PAEDIATRICS

FOR UNDERGRADUATE STUDENTS

Dr Yan Aung
 GENETICS
Genetic disorders are common, with 2% of live-born babies having a significant congenital malformation and about 5% a
genetic disorder.

Terminologies used in genetics

Genes:
are composed of DNA which is coiled around a core of histone proteins and is packaged into
succession of super coils to form the chromosome.
Chromosomes:
the agents for inheritance of characteristics and these are derived from both
parents in equal number. They are thread- like structures found within every cell
nucleus.
Autosome:
any chromosome other than X and Y sex chromosomes. People normally
have 22 pairs of autosomes (44 autosomes) in each cell.
Dominant:
a dominant trait is one that is phenotypically expressed in heterozygotes.
Recessive:
a recessive trait is one that is phenotypically expressed only in homozygotes.
Homozygous state:
Having identical genes or alleles in the same locus on both chromosomes of a pair (one of
maternal and the other of paternal origin) Heterozygous state:
Having a gene at a locus in one chromosome but not at the homologous locus
of the other.
Alleles:
one of the alternative forms of a gene. In a diploid cell there are usually two
alleles of any one gene (one from each parent), which occupy the same relative position (locus) on
homologous.
Barr body:
A microscopic feature of female cells caused by the presence of two X chromosomes in the
female. One of these X chromosomes is inactive, and crumples up to form the Barr body.
Genetically determined diseases
Chromosomal abnormalities
 Single gene defects (Mendelian disorders)
 Mutifactorial disorders (interaction of genetic and environmental factors)

Different types of unifactorial inheritance (Single gene defect) and their examples.
Autosomal dominant inheritance
e.g. Achondroplasia, Marfan syndrome, Myotonic dystrophy, Neurofibromatosis, Otosclerosis
Autosomal recessive inheritance
e.g. Thalassaemia, Cystic fibrosis, Galactosaemia, Oculocutaneous albinism, PKU, Sickle cell disease.
Sex-linked recessive inheritance
e.g. G6PD deficiency, Haemophilia, Duchenne muscular dystrophy
Sex-linked dominant inheritance
e.g. Vitamin D-resistant rickets

Characteristic features of the common disorders due to uni-factorial inheritance

1. Autosomal dominant
• Both sexes are equally affected.
• Heterozygotes are phenotypically affected, i.e. no carrier condition.
• 50 % of children are affected (fig. 1).
• Risk remains the same for each successive pregnancy.
• Variable expressivity and penetrance.
• Rare, and generally less severe than autosomal recessive.
• High new mutation rate - e.g., Achondroplasia, Osteogenesis imperfecta
2. Autosomal recessive
• Both sexes are equally affected.
• Heterozygotes are phenotypically unaffected, i.e. carrier state exists.
• When both parents carry the gene, 1:4 children are affected and 2:4 children
are carriers (fig. 2)
Asymptomatic carriers

• Asymptomatic carriers produce affected children. Those with the disease

do not usually have affected children unless they marry a carrier, i.e. increased risk of disease amongst offsprings of
consanguineous marriages.
• Variable expressivity less of a problem than with autosomal dominant
inheritance, e.g. Thalassaemia, Congenital adrenal hyperplasia

3. X-linked recessive
• Affected cases are usually males carrying the gene and homozygous females (rare).
• Half the sons of carriers are affected, and half the daughters are carriers.
• No male-to-male transmission: condition is transmitted by carrier women who produce affected boys, normal
boys, carrier girls and normal girls with equal frequency (fig. 3)
• Affected males can have only normal sons and carrier daughters.
• Affected cases have affected brothers and affected maternal uncles,
e.g. Haemophilia, Duchenne muscular dystrophy
A
Asymptomatic
carrier s
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m
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4. X-linked dominant
• Affects both sexes, females more than males.
• All children of affected homozygous females are affected.
• Females pass the trait to half their sons and half their daughters.
• All daughters of affected males are affected, but none of their sons,
e.g., Vitamin D resistant rickets, Incontinentia pigmenti

Features of multi-factorial inheritance disorders

They manifest combination of genetic predisposition and environmental factors' Factors which increase the risks to
relatives are:
 More severe forms of disorder
e.g.; the risk of recurrence to sibs is greater in bilateral cleft lip and palate than in unilateral cleft lip
alone
 Close relation to the affected person
e.g.; overall risk to sibs is greater than to more distant relatives
 Multiple affected family members
e.g.; the more sibs already affected, the greater the risk of recurrence
 Sex difference in prevalence
e.g.; in Hirschsprung's disease the male to female ratio is 3:1.
An affected female must have had a greater genetic predisposition than for an affected male, so the risk to sibs is
greater.

Normal and abnormal karyotypes

Karyotyping
The presentation of a cellular chromosome profile, in terms of both the number and structure of the chromosomes.

Cells
Germ cells (Reproductive cells)
 One copy of genetic complement ( haploid cells)
 23 chromosomes ( 22 autosomes + 1 sex chromosome)

Somatic cells
 Two copies of genetic complement ( diploid cells)
 46 chromosomes (22 pairs of autosomes + 1 pair of sex chromosomes)

Normal human karyotype

46 XX in females
46 XY in males
Abnormal karyotype
Abnormal chromosome profile in either number or structure abnormalities, e.g. 45 XO in Turner's syndrome
and 47 XY (+21) in Down syndrome.

Chromosomal abnormalities
Chromosomal abnormalities are either numerical or structural. They usually cause multiple congenital anomalies and
learning difficulties. Single gene (Mendelian) inheritance is a condition or trait resulting from germ line mutation in
DNA

Numerical Abnormalities
Euploidy
describes chromosome constitutions which are multiples of the haploid (n)
number (23 in man).
diploid = 2n = 46
triploid = 3n = 69
Multiples greater than 2n are designated
tetraploid = 4n = 92 polyploid

Aneuploidy
refers to those karyotypes in which the chromosome complete is not an exact multiple of the haploid number. It
includes both the trisomic and monosomic states.

Nondisjunction
is resultant from the failure of homologous chromosomes to separate during cell division. It is the major mechanism
by which monosomic and trisomic states originate.

Translocation
There is a transfer of genetic material from one chromosome to another.

Mosaicism
Some of the cells are normal and some have abnormal cells.

Structural abnormalities
Structural chromosomal abnormalities may be those involving a definite loss or gain of material and may be those in
which the existing genetic material is rearranged in some way.

Deletions
Deletion results when one or more breakages occur along the chromosome with subsequent loss of the fragment.
COMMON CHROMOSOMAL DISORDERS
DOWN SYNDROME
The most common autosomal [Link] most common genetic cause of severe learning difficulties. Karyotype of
Down syndrome is trisomy 21.

Types of Down syndrome

1. Non disjunction (95%)
 Error at meiosis
 Karyotype – 47 XX/XY ( +21)
2. Robertsonian translocation (4%)
 Commonest – 14/21
Down
 Karyotype – 46 XX/XY ( -14,-21) (t14:21)
syndrome
3. Mosaicism (1%)
 Some of the cells are normal and some have trisomy 21
 Karyotype – 47,XY + 21/ 46,XY

Risk of Down syndrome

All ages-1:650 [rises with increasing maternal age]
Clinical Features of Down syndrome
Characteristic physical features
Head and facies
 Small head with flat occiput ( Brachycephaly )
 Flat facies
 Upward slanting of eyes/ palpebral fissures (Mongoloid slant)
 Prominent Inner epicanthic folds
 Small nose with flat nasal bridge
Brushfield
 Low set ears
spots
 Small mouth
 Protruded fissured tongue
 Brushfield spots in iris
 short and broad hands
 Incurved little finger (clinodactyly)
 Wide space between the first and second toes
 Hyperflexibility of joints

Mental retardation (mild to moderate) (trainable)

Hypotonia
Dermatoglyphics
  Single palmar crease ( Simian crease)
 Excess ulnar loops on finger tips,
 Distal location of palmar triradius (angle of triradii >60%)
Growth retardation

Associated problems/ Anomalies

 Congenital heart diseases (40% of cases)
- Most common being AVSD (ECD), VSD, PDA
 Congenital GI tract anomalies
- Duodenal atresia
- esophageal atresia
- Hirschprung's disease
- Imperforate anus
 Prone to infections
 Recurrent respiratory tract infections including pneumonia
 Hypothyroidism
 Increased risk of leukemias
 Atlanto-axial instability
 Alzheimer disease

Management of Down syndrome

 No specific treatment; but many supportive measures.
 Diagnosis should be confirmed by chromosomal analysis (Karyotyping)

Supportive measures
 Early stimulation programme
 Speech therapy in older children
 Special education and occupational training
 Regular check-ups for associated problems
- ENT, ophthalmic, and cardiac evaluations
- Thyroid function tests
 Treatment of associated conditions
- Surgical interventions - e.g. congenital heart disease, GI tract anomalies
- Medical interventions - e.g. recurrent infections, leukaemias, etc
 Parental support / counseling
- Parents need to be informed by discussions and written explanation about:
 Short and long-term implications of diagnosis
 Assistance available from both professionals and self-help groups
 Psychological support
  Genetic counseling:
- how and why the condition has arisen
- risk of recurrence
 translocation-10%
 non-dysjunction-1%
 antenatal diagnosis for future pregnancies

Diagnosis of genetic and chromosomal diseases

Diagnosis of genetic diseases can be reached by (3) ways.
(A) Clinical diagnosis
(B) Chromosomal studies (Karyotyping)
(C) Cytogenetic studies (Gene/ DNA analysis)
(A) Clinical diagnosis
Many genetic diseases can be diagnosed by their clinical features.
For example, Down syndrome can be diagnosed by the following features.
- dysmorphology ( flat facies, upward slanting eyes, brachycephaly, inner epicanthic folds, etc.)
- mental retardation
- hypotonia
- dermatoglyphics (distal triradius, more ulnar loops in finger tips)
(B) Karyotyping
- Study/ analysis of chromosomes from cell cultures.
- Usually peripheral white blood cells are used.
- By karyotyping, we can get the diagnosis of many genetic diseases.
For example- Down's syndrome ( Trisomy 21, 47XYor 47XX
- Turner's syndrome (45 X0)
(C) Cytogenetic studies
-It is study/ analysis of gene or DNA which is extracted from tissues containing nucleated cells such as blood and
chorionic villous material.
Methods of gene analysis
(1) DNA probe hybridization
(2) Gene mapping (Restriction enzymes, Southern blotting )
(3) Gene cloning
(4) Gene sequencing
(5) Polymerase Chain Reaction (PCR)
Principles of prevention of genetic diseases
Prevention of genetic diseases can be achieved by -
(A) Genetic counseling
(B) Prenatal diagnosis
(A) Genetic counseling
Definition:
It is a process of communication and information which deals with the problems associated with a
genetic/hereditary disease in the family.

Aim:
To provide information to allow for greater autonomy and choice in reproductive decisions
Objectives:
- establishing the correct diagnosis
- risk estimation
- reducing anxiety and guilt
- communication and information
- discussing the options available
- prevention of genetic disease
Procedures:
Communication and information is an integral part of counseling. Genetic counseling can be undertaken by any
physician with a proper understanding of the genetic mechanisms of diseases. If there appears to be a risk to the
offspring, counselor discusses the options available such as not having (more) children, ignoring the risk, artificial
insemination, or antenatal diagnosis and termination of pregnancy. The counselor should be non-directive; he or she
only assists in the decision-making process.

Indications for genetic counseling

- Known or suspected genetic disease in a patient or family
- Birth defects in previous children
- Consanguinity
- Identification of malformations by ultrasonography during pregnancy

(B) Prenatal/Antenatal diagnosis

- Prenatal diagnosis has become available for many maternal and foetal or
neonatal diseases including genetic disorders.
Screening tests
Maternal blood
Testing for neural tube defects
 Maternal serum alpha-fetoprotein (MSAFP) is raised in about 80% of open neural tube
defects
Testing for Down syndrome (Triple test)
 MSAFP (lowered)
 Human chorionic gonadotrophin (HCG)
 Unconjugated oestriol (UE3)
(If the risk is high, foetal chromosome analysis is offered)
Ultrasound screening
The following information can be obtained -
 Gestational age
 Multiple pregnancy
 Structural malformations (e.g. anencephaly)
 Foetal growth
 Amniotic fluid volume (Oligohydramios, Polyhydramios)

Tissue samplings (In utero)

Chorionic villous sampling
 done in first trimester (10-12 weeks of gestation)
 tissue used for - chromosomal analysis
- enzyme analysis for inborn error of metabolism
- DNA analysis (e.g. thalassaemia, haemophillia A and B, cystic fibrosis)
 Congenital infection for virus particles using polymerase chain reaction
 2-4% risk of foetal loss

Amniocentesis
 done in second trimester (16-18 weeks)
 Amniotic fluid cells are cultured for the studies:-
- chromosomal analysis
- enzyme analysis for inborn error of metabolism
- alpha fetoprotein and acetyl cholinesterase for neural tube defects
 Lesser risk of foetal loss (0.5-1%)

Fetal blood sampling

 done after 18 weeks of gestation
 used for - rapid chromosome analysis
- severe rhesus isoimmunization-assessment
- congenital infection serology
Fetal tissue sampling
 e.g. Skin biopsy for severe congenital skin disorders, Embryo biopsy (pre-conception)
 NEONATOLOG
TERMINOLOGY
Live birth Complete expulsion from its mother of a product of conception, irrespective of
duration ofpregnancy, which, after such separation, breathes or shows any other
evidence of life, such as beating of the heart, pulsation of umbilical cord, or
definite movement of voluntary muscles.
Stillbirth Born after 22 weeks of gestation but do not breath or show any sign of life after
complete expulsion from its mother.
Perinatal period Commences at 22 completed weeks (154 days) of gestation and ends 7
completed days after birth.
Neonatal period First 28 days of life.
Perinatal death Stillbirth and death with one week after delivery of those born after 22 weeks of
gestation.
Neonatal death death within first 28days of life.
Early neonatal death Deaths within first seven days of life
Late neonatal death Deaths after the seventh day but before the 28th day of life
Gestation age Number of completed weeks measured from the first day of last
normal menstrual period
Low birth weight Birth weight less than 2500g or 5lbs 8ozs at birth.
Preterm infant Born less than 37 weeks of gestation.
Term infant Born from 37 completed to less than 42 completed weeks.
Post-term Born 42 completed weeks or more.
High risk infant An infant who has an increased risk of having, developing or being
adversely affected by a morbid process
ESSENTIAL NEWBORN CARE (ENCC)
Basic preventive care for all newborns, especially warmth, cleanliness, breastfeeding, cord and eye
care, and immunizations.
1. Key Interventions for Essential newborn care:
1. Neonatal Resuscitation ( Refer to Resuscitation chapter )
2. The Clean Chain (clean hands, clean surfaces, clean blade to cut cord, clean cord tie, clean cloth)
3. The Warm Chain (dry baby, warm room, warm mother, warm up, use hat)
4. Breastfeeding
5. Cord, Eye and Skin Care
6. Immunizations
7. Recognition of illness and at-risk conditions, and management or referral

2. Clean chain
Clean delivery (WHO six cleans)
- Clean attendant's hands (e.g. wash with soap).
- Clean delivery surface.
- Clean cord-cutting instrument (i.e., razor blade)
- Clean string to tie cord.
- Clean cloth to wrap the baby.
- Clean cloth to wrap the mother.
After delivery
- All caregivers should wash hands before handling the baby.
- Keep the cord clean and dry.
- Use a clean cloth as a diaper/napkin.
- Wash baby's bottom and your hands after changing diaper/napkin.
3. Warm chain
At delivery
- Ensure the delivery room is warm (25° to 28° C)
- Deliver the baby on a clean surface.
- Dry the baby immediately.
- Wrap the baby with clean dry cloth
- Keep the baby close to the mother (ideally skin-to-skin) to stimulate early breastfeeding.
- Postpone bathing for about 6 hours.
After delivery
- Keep the baby clothed, wrapped with the head covered.
- Minimize bathing, especially in cool water or for small babies.
- Keep the baby close to the mother.

4. Breastfeeding
- Early initiation of breastfeeding (i.e., within the first hour).
- Exclusive breastfeeding for six months.
5. Cord, Eye and Skin Care
Cord Care
- Cut the cord with a clean instrument.
- Tie the cord tightly with clean thread or use a cord clamp.
- Keep the cord clean and dry and wash hands before touching it.
- Fold napkin or diaper below the cord stump.
- Bandages are unnecessary and may delay healing and introduce infection.
- No need to apply any medicine into the cord unless indicated (Alcohol cleansing may delay
healing)
- Applying traditional remedies to the cord may cause infections and tetanus.
Eye Care
- Clean eyes immediately after birth.
- Give prophylactic eye drops (e.g. tetracycline ointment 1%) within 1hr of birth.
- Don’t put anything else in the baby's eyes.
- Watch out for discharge from the eyes especially with redness and swelling around the eyes.

Skin Care
Vernix, the white greasy covering on a term baby's skin, is protective against infections and also
against hypothermia. Simple principles to reduce the risk of skin infections are-
1. Leave vernix on the skin; do not rub vernix off vigorously as this can damage the skin;
2. Change diapers soon after they are wet or dirty;
3. Ensure that caregivers wash their hands before handling the baby.

6. Immunization
- Immunize all babies according to the local policy.

7. Management of newborn illness

Many newborn problems can be prevented by the interventions described above. However, when a
disease occurs, many deaths can be avoided if *danger signs* are recognized early and managed effectively.

*Danger Signs*
Fast breathing (more than 60 breaths per minute), slow breathing(less than 30 breaths per minute),
severe chest in-drawing, grunting, convulsions, floppy or stiff, fever (temperature >38° C), temperature
<35° C or not rising after rewarming, draining pus from umbilicus or umbilical redness extending to skin,
more than 10 skin pustules or bullae, or swelling, redness and hardness of skin, bleeding from stump or cut,
pallor.
NEONATAL RESUSCITATION
A, B, C, D OF RESUSCITATION
A: Anticipation of problem
Establish an Open Airway
B: Initiate Breathing
C: Maintain Circulation
D: Drugs (Medications)

ANTICIPATION
Anticipation of risk factors for which resuscitation team should be present at delivery i.e. prenatal
risk factors, intrapartum and neonatal risk factors.
Check and prepare the resuscitation area and equipment
1. Check that the equipments are available and in working order.
2. Turn on the overhead heater above the resuscitation area.
3. Ensure that warm and clean towels are available.
4. Ensure that the delivery room is warm (>24°C)
5. Draw up naloxone into a syringe if the mother has recently received a narcotic such as pethidine,
within 4 hrs of delivery.
6. Check that all drugs which may be necessary for resuscitation are readily available.

