalous Pulmonary Venous Return (TAPVR)

Refer to:
• Handout 17.1: Normal Heart Circulation
• Handout 17.2: Congenital Anomalies

Acyanotic Congenital Heart Diseases

• Acyanotic Congenital Heart Diseases: A group of cardiac diseases with a left-right
shunt or left heart abnormality
• Acyanotic lesions make up about one third of all CHD

Ventricular Septal Defect (VSD)

• Large defects present between 2 and 6 weeks of life (later at higher altitudes), when the
pulmonary vascular resistance has decreased from high foetal level
• Infants have difficulty in breathing (DIB) and feeding, and as a result, failure to thrive,
due to the large left-right shunt causing overload and heart failure
• Systolic murmur is heard at the left lower sternal edge, below a line drawn through the
nipples, +/_ thrill
• If the shunt is large, a mid-diastolic murmur will be heard at the apex
• CXR - cardiomegaly
• Therapy
o Asymptomatic or small VSD
ƒ No specific treatment needed
ƒ May close spontaneously within the first 2 years of life
o Symptomatic (tachypnea, failure to thrive, difficulty feeding)
ƒ Refer the patient
ƒ Need antifailure medications, and or surgical repair, unless pulmonary
hypertension is present

Patent Ductus Arteriosus (PDA)

• In preterm infants, particularly those with respiratory distress
• The ductus arteriosus often remain patent and a significant left-right shunt develops
usually close to the end of the first week of life, or by the time the infant reaches its
expected term
• Presents with DIB and on examination have tachypnoea
• Continuous machinery murmur on left side of the chest just below the clavicle

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Session 17: Congenital Heart Disease 134
• May close spontaneously or by the use of Indomethacin
• Failure to close, refer to surgery before 6 months of age
• PDA in term infants very rarely closes spontaneously and always requires surgical
removal before 6 months of age, even if it is asymptomatic
• In term infants - continuous machinery murmur just below the left clavicle
• If there is a large flow through the PDA, a mid-diastolic murmur will be heard at the apex
• CXR - cardiomegaly, pulmonary plethora (normal in asymptomatic)
• Refer child to hospital

Atrial Septal Defect (ASD)

• Ostium secundum
• Ostium primum
o Clinically asymptomatic, and may suffer frequent chest infections because of large
shunt into pulmonary circulation
ƒ Show clinical signs of right ventricular hypertrophy
ƒ Ejection systolic murmur is heard at the second left intercostals space
• CXR - cardiomegaly
• Treatment
o Secundum defects
ƒ Surgical closure of the defect during childhood, preferably prior to school
attendance
o Only large primum defects require closure
o Refer to hospital

Cyanotic Congenital Heart Diseases

• Tetralogy of Fallot (ToF) is the most common cyanotic cardiac malformation with
diminished pulmonary blood flow
• The cyanosis in ToF is caused by right to left shunting of blood through the VSD
• 4 components of the malformation:
o Overriding aorta
o Right ventricular hypertrophy
o Ventricular septal defect
o Right ventricular outflow tract obstruction (or pulmonary stenosis)
• Clinical presentation
o Onset in neonatal period
o Cyanosis varies with the degree of outflow tract obstruction and size of VSD
o May be characterized by hypercyanotic (hypoxic) episodes or Tet spells, squatting,
easy fatigability, failure to thrive
o Physical exam- digital clubbing, ejection murmur, located along the mid and upper
(L) sternal border
• CXR- typical boot shaped heart
• Surgical correction- usually at 6-12 months of age (open cardiac surgery) refer to hospital
• Management of anoxic spells
o Try at all costs to maintain a calm environment to lessen child’s agitation
o Place the child in knee-chest position
o Oxygen therapy
o Morphine sulphate 0.1-0.2 mg/kg SC or IM
o Sodium bicarbonate 1meq/kg IV in severe cases
o Propranolol 0.1mg/kg IV in prolonged spells

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 17: Congenital Heart Disease 135
 o Last 3 treatments are usually available at hospital level, so refer the child

Complications and Prevention of CHD

• Complications include thrombosis, cerebral abscess; heart failure is very rare (refer to
hospital)
• Prevention of infective endocarditis prior to dental extraction/surgery

Heart Failure
• Heart failure: The inability of the heart to pump enough blood to meet the body’s
circulatory and metabolic needs
• It does not occur on its own but has various causes

Causes
• Congenital heart diseases
o Ventricular septal defect, atrial septal defect, ToF, etc.
• Acquired heart disease
o Rheumatic heart disease, endocarditis, cardiomyopathies, etc.
• Non-cardiac causes
o Severe anaemia, severe malnutrition, fluid overload, septicaemia, etc.

Clinical Features and Investigation

• Symptoms
o Inability to feed well
o Cough
o Vomiting
o Fast breathing
o Excessive sweating
o Oedema
• Signs
o Tachycardia
o Difficulty breathing (dypnoea)
o Cold extremities
o Murmur
o Cardiomegaly
o Enlarged and tender liver
• Investigation is chest X-ray

Management
• Diuretics
o Furosemide 1 mg/kg IV, should cause increased urine flow within 2 hours
o If the initial dose is not effective, give 2 mg/kg and repeat in 12 hours, if necessary
o Thereafter, a single daily dose of 1 to 2 mg/kg orally is usually sufficient
o Oxygen, if the child has a respiratory rate of ≥70 per minute, shows signs of
respiratory distress or has central cyanosis, however oxygen may cause problems by
inducing pulmonary vasodilation in a child with cyanotic heart disease
o Refer to hospital for further management
• Consider giving Digoxin 0.02 - 0.05 mg/kg/day, start with ½ the dose, then ¼ after 8
hours and then ¼ after 16 hours (at hospital level)
• Supplemental potassium

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 17: Congenital Heart Disease 136
 o Supplemental potassium is not required when furosemide is given alone for treatment
lasting only a few days
o When digoxin and furosemide are given, or if furosemide is given for more than 5
days, give oral potassium (3 to 5 mmol/kg/day)
• Supportive care
o Avoid the use of IV fluids, where possible
o Support the child in a semi-seated position with head and shoulders elevated and
lower limbs dependent
o Relieve any fever with paracetamol to reduce the cardiac workload
• Monitoring
o Monitor respiratory and pulse rates, liver size and body weight to assess the response
to treatment
o Continue treatment until the respiratory and pulse rates are normal and the liver is
normal
o Refer to hospital for further management

Complications
• Renal failure
• Hypokalaemia
• Hyperkalaemia
• Hyponatraemia
• Impaired liver function
• Thromboembolism
• Atrial and ventricular arrhythmias

Key Points
• There are two types of congenital heart disease, cyanotic and acyanotic.
• The most common congenital cyanotic heart disease is Tetralogy of Fallot (TOF).
• The most common congenital acyanotic heart disease is Ventricular Septal Defect (VSD).
• A child should be referred to hospital after congenital heart disease is diagnosed.
• Heart failure is the inability of the heart to pump enough blood to meet the body’s
circulatory and metabolic needs.
• Management of heart failure has to be aggressive since the disease can damage other
important organs like the liver and kidneys.

Evaluation
• What is congenital heart disease?
• What are the top congenital cardiac anomalies?
• How are congenital heart diseases classified?
• What are the causes of heart failure?
• What are the common presenting features of heart failure?
• How is heart failure managed?
• What are the complications of heart failure?

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 17: Congenital Heart Disease 137
References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H.M., et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Mayer, D., & Mullins, C. (1988). Congenital Heart Disease, A Diagrammatic Atlas. New
York: Alan R. Liss, Inc.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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Session 17: Congenital Heart Disease 138
 Handout 17.1 Normal Heart Circulation

Source: Mayer & Mullins, 1988.

Legend:
• AO: Aorta
• PA: Pulmonary Artery
• RA: Right Atrium
• LA: Left Atrium
• RV: Right Ventricle
• LV: Left Ventricle

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Session 17: Congenital Heart Disease 139
 Handout 17.2: Congenital Anomalies

Figure 1: Transposition of Great Vessels

Source: Mayer & Mullins, 1988.

Legend:
1. Tricuspid valve atresia

Features:
• Tricuspid valve atresia
• Transposition of the great arteries
• Ventricular septal defect
• Atrial septal defect
• Small right ventricle (not depicted)

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Session 17: Congenital Heart Disease 140
Figure 2: Tetralogy of Fallot

Legend:
1. Ventricular septal defect
2. Valvular and infundibular pulmonary
stenosis
3. Overriding aorta
4. Right ventricular hypertrophy
5. Atrial septal defect (optional)

Source: Mayer & Mullins, 1988.

Figure 3: Truncus Arteriosus

Legend:
1. Truncus arteriosus (type I)
2. Ventricular septal defect
3. Atrial septal defect (vs. patent foramen
ovale) - optional
4. Truncal valve

Source: Mayer & Mullins, 1988.

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Session 17: Congenital Heart Disease 141
Figure 4: Tricuspid Atresia

Features:
• Tricuspid valve atresia
• Ventricular septal defect (restrictive)
• Hypoplastic right ventricle
• Small atrial septal defect

Source: Mayer & Mullins, 1988.

Figure 5: Atrial Septal Defect (ASD)

Features:
• Tricuspid valve atresia
• Ventricular septal defect (restrictive)
• Hypoplastic right ventricle
• Small atrial septal defect

Source: Mayer & Mullins, 1988.

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Session 17: Congenital Heart Disease 142
Figure 6: Ventricular Septal Defect (VSD)

Legend:
1. Tricuspid valve atresia

Features:
• Tricuspid valve atresia
• Transposition of the great arteries
• Ventricular septal defect
• Atrial septal defect
• Small right ventricle (not depicted)

Source: Mayer & Mullins, 1988.