Management at birth
Time: Start the stop watch
For breech delivery, time is marked for resuscitation when the whole body of the baby up to the neck is
delivered.
Resuscitation is done in steps. One specific step is followed by another specific action steps. These are:
1. INITIAL STEPS
2. BAG AND MASK VENTILATION
3. CHEST COMPRESSIONS
4. ENDOTRACHEAL INTUBATION
5. MEDICATIONS

1. INITIAL STEPS
The initial steps which can be completed within 30 seconds
A). Prevention of heat loss
B). Opening the airway
C). Initiate breathing

A). Prevention of heat loss is critical

Placing the infant under a pre-heated radiant warmer.
This must be turned on 15 minutes before delivery.
The surface in which baby is placed should be warm as well as flat, firm and clean. The baby should be
thoroughly dried first and remove the wet towels.

B). Opening the airway

In a baby whose respiration is irregular or gasping or who is apnoeic
This is done by correct positioning & suctioning
1. Correct position
The newborn infant must be positioned on the back or side, with the neck slightly extended. This
may be accomplished by putting a roll of tower (3/4 to 1") under the shoulder.

2. Suctioning
As soon as the infant is properly positioned, he/she needs to be suctioned to clear off
secretions in the mouth or nose. The mouth should be suctioned first.

Mouth first Then nose

C). Initiation of breathing
Tactile stimulation
If after thermal care, positioning & suctioning, the baby fails to breathe, you may try tactile stimulation
for 1-2 times briefly:
1. By slapping the sole of foot or flicking the heel
2. Rubbing the back up and down over the spine.
Do not slap the back or squeeze the rib cage.
You may omit this step completely and go to bag and mask ventilation. This will save
valuable time in resuscitation.

The
following is useful
algorithm.

Prevent heat loss -Place infant under radiant warmer.

-Dry off amniotic fluid
-Position infant correctly to assure open airway

Open the airway

-Suction mouth first, then nose (To prevent aspiration)

Initiate breathing -If not breathing

-Tactile stimulation(May omit this step)

Evaluate
- Observe respiration, heart rate, color and decide
LOOK AT THE FOLLOWING PICTOGRAM FOR THESE STEPS.

II. BAG AND MASK VENTILATION

Indications for positive pressure ventilation with 100% Oxygen:
 If the infant is apnoeic or gasping
 Respiration is spontaneous but heart rate is below 100 beats per minute
 Persistent central cyanosis despite 100% oxygen
Ventilation of the lungs is the single most important and most effective step in
cardiopulmonary resuscitation.
Most asphyxiated infants pick up well with bag and mask ventilation alone. Promptly to
open the lungs, the ventilation pressure required is 30-40cm water; successive breaths need
only 15-20cm water pressure. Approximately 40 breaths per minute are required. The
facemask used must cover tip of chin, nose and mouth but not the eyes. Adequacy of
ventilation is assessed by observing the chest movements. The best indication of adequate
pressure is seeing the chest rising and falling easily with ventilation.
If supplemental Oxygen is unavailable, room air should be used to deliver positive pressure
ventilation.
III. CHEST WALL COMPRESSION
Chest wall compressions are indicated if after 30 seconds of positive pressure ventilation (with 100%
oxygen), the heart rate is,
1. Below 60 beats per minute
2. Between 60-80 beats per minute and not increasing.

Remember ~ chest compression must always be accompanied by ventilation with 100% oxygen.

Site of compression
On lower 1/3 of sternum just below the nipple line. Give 1/2- 3/4 inch compression i.e.
1/3 of AP diameter
1. Ventilation rate = 30/min
2. Compression rate = 90/min
The compressor counts aloud One-and-two and three- and- BAG.
Either thumb method or two finger method is used for chest compression.
.
 Thumb

Two-finger
method

IV. ENDORACHEAL INTUBATION is indicated when

1. When prolonged positive pressure ventilation is required
2. When bag and mask ventilation is ineffective
3. When tracheal suction is required
4. When diaphragmatic hernia is suspected

V. DRUGS (MEDICATIONS)
1. Epinephrine – 1: 10,000 (0.1-0.3 ml/kg)
IV or per endotracheal tube
2. Volume expanders – normal saline 10 ml/kg, IV
3. Sodium bicarbonate – indicated for documented or assumed metabolic acidosis. 4.2% i.e. 0.5
mmol/ml at a dose of 2 mmol/kg, IV
4. Naloxone hydrochloride – respiratory depression and history of narcotics administered to the
mother within past 4 hrs, IV, ET, IM, SC.
5. Dopamine hydrochloride – begin at 5 μg/kg/min. May increase up to 20 μg/kg/min.

Resuscitation Spiral:

Immediately following delivery- the process of evaluation, action and decision cycle is begun
which moves every 20-30 seconds.

RESUSCITATION SPIRAL

ACTION

20-30 seconds

DECISION EVALUATION
Evaluation consists of:
Lungs : presence or absence of spontaneous respiration
Heart ; rate above 100 or not
Color ; whole body pink, peripheral cyanosis or central cyanosis

Simple (Basic) resuscitation

 Initial steps
 Bag and mask ventilation
 Chest compression
Advanced resuscitation
 Endotracheal intubation
 Medications
When to stop resuscitating
There is no clear information as to the maximum duration of resuscitation that should be
recommended. A newborn that does not start breathing after 20 minutes of adequate ventilation has
probably suffered severe asphyxia. It will probably require intensive care if it survives. If such care is
available, the ventilation could continue for 30 minutes while admission to the intensive care unit is being
arranged. If such care is not available (i.e. in most circumstances) ventilation can be discontinued if there is
no response (no spontaneous breathing) after 20 minutes of ventilation.

The APGAR score:

The Apgar score assesses the status of the infant at birth. A score of 0, 1 or 2 is given for each
parameter depending on the state of the infant. The Apgar score is recorded at 1 minute, 5 minutes, 10
minutes etc., as long as the infant needs resuscitation. But this scoring is not used to decide whether the
infant needs resuscitation or not. Resuscitation is started immediately after delivery within 15-20 seconds.

SIGN SCORE 0 SCORE 1 SCORE 2

Heart rate
Absent <100 /min >100/min
P- Pulse, heart
Respiratory effort Good,
Absent Weak
R- Respiration crying
Muscle tone Some flexion of
Flaccid Well flexed
A- activity extremities

Reflex irritability Cough or

No response Grimace
G- Grimace Sneeze
Color Body pink
Pale or Blue Completely pink
A- Appearance Extremities blue

Normal babies (Apgar score 8-10)

Mild to Moderate Birth Asphyxia (Apgar score 4-7)
Severe Birth Asphyxia (1-3)
Dead but still possible to resuscitate (Apgar score 0)
 Overview of Resuscitation in the Delivery Room

Evaluate respiration
 Place under radiant heater
 Dry thoroughly
 Remove wet linen
 Position
 Suction mouth, then nose
 Provide tactile stimulation

None or gasping Spontaneous

IPPV

With
Evaluation of Heart Rate
100%
Evaluation of Heart Rate
Oxygen
Below 100
15-30 secs

Above 100

Evaluate color
Below 60 60-100 Above 100 Blue
Continue HR not increasing HR Watch for Pink or
increasing
Continue spontaneous
Ventilation Peripheral
Ventilation, Chest Continue respirations
Chest Compression if HR
Cyanosis
below 80 ventilation Then, Observe and
Compression discontinue \ Provide oxygen
Initiate medication if: Monitor
s
ventilation
HR below 80 after 30secs of
PRIMITIVE REFLEXES
COMMON PRIMITIVE NEONATAL REFLEXES
DEMONSTRATION AND INTERPRETATION OF THESE REFLEXES
 Moro's reflex
 Grasp reflex
Value of primitive reflexes
Present in all newborns
Useful in assessing gestational age and clinical condition of the infant
Have to be lost before voluntary control development
Persistence beyond a certain time limit may indicate cerebral palsy

Moro's Reflex
Present at birth. Lost at 3-5 months. Persistence beyond 6 months is always abnormal.
With baby supine, support head on hand a little off table (an inch or so) and released suddenly. The reflex
consists of
 abduction of arms
 extension of arms
 opening of hands
 followed by adduction with or without a cry
Look for presence, absence, symmetry, increase and decrease.
In preterm infants, the arms tend to fall backwards on to the table during the adduction phase because the anti-
gravity muscles are much weaker than in full term infant.
Clinical significance of Moro’s Reflex
Increased – seen in early stages of post-asphyxial encephalopathy
Decreased – due to hypertonus or hypotonus or cerebral damage
Asymmetrical – seen with peripheral nerve injury like Erb's palsy or fracture clavicle or humerus and in spastic
hemiplegia
Persistence – seen in cerebral palsy

Grasp Reflex
Palmar Grasp
Present at birth. Lost after 3 months before the hand can be used for support.
A suitable object or a finger is introduced into the palms from the ulnar side. The fingers flex and grip the
object. It may even be able to lift the arm and body momentarily.
Head should be in midline. Otherwise grasp reflex more easily elicited on the side to which the occiput is
directed. Dorsum of hand should not be touched.

Plantar Grasp
Present at birth. Lost from 8 – 12 months when the foot can bear weight.
The sole of the foot behind the toes is gently stroked. Grasping response of the feet is obtained.
An exceptionally strong grasp reflex is seen in spastic CP and in kernicterus. Asymmetrical grasp is seen in
hemiplegia.
BIRTH INJURIES
Superficial injuries
Abrasions, ecchymosis, forceps blade marks
Traumatic cyanosis – petechiae over face, neck and chest may present from prolonged labour with local anoxia

Intracranial injury
Intraventricular haemorrhage, massive subarachnoid haemorrhage

Others
Cephalhaematoma
Eye injuries
Fractures – long bones, skull
Nerve palsies – e.g. Erb's palsy, Facial nerve palsy
Sternomastoid tumour
Visceral injuries – internal organ rupture

Cephalhaematoma
 SUBPERIOSTEAL HAEMORRHAGE SECONDARY TO RUPTURE OF BLOOD VESSELS
BETWEEN SKULL AND PERIOSTEUM
 LIMITED BY EACH CRANIAL BONE AND IS PROBABLY ALWAYS ASSOCIATED WITH A
HAIRLINE FRACTURE
 NO DISCOLORATION OF OVERLYING SCALP
 COMMONEST SITE IS PARIETAL BONE FOLLOWED BY FRONTAL AND OCCIPITAL
BONES

Sometimes it needs to be differentiated from Caput succedaneum which is a diffuse edematous swelling of the
soft tissues of the scalp that may extend across the suture lines.
It is due to pressure of the uterus or vaginal wall on the areas of the fetal head bordering the caput and usually
resolves within a few days.
PROGNOSIS
 MOST RESORBED WITHIN 2 WEEKS – 3 MONTHS DEPENDING ON SIZE
 WITH RESOLUTION, HARDENING OF EDGE ON PALPATION MIMICS A DEPRESSED
FRACTURE
 A FEW REMAIN FOR YEARS AS BONY PROTUBERANCES, DETECTABLE BY X-RAY AS
WIDENING OF
 DIPLOIC SPACE
 DIFFERENTIATE FROM CRANIAL MENINGOCELE
 With resolution, differentiate from depressed fracture
 Management
 OBSERVATION ONLY
 MASSIVE HAEMORRHAGE MAY NEED
BLOOD TRANSFUSION
 PHOTOTHERAPY FOR
HYPERBILIRUBINAEMIA
 NEVER INCISE OR DRAIN. RISK OF
INTRODUCING INFECTION
 RULE OUT A BLEEDING DISORDER
 REASSURE PARENTS

Cephalhaematoma

Erb's palsy
Also known as Erb-Duchenne Paralysis
 Injury to brachial plexus C 5,6
 Usually follows difficult deliveries- especially breech, shoulder
dystocia
 Paralysis of – deltoid, biceps, brachioradialis & long wrist
extensors
 Biceps jerk absent on affected side
 Absent Moro’s Reflex on affected side Erb's palsy
 Finger movements and grasp reflex are normal
AFFECTED ARM IS:
 LIMP
 ADDUCTED
 INTERNALLY ROTATED
 ELBOW EXTENDED
 FOREARM PRONATED
 WRIST FLEXED

MANAGEMENT
 DO PARTIAL IMMOBILISATION AND APPROPRIATE POSITIONING BETWEEN 7 – 10

DAYS WHEN NERVE OEDEMA IS SETTLED.

 Arm abducted 90°

 Externally rotated at the shoulder
 Full supination of forearm
 Slight extension at the wrist
 Palm turned towards the face
 IMMOBILISATION DONE BY PINNING THE ARM TO THE COT, OR BY USING A BRACE
OR SPLINT
 IMMOBILISATION SHOULD BE INTERMITTENT THROUGH THE DAY WHILE THE
INFANT IS ASLEEP AND BETWEEN FEEDINGS
 IMPROVEMENT IN THE 1ST 1-2 WEEKS PREDICT NORMAL OR NEAR NORMAL
FUNCTION
 If no improvement seen for 6 months denotes permanent deficit.

LOW BIRTH WT INFANTS

Definition
Infant whose birth weight is less than 2500 g (5lbs 8 ounces)
Further divided into
 Very low birth weight – less than 1500 g
 Extremely low birth weight – less than 1000 g
Different types of low birth weight
 Preterm (less than 37 weeks gestation)
 Small for gestational age infants
Babies whose birth weight at any gestation is below 10th percentile for gestational age or more than 2 SD below
the mean for gestational age (SGA)

Clinical signs in differentiating among premature and full-term infants (in order of usefulness):
 creases in the sole of the foot
 size of the breast nodule, nature of the scalp hair
 cartilaginous development of the earlobe
 scrotal rugae and testicular descent in males
 prominence of clitoris and separation of labia majora in females

These signs will give rapid assessment of an infant, especially at delivery.

36 weeks and earlier Full – term infant

Creases in sole one or 2 transverse creases; smooth Multiple creases; anterior two thirds or the
of the feet posterior three fourths of foot entire sole

2 mm; no breast nodule before 33 4 – 7 mm. SGA infants may have retarded
Breast nodule
weeks breast development
Fine and fuzzy to coarse and silky; each hair
Scalp hair Fine and woolly; fuzzy
single-stranded

Earlobe No cartilage; folds easily Moderate to thick cartilage with stiff earlobe

Testes/scrotum Testes fully descended; scrotum has

Testes partially descended; scrotum
prominent rugae and median raphe
small with none or few rugae
Clitoris is prominent with small and
Clitoris/labia Fully developed labia majora completely
widely separated labia
majora covered the labia minora

COMPLICATIONS OF LOW BIRTH WEIGHT INFANTS

Preterm low birth weight

Short term complications
Respiratory
 Respiratory distress syndrome due to deficiency of surfactant (see section on Respiratory distress in
newborn)
 Apnoea of prematurity due to immaturity of respiratory centre
 Poor gag and cough reflex associated with poor coordinated sucking & swallowing may cause
increased risk of aspiration.
Cardiovascular
 PDA–the ductus may remain patent or reopen in many preterm infants. Most common in infants with
RDS and may cause apnoea and bradycardia.
Central Nervous System
 Increased susceptibility to Periventricular haemorrhage especially below 33 weeks of gestation due to
immature brain and fragile vassals.
Haematologic
 Hyperbilirubinaemia due to immature liver
 Anaemia due to erythropoietin deficiency
 Vitamin E deficiency

GI tract
  Paralytic ileus (Ileus of Prematurity) usually on the first 3 days of life & may cause feeding
[Link] usually resolves spontaneously.
 Necrotizing enterocolitis – It is a serious illness mainly affecting preterms in the first few weeks of life.
It is thought to be due to a combination of ischaemia of bowel wall and infection from organisms
colonizing the bowel. Usually presenting with the classical triad of abdominal distention, bile stained
aspirates and bloody mucousy stools.
Metabolic
 Hypothermia- Because of larger skin surface area for weight, reduced subcutaneous fat stores & less
well developed brown fat stores. Maintenance of temperature is most important from the time of birth.
 Hypoglycaemia –due to deficient glycogen stores at birth.
 Late Hyponatremia –due to high renal sodium loss & low intake of sodium.
 Rickets of prematurity –because of increased demand by rapid postnatal growth.
Immunologic
 Because of deficiencies in both humoral and cellular response.

LONG TERM COMPLICATIONS

Retinopathy of prematurity –It may develop in the immature retina in infants less than 32 weeks of gestation
or less than 1500gm birth weight.
Major handicaps
 Cerebral palsy( e.g. spastic diplegia)
 Mental retardation
 Language disorders
 Learning disabilities
 Hyperactivity
 Cognitive delay
Sensory impairments
 Squint and visual defects
 Hearing defects
Poor growth

Small for gestational age/ IUGR

Potential complications-
 Asphyxia
 Meconium aspiration syndrome
 Hypothermia
 Hypoglycaemia
 Hypocalcaemia
 Polycythaemia .etc

Management of preterm infants

  Temperature control
 Nutritional management
 Fluid and electrolyte management
 Haematologic and jaundice management
 Prevention of infection
 Prevention and management of complications

Temperature control
Management to avoid hypothermia
At Birth
Maintain adequate body temperature.
Skin temperature - 36.5 – 37.5C (axilla)
Switch on the lamp / radiant warmer / incubator before the birth of the baby
Dry immediately. Discard the wet towels and wrap in a warm, dry and clean towel.
NO BABY BATHS.
Keep under overhead radiant warmer before transfer to SCBU
Maintain temperature during transport. Use transport incubator for VLBWs.
Precautions to prevent hypothermia in SCBU
Generally for preterm nursing, room temperature should be 28 - 29C, environmental humidity 50%.
Over 1.5 kg
Nurse clothed, in room temp. 24°C-26°C
Less than 1.5 kg (VLBW)
Incubator care, nurse clothed, with a bonnet, temp. 32 - 35C

Nutritional Management
Feeding Preterm Infants
Aims: - To provide the infant with nutrients necessary for the metabolic requirements of growth, replacement
and energy production.
Decision:-
CONSIDER
 Choice of feed
 Route of feeding
 Schedule of feeding
Co- ordinated sucking and swallowing at 34 - 35 weeks gestation only
Caloric requirement = 110 - 130 Cal / kg / day (max: 165)
Fluid ……………. = Start at 60 ml/kg/ day and gradually increase the amount up to maximum of 150 - 200 ml
/ kg /day as tolerated.
Initiation of feeding:-
< 1.5 kg = nil orally on admission. Put an iv line.
> 1.5 kg, > 32 weeks & up to 1.8 kg = Enteral feeds can safely be started if there are no contraindications (eg .,
ill, sick, very immature, paralytic ileus, respiratory distress etc.).

Preferred Milk:
Preterm mother’s milk. Because it has higher electrolyte and protein content necessary for rapid growth of the
baby. The antibodies and other anti - infective factors in mother’s milk are very necessary for the survival of a
preterm baby.

The mother should express her own milk into sterile container and the baby < 32 weeks will need to be given
intragastric feeding (orogastric or nasogastric). If the baby could swallow (bet 32 - 34 wks) this is fed by spoon.
Between 34 - 36 weeks most babies can suckle well at breast. But if gets tired may need supplements by spoon
or cup.

Timing and Frequency of Feeding:

 < 1000 g - needs hrly feeding
 1000 - 1500 g - needs 2 hrly feeding
 1500g - 3 hrly feeding
Feeding should be scheduled because these preterms rarely demand for feeds and demand feeding alone is
impracticable. For bigger preterms give demand feeding or 2 - 3 hrly scheduled feeding, whichever comes 1st.