Figure 7: Patent Ductus Arteriosus (PDA)

Features:
• Vascular ring caused by:
• Pulmonary artery sling (origin of left
pulmonary artery from right
pulmonary artery)
• Patent ductus arteriosus

• Left superior vena cava to coronary sinus

(optional)

Source: Mayer & Mullins, 1988.

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Session 17: Congenital Heart Disease 143
CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 17: Congenital Heart Disease 144
 Session 18: Acute Rheumatic Fever and Infective
Endocarditis
Learning Objectives
By the end of this session, students will be able to:
• Explain the causes of acute rheumatic fever and rheumatic heart disease
• Describe the clinical features of acute rheumatic fever
• Discuss the diagnosis, treatment and prevention of acute rheumatic fever
• Discuss the diagnosis, treatment and prevention of rheumatic heart disease
• Define infective endocarditis
• Outline the management of infective endocarditis

Overview of Rheumatic Fever

• Acute rheumatic fever: A diffuse inflammatory disease of connective tissue, primarily
involving the heart, blood vessels, joints, subcutaneous tissue and central nervous system
(CNS)
• Causes
o Follows 0.3% of cases of group A beta haemolytic streptococcal pharyngitis (throat
infection) in children
o Antibodies made against group A streptococcus cross-react with human tissue leading
to damage of the heart, joints and CNS
• Epidemiology
o Ages 5-15 yrs are most susceptible, rare <3 yrs
o All sexes are equally affected but girls > boys
o Common in developing countries
o Environmental factors include overcrowding, poor sanitation and poverty

Clinical Features of Rheumatic Fever

• Acute rheumatic fever develops 2 to 6 weeks after group A beta haemolytic streptococcal
infection of the throat or skin
• The modified Jones Criteria (revised in 1992) provide guidelines for the diagnosis of
rheumatic fever
• The criteria require the presence of 2 major or 1 major and 2 minor criteria
o Major criteria
ƒ Carditis
ƒ Polyarthritis
ƒ Chorea
ƒ Subcutaneous nodules
ƒ Erythema marginatum.
o Minor criteria
ƒ Fever
ƒ Arthralgia
ƒ Prolonged PR interval on ECG
ƒ Elevated acute phase reactants (increased erythrocyte sedimentation rate (ESR))
presence of C-reactive protein (CRP)
ƒ Leukocytosis

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• Additional evidence of previous group A streptococcal pharyngitis is required to diagnose
rheumatic fever
• One of the following must be present:
o Positive throat culture or rapid streptococcal antigen test result
o Elevated or rising streptococcal antibody titer
o History of previous rheumatic fever or rheumatic heart disease (RHD)
• These criteria are not absolute (diagnosis of rheumatic fever can be made in a patient with
chorea alone if the patient has had documented group A streptococcal pharyngitis)
• After a diagnosis of rheumatic fever is made, symptoms consistent with heart failure may
be indications of carditis and RHD

Major Manifestations
• Arthritis
o Most common symptom, and is frequently the earliest manifestation (70-75%)
o Flitting and fleeting migratory polyarthritis, involving major joints
o Commonly involved joints are the knee, ankle, elbow and wrist
o Occurs in 80% of children who have rheumatic heart disease
o Involved joints are exquisitely tender
o In children below 5 years, arthritis is usually mild but carditis more prominent
o Arthritis does not progress to chronic disease
• Carditis
o Occurs in 5 to 10% of cases
o May predispose individual to long-term valvular heart disease well after acute episode
o Commonly detected by a new murmur and tachycardia out of proportion to fever
o The only manifestation of rheumatic fever that leaves a sequelae and permanent
damage to the organ
o Valvulitis occurs in acute phase
o Chronic phase includes fibrosis, calcification and stenosis of heart valves
o Pancarditis is the most serious and second most common complication of rheumatic
fever (50%)
o In advanced cases, patients may complain of cough, difficulty in breathing or oedema
• Sydenham Chorea
o Occurs in 10 to 30% of patients with rheumatic fever
o Mainly in girls of 1 to15 years of age
o May appear even 6 months after the attack of rheumatic fever
o Presents with difficulty writing, involuntary grimacing, purposeless (choreiform)
movements of the arms and legs, speech impairment, generalized weakness, and
emotional liability
o Physical findings
ƒ Hyperextended joints
ƒ Hypotonia
ƒ Diminished deep tendon reflexes
ƒ Tongue fasciculations
ƒ ‘Milk sign’, or relapsing grip, demonstrated by alternate increases and decreases
in tension when the patient grips the examiner's hand
• Erythema Marginatum
o Occurs in 5 to 13% of cases
o Unique, transient, serpiginous-looking lesions of 1 to 2 inches in size
o Pale centre with red erythematous irregular margin
o More on trunks and limbs, non-itchy; never on the face

CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 18: Acute Rheumatic Fever and Infective Endocarditis 146
 o Exacerbated by heat
o May remain long past resolution of other symptoms
o Has been reported in association with sepsis and glomerulonephritis
• Subcutaneous nodules
o Infrequent manifestation
o Occurs in 0 to 10% of cases
o Painless, pea-sized, palpable nodules
o Mainly over extensor surfaces of joints, spine, scapulae and scalp
o Associated with strong seropositivity
o Always associated with severe carditis

Minor Manifestations
• Fever
• Arthralgia
• Prolonged PR interval
• Raised ESR
• Presence of CRP
• Leukocytosis

Note: Other features (not used in diagnostic criteria but can occur) include pallor, anorexia
and weight loss

Diagnosis, Treatment and Prevention of Rheumatic Fever

Diagnosis
• Rheumatic fever is mainly a clinical diagnosis
• No single diagnostic sign or specific laboratory test is available for diagnosis
• Diagnosis is based on modified Jones Criteria

Differential Diagnosis
• Idiopathic rheumatoid arthritis
• Pyogenic arthritis
• Sickle cell anaemia
• Myocarditis

Treatment and Prevention

• Step I
o Primary prevention (eradication of residual streptococcal infection)
ƒ Give Benzathine penicillin 50,000 mg/kg IM stat OR
ƒ Phenoxymethylpenicillin 250 mg 8 hourly for 10 days OR
ƒ Erythromycin 12.5 mg/kg 8 hourly for 10 days
• Step II
o Anti inflammatory treatment (aspirin, steroids)
ƒ Give Aspirin 10 to 20 mg/kg orally 4-6 hourly OR
ƒ Prednisolone 2 mg/kg/day, tapering to 1mg/kg/day
• Step III
o Supportive management and management of complications
ƒ Bed rest
ƒ Treatment of congestive cardiac failure (digitalis, diuretics)

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 ƒ Treatment of chorea (diazepam or haloperidol)
ƒ Rest to joints and supportive splinting
• Step IV
o Preventive (secondary) and prophylactic therapy is indicated after rheumatic fever and
RHD to prevent further attack
o The initial course of antibiotics given to eradicate the streptococcal infection also
serves as the first course of prophylaxis
o An injection (IM) of 0.6 (if weight < 27kg) to 1.2 million units of benzathine
penicillin G every 3-4 weeks is recommended for secondary prevention
ƒ The prophylaxis should be continued indefinitely for patients at high risk (e.g.
health care workers)
ƒ Patients with rheumatic fever without carditis should receive prophylactic
antibiotics for 5 years, or until age 21 years, whichever is longer
ƒ Patients with rheumatic fever and carditis but no valve disease should receive
prophylactic antibiotics for 10 years or well into adulthood, whichever is longer
ƒ Patients with rheumatic fever and carditis and valve disease should receive
antibiotics at least 10 years or until age 40 years
o Patients with RHD require antibiotic prophylaxis before certain surgical and dental
procedures to prevent bacterial endocarditis
ƒ Patients who have had rheumatic fever without valve disease do not need
prophylaxis for prevention of endocarditis
ƒ Penicillin should not be used for prophylaxis of endocarditis in patients who are
receiving secondary rheumatic fever prophylaxis because of resistance, the
recommended alternative is erythromycin

Rheumatic Heart Disease (RHD)

• The most serious complication of rheumatic fever
• As many as 39% of patients with acute rheumatic fever may develop varying degrees of
pancarditis with associated valve insufficiency, heart failure, pericarditis, and even death
• With chronic RHD, patients develop valve stenosis with varying degrees of regurgitation,
arrhythmias, and ventricular dysfunction
• Like acute rheumatic fever, RHD is thought to result from an autoimmune response, but
the exact pathogenesis remains unclear
• A diagnosis of RHD is made after confirming antecedent rheumatic fever
• Physical findings include cardiac and noncardiac manifestations of acute rheumatic fever
• Some patients develop cardiac manifestations of chronic RHD
• Cardiac manifestations of acute rheumatic fever are carditis, pancarditis, congestive
cardiac failure (CCF) and pericarditis
• If moderate to severe carditis is indicated by cardiomegaly or CCF, oral prednisone
should be added to salicylate therapy (refer to hospital)
• Additional treatment for patients with acute rheumatic fever and CCF include digoxin,
diuretics, oxygen, bed rest, and sodium and fluid restriction (refer to hospital)

Infective Endocarditis
• Infective endocarditis: A microbial infection of the endothelial surface of the heart
• Site of infection and pathogenic risk factors are essential in therapeutic and prognostic
considerations
• Can be seen in children with pre-existing valvular heart disease such as that caused by
rheumatic fever