Vitamin supplements:
All preterm babies must receive injection intramuscular Vit K 1 after birth to prevent haemorrhagic disease of the
newborn. 0.5 mg is given for infants under 34 weeks and 1 mg for those above 34 weeks.

Multivitamins and Folic acid

Compound vitamins are started from day 7 - 14 depending on baby’s condition.
Folic acid deficiency may reduce growth and rarely also causes megaloblastic anaemia. Give 1 mg / day from
day 7 - 14 till 3 months of age.

Iron
Iron supplementation 2 mg / kg of elemental iron is started only at 6 - 8 wks after birth.

Haematological and Jaundice Management:

Anaemia in critically ill neonate should be corrected by blood transfusion to keep the Hct above 40% at all
times.
Anaemia of Prematurity usually presents at about 6 weeks of age mainly due to erythropoietin deficiency.
Hyperbilirubinemia – Close observation for development of jaundice, appropriate investigation and timely
intervention. (Refer to section on neonatal jaundice)

Fluid and Electrolyte Management:

Weight: Weigh daily for management of fluid and electrolytes.
Also look for:
 Urine output
 Physical examination
Plain dextrose is used for day 1. 10% dextrose is the usual dextrose solution for newborns but preterms, esp.
ELBW babies tolerate 10% dextrose poorly - thus 7.5% dextrose is used for those < 1 Kg.

Day 2 onwards:
Depends on changes in body weight, renal function and serum electrolyte levels
From day 2 onwards, use 10 % dextrose in 0.18% saline for > 1000g and 7.5% dextrose in 0.18% saline for <
1000g.
Oral feeds may be started when there is no abdominal distention with audible bowel sounds. Oral feeds are
slowly increased while IVs are gradually withdrawn.

Prevention of infection
 Meticulous hand and arm washing before and after handling babies.
 Avoid overcrowding.
 Practice minimal handling of infants
 Adequate staffing
 Isolation of infected babies
 Proper cleaning and maintenance of nursery.
 Encourage breastfeeding.

Management of Small for gestational age infants / IUGR

 Resuscitation
 Temperature control
 Early initiation of feeding
 Prevention and treatment of hypoglycaemia

Prevention and treatment of hypoglycaemia

Prevention of hypoglycaemia is [Link] is achieved by Close monitoring of blood glucose levels together
with early initiation of feeding. Breastfed babies need prefeed glucose check for the 1 st 48 hours. They may need
breastmilk as well as supplementary feeds.
RESPIRATORY DISTRESS IN NEWBORN

Respiratory Distress in newborn is recognized by

1. Tachypnoea (respiratory rate above 60 per minute)
2. Recession of intercostal spaces, sternal and subcostal areas
3. Expiratory grunting (to try to create positive airway pressure during expiration)

COMMON CAUSES OF RESPIRATORY DISTRESS

Preterm Infants
Respiratory
 Surfactant deficiency
 Pneumothorax
 Pulmonary haemorrhage
Infection
 Pneumonia
 Septicaemia
 Meningitis
Miscellaneous
 Hypothermia
 Hypoglycaemia

TERM INFANTS
Respiratory
 Transient Tachypnoea of Newborn (TTNB / TTN)
 Meconium Aspiration Syndrome (MAS)
 Pneumothorax
 Persistent Pulmonary Hypertension (PPHN)
Cardiovascular
 Congenital heart defects leading to heart failure e.g., hypoplastic left heart syndrome, severe
coarctation
Infections
 Pneumonia
 Septicaemia
 Meningitis
Miscellaneous
 Hypothermia
 Polycythaemia
 Birth trauma and birth asphyxia
Metabolic
 Hypoglycaemia
 Acidosis
Respiratory distress syndrome (RDS)
Commonest neonatal respiratory disease in preterm. It is due to a deficiency of surfactant, the mixture
of lipoproteins excreted by the alveolar epithelium which lowers the surface tension. There is alveolar collapse
and inadequate gas exchange. The more preterm the infant, the higher the incidence of RDS .Surfactant
synthesis increases at about 30-34 weeks of gestation, before that the risk of developing RDS is high. Treatment
involves artificial ventilation, surfactant therapy and intensive care support.

Transient tachypnoea of newborn (TTN)

Transient tachypnoea of newborn (TTN) is attributed to the delayed clearing of the fetal lung liquid
after the onset of respiration. It affects mainly mature babies and more common in those delivered by caesarean
section especially before the onset of labour. Respiratory distress develops immediately after delivery. It is
usually benign, self limiting and responds well to supplemental oxygen but occasionally may need artificial
ventilation. Full recovery is expected within 2 to 5 days.

Meconium aspiration syndrome (MAS)

Meconium aspiration syndrome (MAS) is diagnosed in a baby delivered through meconium- stained
amniotic fluid who subsequently develops signs of respiratory distress in the presence of a supportive chest x-
ray .It is usually confined to mature and postmature babies. Inhalation of meconium causes airway obstruction,
air trapping and overdistension of the lungs with a risk of pneumomediastinum and pneumothorax. Every effort
should be made to prevent this condition by meticulous intrapartum care for early detection and appropriate
management of fetal hypoxia. Routine oropharyngeal and nasopharyneal suctioning of meconium-stained
neonates before the delivery of shoulders (intrapartum suctioning) is no longer recommended. If the newborn
has absent or depressed respiration, heart rate of less than 100 beats per min or poor muscle tone, direct tracheal
visualization and suctioning should be performed to remove meconium from the airway. However vigorous and
active babies need not undergo intratracheal suctioning.
NEONATAL CONVULSIONS
Fits in the newborn period are often subtle. All fitting babies require full biochemical, EEG and
ultrasound investigation as well as a work-up for meningitis.

CAUSES OF NEONATAL CONVULSIONS

Hypoxic ischaemic encephalopathy
Intracranial bleeding
 birth traumas (difficult traumatic delivery)
 intraventricular haemorrhage ( preterm infants )
Metabolic
 hypoglycaemia
 hypocalcaemia
 hyponatremia or hypernatremia
 Pyridoxine dependency
Infections
 meningitis
 sepsis
 TORCH
Structural cerebral anomalies
 hydrocephalus
 cerebral malformations
Toxin exposure
 bilirubin encephalopathy (kernicterus)
 Inborn Errors of Metabolism
 Polycythaemia
 Drug withdrawal e.g. maternal opiates

Management principles of neonatal convulsions

 ABC first (Airway, Breathing and Circulation management)
 Check for hypoglycaemia and correct promptly if noted
 Control seizures. Current first line anticonvulsants are phenobarbitone and phenytoin,with
clonazepam as the second line.
 Fluid and electrolyte balance
 Reduce intracranial pressure if raised ICP noted by fluid restriction and mannitol
 Treatment of underlying cause if treatable

Treatment of Hypoglycaemia:
Take blood for glucose immediately in the convulsing child and give glucose treatment immediately if
hypoglycemic. (Also check with lab true glucose in face of hypoglycaemia though we will not wait for
treatment.) Diagnosis is confirmed by low blood glucose < 2 .6 mmol/ l.
 Give 2 - 4 ml / kg of 10% dextrose followed by maintenance with 10% dextrose infusion of 6 - 8 mg /
kg / min of glucose i.e., about 90 – 120 ml / kg / 24 hour of 10% dextrose. Recheck glucose level after 30 – 60
mins and hourly thereafter until stable to determine for any change in therapy. Continue to check blood glucose
4-6 hrly if it is normalised and maintained.
Stop monitoring if glucose is persistently above 2.6 mmol / l. Avoid frequent boluses of glucose
because it will induce rebound hypoglycaemia especially if the cause is hyperinsulinism.
If hypoglycaemia persists with 10% dextrose, glucose concentration has to be increased to 12.5%
dextrose to avoid fluid overload. (A central line is needed if more than 12.5% dextrose is going to be used.)
Adjust the rate of infusion until plasma glucose is normal and stabilized. Gradually reduce glucose infusion
while increasing volume of enteral feeds.

Treatment of Neonatal Meningitis

(See section on neonatal infections for detailed treatment)
PAEDIATRIC SURGERY
(For full contents see the appropriate section)

Immediate care of important surgical conditions

Choanal atresia
 Congenital imperforate posterior nares by bone or membrane. Infant breathes through mouth
 Diagnosis by passage of catheter or X ray
 Early surgical correction

Oesophageal atresia with or without tracheo-oesophageal fistula

 awareness of its association with maternal polyhydramnios
 to pass stiff oral catheter in all infants born to polyhydramnios mothers to see it goes into stomach
 frothy saliva and mucous at mouth , choking when fed
 do not feed, keep oesophagus clear by frequent suction
 nurse with head up
 prompt referral to surgeon

Diaphragmatic hernia
 Usually severe respiratory distress and cyanosis
 Scaphoid abdomen
 Mediastinal displacement
 Do not hand ventilate
 Pass wide bore orogastric tube and deflate stomach
 Chest X ray
 Lie on affected side
 Prompt referral to surgeon

Intestinal obstruction
 Associated with maternal polyhydramnios
 Down syndrome (duodenal atresia)
 Clinical features vary with level of obstruction. Vomiting, abdominal distension, visible peristalsis
depending on site of obstruction
 Do plain erect abdominal X ray
 Nil by mouth
 Oro gastric suction
 Referral to surgeon

Imperforate anus
 Absence of anal orifice
 Absence of meconium on anal catheter
 No passage of meconium
 Nil by mouth
 Referral to surgeon

Exomphalos and Gastroschisis

 Cover with warm saline to prevent evaporation and drying
 Prompt referral to surgeon

Ambiguous genitalia
 Anticipation for congenital adrenal hyperplasia
 Look out for salt losing symptoms
 Prompt correction of fluid and electrolyte loss in salt losers
 INFANT FEEDING
BREAST FEEDING
Physiology of lactation

PROLACTIN REFLEX
In the third trimester of pregnancy, prolactin secreted by anterior pituitary sensitizes the glandular tissue
with the secretion of small amount of colostrum. The flow of milk after birth is due to let down reflex. After
birth, there’s increase in prolactin level which maintains milk production.

OXYTOCIN REFLEX
The baby rooting at the nipple causes afferent impulses to pass to the posterior pituitary which secretes
oxytocin. This stimulates the smooth muscle fibres surrounding the alveoli to eject the milk into large duct.

Types of breast milk

Colostrum
 milk secreted in the first week
 yellow, thick & contains more antibodies & WBC.
 Epidermal growth factor helps intestine to mature & prevents allergy.
Term milk
 Follows transitional milk, thinned, watery contains all
 The nutrients essential for optimal growth.
Preterm milk
 Contains more protein, Na, iron, Ig G, calories than term milk.

Advantages of breast feeding

ADVANTAGE TO INFANT
BREAST MILK – IDEAL FOOD FOR BABIES
1. Nutritional – complete and perfect
2. Anti-infective properties – protection against ARI, diarrhoea
3. Anti-allergic – ↓ the risk of asthma & eczema
4. Better intellectual attainment
5. Mother and child bonding

Anti-Infective Properties
Immunoglobulin - Ig A- High concentration in colostrum
Cells - macrophages, polymorphs, T & B lymphocytes
Lysozyme - lyse E coli membrane
Lactoferrin - binds iron which is necessary for some bacteria to multiply
L Bifidus factor - together with acidity of stool, encourages lactobacillus to flourish, which has
the effect of inhibiting the growth of [Link].
ADVANTAGE TO MOTHER
 Convenience
 Contraception (lactational amenorrhoea)
 Improve uterine involution and prevent PPH
 Reduced incidence of ovarian, breast cancer and osteoporosis

ADVANTAGE TO FAMILY
 Economical
 More time for other children

ADVANTAGE TO COUNTRY
 Economical
 Reduce child mortality
 Promote health of future generation.

Contraindications of breastfeeding
ABSOLUTE CONTRAINDICATIONS
 Maternal medication
- Radioactive substances
- Ergot
- Anticancer drugs
- Lithium
RELATIVE CONTRAINDICATIONS
 Maternal HIV infection (after counseling)
 Maternal psychosis

BFHI / BHCI / BFHD

10 STEPS TO SUCCESSFUL BREAST-FEEDING
1. Have a written breastfeeding policy, known to all health care staff.
2. Train the staff in the skills necessary to implement this policy.
3. Inform all mothers of the benefits and management of breastfeeding.
4. Help mothers initiate breastfeeding within half an hour of birth.
5. Show mother how to breastfeed and maintain lactation even if separated from their infants.
6. Newborns to have nothing other than breast milk unless “medically” indicated.
7. Mothers and infants to stay together throughout the 24 hours.
8. Encourage breastfeeding on demand.
9. Give no artificial teats or pacifiers to breastfeeding infants.
10. Foster the establishment of breastfeeding support groups and refer mothers to them on discharge from
hospital.
Differences between Human milk and Cow’s milk
Constituents Human milk Cow milk
PROTEIN 1.25% 3.5%
Lactoalbumin 0.75 0.5

Caseinogen 0.5 3.0

LACTOSE 7.5 4.5
FAT 3.5 4.0
CALORIES /oz 20 18-20

Ca content of CM 3-4 times > HM

Phosphate 6-7 times
Sodium 4 times
Osmolality 3 times
WEANING
It is the process by which an infant gradually becomes accustomed to an adult diet. During weaning,
breast milk remains an important part of the diet.

When to wean
Weaning should begin at 6 months old.

HOW TO WEAN
6 Months up to 8 Months
 Breastfeed as often as the child wants
 Add complementary food:-
- Boiled rice with oil (take a teacup full of partly cooked rice from the family pot. Add oil. Make it
soft by adding water and boiling further.)
- Mix rice powder, bean powder (in the ratio of 4:1) and oil and boil.
 Give the food 1-2 tablespoonfuls, one to two times per day after breastfeeding.

8-12 Months
 Breastfeed as often as the child wants.
 Give adequate servings of
- Soft cooked rice, adding oil, mixed with soft boiled egg or chicken liver or fish or meat or bean.
Add mashed vegetables.
- Mashed banana, papaya or mango.
 3 times per day if breastfed.
 5 times per day if not.

12 Months up to 5 Years
 Continue breastfeeding until child is 2 years old.
  Give family food: Rice and curry (egg, fish, meat, beans, vegetables except spicy food), 3 meals each
day
 Give nutritious food between meals.
- Myanmar traditional snacks (made of rice, beans, oil and jaggery) sweet potatoes, ground nut, corn
banana, papaya and seasonal fruits such as mango, pine apple

What food for weaning

Cereals & starchy foods are more widely used, mixing one or two teaspoonfuls of vegetables oil to
each serving, to increase the energy content. Between 6 months & 1 year, pulses, fruit, green vegetables, meat,
fish & milk products should be added to the diet.

Hazards of artificial feeding

1. Acute diarrhoea due to poor sterilization of feeding bottle.
2. Secondary lactose intolerance after having persistent diarrhoea.
3. Infantile or childhood eczema.
4. Excessive renal solute load.
5. Late hypocalcemia, iron, folate deficiencies.

HAEMORRHAGIC DISEASES OF NEWBORN

 Caused by a deficiency of Vit K dependent clotting factors (II, VII, IX & X).
 Vitamin K is produced by the bacterial flora of the GI tract, but as the newborn has a sterile bowel at
birth, there is little production from this source in the first week of life.

Clinical features
Spontaneous bleeding can occur from any site but more commonly as haematemesis and malena on
3rd–5th day of breastfed baby owing to low vitamin K level in the human milk.

Investigations
The diagnosis is confirmed by prolonged PT but normal PTT.

TREATMENT
Whole blood transfusion 30 ml/kg for hypovolaemic shock.

Prophylactic Vitamin K injection to all exclusively breast fed babies.

Routine administration of Intramuscular vitamin K (0.5 – 1 mg) to all newborn babies will prevent
from bleeding due to Vitamin K deficiency.
 NEONATAL INFECTION
INTRAUTERINE INFECTIONS
TORCH INFECTIONS
T - Toxoplasmosis
R - Rubella
C - CMV, Chicken pox
H - H simplex, HIV, Hepatitis B
O - Others such as Syphilis, Entero virus
FEATURES OF INTRAUTERINE INFECTION
1. Small for Gestational Age (SGA) or failure to thrive
2. Microcephaly
3. Hepatosplenomegaly
4. Petechiae or purpura
5. Hemolytic anemia, jaundice and hepatitis

MANAGEMENT OF BABIES BORN TO HBS ANTIGEN (+) VE MOTHER

 Should be given Hepatitis B vaccine (Recombinant DNA) 10 microgram IM shortly after birth (or
within 12 hrs) and again at one month, 2 months and 12 months of age (known as FAST REGIME) 0-
1-2-12 months
Conventional method 0-1-6 months
 Infants of mothers who are e-Ag (+)ve and e-Ab (-)ve should be given Human Hepatitis B Immune
globulin 100-200IU deep IM not later than 12 hrs in addition to Hepatitis vaccine.

BABIES OF HIV POSITIVE MOTHERS

PREVENTION OF MOTHER TO CHILD TRANSMISSION (PMCT)
Core interventions—
 HIV testing and counseling
 ARV prophylaxis to both the mother and baby
 Safe delivery practices e.g. elective caesarean section
 Safe Infant Feeding practices (exclusive breastfeeding vs replacement feeding)

Laboratory Diagnosis of HIV in newborn

 ELISA or Western Blot test may be positive due to transplacental passage of antibody from HIV (+) ve
mother.( HIV antibody test )
 These tests may be repeated at the age of 9 months or more and at least 6-12 weeks after the cessation
of breastfeeding.( negative results exclude HIV infection)
 HIV DNA PCR or HIV RNA PCR or P24 antigen determinations can be done as early as 1 month of
age to exclude HIV infection acquired during delivery ( only > 6 weeks after stopping breastfeeding)

FEEDING OF INFANT OF HIV (+) VE MOTHER

 Infant feeding counselling should be done antenatally or postnatally.
 Recommend avoidance of all breastfeeding if replacement feeding is acceptable, feasible ,affordable,
sustainable and safe (AFASS) .Otherwise recommend exclusive breastfeeding for the first months of
life and support mothers to safely use the replacement feeding when it becomes feasible for them.
Acquired infections
MINOR INFECTIONS
Oral thrush (Candidiasis)
By Candida albican seen in
1. Bottle fed baby
2. Breastfed baby of mother with poor personal hygiene
3. Babies on prolonged board spectrum antibiotics
4. AIDS babies
Clinical features
 White patches adherent to buccal mucosa & tongue with history of refusal to feed.
 Candida oesophagitis & tracheitis in AIDS babies.
It can extend along the GI tract to cause diarrhea with peri-anal excoriation & satellite lesions.
Treatment
1. application of 1% gentian violet or
2. instillation of 1: 10,000 Nystatin oral suspension 1ml 6 hourly x 5 days or ketoconazol oral
gel
No systemic antifungal agents.