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• The overall mortality rate is approximately 16 to 25%, and is mostly due to secondary
congestive heart failure (CHF)
• No predilection for race or sex
• Incidence of bacterial endocarditis in children with congenital heart disease (CHD)
continues to rise
• S aureus is the most common cause of acute bacterial endocarditis
• Factors that increase the risk of complications
o Prosthetic valve endocarditis
o Left-sided endocarditis
o Infection with Staphylococcus aureus or fungi
o Previous endocarditis
o Cyanotic congenital heart disease
o Systemic-to-pulmonary shunts
o Poor response to antibiotic therapy
• Clinical features
o Patients may present with nonspecific symptoms, but 85 to 99% of patients are febrile
o Other features are diverse and may include
ƒ Fatigue
ƒ Chills
ƒ Sweats
ƒ Anorexia
ƒ Malaise
ƒ Cough
ƒ Headache
ƒ Myalgia and/or arthralgia
ƒ Confusion
ƒ Heart failure
ƒ Splenomegaly
ƒ Hepatomegaly
ƒ Renal insufficiency, which may cause hematuria
o Patients with acute bacterial endocarditis present with an acute, toxic, febrile illness
and symptoms that have lasted < 2 weeks
o Extracardiac manifestations are less common in children than in adults
ƒ Petechiae are the most common of these symptoms (20-40%)
o In neonates, endocarditis commonly produces septic embolic phenomena, such as
osteomylitis, meningitis, and pneumonia
o Neonates may also have feeding problems, respiratory distress, tachycardia, or
neurologic symptoms
• Treatment
o Patients with CHD and fever require special consideration
o IV Ampicilin, IV Cloxacillin and Gentamycin
o Refer the child to hospital
• Prophylaxis is given before and after
o Oral surgery (e.g. tooth extraction) - Amoxicillin
o Catheterization/ rectal surgery -Amoxicillin and gentamycin

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Key Points
• Acute rheumatic fever is a diagnosed using the modified Jones Criteria.
• Prevention against further attacks is important.
• Rheumatic heart disease is the most serious complication of rheumatic fever.
• Clinical features for infective endocarditis are diverse, but factors that increase risk of
complications include cyanotic congenital heart disease.
• Antibiotic prophylaxis against bacterial endocarditis is recommended before and after
surgery in children with rheumatic- and congenital- heart disease.

Evaluation
• What is acute rheumatic fever?
• Why should preventative antibiotics be given to children with history of rheumatic fever?
• What are the clinical features of rheumatic heart disease?
• What are the clinical features of infective endocarditis in neonates?

References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H M, et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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 Session 19: Urinary Tract Disorders
Learning Objectives
By the end of this session, students are expected to be able to:
• Describe common urogenital anomalies
• Describe the causes and management of haematuria
• Describe the management of haematuria
• Explain the management of a child with urinary schistosomiasis
• List the risk factors for urinary tract infections
• Describe the clinical features and treatment of urinary tract infections

Balanitis, Phimosis, Paraphimosis and Hypospadias

Balanitis
• The inflammation of the glans penis
• The glans of the uncircumcised penis is protected by a layer of loose skin called the
foreskin or prepuce
• Often associated with phimosis
• Infection can occur beneath the foreskin, and if severe, pus may appears
• Infection may cause considerable redness and swelling of the penile shaft, necessitating
treatment with antibiotics
• Clinical features
o Mild cases - itching and discharge
o Severe cases - glans and foreskin red raw, and pus exudates
o Monilial (fungal) infections are quite common under the prepuce
• Treatment
o Broad spectrum oral or topical antibiotics and anti-fungals
o Local hygienic measures

Phimosis
• Condition in which the opening at the tip of the foreskin has narrowed down to such a
degree that the foreskin cannot be retracted
• The external urethral meatus is not visible
• It can be treated by application of steroid ointment in most boys, and this usually obviates
the need for circumcision
• Marked inflammation, infection, skin splitting and balanitis xerotica obliterans can lead to
marked scarring of the foreskin and phimosis, and in many of these children the treatment
of choice is circumcision
• Sometimes the severity of phimosis is such that there is ballooning of the foreskin on
micturition, and on rare occasions it may even cause urinary retention with a distended
bladder
• Cases of severe urinary obstruction require referral for surgical consultation

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Paraphimosis
• Occurs when a mildly phimotic foreskin has been retracted over the glans and has become
stuck behind the coronal groove, causing oedema of itself and the glans penis
• It is a painful and progressive process
• Treatment involves gentle manipulation of the foreskin forwards (may require a general
anaesthesia)
• Circumcision is not performed at this time, but a few children may need it later if the
phimosis does not respond to topical application of steroid ointment

Hypospadius
• Condition in which the external meatus opens abnormally on the underside (ventral
aspect) of the penis or perineum and the inferior aspect of the prepuce, and it is poorly
developed
• Severe cases can be confused with ambiguous external genitalia
• Most cases should be referred to urologist
• Hypospadius occurs in 1 in 350 male births and is the most common congenital
malformations of the urethra
• Classification and Treatment
o Glandular hypospadius is the most common, and does not need treatment unless the
meatus is stenosed, and then a meatotomy is performed
o Coronal hypospadius
o Penile hypospadius
o Perineal hypospadius most severe
o Refer the last three types for surgery by paediatric urologist
• These children should NOT be circumcised

Congenital Posterior Urethral Valves and Bladder Extrophy

Congenital Posterior Urethral Valves

• Symmetrical folds of urothelium which can cause obstruction of the urethra
• They are found distal to the verumontarum, but may be within the prostatic urethra
• Behave as flap valves so urine does not flow normally, however a urethral catheter can be
passed without difficulty
• Usually presents with recurrent urinary tract infections (UTIs)
• Diagnosis is by ultrasound scanning and voiding cystogram
• Treatment is by insertion of suprapubic catheter to relieve the backpressure, and then
refer for surgery

Bladder Extrophy
• Congenital anomaly characterized by exposure and protrusion of posterior wall of the
bladder
• The trigone of the bladder and the ureteric orifices are exposed and urine dribbles
intermittently from the everted bladder
• Epispadias and separation of pubic bones are associated with complete bladder extrophy
• In some cases, the penis is divided in two parts and the halves of the scrotum are widely
separated
• Causes
o Incomplete median closure of inferior part of the anterior abdominal wall

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 o Results from failure of mesenchyme cells to migrate between the ectoderm of the
abdomen and cloaca during the 4th week of gestation
o Then the inferior parts of the rectus muscles are absent, and the external and internal
oblique and the transverse abdominal muscles are deficient
o No muscle or connective tissue form in the anterior abdominal wall over the urinary
bladder, hence the thin epidermis and anterior wall of the bladder rupture, causing
wide communication between the exterior and the mucous membrane of the bladder
• Types
o Presence of an intravesical septum to complete bladder duplication
o Exstrophy of one or of the bladders duplicated

Haematuria
• The presence in urine of five or more red blood cells per high power field (≥ 5/hpf)
• Can be macroscopic (seen with naked eye) or microscopic (seen with aid of microscope)
• Can be symptomatic or asymptomatic
• Causes
o Renal
ƒ Acute glomerulonephritis (AGN)
ƒ Infections (e.g. pyelonephritis)
ƒ TB of kidney
ƒ Sickle cell anaemia
ƒ Wilm’s tumour
ƒ Trauma
o Ureter – rarely stones
o Urinary bladder
ƒ Infections (e.g. cystitis, schistosomiasis)
ƒ Trauma
o Urethra
ƒ Urethritis
ƒ Trauma
• Diagnosis
o History
ƒ Duration and recurrence
ƒ Features suggestive of UTI (e.g. dysuria and frequency)
ƒ Terminal haematuria suggests urinary schistosomiasis
ƒ Loin pain suggests pyelonephritis
ƒ Recent sore throat or skin infection suggests post-streptococcal AGN
o Physical findings
ƒ Fever suggests UTI
ƒ Facial puffiness and high blood pressure suggests AGN
ƒ Abdominal mass suggests Wilm’s tumour
ƒ Tenderness at suprapubic region suggests cystitis
• Investigations
o Urine analysis
ƒ Macroscopic – gross haematuria
ƒ Microscopic – red blood cells
ƒ Pus cells and or white blood cells
ƒ Casts
ƒ Protein

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 ƒ Leukocyte esterase or nitrites (if available on urine dipstick)
ƒ Urine culture, abdominal ultrasound, creatinine, urea and electrolytes – can be
done at hospital level
• Treat the cause according to presentation and investigation findings

Urinary Schistomiasis
• A chronic parasitic infection caused by blood flukes of the genus Schistosoma, and the
specie Schistosoma haematobium
• The flukes live in the vesicle veins of the pelvic plexus, lay eggs that are passed in urine,
thus the name urinary schistosomiasis
• Most common form of schistosomiasis found in children
• The disease is only found in the tropics
• Transmission
o The life cycle of schistosomias is divided into two phases
ƒ The sexual phase in the vascular system of the definitive host
ƒ The asexual phase in the intermediate aquatic snail host
ƒ Refer to the life cycle in Communicable Diseases Module Session 20
o The schistosoma migrate to portal blood in liver, and mature into adults
o Male and female schistosomes pair and migrate to the preferred site, the vesicle and
pelvic plexus of veins, and start laying eggs
• Clinical Features
o Swimmer’s itch (cercarial dermatitis) at the site of cercariae penetration
ƒ Persists for up to 72 hours after exposure
o Acute infection may present with Katayama fever (4-8 weeks after exposure)
o Pain when passing urine
o Frequency
o Lower abdominal pain
o Recurrent painless terminal haematuria
• Investigations and Treatment
o Investigations
ƒ S. haematobium ova (eggs) ovoid with a terminal spine in urine
ƒ Maximum excretion of ova occurs at midday
o Treatment
ƒ Praziquantel 40mg/kg/day in two divided doses
• Complications
o Ureteric orifice obstruction
o Ureteric stenosis
o Bladder calcification
o Renal failure
o All of the above can lead to obstructive uropathy
o Predisposition to E. coli or Salmonella urinary tract infections that can lead to chronic
pyelonephritis and Gram negative septicaemia

Urinary Tract Infections (UTIs)

• Infection of the urinary tract which comprises the kidneys, ureters and urinary bladder
• Microorganisms reach the urinary tract system by either ascending from the urethra, or
spreading to the kidney from the bloodstream
• Risk factors
o At young ages, more common in girls than boys

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 o Increased frequency of UTI in malnourished children in the tropics
o Congenital anatomical abnormalities of the urinary tract or vesico-ureteral reflux, also
those with bladder outlet obstruction and patients with indwelling bladder catheters
o Diagnosis of UTI in an infant or a child may be a possible indicator of an underlying
structural or functional abnormality, which may require specific therapy to prevent
progressive renal damage
• Causes
o Majority of uncomplicated UTIs are caused by Escherichia coli
o Other bacteria include Klebsiella in neonates, proteus in older boys, and coagulase-
negative staphylococcus in pubertal children
o Where an underlying structural abnormality is present, pseudomonas, enterococcus
and even Candida albicans may be the invading organisms
• Clinical Features
o Symptoms of UTI are influenced by age and sex of the patient, presence of
complications, site of infection, and a number of previous infections
o Infants tend to present with non-specific symptoms such as fever, vomiting and
diarrhoea, failure to thrive, feeding problems and irritability
o In addition to the above, a young child may complain only of abdominal pain
o The older child may have loin pain or pain over the kidney area, or symptoms directly
related to urination such as frequency, urgency, dysuria, enuresis or cloudy urine
o Constipation may be present as the child may avoid defecation due to fear of pain
o Careful clinical examination may:
ƒ Reveal enlarged kidneys due to hydronephrosis, with or without distended bladder
due to bladder outlet obstruction
ƒ Identify abnormalities causing obstruction of the flow of urine such as in
congenital posterior urethral valves (rare in infant boys), or in chronic
unrecognized phimosis
o UTI may also occur in child with neurological abnormalities such as spinal bifida or
spinal injury with paraplegia, therefore these must be excluded
o Local features such as pain or discomfort on passing urine (dysuria) may be due to:
ƒ Vulvitis in girls or uncommon balanitis in uncircumcised boys
ƒ Injury/trauma to the urethra from young children inspecting their urethral
openings and inserting foreign bodies or sexual abuse
• Investigations
o Urinalysis (urine for microscopy) - take a fresh, clean mid-stream urine
ƒ More than 15WBC/HPF in centrifuged (or 5 WBC/HPF in uncentrifuged) urine,
almost always combined with proteinuria suggests UTI
o Urine for culture and sensitivity
o Ultrasound scan and/or intravenous urethrogram
Note: Ensure the child is well hydrated, and is drinking an adequate amount of water
• Treatment
o Cotrimoxazole
ƒ 120mg BD for children 6 weeks to 5months old
ƒ 240mg BD for children 6 months to 5 years old
ƒ 480mg BD for children 5 years of age and up
ƒ Duration of treatment is 7 to 14 days
o Nitrofurantoin
ƒ 5mg/kg/day in three to four divided doses for 7days, in lower UTI with pain and
dysuria without fever
ƒ Not to be given to a child with G6PD deficiency

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Session 19: Urinary Tract Disorders 155
 o When upper urinary tract involvement is suspected, parenteral antibiotics such as
gentamicin should be used
ƒ Dosage: injection Gentamicin (2.5 mg/kg per dose b.i.d or 5-7.5mg/kg once daily)
for 7-10 days
ƒ If renal impairment is present, use alternative drugs or adjust the dosages
ƒ A 3rd generation cephalosporins with less nephrotoxic side-effects may be safe
Note: Chronic UTI will permanently damage the kidneys, so if UTI has not cleared up after 2
weeks of treatment refer the child to hospital

Activity: Case Study

Instructions
Read the following scenario. In small groups, based on information from the scenario, discuss
the recommended treatment.

Scenario
James, a seven year old boy, presents to you following two episodes of balanatis. He also
complains of discomfort during urination. Examination revealed a tight foreskin that could
not be retraced, the urethral meatus could not be seen and laboratory urine analysis revealed
20 WBC/HPF.

Key Points
• Balanitis is often associated with phimosis.
• Paraphimosis is a painful and progressive process.
• Hypospadia is an abnormal location of the external urethra meatus on the ventral aspect
of the penis.
• Diagnosis of posterior urethral valves is by radiological methods, and surgery is the
treatment of choice.
• In bladder extrophy urine dribbles intermittently from the everted bladder.
• Treat a child with haematuria according to the underlying cause.
• The main presenting feature of urinary schistomiasis is terminal haematuria.
• Early diagnosis and treatment of UTIs is very important to avoid permanent renal
damage.

Evaluation
• What is balanitis?
• How do we treat phimosis?
• At what age do we correct hypospadius?
• What are the investigations for posterior urethral valve?
• What are the types of bladder extrophy?
• What are the non-renal causes of haematuria?
• How does the transmission of urinary schistosomiasis occur?
• What are the clinical features of UTIs?

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References
• Beattie, J., Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia H.M., et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Mayer, D., & Mullins, C. (1988). Congenital Heart Disease, A Diagrammatic Atlas. New
York: Alan R. Liss, Inc.
• Russell, R.C.G., et al. (2004). Baily and Love’s Short Practice of Surgery. (24th ed.) USA:
Oxford University Press.
• Stanfield, P., Bwibo, N. (2005). Child Health: A Manual for Medical and Health Workers
in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M., Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA: Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 19: Urinary Tract Disorders 158
 Session 20: Nephrotic Syndrome and Acute
Glomerulonephritis
Learning Objectives
By the end of this session, students are expected to be able to:
• Define nephrotic syndrome
• Describe the diagnosis, investigations and treatment of nephrotic syndrome
• List the complications of nephrotic syndrome
• Define acute glomerulonephritis
• Describe the causes, clinical presentation and management of acute glomerulonephritis

Epidemiology and Causes of Nephrotic Syndrome

• Nephrotic Syndrome (NS) is primarily a paediatric disorder
• The syndrome is characterized by excessive proteinuria, hypoalbuminemia,
hyperlipidemia/hypercholesteremia and oedema
• Conditions that cause NS always affect the glomeruli and so there is structural damage to
the glomerular basement membrane leading to increase in size and number of pores and
reduction in fixed charge

Epidemiology
• Incidence is 2 to 3cases per 100,000 children per year
• Age related differences in incidence of different causes
o Congenital NS in neonates
o Minimal change disease in older children
o Sclerotic lesions common in black races
o Focal segmental and membranous lesions- later in life
• Most children (90%) with NS have idiopathic NS
• Histopathological presentation of idiopathic NS
o Minimal change disease- 85%
o Mesangial proliferation- 5%
o Focal segmental glomerulosclerosis- 10%
• The remaining 10% of children with NS have secondary NS related to glomerular
diseases
o Glomerulonephritis
o Systemic disorders with glomerular involvement
o Disorders due to mechanical causes producing elevated renal venous pressure
o Primary NS

Causes of Nephrotic Syndrome

• Glomerulonephritis
o Glomerular disease of acute onset
o Glomerular disease of acute onset with rapid progression
o Slowly progressing glomerular disease
• Systemic disorders with glomerular involvement
o Diabetes mellitus (DM)
o Systemic lupus erythematosus (SLE)
o Amyloidosis

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 o Multiple myeloma
• Infections
o Malaria
o Bacterial infections
o Viral (e.g. hepatitis, HIV)
o Syphilis
• Disorders caused by allergens/drugs
o Bee sting(s)
o Pollens
o Heavy metals and poisons (e.g. penicillamine, gold, mecury)
• Disorders due to mechanical or other causes producing elevated renal venous pressure
ƒ Renal vein thrombosis
ƒ Tricuspid disease
ƒ Constrictive pericarditis
o Primary nephrotic syndrome
o Congenital nephrosis
o Acquired nephrosis (minimal change, sclerosing and proliferative lesions)

Diagnosis, Investigation and Treatment of Nephrotic Syndrome

Diagnosis
• History of generalized body swelling
• May also have anorexia, weakness/malaise, morning swelling of the eye lids and or frothy
urine
• Examination reveals facial puffiness and periorbital oedema, ascites, lower limb oedema,
or anasarca
• Features of the underlying disorder (e.g. butterfly rash of the face in SLE)

Investigations
• Urine
o Urine for analysis and culture
o 24 hour urinary protein- heavy protenuria (+3 or +4 protenuria, or > 40mg/m2/hr)
o Protein excretion exceeds 2g/24 hr
• Blood tests
o Plasma albumin, lipids/cholesterol, electrolytes
o Renal function test (BUN and creatinine)
o Full blood count and ESR
o Hepatitis B surface antigen, hepatitis C antibody
o Serum ASO titre (ASOT)
o Complement (C)3 and C4 components of complement
o Antinuclear factor in selected cases
• Throat swab for culture (group A Streptococcus)
• Selective protein clearance
• Renal biopsy (at hospital level) if:
o Onset at less than 6 months of age or congenital NS
o Persistent microscopic haematuria if associated with hypertension and/or low plasma
C3