CONJUNCTIVITIS
Gonococcal conjunctivitis
 1-3 days of life, corneal ulceration & blindness
 treated with Injection C-pen – 0.5-1l/kg 6-12 hourly for 5 days & C-pen eye drop 1:10,000 or
 Injection Ceftriaxone ( 50mg/kg single dose ) or Cefotaxime (100mg/kg single dose ) with
erythromycin eye ointment
Staphylococcal conjunctivitis
 3-7 days of life
 treated with injection Cloxacillin (25-50 mg/kg 6-12 hourly) for 5 days
 Chloramphenicol or Gentamycin eye drops
Chlamydial conjunctivitis
 after 7 days of life
 corneal involvement (+) leading to blindness
 treated with Erythromycin 10-20 mg/kg 8 hourly for 21 days
 Tetracycline eye ointment or chloramphenicol eye drops
Investigations for Ophthalmia neonatorum
 Eye swabs for Gram stain or culture

Umbilical sepsis
By Staphylococcal aureus predisposed by application of local remedies to umbilical cord

Clinical features
 Foul smelling purulent discharge from umbilicus
 In severe cases, periumbilical cellulitis
Complications
 portal pyemia
 septicemia
Treatment
 Injection Cloxacillin (25-50mg/kg/dose 6-12 hourly) +
Injection Gentamycin (2.5mg/kg/dose 12 hourly) x 7 days
 Umbilical toileting with methylated spirit.

STAPHYLOCOCCAL SKIN INFECTION

 Usually by Staphylococcal aureus
 Usual skin lesions are crops of pustules with golden centres surrounded by erythema on any part of
the body.
 Localized areas of pustules & crusts & sometimes large blister as impetigo.
 The more severe skin infection is “Staphylococcal Scalded Skin Syndrome” due to coagulase
positive phage type II.
 Paronychia & breast abscess can also be seen.
Complications
- Staphylococcal pneumonia where pneumatocele is pathognomonic in CXR & may lead to
pyopneumothorax
- Osteomyelitis: head of femur is often involved but any bone can be affected

Treatment
 Most skin & nail bed lesions can be treated by
local cleaning & application of 1 % aqueous gentian violet or
some antibiotic ointment e.g. Bacitracin
 Systemic antibiotics are required for scalded skin syndrome or systemic infection.
MAJOR INFECTIONS
NEONATAL TETANUS
Causal organism - Cl. tetani (Gram (+) motile anaerobic spore forming bacilli)
Incubation period - 3-10 days
Portal of entry - umbilical cord
Predisposing factors
- Unsterile technique of cutting of the cord.
- Unnecessary application of local remedies
- Untimely injection of 2nd dose of TT to mother during pregnancy
Clinical features
 excessive unexplained crying with refusal to feed and apathy are common initial symptoms
 later- trismus , repeated attack of spasm, risus sardonicus, opisthotonus,
 pharyngeal spasms – dysphagia, choking
 laryngeal and respiratory muscle spasm – apnoea, cyanosis
 In severe cases, aspiration pneumonia and fracture vertebra.
Management
 General
- baby should be placed in well-lighted, quiet room
- minimal handling
- prevention of hypoglycemia & hypothermia
- avoid IM injection
- suction of oropharyngeal secretions periodically
 Specific
- to neutralize free toxins
 ATS 10,000 IU IV stat or
 Human tetanus Immunoglobulin 3,000- 6,000 units IM single dose
- to eradicate organisms
 IV C-pen 2.5 L 6/h x 10 days
- to control muscle spasms
 IV diazepam or PR diazepam 0.5 mg/kg or injection phenobarbitone 10-20 mg/kg
 followed by oral diazepam 0.5 mg/kg 8-12 hourly + phenobarbitone 10 mg/kg
 add chlorpromazine if spasms are not controlled
 Feeding
- IV for calories , fluid & electrolytes
- after 3-4 days oral feeding may be started
- Assisted ventilation & tracheostomy in very severely ill cases.

Prevention
1. Proper sterilization of instrument for cutting of cord
2. Proper care of umbilical cord (See ENCC)
3. 2nd dose TT should be injected 2-4 weeks before delivery
4. TT 5 to reproductive age group (5-45 years of age 0- 1- 6- 12- 24 months)

The prognostic criteria of neonatal tetanus

Unfavourable factors
 Short incubation period (< 7days)
 Period of onset <48 hours
 Generalised spasms
 Hypo/ hyperthermia
 Jaundice
NEONATAL SEPSIS
Definition
It is a clinical syndrome of systemic illness accompanied by bacteremia occurring in the first month of
life.

Clinical Presentation
 Non specific and subtle
 May evolve differently in each baby
 Workup of any ill infant must include a sepsis screen

Most frequent signs and symptoms

 Poor feeding
 letharg,irritability
 Does not look well
 Temperature instability (hypothermia or hyperthermia)
 Apnoea and bradycardia
 Respiratory distress
 Vomiting
 Jaundice
 Abdominal distension
 Seizures
 Diarrhoea
 Hypoglycaemia/hyperglycaemia, ect.

Routine septic screen

 Full blood count, including film
 Blood culture
 Swab from any site of inflammation
 Throat ,ear ,nose and umbilical swab (in case of suspected early-onset infection)
 Urine microscopy and culture
 Chest X-ray
 C-reactive protein
 CSF microscopy and culture if indicated

Supportive care
 to normalize the temperature
 stabilize the cardiopulmonary status
 correct hypoglycemia
 prevent bleeding tendency
Treatment
 Early Onset Sepsis (within 72 hours of life) - Caused by GBS, Esch. coli, and Listeria - The drug of
choice is the combination of Injection Penicillin or Ampicillin and injection Aminoglycoside for 7-
10 days.
 Late Onset Sepsis (after 72 hours of life) – caused by Staph aureus, Staph albus, Proteus, Klebsiella,
and Pseudomonas - The drug of choice is the combination of Injection Cloxacillin and
Aminoglycoside for 7-10 days.

NEONATAL MENINGITIS
 Signs of meningial irritations are rarely seen in newborn
 All babies with suspected sepsis, fits, or apnoea must have CSF examination
Normal CSF – WBC up to 30/cumm, polymorph 60%, protein up to 150 mg/dl, glucose 35-125 mg/dl
 Causal organisms (Esch. coli, GBS, Listeria )
Treatment
 With injection Penicillin or Ampicillin and 3rd generation Cephalosporin for 14 days if the causal
organisms are Gram (+)ve and
 For 21 days if the organisms are Gram (–)ve.

NEONATAL JAUNDICE
Bilirubin metabolism
 The initial breakdown product of haemoglobin is unconjugated bilirubin (indirect bilirubin) which is
insoluble in water but soluble in lipids. It is carried in the blood bound to albumin. It is taken up by the liver and
conjugated by the enzyme glucoronyl transferase to conjugated bilirubin (direct bilirubin), which is water
soluble and excreted in bile into the gut and is detectable in urine when blood levels raised. Re-absorption of
bilirubin from the gut (enterohepatic circulation) is increased when milk intake is low.

Causes of neonatal jaundice

CAUSES BY DAY OF ONSET
Day of onset - Causes
1st 2 days - ABO incompatibility
- Rh incompatibility
- G6PD deficiency
- Congenital infection

3rd – 6th day - Physiological jaundice

- Birth injuries – cephalhematoma, bruises
- acquired infection
- ABO incompatibility
- Rh incompatibility
- G6PD deficiency
- Congenital infection

> 7 days - Acquired infection

- Breast milk jaundice
- Hypothyroidism
- Neonatal hepatitis syndrome
- Congenital biliary atresia
- Choledochal cyst Normal Jaundice
- UTI
- Alpha 1 anti-trypsin deficiency

Physiological jaundice
Causes
(i) Shortened RBC life span
(ii) Immaturity of live
(iii) Increased erythrocyte volume
It appears on 3rd day, peaks on 5th day and disappears by 7th day in term but 2 days later in preterm.

Pathological jaundice
1. Clinical jaundice detected within 24-48 hours of life.
2. Clinical jaundice persists beyond 14 days of life in term or 21 days of life in preterm.
3 Rise of Serum bilirubin more than 5 mg% per day.
4. History of clay coloured stool and high coloured urine
5. Direct bilirubin – more than 2 mg% of any time.
ABO incompatibility
 Most common cause of isoimmune hemolytic disease in newborns.
 Neonatal jaundice appears when the mother’s blood group is group O and baby’s blood group is
group A or B.
 Haemolysis is less severe than Rh incompatibility.
 Direct Coomb’s test is weakly positive or negative.
 Blood film typically shows microspherocytes ,polychromosia and normoblastosis

Rh incompatibility
 Neonatal jaundice appears when mother is Rh(-) and the baby is Rh (+) .
 Rh incompatibility can also present as hydrops.
 Direct coomb’s test is strongly positive and blood film shows polychromasia and
normoblastosis .Spherocytes are not usually present.

G6PD deficiency
 Most common and clinically significant red cell enzyme defect
 X-linked recessive inheritance
 Usually affecting male but rarely female.

Substances to be avoided are

1. Sulphur containing drugs e.g. Co-trimoxazole , Sulphamethoxazole,
Sulphonamides
2. Antimalarial drugs e.g. Primaquine, Chloroquine, Quinine
3. Antipyretics e.g. Salicylates, Phenacetin
4. Dapsone
5. Nitrofurantoin
6. Nalidixic acid and other Quinolones
7. Naphthalene balls
8. Fava beans
Clinical estimation of serum bilirubin
KRAMER’S RULE

SB (unconjugated)
Jaundice
Zone Average (mg/dl)

1 Limited to Head & Neck 6

2 Over upper trunk 9

3 Over lower trunk, thighs 12

4 Over arms, legs, below knees 15

5 Hands, feet >15

Complications of neonatal jaundice

KERNICTERUS
– IS BILIRUBIN ENCEPHALOPATHY DUE TO STAINING OF UNCONJUGATED BILIRUBIN IN
BASAL GANGLIA

Stages of Kernicterus
 Early Kernicterus – refusal to feed, high pitched cry, impaired Moro’s reflex.
 Late Kernicterus – Fits, Opisthotonus, absent Moro's reflex
Late neurological squeal
 Choreoathetoid Cerebral Palsy
 High tone deafness

Management of significant neonatal jaundice

APPROPRIATE INVESTIGATIONS
1. ABO & Rh blood grouping of both mother and baby
2. Serial estimation of serum bilirubin
3. PCV
4. Split serum bilirubin – total and direct bilirubin
5. G6PD assay
6. Serology test for syphilis
7. Infection screening

PHOTOTHERAPY
Indications
1. In the term baby SB level > 15 mg%
2. In the preterm baby SB level > 10-12 mg% but it is adjusted by gestational age or body weight.
3. Before exchange transfusion for prevention of further rise of SB.
Methods
 Blue tube photo (wavelength 450-475 nm) is better than white light (ordinary day light fluorescent)

 4 or 6 in numbers of 2’ or 4’ fluorescent tube 18” from the cot or incubator.

 Phototherapy should be given continuously except feeding & toileting.

 Expose the whole body. Cover the eyes.

 Turn the baby every 2-3 hours.
Extra fluid – 20-30 ml/kg/24 hour is given by more frequent breastfeeding.

COMPLICATIONS
1. Retinal damage – Retinopathy – Blindness
2. Hyperthermia/ Hypothermia
3. Fluid loss – dehydration
4. Diarrhoea due to isomers which are hygroscopic
5. Skin rashes due to histamine release
6. Bronze baby syndrome if phototherapy is given to the patient with conjugated hyperbilirubinaemia.

Exchange transfusion
Indications
1. Rule of thumb - Term > 20 mg%
2. Use bilirubin charts according to birth weight, gestational age, age of the baby.
3. Consider exchange at lower SB level if the baby has hypoxia, hypoglycaemia, hypothermia, asphyxia,
septicaemia.
4. Rate of rise of SB is > 1mg% /hour or > 5 mg% /day
5. Severe clinical jaundice associated with impaired Moro’s reflex , refusal to feed and
lethargy(impending bilirubin encephalopathy).

Method
1. Doubled volume exchange transfusion
85ml/kg x 2 = 170 ml/kg
Topping up transfusion for correction of anaemia- 10 ml/kg – 20 ml/kg
2. For safe blood transfusion, fresh whole blood or < 3 days old blood free from malaria, syphilis,
hepatitis B/C, HIV.
3. For ABO incompatibility - use blood group O
Rh incompatibility - use O (-)ve
Other disease - exchange with child’s blood group
4. Route of exchange – umbilical vein
5. Aliquots of 5 ml for preterm & 10 ml for term
6. After 100 ml - 1 ml of 10% Ca gluconate is given to correct hypocalcemia.
7. Before & after exchange transfusion, omit one feed each.
Complications
1. Catheter induced
 infection (portal pyaemia)
 Air & blood clot thrombosis and embolism
 Arrhythmia
2. Metabolic changes
 Hyperglycemia followed by rebound hypoglycemia.
 Hypocalcaemia
 Acidosis
 Hyperkalaemia
3. Incorrect calculation
 Hypervolaemia
 Hypovolaemia
4. Necrotizing enterocolitis
5. Hazards of blood transfusion – including infections: syphilis, CMV, HIV, Hepatitis B, hepatitis C, malaria
infections.

Prolonged neonatal jaundice

Jaundice persisting beyond 14 days in a term infant and beyond 21 days in a preterm infant.

CAUSES
1. Hypothyroid
2. Biliary atresia
3. Neonatal hepatitis
4. Congenital syphilis
5. Breast milk jaundice
6. Urinary tract infection

Hypothyrodism
Mainly unconjugated hyperbilirubinaemia and may present as temperature instability, poor tone, poor
feeding, lethargy,less cry, less active , constipation, delayed passage of meconium & prolonged
neonatal jaundice. Confirmed by ↓T3, ↓T4 & ↑TSH and X-ray knee joint shows absent epiphyses.

Breast milk jaundice

Prolonged unconjugated hyperbilirubinaemia (beyond age 2 to 3 week) in 20 % to 30% of all breastfed
babies and may persist for up to 3 months in some infants.

Congenital biliary atresia & Neonatal hepatitis

Mainly conjugated hyperbilirubinaemia (>15% of total bilirubin)
 Growth and development

Definitions
Growth implies increase in number and size of cells. It is typically coupled with cell division and enlargement of
protoplasm.
Development is maturation in function due to maturation of the nervous system.
Physical growth & development: Change in size and function of body and organs
Mental development: Change in behaviour, intellectual and abstract material.
Emotional development: Development of effective bonds and feelings, sociocultural development
Principles of growth
· Growth is the continuous process starting from conception.
· Depends on maturation and myelination of the nervous system
· Sequence of growth and development is the same for all children but rate of growth is not always
uniform
· Certain primitive reflexes have to be lost before voluntary control development
· The direction of growth and development is cephalo-caudal
· General mass activity given may be replaced by specific individual response

Pattern of growth
There are 4 main types:
General type
The body as a whole except head and neck follows this pattern. Rate of growth is maximum in utero. Slow
deceleration starts from one year except for mid childhood growth spurt which occurs between 6 and 9 years,
attributed to adrenal gland activity.
Neural type of growth
Growth of nervous system is most rapid during the latter months of foetal life and early postnatal life (in the first
2 years)

Brain weight New born 25% of its adult weight

5 years 90% of its adult weight
10 years 95% of its adult weight

Lymphoid type of growth

Maximum at 10 to 12 years and then declines to it’s adult value.
Genital type of growth
Rapid growth with the onset of puberty.

Variability in Body Proportions

Body proportion varies because of different rates of growth of the body tissues at different times.
Head Newborn ¼ of crown-heel length
Adult 1/ of adult height
7
Legs Newborn 3/ of crown heel length
8
Adult ½ of adult height
Upper segment/lower segment ratio
Newborn 2 years adult
Upper segment 1.7 1.44 1
Lower segment 1 1 1

Determination of growth
1. Factors regulating growth
Adequate calorie intake

Digestion by enzymes

Absorption

Metabolism

Hormone End-organ responsiveness

Genetic factors
Psycological factors

Growth

3. Phases of somatic growth in children

Three distinct phases of somatic growth in children

Phase Growth pattern Determinant
1 Infancy Rapid growth of infancy but is less than foetal growth rate Nutrition
2 Childhood Slow deceleration from 1 year old, except for the mid Growth hormone
childhood adrenal spurt
3 Puberty Pubertal growth spurt Sex steroid and growth
hormone

3. Factors influencing physical growth and development

a. Genetic
 Phenotypes
 Parental constitution: tall parents – tall children
 Race
  Boys – Taller, heavier
 Chromosomal defect - Down’s Syndrome
b. Environmental
* Prenatal Period
- Maternal nutrition, smoking, alcohol – maternal malnutrition - IUGR
- Maternal illnesses - hypertension, toxemia, Irradiation (X-rays)
infection - TORCH
chronic medical disease - CRF
- Hormones
o The principle hormones influencing early growth are growth hormone and thyroid hormone.
o Thyroxin does not affect linear growth, it affects skeletal maturation
o Insulin stimulates the foetal growth, Baby of diabetic mother is usually big
o Somatomedin (Insulin like growth factor) deficiency – small length of baby
o Growth hormone - not essential for foetal growth in utero
* Natal Period
- Asphyxia, hypoglycemia, hypoxia, hypothermia
* Post-natal period
- Nutrition - PEM, anaemia, Vitamin deficiencies
- Hormone – Androgen ® initially increases skeletal growth, ultimately- final height affected
- Iatrogenic – steroid
- Trauma - fracture ends of long bones
- Infections and infestations
o whooping cough
o measles
o diarrhoea
o TB
o malaria
o various worm infestations
* Major organ diseases
- Respiratory
- GI
- Heart
- CNS
- Musculo-skeletal disorder
* Socio-psychological factors
- Children from broken families do not have optimal growth and development because of socio-
psychological factors like anxiety, insecurity, lack of support and care.
* Others
- Children of multiple pregnancies

ASSESSMENT OF PHYSICAL GROWTH

There are a number of growth charts and anthropometric data which permit comparison of an
individual child’s weight and length against the population norms of children of same age to assess the health
and nutritional status of a child.
v Growth chart used in Myanmar.
In Myanmar, a locally adopted weight chart is in use, which is based on international reference values. The
nutritional status is categorized in colour codes, red, yellow and green. The direction of growth is more
important than single measurement. (See in nutrition chapter)

EXPECTED WEIGHT
Age kg Pound
3 - 12 months Age (m) + 9 Age (m) +11

1 - 6 years Age(yr) x 2 + 8 Age(yr) x 5 + 17

6 - 12 years (Age(yr) x 7 – 5) / 2 Age(yr) x 7 + 5
EXPECTED HEIGHT
Birth 50cm
1 year 75 cm
2-12 yr Age (yr) x 6 + 77 cm

OCCIPITO FRONTAL CIRCUMFERENCE

OFC 1.5 cm/ month for the first 6 months, 0.5 cm a month for the 2 nd 6 months
Birth 35 cm
3 months 40 cm
6 months 43 cm
9 months 45 cm
1 year 47 cm
2 years 49 cm
3 years 50 cm
5 years 51 cm
* Increase in head circumference of more than 1 cm/week is abnormal.