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Treatment
• Identify and treat the underlying cause
• Treat/manage symptoms
• Prevent complications
• General measures:
o Dietary protein and salt restriction (controversial)
o Salt free albumin infusion (not done in Tanzania)
o Input/Output -Restrict fluid 300 to 400 ml/m2
o Monitor vital signs (BP, body weight) and urine output
o Child should be actively mobilized and bed rest avoided
o Diuretics are rarely needed and must be used cautiously to avoid intravascular volume
contraction
o Hypertension is relatively uncommon, even during corticosteroid therapy, but when
persistent, antihypertensives are required
o A major aspect of the initial management is parental education
• Specific measures
o Minimal change disease is treated with corticosteroid therapy in which prednisolone
for 8 weeks is used
o Initial episode
ƒ Prednisolone 60mg/m2/day until remission, followed by 40mg/m2 on alternative
days for 4 weeks
o Relapse
ƒ First two relapses treat as above and then maintenance prednisolone 0.1-0.5mg/kg/
alt days for 3 to 6 months then reduce
ƒ Relapse on prednisolone more than 0.5mg/kg/ alt day give Levamisole 2.5mg/kg/
alt day for 4 to 12 months
ƒ Relapse on prednisolone more than 0.5mg/kg/alt day and Levamisole use
cyclophosphamide or cyclosporine (hospital level in order to monitor side effects)
ƒ Cyclophosphamide 3mg/kg/day for 8 weeks
ƒ Cyclosporine A 5mg/kg/alt day for 1 year
o SLE - give steroids, azathioprine or cyclophosphamide
o For discussion with paediatric nephrologists
ƒ Onset of NS between 6 and 12 months of age or congenital NS
ƒ Persistent hypertension, microscopic haematuria, or low plasma C3
ƒ Renal failure, persistent and not attributed to hypovolemia
o Post treatment- steroid resistance
ƒ Persistence of protenuria after 4 weeks daily prednisolone (2mg/kg/day) or
equivalent, a biopsy should be arranged if practicable (hospital level)

Complications and Prognosis of Nephrotic Syndrome

Complications
• Infections
o Many different types of infections possible, including upper respiratory infection,
urinary tract infection, peritonitis, pneumonia, emphysema, gastroenteritis
o Acute bacterial infections are relatively common, and most commonly caused by
Streptococcus pneumoniae
o Occasionally, other encapsulated organisms and gram-negative E. coli are isolated
o Abnormalities associated with NS that predispose patients to bacterial infections
ƒ Abnormalities of cellular and humoral immunity

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 ƒ Low serum IgG (only partly explained by urinary losses)
ƒ Decreased rates of immunoglobulin synthesis and increased catabolism
ƒ Decreased serum levels of complement components of the alternative pathway
impair plasma bacterial opsonic activity
ƒ Local factors related to tissue oedema, breakdown of the skin barrier, and the
presence of peritoneal fluid which is a rich culture medium, might also facilitate
infections
ƒ These factors are compounded by the use of immunosuppressive drugs
• Thrombotic disease
o Most serious potential complication
o Virtually all nephrotic patients have hypercoagulable state
o As many as 20% experience thrombotic events that are often clinically silent
• Cardiovascular disease
o Children with chronic relapsing NS are at increased risk of developing premature
atherosclerotic disease.
ƒ Adequate data for this is currently not available
o Children as young as 5 years old who have died from NS have been found on autopsy
to have atheromatous lesions

Prognosis
• Before introduction of antibiotics and corticosteroids, 40% of cases died within 5 years of
diagnosis
• Deaths were mostly caused by infectious complications
• Nowadays more than 95% of these children are still alive at 20-25 years, although
mortality has not been eradicated
• Roughly 30% of children will respond to a single course of steroids and thus be ‘cured’
• A young age at onset, along with several relapses in the first year after diagnosis, indicate
poor prognosis
• 8 to10 years after diagnosis, 80% achieve a permanent remission
• A small number continue to experience relapses even into adulthood

Acute Glomerulonephritis
• Acute glomerulonephritis (AGN): A clinical condition caused by inflammatory changes
in the glomeruli and is characterized by:
o Oedema
o Hypertension
o Haematuria
o Proteinuria
• Most common cause is post group A β haemolytic streptococcal throat and skin infection
• Rare causes include systemic lupus erythematosus (SLE) and IgA nephropathy

Clinical Features
• Oedema (puffiness of the face/periorbital swelling that is more marked on waking up)
• Hypertension
• Haematuria (dark urine)
• Oliguria
• Evidence of preceding streptococcal infection

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Complications
• Nephrotic syndrome
• Cardiac failure
• Uraemic encephalopathy (presenting with convulsions)
• Acute renal failure

Investigations
• Urine
o Protein
o Red blood cells
o Casts
• Other tests (performed at hospital level)
o Abdominal ultrasound
o Creatinine
o BUN
o Electrolytes

Treatment and Monitoring

• Eradicate residual streptococcal infection
• Penicillin/Erythromycin for 10 days/single dose of Benzathine penicillin
• Treat hypertension (Furosemide 1 to 2 mg/kg/day, Nifedipine 0.25 mg/kg/day)
• Monitor blood pressure, fluid intake and output, other vital signs
• Refer to hospital

Prevention
• Prompt systemic antibiotic therapy for streptococcal throat and skin infections
• Treat family members

Key Points
• Nephrotic syndrome is characterized by excess proteinuria, hypoalbuminemia,
hyperlipidemia and oedema.
• Nephrotic syndrome is primarily a paediatric disorder and is 15 times more common in
children than adults.
• Most of the deaths attributed to nephrotic syndrome are because of infectious
complications.
• Acute glomerulonephritis is a clinical condition caused by inflammatory changes in the
glomeruli.
• Some children with glomerulonephritis may complicate to nephrotic syndrome.

Evaluation
• What are the presenting features and causes of nephrotic syndrome?
• What are the common medical complications of nephrotic syndrome?
• What are the clinical features of glomerulonephritis?
• How is glomerulonephritis managed?

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References
• Beattie, J., & Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., & Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia, H.M., et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., & Bwibo, N. (2005). Child Health: A Manual for Medical and Health
Workers in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M.,& Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA:
Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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 Session 21: Disorders of the Musculoskeletal System
Learning Objectives
By the end of this session, students are expected to be able to:
• Define and list the causes of acute flaccid paralysis (AFP)
• Define poliomyelitis, acute osteomyelitis and septic arthritis
• Describe clinical presentation of poliomyelitis, acute osteomyelitis and septic arthritis
• Describe the management of poliomyelitis, acute osteomyelitis and septic arthritis
• Describe the follow up and prevention of patients with poliomyelitis

Overview of Acute Flaccid Paralysis (AFP) in Children

• Focal weakness or paralysis characterized as flaccid (reduced tone) without other obvious
cause (e.g., trauma)
• AFP surveillance is conducted in an attempt to:
o Identify cases of AFP (including GBS and transverse myelitis)
o Investigate all reported cases for evidence to rule out or to confirm paralytic
poliomyelitis

Clinical Presentation
• Presents with weakness of skeletal or cranial muscle groups
• AFP with deeper brain involvement presents with:
o Spasticity, hypertonia
o Respiratory and cardiac arrhythmias, blood pressure and vasomotor changes
o Bladder and bowel dysfunction

Causes
• May be caused by a number of agents including enterovirus, echovirus or adenovirus
• Paralytic polio caused by wild or vaccine-associated poliovirus
• Campylobacter jejuni has also been associated with AFP in the form of GBS
o AFP is a paralysis caused by the infection while the GBS is a post infectious
complication
• Other causes of AFP
o Congenital disorders (e.g. spina bifida)
o Tuberculosis of the spine
o Trauma
ƒ Injuries during delivery, facial nerve and brachial plexus injury
ƒ Cranial birth injury (e.g. cerebral palsy)
ƒ Fracture/dislocations of vertebrae (falls, road traffic accidents, etc.)
o Disease of the muscles (e.g. Duchenne muscular dystrophy)
• It is essential to report all cases of AFP to local district medical officer

Overview of Poliomyelitis in Children

• An acute viral infection of the anterior-horn cells of the spinal cord and sometimes of the
lower part of the brain
• Polio virus types 1, 2, and 3 are usually spread by faeco-oral contamination

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 o Humans are the sole natural reservoir
• Incubation period is about 10 days and the first week of disease is the most infectious
• Polio (poliomyelitis) mainly affects children under five years of age
• One in 200 infections leads to irreversible paralysis (usually in the legs)
• Among those paralysed, 5% to 10% die when their breathing muscles become
immobilized

Clinical Presentation

Figure 1: Clinical Features of Poliomyelitis

Type of Infection Clinical Presentation

Asymptomatic infection 95% of infected persons are asymptomatic

Abortive form (non Fever, malaise, anorexia, nausea, vomiting, headache,
specific febrile illness) pharyngitis, abdominal pain
Similar to the abortive form plus stiff neck and signs of
meningeal inflammation, soreness of back muscles, tripod sign,
Nonparalytic form
positive kerning and brudzinski signs, and bulging fontanel;
(aseptic meningitis)
decrease in both superficial (cremasteric, abdominal) and deep
tendon reflexes heralds paralysis
Paralytic forms (see below)
Axial and extremity muscle weaknesses that may involve
Spinal form
intercostals muscles and diaphragm
Cranial nerve weakness and respiratory and circulatory
Bulbar form
disturbances
Encephalitic form Irritability, disorientation, drowsiness and tremors