MID-ARM CIRCUMFERENCE
Birth 10.5 cm
1 yr 16 cm
1-5 yr 16-17 cm

MAC 13.6 - 14.5 cm (green)

12.5 - 13.5 cm (yellow)
< 12.5 cm (red)
** MAC is used for screening the nutritional status of children of 1-5 years

Catch up growth
It is the acceleration of growth following removal of retarding effects: e.g. illness, malnutrition or following
institution of effective treatment.

DEVELOPMENT
A process of child’s development represents the interaction of heredity and environment.

Hereditary Potential
Warmth, clothing and shelter

Functioning senses PHYSICAL NEEDS Activity at rest

Food Good health

Personal identity

Functioning senses Self respect and independence Activity at rest

PSYCHOLOGICAL NEEDS

Food Opportunity to learn Good health

from experience
BASIC EMOTIONAL NEEDS
Love, security, progressive permissiveness, discipline and punishment, recognition as an individual, praise.

Developmental process in children 1-5 years

Age Gross motor Fine motor/vision Hearing and speech Social behaviour
months
0-4 Head control Eyes follow an object/ Responds to sound Social smile
follow Mum’s face. Cooing (6 weeks)
Grasps a rattle or rings Recognizing mother
when placed in hand
6 (5-7) Rolls over Reaches out to an Turns to voice Put solid food into
Sit with support (6 object and hold it with mouth
months) both hand
Transfers and mouths
9 Crawls /Creeps Points with index finger Bi-syllables (mama, waves bye bye
(9-10 months) baba) Play peek-a-boo
Responds to own name
Distraction hearing test
12 Pulls to stand A good pincer Turns to sound of name Drinks from cup
Stands without support Casting Understands several Indicates wants
Walks holding furniture words Claps hands (play pat-
a-cake)
Wary of strangers
18 Climbs onto chairs Scribbles Utters 3 or more words Indicates toilet needs
Runs Builds tower of 3 Points to ‘ear’ ‘nose’ Follows simple
‘mouth’ command

24 Climb stairs (2 feet per Tower of 6 cubes Complete sentences Can remove garment
step) Imitates vertical stroke Knows own name
Turns book pages
singly
36 Climbs on alternate feet Copies a circle Knows full name, sex, Dry throughout day
Riding tricycle Matches 2 colours age.
Normal speech
60 Bounce & catch ball Copies triangle Speaks fluently Chooses own friends
Name 4 colours Dress with supervision

Salient points regarding development

1. Mental retardation causes delay in all fields of behaviour.
2. Isolated delay in one behaviour alone should not be classified as mental retardation.
Time of eruption of teeth (permanent and deciduous)
Deciduous teeth
Deciduous teeth starts to erupts at 6 months. Complete at about 2 years.
Delayed in eruption occurs in hypothyroidism and other nutritional and growth disturbances.
Permanent teeth
Permanent dentition starts at about 6-7 years.
Some important markers:
6 – 8 years Central incisor
6 years 1st molars
12 years 2nd molars
18 years 3rd molars

Osseous maturation
Skeletal maturity
Some important markers:
Birth (term) – Lower end of femur and upper end of tibia, cuboid
1 year - Head of humerus, head of femus, 2 carpal bones

Puberty
Refers to the passage from childhood to adult.
Early adolescence ( 10 - 14 years ) - This refers to the first stage of puberty. ( SMS (sexual maturity staging)
2)
Middle adolescence ( 15 - 16 years ) - This is defined as SMS 2 and 3. Onset of menarche is the most dramatic
event in this period.
Late adolescence ( 17 - 20 years ) – This refers to SMS 5.

Common causes of failure to thrive

1. Genetic diseases - e.g. chromosomal disorder
2. Physical defects - e.g. cleft palate
3. Major organ diseases - e.g. malabsorption
4. Metabolic disorders
5. Chronic diseases - e.g. TB, intestinal parasitosis

Causes of short stature

1. Genetic – e.g. familial dwarfism
2. Endocrine - e.g. hypothyroid
3. Chromosomal - e.g. Down’s syndrome
4. Nutritional - e.g. Protein-energy-malnutrition
5. Metabolic - e.g. Rickets
6. Major system diseases - e.g. Congenital heart disease
7. Bone diseases - e.g. achondroplasia
Variations of growth and development

1. Dwarfism (short stature) - defined as the child whose height is less than the 3rd percentile.

2. Gigantism - means height is greater than the 97th percentile.

3. Infantilism - means dwarfism with delayed sexual growth.
4. Precocious puberty - is generally defined as the onset of secondary sexual characteristics before 8 years of
age in girls and 9 years in boys
5. Premature thelarche - applies to transient condition of isolated breast development that most often appears
in the first 2 years of life. (thelarche >3 yrs – not benign precocious thelarche)
6. Adrenarche - means onset of pubic hair development. Adrenal androgens are responsible for development of
sexual hairs especially in girls and contributes to development of sexual hairs in boys. Adrenarche is mainly
mediated by testosterone in males.

Mental retardation
Mental retardation is defined as sub-average mental intelligence, manifesting during early developmental
period.

Categories of Mental Retardation (Ghai OP)

Mental Retardation Range Intelligence Quotient (IQ)
Mild 51-70
Moderate 36-50
Severe 21-35
Profound < 20

Causes of mental retardation

1. Prenatal
 GENETICALLY DETERMINED - CRANIAL ABNORMALITIES, CHROMOSOMAL
DISORDERS
 Intra-uterine infections – rubella, syphilis, toxoplasmosis, cytomegalovirus infection
 Cretinism
 Foetal irradiation

2. Natal
 Birth injuries
 cerebral trauma
 haemorrhage
 anoxia
 infection

3. Postnatal
 cerebral infection
 cerebral trauma
 hypoglycaemia
 hyperbilirubinaemia
 poisoning (CO, lead & others)
 CVA
 COMMUNITY PAEDIATRICS
ADOLESCENT HEALTH
 Adolescent is considered as a period of transition from childhood to adulthood.
 Adolescents are no longer children yet not adults. It is characterized by rapid physical growth with
significant emotional, psychological and spiritual changes.
 The problems of adolescents are multi- dimensional in nature and require holistic approach.

 Adolescence is defined by AGE according to World Health Organization as follows

Adolescence 10 – 19 years
- Early Adolescence 10 – 13 years
- Middle adolescence 14 -16 years
- Late adolescence 17 -19 years

Characteristic features
Early adolescence (10 -13yrs)
 Spurt of growth of development of secondary sex.
Middle adolescence (14-16yrs)
 Separate identity from parents, new relationship to peer groups, with opposite sex and desire for
experimentation.
Late adolescence (17-19yrs)
 Distinct identity, well-formed opinion and ideas.
The following changes are taking place during adolescent period
 Biological changes – onset of puberty
 Cognitive changes – emergence of more advanced cognitive abilities
 Emotional changes – self image, intimacy, relation with adults and peers group
 Social changes – transition into new roles in the society

Main health problems among adolescents

 Anorexia nervosa
 Obesity & overweight
 Reproductive Health Problems
 Early marriage
 Teenage pregnancy
 Abortion
 STD/HIV-AIDS
 Substance Abuse and
 Use Intentional & Non-Intentional Injuries
 Mental Health & Illness
 Violence & Sexual abuse
Underlying factors contributing to adolescent health issues and concerns
 Lack of Information
- about the physical, psychosocial changes
- potential risks to health & development
- of risky behaviors
- rights to health, education ,
- availability of services
 Lack of Life Skills
- Lack the necessary skills such as communication, decision making, negotiation, critical
- Thinking skills to make responsible decision
 Lack of access to health services
- Need services that are adolescent friendly with emphasis on confidentiality
- Non-judgmental attitude & convenient hours of operation
 Lack of Safe and Supportive environment

Hindering factors to access & utilization of health services

 Most don’t recognize illness
 Not aware of serious consequences of illness
 Don’t know they can get help to prevent or treat illness
 Lack of skills of service providers to deal with adolescent concerns

Prevention
 Health education
 Skill based health education
 Life skill education
 Family life education
 Counseling for emotional stress
 Nutritional education
 Early diagnosis & management of medical and behavioural problem
INTEGRATED MANAGEMENT OF MATERNAL AND CHILDHOOD ILLNESSES
(IMMCI)
IMMCI is a strategy, which combines improved management of important and common maternal and
childhood illnesses responsible for high mortality. The term IMMCI is comprehensive since it is not merely
focused on treatment of illness or their combination. The IMMCI is an approach which also emphasizes
prevention of disease and promotion of health by dealing with feeding advice, immunization and other
important factors having a positive impact on child health and development.
IMMCI requires improvement of training, supplies, planning, implementation, monitoring and
supervision, which necessitate co-ordination and linkages amongst different existing programs. Therefore,
IMMCI is an approach and not a new program.

Components of IMMCI interventions

There are four important considerations in the implementation of IMMCI.
1. Improvement of case management skills of health workers and doctors through the use of locally
developed guidelines on IMMCI and through promotion of activities, which enable the use of these
guidelines.
2. Improvement and strengthening of the health systems needed to promote the use of the IMMCI
guidelines.
3. Improvement of family and community practice through the promotion of IMMCI by the basic health
workers.
4. Strengthening of the referral support for treatment of serious illness or their complications.

THE IMMCI CASE MANAGEMENT GUIDELINES

ASSESS the child
Check the child for general danger signs:
Then ask:
 Does the child have cough or difficult breathing?
 Does the child have diarrhoea?
 Does the child have fever?
 Does the child have an ear problem?
Then check the child for malnutrition and anaemia
Then check the child's immunization status.
FURTHER assess the child and classify the illness:
 Does the child have cough or difficult breathing?
 Does the child have diarrhoea?
 Does the child have fever?
 Does the child have an ear problem?
For any "YES" answer, ask further question, LOOK, LISTEN, and FEEL. Based on this classify the illnesses.
For all children classify the nutritional status.
TREAT the child
  Teach the mother to give oral drugs at home (antibiotics, antimalarials, paracetamol, iron, vitamin
A, mebendazole)
 Teach the mother to treat local infections at home (ear, eye, mouth, throat)
 Give intramuscular drugs in clinic (Quinine, Chloramphenicol)
 Give increased fluids for diarrhoea and continue feeding.
Counsel the mother
About
 Food and feeding problems
 Fluid intake during illness
 When to return to health center
 Her own health

Use the process: ASK, PRAISE, ADVICE & CHECK

Benefits of IMMCI
1. It addresses the major health problem including the most important and common diseases.
2. It responds to demand because at least 75% of children suffer from one of the IMMCI target diseases.
3. It is likely to have a major impact on health status.
4. It is cost effective.
5. It promotes prevention as well as cure. E.g. Immunization.
6. It promotes cost saving and less wastage.
7. It improves equity in global health care between developed and developing countries as well as rual
and urban.

UNDER 5 HEALTH
Fifty percent of all deaths in developing countries may be attributable to deaths of children under 5
years of age. In Myanmar under 5 mortality rate (U5 MR) was 77.7 in 2000. According to nation wide under 5
mortality survey in Myanmar in 2003, under 5 mortality rate was 66.1.
At the Millennium Summit in 2000, representatives from 189 countries formulated the Millennium
Development Goals. There are 8 Goals. Goal 4, 5, 6 and 7are related to Health. Among them Goal 4 and 5 are
related to Maternal and Child Health. Goal 4 is to reduce under-five mortality rate by two thirds, between 1990
and 2015.
Leading causes of under 5 deaths according to nation wide under 5 mortality survey in Myanmar in
2003 are-
1. ARI
2. Diarrhoea
3. Brain infection
4. Malaria
5. Beri beri
6. Septicaemia
7. Accident & poisoning
Strategies to reduce under 5 mortality
3.9 million of the 10.8 million under 5 deaths occur in the newborn period.
The two- thirds phenomena
 The neonatal mortality is 2/3 of infant mortality
 Early neonatal mortality is 2/3 of neonatal mortality
 First day mortality is 2/3 of early neonatal mortality
 IMR is 49.7
Therefore, we must reduce newborn mortality to reduce U5MR.
Leading causes of neonatal deaths
1. Sepsis
2. Birth asphyxia
3. Prematurity
4. Neonatal jaundice

Intervention Areas
1. Improvement in vital & health statistics
 Routine reporting & recording system
 Compulsory registry of all births & deaths including SB.
2. Birth weight measurement
 Neonatal mortality rates were highest among preterm infants with birth weight below 2000
grams.
 There is progressive decrease in mortality with increasing birth weight.
 These data emphasize the importance of obtaining information on birth weight and maturity.
3. Women’s health
 Preventive care before pregnancy
 Improve women’s health
 Birth spacing
 Tetanus toxoid immunization.
4. Antenatal care
 Adequate & quality AN care
 Tetanus immunization (2 doses)
 Timely referral for the at risk
5. Birth sites and birth attendants
 Improve Skills of Health Care Providers
 Emergency Obstetric Care
 Capacity Building
 Encourage for hospital delivery
 Separate clean birthing place
 Intrapartum Period
Five cleans to prevent infection
- Clean surface
- Clean hands
- Clean cord
- Clean blade
- Clean Cord tie
 Clean Resuscitation
6. Improvement in midwifery kid
 Every midwife must have a fully equipped kit for clean delivery and resuscitation
 Plus equipment for birth weight measurement.
 7. Better coordinated maternity services
 2 way referral system between community and facility
8. Trainings
 Competency based neonatal Resuscitation, essential neonatal care, breastfeeding
 Counseling
 Maintenance of quality through assessments, re-assessments and evaluation
 A coordination of paediatricians, obstetricians and community midwives who are highly
 Trained to leadership position.
 Regional training centres at all States and Divisions
 Revision of medical and nursing curriculum.
9. Strengthen the present intervention strategies
 BFHI/BFHD, IMMCI, WCHD, SAFE MOTHERHOOD
10. Improve literacy rates of women
11. Improve exclusive breastfeeding rates
 Strengthen Baby Friendly Hospitals
 Strengthen Baby Friendly Home Delivery
 Breastfeeding Counseling
 Private sectors participation
 Constant media support
 Community participation
12. Upgrading of present hospitals for neonatal care
Develop fully functioning
 level I hospitals (Station, Township and District Hospitals, fully equipped for “Normal Care”),
 level II hospitals (Essential neonatal care including universal AN care/tetanus toxoid, delivery
by trained personnel, full facilities for basic resuscitation, early & exclusive breastfeeding,
prevention of infection, early detection of illness & prompt treatment, referral for those in need
optimal neonatal transport) and
 level III hospitals (at central, some teaching hospitals including facilities for-
- Level 1Intensive Care (Maximal Intensive Care)
- Level 2 Intensive Care (High Dependency Intensive Care) and
- Special Care.
MATERNAL AND CHILD HEALTH SERVICES

Aims and Objectives of MCH Services

1. To reduce reproductive morbidity and mortality
2. To reduce infant and childhood morbidity and mortality
3. To permit the provision of integrated and comprehensive health services
4. To promote the concept of family oriented comprehensive health responsibilities

Functions of MCH
1. Promotion of reproductive health, antenatal care, international care, and postnatal care
2. Prevention, identification and management of prevalent disease in the areas particularly those
affecting mothers and children
3. Advice on and care for fertility regulation, counseling and birth spacing
4. Health care of under 5 years children
5. Improvement of environmental sanitation
6. Impartation of Health knowledge
7. Collection of vital statistics
8. Prevention and control of diarrhoeal diseases
9. Nutrition promotion
10. Prevention and control of acute respiratory tract infection
11. Immunization
12. Infant care
13. Supervision of physical and psychological development and maturation of child and adolescent
14. Record keeping and reporting
15. Training of health personnel
16. Collaboration with local maternal and child welfare association
17. Record work

DUTIIES AND RESPONSIBILITIES OF MCH STAFF

Duties of MCH Medical Officer (MCHO)
MCHO is responsible for the comprehensive health care of the mothers and children in her area. One MCHO
has to take responsibilities of 10,000 to 15, 000 populations.
1. Supervision of MCH clinic (Reproductive care and child care)
2. Supervision of MCH staff
3. Communicable disease control
4. Health education
5. Nutrition
6. Birth & death registration
7. Recording and reporting of MCH activities
8. Research work
9. Training of health personal
Duties of Lady Health Visitors
1. Clinic work (Mother & Children care)
2. Supervision of MWs & AMWs activities
3. Communicable disease control
4. Family Health Care & home visiting
5. Health education
6. Environmental sanitation
7. Nutrition promotion
8. Collection of vital statistics
9. Record keeping and reporting
Duties of Midwife
Work under the direct supervision of MCHO / LHV
1. Assisting clinic work
2. Communicable disease control
3. Home visiting domicilliary care of pregnant woman
4. Domicilliary delivery of normal labour cares- Postnatal care
5. Environmental sanitation
6. Health education
7. Nutrition promotion
8. Collection of vital statistics
9. Recording & Reporting

Under 5 clinics (UFC)

The clinic for under five attempts to offer comprehensive and integrated health care for all children
under the age of five. Its aim is to extend low cost curative and preventive care to large proportion of the
population as much as possible. It is different from the traditional out - patient clinic in attempting to offer both
preventive and curative service.

Activities of Under Five Clinics

1. Supervision of the health of all, children up to age 5 years
2. Prevention of diseases by immunization
3. Provision of treatment for diarrhoea, ARI and other common childhood diseases
4. Nutrition education to mother and nutrient supplementation to mothers.
 All newborn will be weighted and recorded on growth chart.
 All infants under 1 year will be weighted monthly and health education given to mothers
 All 1-3 years will be weighted every 3 months. For unsatisfactory weight gain or no weigh gain,
monthly weighing will be done.
 All severely malnourished children will be given appropriate treatment or referred to higher centers.
 Immunization of children
 Prevention and control of Acute Respiratory Infections (ARI) through immunization, early diagnosis
& treatment
 Curative treatment for all illness that need treatment
 Prevention and control of diarrhoeal disease; breasting feeding, proper weaning, health education to
mothers, selective deworming.
 Appropriate rehydration therapy for diarrhoeal and gastroenteritis cases.
 Health and nutrition education to mothers, nutrition supplements, prevention of vitamin A deficiency
by giving high potency vitamin A capsules, and supplementary feeding given to children through
community nutrition centre.
 The under 5 clinic will be a major part of the MCH & if possible it should be run in conjunction with
AN clinic.
5. Improvement of environmental sanitation
6. Impartation of Health knowledge
7. Collection of vital statistics
8. Records keeping and reporting
9. Training of health personnel
10. Research work
SCHOOL HEALTH SERVICES
Aims and Objectives
1. Promotion of healthful living through development of desirable habits and understanding of factors
relating to individual and community health
2. Health supervision and provision of health care through early detection and correction of physical
defects, early diagnosis and treatment of disease and control of communicable diseases.
3. Provision of a healthy environment by ensuring a healthful environment in the school
4. Promotion of physical development in co-operation with the department of sport and physical
education
5. Promotion of mental well being and sound character
6. Impartation of health knowledge through the health education program for children, teacher and
parents.