Paralytic Polio
• Most common in children
• In around 1% of infections, poliovirus spreads along certain nerve fibre pathways,
replicating in and destroying motor neurons within the spinal cord, brain stem or motor
cortex
• This leads to the development of paralytic poliomyelitis, the various forms of which
(spinal, bulbar and bulbospinal) vary only with the amount of neuronal damage and
inflammation that occurs, and the region of the CNS that is affected
• Early symptoms of paralytic polio
o High fever
o Headache
o Stiffness in the back and neck
o Asymmetrical weakness of various muscles
o Sensitivity to touch
o Difficulty swallowing, muscle pain
o Loss of superficial and deep reflexes
o Paresthesia (pins and needles)
o Irritability
o Constipation or difficulty urinating

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• Paralysis generally develops 1 to 10 days after early symptoms begin, progresses for two
to three days, and is usually complete by the time the fever breaks
• The paralysis of poliomyelitis is characteristically asymmetric, the legs are affected more
often than the arms
• The likelihood of developing paralytic polio increases with age, as does the extent of
paralysis
• In children, non-paralytic meningitis is the most likely consequence of CNS
involvement, and paralysis occurs in only 1 in 1000 cases
• In children under five years of age, paralysis of one leg is most common

Diagnosis
• History
• Clinical presentation
• Investigations
o Stool to recover the virus
o Pharyngeal secretions for recovering polio virus
o Lumbar puncture to exclude meningitis

Differential Diagnosis
• GBS
• Transverse myelitis
• Traumatic neuritis

Care, Follow Up and Prevention of Poliomyelitis in Children

Care
• Strict bed rest
• No injections, may cause paralysis
• When the acute stage is settled, gentle exercise of the affected limbs should be
commenced
• Prevention of contractures (e.g. splinting, supporting limbs)
• Initiate passive exercises of the paralyzed muscle groups
• Prevent bed sore by changing position frequently
• Provide warmth in paralyzed limb to improve circulation
• Active physiotherapy after acute stage
• After discharge from the hospital, the child should be seen regularly to ensure flexion
deformities are not occurring
• Special shoes and callipers may help severely affected children walk again

Follow Up
• Regular out-patient supervision in regard to the physical and emotional state
• Social and economical support is frequently necessary
• Orthopaedic surgeon will advise on the adjustment of appliances to prevent deformity and
improve function
• Surgical treatment may be needed to overcome soft tissue contractures, improve function
and prevent deformity
• Leg length inequality may need correction

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Prevention
• If polio occurs in your area, notify the district medical officer immediately
• Sabin oral vaccine effectively prevents children from getting poliomyelitis
• There are four core strategies to stop transmission of the wild poliovirus in areas that are
affected by the disease or considered at high risk of re-infection:
o High infant immunization coverage with four doses of oral poliovirus vaccine (OPV)
o Supplementary doses of OPV to all children under five years of age
o Surveillance for wild poliovirus through reporting and laboratory testing of all acute
flaccid paralysis (AFP) cases among children under fifteen years of age
o Targeted “mop-up” campaigns once wild poliovirus transmission is limited to a
specific focal area (not done in Tanzania)

Overview of Joint Swelling in Children

• Joint swelling: The pathological enlargement or growth of one or more of the body joints
• It may or may not be associated with pain

Osteomyelitis in Children
• An acute or chronic inflammatory process of the bone and its structures secondary to
infection with pyogenic organisms
• Acute osteomyelitis is commonly caused by Staphylococcus aureus
• Pathophysiology of acute osteomyelitis
o The infection associated with osteomyelitis may be localized or it may spread through
the periosteum, cortex, marrow, and cancellous tissue
o The bacterial pathogen varies on the basis of the patient's age and the mechanism of
infection
o Two primary categories of acute osteomyelitis:
ƒ Hematogenous osteomyelitis- caused by bacterial seeding from the blood,
characterized by an acute infection of the bone, primarily occurs in children, site
of infection is commonly the metaphysic where blood supply is richest in the
growing bones of young children
ƒ Direct or contiguous inoculation osteomyelitis
• Clinical presentation of acute osteomyelitis
o High fever
o Rigors malaise and anorexia
o Localized intense pain
o Tenderness is confined to infected area of bone
o Movement at joint is not restricted
o Acute hematogenous osteomyelitis, despite its name, may have a slow clinical
development
• Complications include chronic osteomyelitis, leg-length discrepancy, spreading of
infection, septicaemia

Septic Arthritis in Children

• Inflammation of a synovial membrane with purulent effusion into the joint capsule,
usually due to bacterial infection
• Also referred to as bacterial, suppurative, purulent, or infectious arthritis
• Septic arthritis is a rare but important disease that typically affects monoarticular joints
• The age range of those affected is broad, from the neonatal period to advanced age

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• Acute septic arthritis, arising directly from the blood stream, is commonly seen in young
infants
• The infection is usually secondary to an infection elsewhere in the body
• Treatment consists of a combined medical and surgical approach
• Septic arthritis usually is divided into gonococcal and nongonococcal arthritis, as clinical
and treatment regimens differ
• In children, infection into the hip joint predominates
• Despite advances in diagnostic studies, powerful antibiotics, and early drainage,
significant joint destruction commonly occurs
• It is caused by staphylococcus, and beta haemolytic streptococcus and presents with:
o Fever
o Anorexia
o Pain
o Irritability
o Swollen and tender joint
o Limited joint movement due to pain and muscle spasms
• Treatment
o IV antibiotics (penicillinase-resistant synthetic penicillin or and a third-generation
cephalosporin)
o Refer child to hospital

Trauma
• Physical injury to a joint which can be associated with bleeding into a joint
• Trauma may also be associated with:
o Sprains
o Dislocation
o Fracture
• Refer the child to hospital for further management

Juvenile Rheumatoid Arthritis

• A systemic autoimmune disease characterized by inflammation of the joints and
characterized by:
o Swelling of the joints (large and small)
o Fever
o Transient rash
o Pain
o Anaemia
o Lymphadenopathy
o Hepatosplenomegaly
• Treatment
o Nonsteroidal anti-inflammatory drugs (NSAIDs)
o Team based approach
o Refer child to hospital

Acute Rheumatic Fever Arthritis (covered in Session 16: Acute Rheumatic Fever)

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Assessment and Management of Joint Swelling
Assessment
• History
o Pain
ƒ Onset
ƒ Duration
ƒ Location
ƒ Character
ƒ Intensity
ƒ Frequency
ƒ Aggravating/alleviating factors
o Limitations in daily activity
o Trauma, injury
o Sexual history or sexual abuse (gonococcal disease)
o Morning stiffness
o Limpness
o Swelling/redness of joints
o Heat
o General
ƒ Fever
ƒ Rash
ƒ Fatigue
ƒ Weight loss
ƒ Cough
ƒ Chest pain
ƒ Hair loss
o Family history
ƒ Arthritis
ƒ Bleeding disorders
• Physical exam
o Complete physical exam
o All joints
ƒ Inspection
ƒ Palpation
ƒ Range of motion
o Skin findings:
ƒ Rash
ƒ Cellulitis,
ƒ Rash of disseminated gonococcal infection
o Gait, leg length discrepancy
o Tenderness over tendons or tendon insertion sites
o Muscle weakness or atrophy

Management
• Treat the cause
• Refer to hospital

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Key Points
• Polio can present sub-clinically or as acute flaccid paralysis.
• Polio prevention is achieved by vaccinating children using the oral poliovirus vaccine.
• Acute hematogenous osteomyelitis can cause localized bone pain and fever and requires
aggressive antibiotic therapy and sometimes surgical drainage.
• Septic arthritis is one of the causes of a joint pain and swelling which needs aggressive
management as the complication can be fatal.
• In assessment of a child with joint pain and swelling it is important to examine all joints.
• Acute septic arthritis, arising directly from the blood stream, is commonly seen in young
infants

Evaluation
• What is poliomyelitis?
• How can you diagnose poliomyelitis?
• What are the common causes of swelling and pain in joints?
• How can you assess a child with joint swelling?
• How can you manage a child with joint swelling/pain?

References
• Beattie, J., & Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., & Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia, H.M., et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., & Bwibo, N. (2005). Child Health: A Manual for Medical and Health
Workers in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M.,& Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA:
Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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CMT 05103 Paediatrics and Child Health NTA L 5 Semester 1 Student Manual
Session 21: Disorders of the Musculoskeletal System 172
 Session 22: Common Skin Conditions and Leprosy
Learning Objectives
By the end of this session, students will be able to:
• Identify common skin conditions
• Describe clinical features of common skin conditions
• Describe management of each skin condition
• Define leprosy and its causative agent
• Explain the clinical features and management of leprosy
• Explain the prognosis and prevention of leprosy

Impetigo, Tropic Ulcer, Abscess and Cellulitis

Impetigo
• A superficial contagious infection of the skin caused by streptococci or staphylococci,
and spreads readily between children
• May develop after trauma or irritation to the skin
• Flies can also transmit the infection
• Streptococcal infection of the skin can be responsible for rheumatic fever or acute
glomerulonephritis
• Clinical Presentation
o Lesions are rapidly enlarging thin-walled vesicles or bullae on erythematous or dusky
bases that quickly become pustular, rupture and spread by contact
o The raw, broken surfaces are covered with yellowish, ‘honey-crusted’, brown or
haemorrhagic exudates which dry to form scabs and crusts
o Sites commonly affected are the exposed parts
ƒ Face (around the nose, mouth and cheeks)
ƒ Neck
ƒ Scalp
ƒ Extremities (hands and feet)
ƒ However, covered parts may also be affected
o Impetigo is more common in malnourished and newborn children
o Occasionally in young infants, large loose blisters having yellow fluid involving large
areas of the body, especially the skin folds, may occur
ƒ This is staphylococcal bullous pemphigus, and the infant can die of septicaemia
• Treatment
o Remove scabs and crusts with soap and water, or half-strength (1.5%) hydrogen
peroxide
o Cut hair away from scalp lesions
o Apply antiseptics (e.g. GV 1% aqueous solution), or topical antibiotics such as
neomycin, fucidin or bacitracin to the lesions
o Systemic antibiotics such as penicillin are indicated when lesions are widespread, and
in newborns if proper follow-up is not possible
o Cloxacillin or erythromycin is preferred for staphylococcal infection

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Tropical Ulcer
• An ulcer is a lesion of the skin or mucous membranes marked by inflammation, necrosis
and sloughing of damaged tissues
• Tropical ulcer often follows a cut or abrasion of the skin which becomes infected with
bacteria
• Results from neglect or wrong treatment of small injuries in hot, humid unhygienic
settings leading to rapidly growing, necrotic painful ulcers often with raised or
undermined edges
• Feet and lower limbs are commonly affected
• Treatment
o Rest the affected limb, and clean the ulcer at least once daily with Eusol, hydrogen
peroxide or potassium permanganate solution
o Dress daily with medicated dressings (e.g. wet Eusol gauze and bandage)
o Systemic antibiotics - Fortified Procaine Penicillin (FPP) 30mg/kg/day for 5 days
o Skin grafting may be necessary after good granulation tissue has formed

Note: Occasionally diphtheria can infect or cause skin ulcer, the ulcer is seen to be covered
by a grey-white membrane, and is highly infectious

Abscess
• A localized collection of pus in any body part resulting from invasion of a pyogenic
bacterium or other pathogens
• Staphylococcus aureus is a common cause
• The abscess is surrounded by macrophages, fibrin and granulation tissue
• If left untreated, pathogens may spread to adjacent tissues or to other parts of the body via
the blood stream
• Appearance of fever may indicate sepsis
• Treatment
o Surgical drainage is the most important treatment for an abscess
o Antimicrobial agents especially penicillins (e.g. cloxacillin) are often used if there is
significant surrounding soft tissue involvement (e.g. cellulitis) or systemic infection
o In most situations, surgical incision and drainage is mandatory

Cellulitis
• Usually a streptococcal infection which may be acute, subacute or chronic, affecting the
skin and subcutaneous tissue
• May follow a scratch, pin or thorn prick, cut, bite, fissure, wound or ulcer, area of an IV
line, but may also develop on apparently normal skin
• Begins as a red or dusky patch which becomes hot, indurated or oedematous and tender
• May spread along lymphatics to regional lymph nodes which become swollen and tender,
there may be associated fever and malaise
• Complications include necrosis, gangrene and septicaemia
• Treatment
o Prompt, adequate treatment with Penicillin G until antibiotic culture and sensitivity
test results indicates more specific treatment
o Failure to respond to initial antibiotic therapy in several days should prompt
consideration of second-line therapy such as with Cloxacillin, Doxycycline or
Cephalosporin
o Affected part should be rested and any underlying systemic disease treated

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Eczema
• Eczema is a distinctive inflammatory reaction in the skin characterized in the acute stage
by erythema or duskiness, papules, vesicles and bullae, and accompanied by itching
• In the subacute stage, the vesicles and bullae break are scratched open, and exudation,
scabs, crusts and scales develop
• In the chronic stage, scaling is more prominent and lichenification and hyper-
pigmentation may develop
• Eczema or dermatitis may be caused by exogenous factors, inherited factors or acquired
factors which predispose the body to act in a hypersensitive way to substances which
would not normally be antigenic

Endogenous Eczema
• A disorder in which the precipitating causes are difficult to identify
• Is more common in children than exogenous eczema or dermatitis which is found more
in adults who are exposed at work or home to various allergens
• Forms of endogenous eczema seen in children include atopic eczema, seborrhoeic
eczema, nummular or discoid eczema and flexural infective eczema

Infantile Eczema
• Presents at about 3 to 6 months of age with erythema or duskness on cheeks and forehead
associated with itching
• Papules and vesicles develop later, and flexures (neck and elbows and knees in particular)
become involved
• In the subacute stage, exudation and scaling occur, and secondary bacterial infection may
follow
o The trunk and other parts of the limbs may become affected
• The condition tends to wax and wane over years, responding positively but irregularly to
appropriate treatment
• The child may grow out of it in late childhood or the condition may become chronic with
thick scaling, lichenification and hyperpigmentation
• It is comparatively rare in rural tropical areas possibly due to prolonged breastfeeding
which reduces the degree of foreign antigen exposure at an early age

Atopic Eczema
• An atopic child develops IgE-mediated hypersensitivity reaction, this may present as
infantile eczema or as atopic eczema in childhood or in adolescence
• Family history of atopic conditions like bronchial asthma, urticaria and hay fever (allergic
rhinitis) may be found
• A child with atopic eczema may develop bronchial asthma or other atopic conditions
while the eczema is active, or after it has cleared up

Treatment
• Atopic eczema responds to corticosteroid lotions in the acute stage, creams in the
subacute stage and ointments in the chronic stage (these should be used in the lowest
possible concentration)
• Start applications 3 times daily, treatment should be tailed off weekly to daily
applications
• In mild cases or when corticosteroid preparations cannot be afforded, calamine lotion
may be used

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Session 22: Common Skin Conditions and Leprosy 175
• Antihistamines may be given for the relief of itching, and sedatives may be given if
itching or distress disturbs sleep
• It is important to advise against the use of irritant soaps and disinfectants and undue
scratching
• For severe eczema that is not responding to topical therapies, oral corticosteroids can be
used
• Careful attention should be paid to the possibility of super-infection of eczematous
lesions with bacteria (e.g. staphylococcus or streptococcus) or viruses (e.g. eczema
herpeticum)

Urticaria
• Urticaria is marked by sudden or gradual appearance of itchy evanescent raised wheals of
variable sizes and shapes on the skin or mucosa
• Wheals are produced following histamine release from mast cells in the dermis which can
be provoked by antigens, immunoglobulins or complement
• Histamine, bradykinin, acetylcholine and prostaglandins cause cutaneous vasodilatation
and localized tissue oedema
• This fluid accumulation stretches the skin into familial pattern of wheals
• Wheals may be pale, skin-coloured or erythematous
• They may be circular, ovoid, annular or irregular in shape
• Wheals may last minutes, hours, days or weeks, and some may become chronic or
recurrent
• Severity of wheals varies from the mildest inconvenience of burning, to uncontrollable
itching to anaphylaxis with peripheral vascular collapse and impending death
• There is no tissue destruction, and after the reaction has subsided or when is counteracted
with antihistamines or vasoconstrictors, the affected skin returns to normal

Aetiology
• Causes of urticaria include allergic and non-allergic factors
• Often times an exact cause is not found
• Allergens may enter the body by:
o Ingestion (food, drinks, drugs, parasitizes, microorganisms)
o Inhalation (chemical fumes, insecticides)
o Injection or inoculation
• Chronic urticaria may be associated with systemic diseases, infections, autoimmune
diseases and neoplasms
• Non-allergic or mixed factors include mechanical pressure, heat or cold, sunlight, familial
and hormonal factors
• Differential diagnosis
o Insect bites or stings
o Erythema multiforme
o Localized lymphoedema

Papular Urticaria
• Seropapular itching that is very common in small children
• Can get secondarily infected
• Bites of insects make sensitized areas of the skin to flare up
• It is not contagious

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Treatment
• The most important measures are identification, elimination and avoidance of the cause
• Antihistamines should be given orally or parenterally (depending on the severity)
• In severe cases, adrenaline (1 ml of 1/1000 solution) is given SC slowly

Drug Eruptions, Warts and Pyoderma

Drug Eruptions
• Like adults, drug reactions also occur in children
• Commonly used drugs can bring about these eruptions from overdose, hypersensitivity or
idiosyncrasy
• There may be mild transitory rash or a more severe reaction like urticaria, or even
generalized eruptions with fever and anaphylactic shock
• Urticarial eruptions may result from treatment with salicylates, penicillin, sulphonamides,
antitetanus serum, laxatives, antimalarials and barbiturates
• Fixed drug eruptions present as bullae, erosion and residual hyperpigmentation which
tend to recur in exactly the same anatomical location with repeated administration of the
same or related drugs
• Implicated drugs include sulphonamides, antimalarials, salicylates and barbirurates
• Treatment
o Find out the offending drug and stop using it
o In severe reactions, antihistamines, hydrocortisone and even adrenaline are indicated
and should be given systemically
o Do not give antihistamines topically as they may provoke drug eruptions

Warts
• Are benign tumours resulting from epithelial hyperplasia of skin or mucous membrane
invaded by DNA human papilloma viruses (HPV)
• They start as small papules and develop various patterns, depending on the site, skin
texture, moistness or dryness, and pressure on the skin
• Plane, flat or juvenile warts (verruca plana) present on the face, hands and fingers as
small, flat, smooth skin-coloured papules which may coalesce or remain discrete
o Many regress or resolve spontaneously
• Common warts (verruca vulgaris) are skin-coloured, brown or greyish papules or rough
verrucous plaques that develop mainly on the exposed parts
o They are itchier and more chronic than plane warts but may regress spontaneously
• Filiform and digitate warts develop in thread or finger-like pattern that grow more rapidly
than common warts
• Plantar warts and palmar warts present as hard hypertrophic nodules on the soles or palms
o Because of the pressure they do not project much above the surface, and are painful
and tender
• Anogenital warts grow profusely into moist dusky clusters which if neglected may
become secondarily infected and malodorous
• Certain types of warts are associated with cervical, anal, and oropharyngeal cancers
• Diagnosis is based on the history and characteristic clinical picture
o HPV infection can be diagnosed by detection of specific viral DNA by special
techniques
• Treatment