Functions of School Health Team

1. Medical examination of school children
 Periodic physical medical examination
 Special and re-examination of children with long standing defects and illness
 Examination of dental health
 Assessment of mental health
2. Remedial measure and follow-up
3. Prevention and control of communicable diseases
4. Health education
 Personal hygiene
 Environmental health
 Communicable diseases
 Family life
5. Nutritional services
6. Training and research work
 NUTRITION

PRINCIPLES OF NUTRITION
Essential nutrients
1. Protein
2. Carbohydrate
3. Fat
4. Vitamin
5. Mineral
6. Water

Daily requirement of major essential nutrients

1. Protein - 2-4 G/kg/day
2. Calories
- 0-6 months - 120 kcal/kg/day
- 7-12 months - 100 kcal/kg/day
- >1yr - 1000 + 100 (age in year – 1) kcal /day
 10 – 20 % of calories from protein
 40– 60 % from carbohydrate
 30 - 40% from fat.
3. Water
- 100 ml/kg for 1st 10 kg
- 50 ml/kg for next 10 kg
- 20 ml/kg thereafter

Essential amino acids

1. Threonine
2. Valine
3. Leucine
4. Isoleucine
5. Lysine
6. Tryptophan
7. Phenylalanine
8. Methionine
9. Histidine
During infancy
10. Arginine

Nutritional Disorders
 Over nutrition e.g. obesity
 Under nutrition
 Micronutrient deficiency - Vitamin deficiency, Mineral deficiency
 Macronutrient deficiency - Protein Energy Malnutrition (PEM)
SEVERE PROTEIN ENERGY MALNUTRITION (PEM)
Severe Protein Energy Malnutrition (PEM) according to WHO criteria
 Presence of severe wasting - (<70% weight for height or – 3SD) and / or bilateral oedema

Clinical types of PEM by Wellcome classification

 60 – 80 % of standard weight for age
- Without oedema – underweight
- With oedema – Kwashiorkor
 < 60 % of standard weight for age
- Without oedema – Marasmus
- With oedema – Marasmic-kwashiorkor

Clinical features of PEM

Kwashiorkor
Four cardinal criteria
1. Generalized pitting oedema
2. Psychological changes: apathetic, miserable and irritable
3. Muscle wasting with some retention of subcutaneous fat
4. Growth retardation ( 60 – 80 % of weight for age ).
Other features of Kwashiorkor
 Skin changes
- Hypopigmentation
- Hyperpigmentation
- Desquamation and ulceration
- Crazy pavement dermatosis
- Fissures and blisters.
 Hair changes
- Thin, dry, silky, depigmented areas of pigmented and depigmented segments (Flag sign)
 Liver enlargement
 Haematological changes
- Iron deficiency anaemia, folic acid deficiency
 Signs and symptoms of vitamin deficiencies

Marasmus
Characteristic features
 Growth retardation (< 60 % of weight for age)
 Muscle wasting.
 Loss of subcutaneous fat

Other features of marasmus

 Old man facies
 Hungry looking, listless, anxious and sleep very poorly
 Mucus diarrhoea (hunger diarrhoea)
Marasmic-kwashiorkor
Characteristic features
 Growth retardation (< 60 % of weight for age)
 Oedema
 Muscle wasting
 Loss of subcutaneous fat

Causes of PEM
Inadequate or improper food intake quantitatively or qualitatively
 Low socio-economic condition
 Predisposing factors for reduced intake
- Infections and infestations
- Emotional factors
- Inappropriate weaning and improper feeding practices
- Lack of nutritional education

Common complications of PEM

1. Hypoglycaemia
2. Hypothermia
3. Severe dehydration and hypovolaemic shock
4. Electrolyte imbalance
5. Septicaemia
6. Anaemic heart failure
7. Growth retardation and mental retardation

10 essential steps in management of PEM

1. Treat / prevent hypoglycaemia
 Give 50 mls of 10% glucose or sucrose solution orally or by nasogastric tube followed by the first
feed. Give 2 hourly feeds, day and night.
2. Treat / prevent hypothermia
 If axillary temperature is <35°C (95 °F) feed the child immediately. Rewarm the child.
3. Treat / prevent dehydration
 Do not use the intravenous route except in shock
 Give ReSoMal 5ml/kg every 30 min for 2 hours orally or by nasogastric tube then 5-10 ml/kg/hr
for next 4-10 hours
 Replace ReSoMal doses at 6th and 10th with equal amount of F-75 formula.
4. Correct electrolyte imbalance
 Give - extra potassium 3- 4 mmol /kg/day
- extra magnesium 0.4-0.6 mmol/kg/day
- low sodium rehydration fluid (eg ReSoMal)
- prepare food without salt
5. Treat / prevent infection
 Give routinely broad-spectrum antibiotics
- If the child has no complications, give Co-trimoxazole (Trimethoprim 4 mg/kg/dose) orally
twice daily for 5 days
- If the child is severely ill or has complications give Ampicillin 50 mg/kg IM/IV 6 hourly for 2
days, then oral Amoxicillin 15 mg/kg/dose 8 hourly for 5 days, and Gentamycin 7.5 mg/kg
IM/IV once daily for 7 days
- If the child fails to improve clinically within 48 hours, add Chloramphenicol 25 mg/kg/dose
IM/IV 6 hourly for 5 days
- Measles vaccination if child is > 9 months and not immunized
6. Correct micronutrient deficiencies
 Give daily – Multivitamin supplement
- Folic acid 1 mg/day (give 5mg on day 1)
- Zinc 2 mg/kg/day
- Copper 0.3 mg/kg/day
- Once weight gain is observed, give iron 3 mg/kg/day
- Vitamin A orally on Day 1 (if age>1year give 200,000 IU, 6-12 months give 100,000 IU, 0-5
months give 50,000 IU)
7. Initiate refeeding
 Give small frequent feeds of low osmolarity and low lactose formula
- Oral or nasogastric feeds 100 kcal/kg/day
- 1-1.5 g of protein/kg/day
- 130 ml/kg/day of Starter F75 (100 ml/kg/day if child has oedema)
- if the child is breastfed, continue to breastfeed but give Starter formula first

8. Facilitate catch-up growth

  Return of appetite is a sign for entering the rehabilitation phase
- Replace Starter F-75 with the same amount of catch-up formula F-100 for 48 hour
- Then increase each successive feed by 10 ml until some feed remains uneaten.
9. Provide sensory stimulation and emotional support
 Provide
- tender loving care
- a cheerful stimulating environment
- structured play therapy
- physical activity as soon as the child is well enough
- maternal involvement when possible
10. Prepare for follow-up after recovery
- A child who is 90% weight-for-length can be considered to have recovered.
- Good feeding practices and sensory stimulation should be continued at home.

Show the parent how to:

- feed frequently with energy-rich and nutrient-dense food
- give structured play therapy
Ask the parent to bring the child back for regular follow up at 1, 2 and 4 weeks, and then monthly for 6 months.

Recipes for starter and catch-up formulae

Prevention of PEM
1. Proper breast feeding
2. Growth monitoring and early referral
3. Timely and proper weaning practices
4. Immunization
5. Birth spacing
6. Female education
VITAMINS
Different types of vitamins
Water soluble vitamins
 Vitamin B1 (thiamine)
 Vitamin B2 (riboflavin)
 Nicotinic acid (Niacin)
 Pyridoxine (B6)
 Folic acid
 Vitamin B12
 Vitamin C

Fat soluble vitamins

 Vitamin A
 Vitamin D
 Vitamin E
 Vitamin K

Daily requirement of commonly deficient vitamins

 Vitamin B1 0.5 – 1.5 mg
 Folic acid 20 –
 Vitamin A 1500 IU
 Vitamin D 400 IU

Sources of vitamins
 Liver – Vitamin A, D, E, B1, B2, B6, niacin, folic acid
 Milk and milk product – Vitamin A, D, B1, B2, B12, niacin, folic acid
 Egg – Vitamin A, B12, B2
 Vegetables – Vitamin A, E, K, B2, C, folic acid
 Meat and meat products - niacin, folic acid, B2, B12, Vitamin E
 Fruits – Vitamin C

VITAMIN B1
Physiological functions of vitamin B1 (Thiamine)
 Acts as a co-enzyme in carbohydrate metabolism
 Required for synthesis of acetylcholine

Clinical features of vitamin B1 deficiency in infancy (Beriberi)

 Age 2 -3 months
 Breastfed babies of thiamine deficient mothers
 Cardiac form
- Sudden onset of cyanosis, dyspnoea, tachycardia, tachypnoea, puffiness of face, oedema,
hepatomegaly and low urine output.
 Aphonic form
- Continuous crying which becomes thin followed by aphonia within 24-48 hours
 Pseudomeningitic form
- Restlessness, convulsions and coma.

Diagnosis of infantile beriberi

- Therapeutic diagnosis – clinical response to administration of Thiamine such as improve general
condition, reduced heart rate and size of liver, diuresis within 2 hours
 - Iincreased blood lactic and pyruvic acid level
- Decreased red cell transketolase

Treatment and prevention

- Treat both mother & infant
- Vitamin B1 50 mg IM stat to infant followed by 10 mg of vitamin B 1 orally
- Oral vitamin B1 50 mg or B complex 1 tablet OD to mother
- Maternal diet containing sufficient amount of thiamine - pork, bean sprout
- Avoid thiaminase containing fish

VITAMIN A
Physiological functions
- Formation of photosensitive pigment of rods and cones in retina
- Integrity of epithelial tissue
- Anti-oxidant property

Clinical features of deficiency

- Xerophthalmia
- Retardation of physical and mental growth
- Follicular hyperkeratosis
- Prone to get infections due to reduced immune response

WHO classification of xerophthalmia

- XN – Night blindness
- X1a – Conjunctival Xerosis
- X1b – Bitot’s spot
- X2 – Corneal Xerosis
- X3a – Corneal ulcer / Keratomalacia less than 1/3 of corneal surface
- X3b – Corneal ulcer / Keratomalacia more than 1/3 of corneal surface
- XS - Corneal scar
- XF- Xerophthalmia fundi

Treatment and prevention

- Oral vitamin A Day 1, 2 and 14 (if age >1year give 200,000 IU, 6-12 months give 100,000 IU, 0-5
months give 50,000IU)
- Local antibiotic treatment for eye infection.
- High potency Vitamin A 6 monthly for prevention (< 1 year 100,000 IU, > 1year 200,000 IU).
- Vitamin A rich food (e.g. fish, liver, milk, egg yolk, green leafy vegetables, yellow foods.

VITAMIN D
Physiological function
- Antirachitic function
- Homeostasis of calcium and phosphorus in body fluids and tissues
Clinical features of deficiency
Rickets
- Early signs of Rickets - restlessness, generalized muscular hypotonia , abdominal distension (pot
belly), excessive head sweating , craniotabies , rachitic rosary , thickening and flaring of wrist and
ankles.
- Advanced Rickets - caput quadratum, pigeon chest deformity, Harrison’s groove, kyphosis, scoliosis,
lordosis, pelvic deformity, bow leg, knock knee , genu varum, genu valgum, green stick fracture,
rachitic dwarfism.
Investigation
- Serum calcium level – low or normal (normal 9-11 mg/100ml )
- Serum phosphorus level – low (<4mg/dl)
- Serum alkaline phosphatase level – high (normal 250-800 IU /L for growing child).
- Roentgenographic changes
- Cupping, fraying and widening of distal end of the bone.
- Increased distance between epiphysis and diaphysis
- Raised periosteum and double contour along the shaft
- Reduced bone density with prominent trabeculae
- Delayed bone maturation
- Healing state –Zone of preparatory calcification

Treatment
- IM vitamin D 600000 IU stat and oral vitamin D 400 IU/day after the process of healing has started.

Prevention
- Exposure to sunlight
- Vitamin D supplementation
- Vitamin D rich foods – cereals, milk and milk products, meat, oily fish

THE WEIGHT CHART OR ROAD TO HEALTH CHART

Main features of a Weight Chart
1. Calendar to record the child’s age.
The child’s age is ascertained and this is written into a first box for each year. Using this method worker
can accurately and quickly record the weight curve without calculating the age of the child at each visit.
2. The use of weight standards to construct a Road to Health.
a. Two curved lines are drawn in these cards. They represent the accepted standards of growth and their
direction. It is more important than their precise position on the chart.
b. The line between Green and Yellow is weight for age 80% of Harvard medium and line between
Yellow and Red is weight for age 60% of Harvard medium.
c. The channel between the lines is known as the “ROAD TO HEALTH’’ .If over several months the
child’s weight curve is moving away from the “ROAD’’ downwardly there is need for concern and
 action. If the direction of growth static in Green band is important because it can go downward in
anytime. Upward direction in Yellow band is a good sign for children’s health.
d. The Green band show weight for age 90%.Yellow band show 60-80% weight for age and Red band
show less than 60% weight for age.
3. The chart is a graphic representation of the Growth monitoring, Clinical and Nutritional Status.
In the weight chart the doctor or nurse enters the weight of child illness or other points relevant to the
Child’s Health. In this chart the growth curve can be seen in relation to a child’s age and illness.
4. Health Education and Nutritional guidance for Maternal and Child Health.
On weight chart there is pictures of Nutritious food , direction of growth and interpretation, advice
encouraging breast feeding, introduction of weaning foods, Health Education about certain disease e.g.
Dengue, Malaria, Gastroenteritis etc. and health advice for pregnant mother.
5. Immunization.
On the back of the chart is a panel listing the different immunization. The boxes should be filled in as the
child completes the various primary courses and booster doses for 6 common communicable diseases. E.g.
BCG, DPT, Polio and measles.
6. Reasons for special care.
Children with significant family history of parental problems are known to be ‘AT RISK` and should be
brought under closed observation and more frequent medical supervision e.g. birth weight less than 2 ½ kg
etc.
7. Parent retention of the chart
This is important because it is essential to secure parental participation in promoting the health of children.

Values of weight chart

1. It helps mothers to visualize whether the child is having adequate growth
E.g. the direction of growth curve is ascending
2. Early detection of malnutrition.
E.g. stationery weight is a sign of growth faltering
Descending growth curve means decline in nutritional status
3. Early detection of chronic illness/ disease.
E.g. children in yellow or red zones should be screened for major organ disease or chronic illnesses.
4. Record the immunization status.
5. It helps the parents to identify high risk infants who need special care.
6. It serves as a starting point for health education.
7. It helps the parents/caregiver to participate in monitoring their children’s health.
8. It helps the mothers to remember the date of birth and birth weight.
 INFECTIONS
BACTERIAL INFECTIONS
CONGENITAL SYPHILIS
Mode of spread of Syphilis
 Transplacental transfer of Treponema pallidum from the infected mother to the foetus
 During passage through the birth canal (rare).

Various presentation of congenital syphilis

Clinical manifestation of early congenital syphilis
 Mucocutaneous manifestations
 Nasal snuffles (profuse mucopurulent nasal discharge)
 Excoriation of skin over the upper lip.
 Sole and palm shows bullous lesion and desquamation and denuded area (washer women hands).
 Mucous patches, ulceration and fissures in mouth and anus.
 Skin lesion is most prominent over back, buttock and posterior aspect of thigh.
 Hepatosplenomegaly
 Generalized lymphadenopathy
 Haematologic manifestations – Anaemia
 Skeletal lesions – pseudoparalysis

 Failure to thrive

Skin peeling Syphilitic dactylitis

Clinical manifestation of late congenital syphilis

 Stigmata - Hutchinson's teeth, saddle nose, rhagades, saber shin & mulberry molars
 Interstitial keratitis , nerve deafness , Clutton's joints
Radiological changes
 X-Ray long bone – Periosteitis
 Dactylitis
 Osteochondritis & Syphilitic metaphysis
Wimberger sign – symmetrical destruction (“bite”) over the medial aspect of upper part of tibia.

Syphilitic periosteritis Nasal Snuffle

Laboratory tests for syphilis

1. Serology test (VDRL) High titre dilution of antibody i.e. positive VDRL
2. IgM antibodies against 47-KD antigen
3. Dark Ground Illumination - Demonstration of causal organism.
4. Radiology- X-ray long bones - periosteitis, dactylitis, Wimberger sign. etc.

Antibiotic treatment
 IV Crystalline Penicillin G 100,000 – 150,000 units/kg/day in divided doses (6Hourly) for 10 - 14 days.
 IM Procaine Penicillin 4-6 L per day x 7-10 days for early/mild case and 14 to 21 days for late case.
 If CSF is abnormal, IM or IV Crystalline Penicillin G 150,000 units /kg/day in 2 or 3 divided dose for
minimum of 21 days.

Preventive measure
 Routine prenatal screening for Syphilis

Prognosis
 Early treatment – Good.
 Delay treatment – Stigmata is high
DIPHTHERIA

Causal organism
 Gram (+) ve bacillus – Corynebacterium diphtheriae
Mode of transmission
 Contact or droplet infection
Incubation period
 2 - 5 days

Pathogenesis
 Exotoxin is the principal cause of local & systemic lesions.

Clinical presentation of different clinical types of diphtheria

 Constitutional symptoms
- Sore throat, difficulty in swallowing
- Restless, general malaise and prostration
- Fever, tachycardia
- Cervical lymphadenopathy
 Local manifestations
- Faucial
- Laryngotracheal
- Nasal and
- Cutaneous diptheria (unusual sites).

Faucial Diphtheria
Whitish gray membrane (pseudomembrane) firmly attached over tonsils, anterior pillars and uvula. It may
extend over the pharynx. It is difficult to remove the membrane without damaging the mucosa.

Fig. Diphtheritic pseudomembrane

Laryngeal Diphtheria
Membrane is usually extension from the throat, lower into the larynx. It is most serious but less common. The
manifestations are hoarseness, aphonia and croup, brassy cough, dyspnoea, cyanosis, respiratory distress, Bull-
neck (gross cervical lymphadenopathy and brawny oedema of the neck).

Nasal Diphtheria
It is uncommon but it is a source of spread of infection to others. It manifests as visible membrane over
turbinates, serosanguinous and foul smelling discharge which may be unilateral or bilateral.

Cutaneous Diphtheria
Diphtheria membrane may be found on skin, open wound, genitalia, conjunctiva and in ear. Underlining ulcer is
often painless and chronic.

Diagnosis
 Based on clinical features and identification of organisms from site of lesions
 Throat swab – Albert’s stain, and culture, FAT (fluorescent antibody technique)
 Demonstration of bacilli in smear alone is not adequate for precise diagnosis.
 Negative culture or staining does not exclude Diphtheria.