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 o In children spontaneous regression occurs in up to 60% of cases
o The remainder may require topical applications, chemical destruction, cold surgery,
diathermy or excision
ƒ Topical applications include: 25% podophyllin in alcohol, 25-40% salicylic acid
(with or without adhesive plaster), wart paste
ƒ 10% benzoyl peroxide cream is effective against juvenile warts
ƒ Chemical destruction with formalin, phenol or nitric acid for common warts and
plantar and palmer warts after paring with a scalpel or razor blade
ƒ Excision, diathermy or curetting under local anaesthesia may be needed for
digitate, plantar and palmar warts, while filiform warts can be tied off with a black
thread or suture

Pyoderma
• A mixed picture of impetigo, cellulites, folliculitis and furunculosis with ulceration and
granulation may complicate simple bacterial infections or scabies, pediculosis or other
infestations, or may complicate a systemic disease
• Antibiotics should be given and an underlying disease treated

Overview of Leprosy
• Leprosy is a nonfatal, chronic infectious disease caused by Mycobacterium leprae, whose
clinical manifestations are largely confined to the skin, peripheral nervous system, upper
respiratory tract, eyes and testes
• It has an affinity for the skin, particularly in the cool areas of the body, and a unique
ability to invade peripheral nerves, sparing warmer areas of the skin (the axilla, groin,
scalp & midline of the back)
• M. leprae produces no known toxins
• It is found in the skin predominantly in macrophages, and in peripheral and dermal nerves
in Schwann cells, yet it may survive outside the body for 7 to 10 days
• The most severe form, lepromatous leprosy is rarely encountered in children

Epidemiology
• The incubation period varies between 2 and 40 years, although it is generally 5 to 7 years
in duration
• The time of peak onset is in the 2nd and 3rd decades of life

Spread of Leprosy
• M. leprae has been identified not only in skin and nerves but also in virtually every form
of human secretion and excretion
• It is generally accepted that the most important means of spread is by droplet transmission
from the nose of infectious lepromatous patients
• Skin-to-skin transmission generally not considered an important route of transmission,
relevant mostly in the transmission from mother to child
• Sexual transmission has been suggested to explain unusual presence of mycobacterium in
amniotic fluid
• Of greatest significance to children is the possibility of transplacental transmission and
transmission through breast milk

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Session 22: Common Skin Conditions and Leprosy 178
Pathogenesis of Leprosy
• It has been taught that the type of leprosy most frequently seen in children is
indeterminate or tuberculoid
• Indeterminate leprosy may undergo spontaneous healing or progress to clinical leprosy,
depending on the host’s immune response, and factors influencing it
• Tuberculoid leprosy may undergo spontaneous healing
o The patient may destroy the bacilli in the skin and nerve lesions, but develop leprosy
neuritis, (e.g. within the lateral popliteal nerve) resulting in foot drop
o The foot drop will be permanent unless high doses of steroids are given for several
months in addition to antileprosy drugs
• Another presentation of leprosy in children is a single tuberculoid macule in the vicinity
of a BCG scar
o It is thought that the sensitized lymphocytes and macrophages aggregate to ‘mop up’
the circulating M.leprae in a child with subclinical or early indeterminate leprosy,
causing the appearance of a single lesion
o The subclinical/inderminate leprosy would become overt tuberculoid and self-healing
o This is probably the reason for an apparent increase in tuberculoid leprosy following
mass BCG campaigns, with a decrease in the incidence of lepromatous leprosy

Clinical Features of Leprosy

• Diagnose leprosy if one of the three cardinal signs is positive:
o Loss of or diminished sensation in a skin patch/macule (tested with cotton wool)
o Enlargement of one or more peripheral nerves
o Presence of acid-fast mycobacteria in the skin (demonstrated with a skin smear)
• Special features of leprosy in children
o In young children the lesions are often very small and tend to be of the indeterminate
or tuberculoid form
o The patches are often single and tend to disappear spontaneously (self-healing) after 4
to 6 months
o Appearance of tuberculoid macule in the vicinity of the BGC scar following BCG
campaigns
o Children with leprosy (especially early leprosy) usually do well and tolerate treatment
without problems
o Children without disability grading at the start of treatment are unlikely to develop
any disability if they are put immediately on to a full multidrug therapy with
prednisolone should they develop neuritis
o Any child who has a disability grading (evidence of loss of sensory or motor nerve
function) should be referred to a leprosy treatment centre for supervised treatment

Symptoms of Leprosy
• Covered in the Communicable Disease module

Examination of the child

• The child should be examined in a well-lit room
• The skin should be palpated with the flat of the hand and fingers, to detect changes in skin
texture, and dryness of palms of hands or soles of feet
• Loss of light touch sensation is detected using a wisp of cotton wool
• Peripheral nerve trunks are palpated where they lie close to the skin

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Session 22: Common Skin Conditions and Leprosy 179
• If the child has generalized skin infestation, such as scabies masking the skin lesions of
leprosy, it is advisable to treat the generalized skin infestation/infection first and then to
re-assess the child a week or two later for signs of leprosy

Diagnostic Tests
• Slit skin smears for bacteriological index (BI) and morphological index (MI)
• Skin biopsy
• Nerve biopsy
• Additional diagnostic tests are covered in the Communicable Disease Module

Treatment and Prognosis

• If the diagnosis is made early, and the child adequately and properly managed, cure can
be attained and deformity prevented
• Supervision from a health facility is needed
• The child will be non-infectious within a few days of first taking rifampicin and so is not
a danger to other people
• The basis of modern treatment is multidrug therapy (MDT) using Dapsone, Rifamicin and
Clofazimine
• Episodes of acute reaction should be treated with anti-inflammatory drugs
• If evidence of reaction, refer the child to a specialist leprosy clinic
• Nerve damage in lepromatos leprosy tends to get better with treatment, and full recovery
of sensation may will occur
• Even when irreversible nerve damage is present at the first visit, much can be done to
prevent progression of nerve damage and to minimize its consequences
• Protective footwear, physiotherapy, reconstructive surgery and vocational training may
all help to preserve the personality of the child and to ensure that the child takes, or
resumes, a place in society
• Health education
o At an early age the child should be taught:
ƒ Eye exercises
ƒ To soak dry hands and feet in water every day, which are then patted dry, then
petroleum jelly, baby oil is applied to retain the moisture
ƒ For insensitive feet, footwear must be worn (plastic shoes should not be worn)
ƒ Care should be taken with regards to hot cooking stoves and utensils, and with
garden, agricultural and building instruments and thorns
ƒ Minor injuries and traumas should be managed promptly
ƒ Girls should be watched as they approach puberty as hormonal effects may affect
their leprosy if it is not well controlled

Activity: Leprosy Card and Medications

Instructions
The tutor will bring leprosy cards ‘LEP02’ to class (and leprosy patient record card ‘LEP01’
if possible), or photocopy a card for the class. The tutor will also bring medicines used for
treatment of leprosy in blister packs. Closely examine the cards and medicines. Look at the
back of the blister packs and locate the information that dictates when to give the medicines.
You will be given opportunity to practice filling out the cards.

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Session 22: Common Skin Conditions and Leprosy 180
Prevention
• Identify and treat people (adults and children) with infectious disease
• Conduct contact tracing and regular examination of babies of mothers with leprosy

Key Points
• Most skin conditions are due to infections (by bacteria, fungi, viruses) or invasion of the
skin by insects.
• Washing with soap and water is the best practice to prevent skin infections.
• Common skin diseases include impetigo, tropical ulcer, abscess, cellulitis, eczema,
pyoderma, drug eruptions, warts and urticaria.
• Leprosy is rare in children, but can occur, most commonly via mother to child
transmission.
• The basis of effective leprosy treatment is multidrug therapy (MDT).

Evaluation
• Name at least 5 common skin infections.
• What are the clinical features of the infections you have named?
• How can skin diseases be managed?
• What are the 3 cardinal signs of leprosy?
• How can leprosy be treated?

References
• Beattie, J., & Carachi, R. (2005). Practical Paediatric Problems (International student
Edition) London: Hodder Arnold.
• Behrman, R.E., & Kliegman, R.M. (2002). Nelson Essentials of Paediatrics. (4th ed.)
Pennsylvania: Saunders Company.
• Coovadia, H.M., et al. (2001). Paediatrics and Child Health: A Manual for Health
Professionals in the Third World. (4th ed.). Cape Town, South Africa: Oxford University
Press.
• Stanfield, P., & Bwibo, N. (2005). Child Health: A Manual for Medical and Health
Workers in Health Centres and Rural Hospitals. (3rd ed.) Nairobi: AMREF.
• Swash, M.,& Glynn, M. (2007). Hutchinson’s Clinical Methods. (22nd ed.) USA:
Saunders.
• Swai, M., et al. (2009). KCMC Paediatric Management Schedule. (7th ed.) Moshi,
Tanzania: Kilimanjaro Christian Medical Centre.

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Session 22: Common Skin Conditions and Leprosy 182
The development of these training materials was supported through funding from the President’s Emergency Plan for AIDS Relief
(PEPFAR) through the U.S. Department of Health and Human Services, Health Resources and Services Administration (HRSA)
Cooperative Agreement No. 6 U91 HA 06801, in collaboration with the U.S. Centers for Disease Control and Prevention’s Global AIDS
Programme (CDC/GAP) Tanzania. Its contents are solely the responsibility of the authors and do not necessarily represent the official
views of HRSA or CDC.