Differential diagnoses of different types of diphtheria

 Nasal diphtheria
o Foreign body
 Faucial diphtheria
o Acute streptococcal membranous tonsillitis
o Thrush
o Infectious mononucleosis
o Post tonsillectomy faucial membrane
 Laryngeal diphtheria
o Croup
o Acute epiglotitis
o Laryngotracheobronchitis
o Retropharyngeal abscess
o Post tonsillar abscess

Complications
 CVS - Myocarditis
 Neurological complications - Pharyngeal and palatal paralysis, ocular paralysis
 Renal complications - Nephritis
 GI & Liver – Gastritis, Hepatitis

Treatment of Diptheria and its complications

Specific treatment
  Anti-toxin – IM or IV Anti diphtheritic toxin 20,000-40,000 units
 Antibiotics for eradication of organism. It will stop the production of toxin and prevent their spread
- IV C Pen 0.5 L/kg/dose 6 hourly x 7-10 days.
- Oral Erythromycin 50 mg/kg/day 6 hourly x 10 days (to those who are hypersensitive to
Penicillin)

Supportive treatment
 Bed rest for 2 weeks
 Isolation
 Nasal feeding
 Antipyretic
 Maintenance of fluid and diet

Treatment of complications
By tracheostomy and mechanical respirator for respiratory obstruction or paralytic diaphragm

Prevention
 Active immunization according to EPI – 3 doses of DPT immunization.
 Contact person –
- Immunized person – booster dose of Toxoid and oral Erythromycin 40-50 mg/kg/day x 7 days
(or) IM Benzathine Pen 60,000-120,000 unit
- Unimmunized person – 1st dose Toxoid 5000 to 10,000 of ADS (Antidiphtheritic serum)
MENINGOCOCCEMIA
Causal organism
 Neisseri Meningitidis – Gram negative diplococci
Mode of transmission
 Droplet infection
Incubation period
 2-10 days

Clinical features
 Acute meningococcemia – influenza like symptom, morbilliform rash, petechial or purpuric spots,
hypotension, DIC, renal failure and coma. Very high mortality if undiagnosed early
 Meningococcal meningitis.
 Acute endocarditis, myocardits, pericarditis.
 Chronic meningococcemia – anorexia, weight loss, rash, arthritis, erythema nodosum.

Fig. Meningococcemic rash

Investigations
 Gram stain and culture from skin lesion, nasopharynx, blood & CSF
 CSF examination if meningitis is suspected
 Blood for CP – Neutrophil leucocytosis
 Rapid diagnostic test – by Counter current immunoelectrophoresis, immunoassay.

Treatment
 Antibiotics
- IV Crystalline Penicillin 1 L/kg/dose 6 hourly (or)
- 3rd generation cephalosporin (e.g. Cefotaxime 50mg/kg/dose 6hrly) for 7 -10 days.
 Fluids – colloid and inotropes in shock
 Steroid –IV hydrocortisone in adrenal haemorrhage.
 DIC – fresh whole blood, fresh plasma
Prognosis
 Very high mortality if undiagnosed early

Prevention
 Vaccination – meningococcal vaccine to household and day care nursery contacts. Booster after 3
month and 12-18 month.
 Drugs such as Rifampicin10mg/kg bd x 2 days to household and day care nursery contacts.
Ciprofloxacin 500mg single dose (adult contacts)

PERTUSSIS
Causal organism
 Bordetella pertussis – Gram negative bacilli.
Mode of transmission
 Droplet infection
Incubation period
 7 to 14 days

Common clinical manifestations

Three stages of clinical manifestations
 Catarrhal stage:
- Insidious onset
- Rhinitis, sneezing, lacrimation
- Fever and cough, which is nocturnal in the beginning and diurnal in later stage.
 Paroxysmal stage:
- Cough comes in paroxysms and is accompanied by vomiting, Cough is repeated series of
many coughing spasms – with an expiration followed by a sudden deep violent inspiration
with characteristic crowing sound (whoop) .
- Congestion of the face
- Sweating
- Periorbital oedema
- Subconjunctival haemorrhage
- Ulceration of frenulum of tongue
- In the young infants there is no characteristic whoop and may present with apnoeic attack.

Subconjunctival haemorrhage
 Convalescent stage:
- Cough and vomiting stop.
- Duration of cough may persist for weeks or months.
- Appetite becomes improved.
Complications
Respiratory
- Air leak syndrome
- Lung collapse
- Secondary bacterial infection
- Bronchiectasis
- Flaring of pulmonary tuberculosis
Neurological
- Encephalopathy
- Cerebral haemorrhage
- Convulsion
Gastrointestinal
- Hernia
- Rectal prolapse
Haematological
- Leucocytosis with absolute lymphocytosis
Others
- Severe PEM, otitis media, subconjunctival haemorrhage, Frenular ulcer.

Investigations
Bacteriological
 Per-nasal swab for organism
 Cough plate culture (Bordet Gengou Media) for organism
Haematological
 T&DC shows leucocytosis with absolute lymphocytosis.
Radiological
 CXR - perihilar infiltration, actelectasis emphysema.
ELISA test
 To detect serum IgM, IgG & IgA, pertussis toxin.

Treatment
Specific
 Antibiotics are effective only in catarrhal stage, reduce transmission if given.
- Oral Erythromycin 40 – 50 mg/kg/day in 3-4 divided doses x 14 days or
- Chloramphenicol 25-50 mg/kg/day in 4 divided dose x 7-14 days.
Supportive care
 Cough suppressant
 Bronchodilator – Oral Salbutamol 0.3 – 0.5 mg/kg/day in 3 divided doses

Preventive measures
 Active immunization (with triple antigen - DPT) according to EPI program.
  For close contact: -
- Neonate of mother with pertussis – Erythromycin x 2 wks.
- Children under 7 years previously immunized – give booster dose of DPT.
- Unimmunized person – erythromycin x 2 wks after the contact cases or cough in index case
are ceased. Then immunized.

SALMONELLOSIS
Causal organism
 Salmonella typhi
 Salmonella paratyphi A & B
Incubation period
 10-14 days.

Clinical features
Enteric fever
 Sudden rise of temperature
 Malaise, anorexia
 Headache
 Liver and spleen enlargement
 Bradycardia (uncommon)
 Rash (rare)

Salmonella gastroenteritis
 Diarrhoea is more common in children rather than constipation.

Dysentery
Food poisoning – Abdominal pain with vomiting

Gas under diaphragm indicates gut

perforation

Complications of enteric fever

1. GIT – Intestinal haemorrhage, Perforation.
2. CVS – Toxic myocardits, pericarditis.
3. Respiratory – Pneumonia, empyema.
4. Haematology – Haemolytic anaemia, haemolytic uremic syndrome
5. CNS – Toxic encephalopathy, Guillian Barre Syndrome
6. Miscellaneous – Metastatic abscesses, Otitis media, Tonsillitis
Investigations
1. CP – Leucopenia with relative lymphocytosis.
2. Blood culture (1st wk) - positive organism detected.
3. Widal test (Serological test) (2nd week) – for `O’ Antibody, positive mean Titre 1/160 or Four fold rise
after 10 days.
4. Culture of stool (3rd wk) - organism detected.

Treatment
 Antibiotics
- Chloramphenicol 50-100 mg/kg 6hrly x 10-14days.
- Other antibiotics - Amoxicillin, Ampicillin, Cotrimoxazole, Amoxi-clav and Quinolones.
 Correction of dehydration and electrolyte disturbances
 Treatment of complications.
 General measure – light fluid, semisolid diet and careful disposal of excreta.
 Treatment of chronic carrier – High dose of Ampicillin x 4-6 wks, Quinolones and Cholecystectomy.

Preventive measures
 Proper hand washing and personal hygiene especially for food handlers
 Environmental sanitation
 Availability of safe water
 Immunization by using Typhoid vaccine.
 Health Education.
 Detection and treatment of carrier.
Differential diagnosis of enteric fever
1. UTI
2. Tuberculosis
3. Malaria
4. Malignancies

Prognosis
 Generally good
 When malnutrition is present – bad

STAPHYLOCOCCAL INFECTIONS
Causal organism
Groups of staphylococcus – Gram positive cocci
 S. aureus – coagulase positive ( ß lactamase producer)
 S. epidermidis – coagulase negative
 Staphylococcus phage group II – producing exfoliative toxin
Clinical manifestations
Skin
 Impetigo, folliculitis, furunculosis, carbuncles
 Cellulitis, bullous impetigo (pemphigus neonatorum)
 Scalded Skin Syndrome
- Commences with macular erythema initially on the face, major flexures and then becomes
generalized.
- After 2 days bullae develop.
- Skin wrinkles and shears off (positive Nikolsky’s sign)
- Erosion, crust and dry, and healed with desquamation over next 4-8 days.
- Differential diagnosis – toxic epidermal necrolysis (due to Herpes)
Respiratory Tract
 Otitis media
 Sinusitis
 Staphylococcal pneumonia in infancy
 Empyema
Heart
 Acute bacterial endocarditis
 Pericarditis
CNS Scalded skin syndrome
 Brain abscess
Bones & Joints
 Osteomyelitis
 Septic arthritis
Intestinal Tract
 Food poisoning
Bacteraemia
Septicaemia

Investigations for Staphylococcal skin infection

 Skin swab
 Wound swabs
 Blood culture – for isolation and identification of the organism
 CSF culture – for isolation and identification of the organism
 For staphylococcal food poisoning- test for enterotoxin

Treatment
 Incision and drainage of abscess cavities.
 Antibiotics - Penicillinase resistant penicillin e.g. cloxacillin 25mg/kg/dose 6 hourly x 7-10 days, (or)
flucloxacillin, oxacillin, methicillin, clindamycin, etc.

Prevention
 Strict attention to hand washing techniques.
TETANUS
Causal organism
 Clostridium tetani – Gram positive spore bearing bacillus, drum-stick appearance.
 Vegetative forms are killed by heat and antiseptic but the spores are highly resistant.

The toxins produced by Clostridium tetani

 Tetanospasmin (Neurotoxin )
 Tetanolysin (Neurotoxin).

Common sources of infection

 Deep injuries
 Chronic otitis media

Characteristic features
 Muscle stiffness and rigidity (stiffness of jaw muscle – trismus)
 Risus sardonicus
 Muscle spasms
 Opisthotonus

Risus sardonicus Opisthotonus

Diagnostic criteria
 Clinical features mainly
 Identified organism from wound swab

Complications of tetanus
 Pulmonary complications – aspiration pneumonia, actelectasis.
 Laryngeal spasm – apnoea and cyanosis

Treatment
 Childhood Tetanus
- Eradication of the organism by IV Penicillin G - 100,000 U/kg/24hrs divided and administered
in 4 – 6 hrs x 10 – 14 days
- Neutralization of accessible tetanus toxin by Antitoxin:
o Passive immunization by IM or IV Anti Tetanus Serum 100,000 IU to children and
30,000 to 50,000 IU to newborn.
o Active immunization: Tetanus Toxoid (TT) initially 0.5-1 ml simultaneously with
passive immunization.
o IM Human Tetanus immune globulin (HTIG) 500 to 3,000 IU. It is safe and causes
no allergy.
- Control of muscle spasm by – Diazepam
 - Meticulous supportive care:
o Sedation round the clock.
o Oxygen inhalation
o Artificial ventilation may be required
- Surgical wound excision and debridement.
- Active immunization of patient on discharge.
- General measure- isolation of patient in quiet dark room
o Provision of good nursing care
o Adequate fluid and nutrition by intragastric or intravenous route.

PREVENTION THE OF TETANUS

 Active immunization when discharge;
- For non-immunized patient – give IM Tetanus Toxoid and another 2 doses of Toxoid in 1
month interval.
- For immunized patient – give a booster dose
 Routine immunization according to National Immunization Schedule
 Passive immunization in highly prone wounds – IM ATS 1000 to 3000 IU.
 Tetanus Toxoid should always be given after being bitten by a dog or other animals

TUBERCULOSIS
Causal organism
 Mycobacterium tuberculosis (human)

Major route of infection

 Droplet infection by inhalation
 Ingestion (swallowing of infected sputum)

Natural history of childhood Tuberculosis

Clinical features of primary complex

 Asymptomatic
 Non-specific symptoms / constitutional symptoms
- Fever (evening rise in nature)
 - Anorexia, weight loss, irritability, malaise, easy fatigability, night sweat and signs and
symptoms of upper respiratory tract infection.

 Hypersensitivity reactions
- Erythema nodosum
- Phlyctenular conjunctivitis
- Primary pleural effusion
- Positive Tuberculin test
- Repeated episodes of wheezing

Clinical features of Tuberculous pneumonia

Symptom – high fever, cough, respiratory distress and cyanosis
Sign – dullness on percussion, vesicular or bronchial breath sound/crepitation

Clinical features of Tuberculous pleural effusion

Symptoms – cough, pleuritic pain, shortness of breath
Signs – signs of fluid in chest such as reduced air entry, stony dullness on percussion

Clinical features of bronchial obstruction

Partial obstruction - localized wheezing
Complete obstruction - tachypnoea and dyspnoea, atelectasis of distal segment, dullness on percussion,
reduced breath sound

Clinical features of miliary TB

Fever, fatigue, malaise, anorexia, weight loss, dyspnoea, cyanosis, coarse crepitation, enlargement of
liver, spleen, lymph node and involvement of bone marrow

Clinical features of Tuberculous meningitis

- Insidious onset.
- 3 Clinical staging
Stage 1 – Prodromal Stage – Non-specific symptoms - apathy, mood changes, declining
school performance, loss of appetite, nausea, vomiting and low grade fever.
Stage 2 – Stage of meningitis – Appearance of neurological signs and symptoms - increased
irritability, headache, neck stiffness, Kernig’s sign, Brudzinski’s sign, cranial nerve palsies,
aphasia, slurred speech, disorientation, hemiplegia, ataxia, involuntary movement, convulsion,
features of increased ICP
Stage 3 – Stage of coma - Alteration in level of consciousness – proceeding from stupor to
coma, decerebrate or decorticate posture

Clinical features of TB abdomen

- Follows after ingestion of infected sputum
- Different types are
1. Peritonitis
2. Mesenteric lymphadenitis
3. TB enteritis
- Abdominal pain, chronic diarrhoea, constipation, weight loss, anaemia, enlargement of abdominal
lymph nodes, intestinal obstruction, peritonitis, ascities and doughy abdomen.

Clinical features of TB lymphadenitis

- Cervical lymph nodes – multiple and matted together
- Sinus formation.

Other manifestations
- Bone and joint mostly vertebrae:
- Pott’s spine
 - Gibbus and Kyphosis.
- Genitourinary TB
- Cutaneous TB - Lupus vulgaris
- Congenital TB

Complications of primary complex

 TB bronchopneumonia
 Complication arising from caseous lymph node
o pressure on the bronchial tree
o TB bronchopneumonia
o Bronchiectasis
o Pleural effusion.
o TB pericarditis and pericardial effusion
 Haematogenous spread from the primary and lymph node focus e.g. miliary tuberculosis, tuberculous
meningitis, TB bone, renal tuberculosis.

Less severe extrapulmonary TB

 Lymph node
 pleural effusion (unilateral)
 bone (excluding spine)
 peripheral joint
 adrenal gland
 skin

Severe extrapulmonary TB
 Meningitis
 Military
 Pericarditis
 Peritonitis
 bilateral or extensive pleural effusion
 spinal
 intestinal
 genitourinary

Risk Factors for Developing Childhood Tuberculosis

Presence of one or more of the following risk factors favours a diagnosis of TB in a child with suggestive
clinical presentation.
 Close contact (household, close relatives, caregiver, neighbour and teacher) with a newly diagnosed
smear-positive case as well as smear negative-culture positive case
 Age < 5 years of age
 HIV infection
 Severe malnutrition, measles and immunosuppressive drugs or illnesses
 Absence of BCG vaccination
General approach to diagnosis of TB in children

Symptoms with or without risk factors

Physical examination

Pulmonary disease Extra-pulmonary disease

Child ≥ 8 Child < 8 Cervical Other

years of age years of age glands EPTB

Biopsy
sputum
Request Request or
smear -
 Pleural aspirate
sputum smear test CXR  Lumbar puncture
 Joint aspirate
sputum
CXR + CXR -  Pericardial
smear + aspirate
plus CT scan/
Refer for expert
opinion and X-ray/US
follow up

Treat for TB

Criteria for TB-Suspect in Children

The child can be considered as a TB-suspect if 2 out of 3 following features are present.
 Fever and/ or cough for 3 weeks
 Failure to gain weight or weight loss if known
 History of contact with suspected or diagnosed TB patient

Clinical features
Symptoms suggestive of childhood TB:
 Chronic cough - Cough for more than 3 weeks which is not improving
 Fever (38ºC) - For more than 2 weeks after exclusion of common causes of fever (e.g. malaria)
 Failure to gain weight (Weight loss if known) - see weight chart
 Unexplained loss of appetite or lethargy
Signs suggestive of childhood TB:
 Pulmonary tuberculosis
o Signs of persistent pneumonia after full course of appropriate antibiotics
 Extra-pulmonary tuberculosis
o Highly suggestive
 Pleural effusion
 Acute vertebral gibbus
 Non-painful glands with draining sinus
o Suggestive
 Meningitis not responding to antibiotics
 Pericardial effusion
 Swollen non-painful joints
 Non-painful enlarged lymph glands present for longer than 2 weeks with no known
local cause and not responding to usual antibiotics.
 Distended abdomen with ascites
 Clinical features indicative of Tuberculin hypersensitivity (e.g.
erythema nodosum, phlyctenular conjunctivitis)

Microbiological confirmation
Definitive diagnosis of TB can be achieved only by the demonstration of presence of mycobacterium bacillus in
the lesion or its product. Bacteriological confirmation is desirable and should be tried in all cases.
The following recommendations are mainly for pulmonary tuberculosis. For extra-pulmonary tuberculosis,
Mycobacterium can be detected in the involved tissue.

Sputum examination
 Early morning spot sputum examination is essential in children older than 8 years of age

Recommendations for gastric lavage (aspiration) for TB diagnosis

 Indicated in children less than 5 years of age
 Should be carried out after 4 hours of not eating or drinking (starvation)

Radiological features
Criteria for the diagnosis of TB on the chest radiograph
No specific radiological signs exist for tuberculosis.
The following features highly assist in the diagnosis of tuberculosis when considered together with clinical
features and epidemiological context.

1. Unequivocal hilar lymph gland enlargement with or with out parenchymal opacification
2. Miliary mottling (especially in HIV-uninfected children)
3. Large pleural effusion (  1/3 of pleural cavity) in children older than 5 years of age
4. Apical opacification with cavitation (adult type disease; very rare in children, common in adolescents)

The following tests are not still recommended for clinical diagnosis of childhood TB
 Antibody serology tests
 Nucleic acid amplification tests (PCR tests)
 Gamma interferon immunoassay tests

Immunological evidence of infection

Tuberculin skin tests (TST)
Tuberculin skin tests are useful in the diagnosis of TB infection in young children for contact tracing. It is also
useful as an adjunct test where the diagnosis of TB is uncertain. A negative TST never rule out TB in children.
Interpretation of result:
  TST should be regarded as positive if induration is equal to or larger than 10 mm irrespective of
whether BCG has been administered.
 In HIV infected children induration of 5 mm or larger is taken as positive.

Diagnosis of extrapulmonary tuberculosis

Diagnosis of extra-pulmonary tuberculosis depends largely on site of the disease. .

Diagnostic criteria for TB pleural effusion

 Large pleural effusion ( 1/3 of pleural cavity) in children older than 5 years of age.
 Pleural tap indicates a lymphocyte rich exudates
 Clinical picture suggestive of TB

Diagnostic tests for other Extra-pulmonary TB

Disease Special investigations
Cervical/other lymph glands Biopsy / Fine needle aspiration cytology (FNAC)
TB Meningitis Lumbar puncture, CT brain scan
TB Arthritis Aspiration, biopsy
TB Abdomen/ascites Ultrasonography, aspiration
TB Vertebra Vertebral X-ray

Treatment of tuberculosis in children

Main Objectives
 cure the patient of TB
 prevent death from active TB or its late effects
 prevent relapse of TB
 prevent the development of drug resistance (by using a combination of drugs)
 decrease TB transmission to others

Recommended treatment regimens

Two phases:
 Intensive phase - to rapidly eliminate the majority of organisms and to prevent the emergence of drug
resistance
 Continuation phase - to eradicate the dormant organisms
In either phase, treatment is to be given daily.

First line (or essential) anti-TB drugs and their recommended doses
Drug Daily
Dose and range Maximum
(mg/kg body (mg)
weight)
Isoniazid (H) 5-10 300
Rifampicin (R) 10 (8-12) 600
Pyrazinamide (Z) 25 (20-30) –
Ethambutol (E) 25 (15-25) –
Streptomycin (S) 15 (12-18) –
Recommended treatment regimens
TB diagnostic Regimen
Category TB cases
Intensive phase Continuation phase
 New smear negative pulmonary TB (Other than
III in category I) 2HRZ 4HR
 Less severe forms of extra-pulmonary TB
 New smear positive pulmonary TB
 New smear negative pulmonary TB with
extensive parenchymal involvement
I 2HRZE 4HR
 Severe forms of extra-pulmonary TB (other than
TB meningitis – see below)
 Severe concomitant HIV disease

I TB meningitis / Disseminated TB disease 2HRZE(S) 7HR

 relapse
II  treatment after interruption 2HRZES/1HRZE 5HRE
 treatment failure

Specially designed standardized

IV Chronic and Multi-drug Resistant TB
or individualized regimens

Corticosteroids
Corticosteroids may be used for the management of some complicated forms of TB, e.g. TB meningitis,
TB glands causing airway obstruction, and TB pericardial effusion. In cases of advanced TB meningitis,
corticosteroids have been shown to improve survival and decrease morbidity, and thus are indicated in all cases
of TB meningitis. The drug recommended for use is prednisolone, in a dosage of 2 mg/kg daily, is increased up
to 4 mg/kg daily in the case of the most seriously ill children, with a maximum dosage of 60 mg/day for 4 weeks
(refer to Chapter 5). The dose should then be gradually reduced (tapered) over 2-4 weeks before stopping.

Management of tuberculous meningitis and miliary tuberculosis

TB meningitis and miliary TB are more common in young children and are associated with high rates of death
and disability, particularly if the diagnosis is delayed. It is therefore important to consider these diagnoses in
young children as early as possible, especially in children who have a history of contact with an adult with
infectious TB.

Diagnosis
Miliary or haematogenously disseminated TB has a high risk (60–70%) of meningeal involvement and should
therefore be managed similarly to TB meningitis. For this reason, many experts recommend that all children
with miliary TB (or suspected of having miliary TB) should undergo a lumbar puncture to test for the presence
of meningitis.

Treatment
Children with TB meningitis or miliary TB should be hospitalized, preferably for at least the first 2 months.
Level of service for these cases is as follows:

 District hospitals (first referral level)

 Tertiary level specialist hospital for further investigations when there is no response to treatment within 2
weeks or there are complications requiring further investigations.

Preventive measures
 Tracing the source of infection and treat properly
 BCG vaccination
 Isoniazid prophylaxis to neonate whose mother is an open case of tuberculosis
 Health education
PARASITIC INFECTIONS
MALARIA
Causal organism
1. Plasmodium falciparum
2. Plasmodium vivax
3. Plasmodium malariae
4. Plasmodium ovalae

Life cycle
 2 phases – Asexual cycle a. pro-erythocytic
b. erythocytic
- Sexual cycle
 Exo-erythocytic ( P. vivax, P. malaria, P. ovalae)
 P. vivax and P. ovalae (Young red cell)
 P. falciparum (all ages of RBC)

Fig. Plasmodium falciparum Fig. Plasmodium vivax

Common malaria infections prevalent in Myanmar

1. Plasmodium falciparum
2. Plasmodium vivax

Common clinical features

1. Intermittent fever characterized by the presence of chills, cold and hot stages (may be atypical in
children)
2. Anaemia of varying degree
3. Jaundice – tinge to mild
4. Hepatosplenomegaly

Complications of falciparum malaria

1. Cerebral malaria
2. Hyperpyrexia
3. Hypoglycaemia
 4. Severe anaemia
5. Black water fever
6. Acute renal failure (ARF)
7. Algid malaria
8. Gastrointestinal involvement
9. Disseminated intravascular coagulation (DIC)
10. Hepatitis

Investigations
1. Blood for MP
2. Rapid diagnostic test (RDT) by malaria antigen detection
3. Hb% estimation
4. CSF – routine examination in cerebral malaria
5. Blood urea level in acute renal failure

SUSPECTED CASES

(Clinical Criteria)

RDT/Microscopy

Positive Negative

High suspicion

Falciparum Non-falciparum
Of malaria

Chloroquine

+Primaquine

Uncomplicated
Treat while Look for other
Severe malaria
malaria
Excluding Illness
Treatment Treatment
Other illness Review/Refer
ACT ACT
Chloroquine

Management
Treatment regimen
Uncomplicated Plasmodium falciparum Malaria
First-line treatment for microscopy- or dipstick- confirmed cases of uncomplicated Plasmodium falciparum
malaria is a 3-day artemisinin-based combination.
Monotherapy of Plasmodium falciparum malaria is strongly discouraged.

Artesunate-mefloquine or artemether-lumefantrine (co-artem) is the combination therapy of choice:

Artesunate (4 mg/kg/day for 3 days) + Mefloquine 25 mg base/kg as either 15 mg/kg followed 8-24 hrs later by
10 mg/kg or 25 mg base/kg equal divided doses in 3 days.
Artemether-lumefantrine: 1.2/8 mg/ kg twice daily for 3 days.

ACT for confirmed P.f cases

First - Oral AS 4 mg/kg + MQ 25 mg/kg over 3 days

Treatment failure cases

AS 4 mg/kg immediately followed by 2 mg/kg for 6days + Doxycycline 3 mg/kg/day (or) Tetracycline 4
mg/kg/day
* Doxycycline and Tetracycline are contraindicated in children under 8 year, and during pregnancy
Recommend alternative for these two groups - Clindamycin 10 mg/kg BD x 7Days

Severe and Complicated Malaria

Inj Aretsunate 2.4 mg/kg immediately followed by 1.2 mg/kg for 6 days (or)
Inj Artemether 3.2 mg/kg immediately followed by 1.6 mg/kg for 6 days (or)
iv slow infusion Quinine dihydrochloride 20 mg(salt)/kg as loading dose over 4 hours followed by 10 mg/kg 8
hourly for 6 days (until patient can tolerate oral medication.) (+)
Doxycycline or Tetracycline or Clindamycin x 7 days

Plasmodium vivax and Plasmodium ovale Malaria

Chloroquine (total dose 25 mg base/kg)
Chloroquine 10 mg/kg in 1st day + 10 mg/kg in 2nd day + 5 mg/kg in 3rd day followed by

Radical cure
Primaquine - 0.25 mg/kg for 14 days
- 0.75 mg/kg once weekly for 8 weeks for mild G6PD deficiency cases

Plasmodium malariae
Chloroqune +/- Primaquine
Chloroqune 25 mg/kg over 3 days followed by Primaquine 0.75 mg/kg stat

* Primaquine is contraindicated in severe G6PD deficiency, during pregnancy and infancy.

Symptomatic Treatment
 Maintain fluid and electrolytes balance
 Anticonvulsant therapy with diazepam or phenobarbitone
 Antipyretics for fever – Paracetamol 15 mg/kg/dose 4-6 hourly
  Tepid sponging
 Blood transfusion for severe anemia (if haematocrit is less than 15% or Hb% less than 6 g/dl) - to give
10 ml of packed cells or 20 ml of whole blood per kg of body weight and haematenics to correct
anaemia

Prevention
Prevent contact of vector with man
 Screening of house
 Use of mosquito-nets
 Protective clothing
 Use of insect repellent cream on exposed parts of the body
 Insect repellent tablets (Heat slowly)
Destruction of mosquitoes
 Residual spraying with aerosolized insecticides such as pyrethrum
Destruction of larvae
 Good sanitation around the house
 Applications of oil or larvicidal compounds in water storage places
Reduction of mosquito sources
 Special care of overhead tanks, desert coolers, water chambers, water storage bins and irrigation
channels
Chemoprophylaxis
 Chloroquine 5 mg/kg every week
 Mefloquine 3.5 mg/kg every week (if chloroquine resistance is endemic)
Immunoprophylaxis – Still in research stage

CEREBRAL MALARIA
Clinical Features of cerebral malaria
 Sudden or gradual onset
 Generalized or partial convulsions
 Deep coma
 Tone and reflexes are variable
Poor prognosis signs
 Up-going planter response
 Loss of corneal reflex
 Retinal haemorrhage

Management of cerebral malaria

 See treatment of severe and complicated malaria
 General measures
- Blood transfusion
- Anticonvulsants
- General care of unconscious patients
ASCARIASIS
Causal organism
 Ascaris lumbricoides

Clinical features
Due to presence of adult worms
 Intestinal symptoms (in heavily infected children)
- Colicky abdominal pain (intermittent) and distension
- Abdominal mass
- Intestinal obstruction (partial or complete)
 Migration of worms
Biliary trees (Cholangiohepatitis)
- Acute onset of colicky abdominal pain
- Nausea, vomiting and fever
- Jaundice
Appendicitis
Liver abscess
Peritonitis

Due to larvae
 Loeffler’s syndrome
- Cough
- Blood stained sputum, and eosinophilia
- Transient infiltrates on CXR
 Convulsion – due to larvae in the circulation

Complications
 Intestinal obstruction from adult worms
 Appendicitis
 Peritonitis
 Steatorrhoea decreased vitamin A absorption may occur in heavily infected children.
 Cholangiohepatitis
 Obstructive jaundice
 Liver abscess
 Pancreatitis
 Malnutrition

Investigations
1. Stool RE for characteristic eggs are diagnostic.
2. USG abdomen for complications e.g. obstructive jaundice
Treatment
 Levamisole (<5 years - 1 tab, 5-15 yr - 2 tabs, >15 years – 3 tabs) or
 Mebendazole 100mg BD for 3 days or 500mg single dose or
 Albendazone 200mg single dose for <10 kg bodyweight, 400mg single dose for >10 kg BW or
 Pyrantal pamoate 10 mg/kg/dose as single dose

Preventive measures
1. Personal hygiene - Sanitary practices and hygienic sewage disposal facilities
2. Avoidance of ingestion of partially cooked foods and unhygienic foods and drinking of
contaminated water.

TRICHURIASIS
Causal organism
 Trichuris trichiura

Clinical Features
 Light infections
- Asymptomatic
 Heavier infections
- Abdominal pain
- Tenesmus
- A bloody or mucoid diarrhoea and weight loss
- Rectal prolapse
- Anaemia and growth retardation

Investigation
 Stool RE - eggs of T. trichiura

Treatment
 Supportive treatment (anaemia, nutrition)
 Specific treatments
- Mebendazole 100mg BD for 3days.

Preventive measures
See ascariasis
ENTEROBIASIS
Causal organism
 Entrobia vermicularis

Clinical features
 Nocturnal anal pruritus
 Sleeplessness
 Vaginitis and salpingitis
 Anorexia, weight loss
 Irritability
 Anuresis

Investigations
Eggs can easily be detected on adhesive cellophane tape pressed against the perianal region early in the
morning.

Treatment
 Mebendazole 100 mg orally single dose with a repeat dose in 2 weeks
 Albendazole – 400 mg orally single dose with a repeat dose in 2 weeks, 200 mg for children <2
years (<10 kg body weight)
 Pyrantal pamoate – 10 mg/kg, repeat in 2 weeks
** Treat all family members simultaneously to prevent re-infection

Preventive measures
Same as ascariasis
GIARDIASIS
Causal organism
Causal organism - Giardia Lamblia

Clinical Features
 Asymptomatic
 Symptomatic - more frequent in children acute, subacute or chronic infection.
In acute infection
Sudden onset of explosive diarrhoea (profuse, watery, greasy, foul smelling and may float) low grade
fever, nausea and anorexia. Stool may not contain blood, mucus, or fecal leukocytes.
In chronic persistent diarrhoea
 Intermittent diarrhoea and constipation
 Malabsorption
 Crampy abdominal pain and bloating or failure to thrive or weight loss

Complications
 Malabsorption of xylose and disaccharides, fat, fat soluble vitamin
 Failure to thrive

Investigations
 Stool RE - simple wet film microscopy of fresh stool shows trophozoite or cysts
 Duodenal sampling and biopsy - Aspiration or biopsy of the duodenum or upper jejunum

Treatment
Supportive treatment
 Correction of fluid and electrolyte imbalance
 Correction of any deficiency state and nutritional support
Specific treatment
 Metronidazole (15-20 mg/kg/day) 3 times daily for one week or
 Tinidazole (50-70 mg/kg/day) once daily for 3 days

Prevention
 Personal hygiene
 Hand washing after toileting
 Environmental sanitation
 Purify public water supplies.
AMOEBIASIS
Causal organism
 Entamoeba histolytica
Mode of spread
 Faecal-oral route

Clinical features
Intestinal amoebiasis
 Asymptomatic
 Symptomatic amoebiasis
- Colicky abdominal pain
- Diarrhoea with tenesmus
- Blood stained stool with mucous
- Generalized constitutional symptoms and signs

Extraintestinal Amoebiasis
 Liver
- Hepatitis
- Hepatic amebiasis - Fever with chills and rigors, toxaemia, abdominal pain, distension, and
tender enlarged liver. Jaundice is uncommon.

Amoebic liver abscess

Complications
Intestinal complications
 Severe diarrhoea which may result in dehydration and electrolyte disturbance
 Perforation
 Peritonitis
 Amoeboma
 Toxic mega colon

Hepatic Complications
 Amoebic liver abscess
 Frequently in the right lobe (Single or multiple)
 - Complications: Rupture into the peritoneal cavity, the pleural cavity and/or the lung and
through the skin. Blood-borne spread may result in a brain or lung abscess

Investigations
 Stool RE - Identification of E. histolitica from freshly passed warm stool. Trophozoites can be seen
in feces.
 Proctoscopy or sigmoidoscopy - Scraping of ulcerated area of rectal mucosa
 Aspiration of a liver abscess
 Serological tests: Antibody titers are usually high.
Different methods can be used such as indirect heamagglutination test, counter
immunoeletrophoresis (CIE) and ELISA.

Treatment
 Supportive treatment
Correction of fluid and electrolyte imbalance and nutritional support
 Specific treatment
- Luminal amoebicides: Diloxanide furoate
- Tissue amoebicides: Metronidazole and Tinidazole
 Metronidazole 35-50 mg/kg/day and Diloxanide furoate 20 mg/kg/day in three divided
doses for 10 days, or
 Tinidazole 50-60 mg/kg/day once daily for 3 days
 Diloxanide furoate 20 mg/kg/day in three divided doses for 10 days
 Secnidazole once daily for 3 days
 Aspiration of the liver abscess guided by ultrasound scan.

Prevention
 Personal hygiene
 Environmental hygiene
 Food hygiene
VIRAL INFECTIONS
DENGUE HEMORRHAGIC FEVER (D.H.F)
DENGUE SHOCK SYNDROME (D.S.S)

Epidemiology
Agent - Flavi virus, DHF virus serotype 1,2,3 and 4
Vector - Aedes aegypti - bite during daytime, grow in clear water.
Host - Common among age less than 15 year
Environment - Epidemic in rainy season
- Urban and satellite townships
Incubation period - 5 – 8 days (range 3 – 14 days)

WHO case definition of DHF

1. Acute sudden onset of high fever for 2–7 days.
2. Haemorrhagic manifestations with at least a positive tourniquet test.
3. Platelet count <100 x 109/l.
4. Haemoconcentration (rising packed cell volume >20%) or other evidence of plasma leakage—for
example, ascites, pleural effusions, low level of serum protein/albumin.
The illness usually begins abruptly and has three phases, namely Febrile, Critical and Convalescent.

Febrile phase - sudden rise in temperature accompanied by facial flushing, skin erythema, headache and muscle
pain. Haemorrhagic manifestations are usually present. Massive GI bleeding may occur later as a result of
prolonged shock leading to DIC. Tender hepatomegaly is often present.

Critical phase, which lasts about 24 – 48 hours during which plasma leakage occurs.
Features of plasma leakage
 Circulatory disturbances (low blood pressure, tachycardia, narrow pulse pressure, and poor capillary
refill time).
 Periserositis (pleural effusions, ascites sometimes pericarditis).
 Disseminated intravascular coagulation leading to massive bleeding.
Features of shock
1. Abrupt fall in temperature (usually on or after 3 rd day of fever)
2. Acute abdominal pain
3. Restlessness or drowsiness
4. Cold clammy extremites
5. Sweating
6. Rapid thready pulse
7. Capillary refill time > 3 seconds
8. Narrow pulse pressure (<20 mmHg) or Hypotension

Complications
- Encephalopathy and encephalitis
- Liver failure
- Myocarditis
- DIC leading to massive bleeding

The Convalescent phase - usually short and uneventful even in those with shock. Diuresis ensues as shock
resolves and the patient rapidly regains appetite. Some may have a confluent petechial rash with characteristic
scattered round areas of pale skin on the extremities, which may be itchy. Bradycardia is a common finding.

Dengue Recovery Rash - Confluent petechial rash with typical circular areas of normal skin in between is
pathognomonic of DHF and usually appear on the extremities. They are seen in DSS patients, 1-2 days after
recovery from shock and in patient without shock, 1-2 days after fall of temperature. The significance of this
rash is that prognosis is good, and is a retrospective diagnosis of DHF.

Pathophysiology
The major pathophysiological hallmarks of DHF
1. Plasma leakage as a result of increased vascular permeability leading to hypovolemic shock
2. Abnormal haemostasis as a result of increased capillary fragility (positive tourniquet test and tendency
to bruise), impaired platelet function, thrombocytopenia and in most severe form, disseminated
intravascular coagulation leading to varying degrees of haemorrhagic diathesis.

Severity Grading (WHO Classification)

The disease severity of DHF has been classified into four grades according to the clinical hallmarks of bleeding
and plasma leakage.
• Grade I - Only positive tourniquet test
• Grade II - Positive tourniquet test with spontaneous superficial bleeding
• Grade III - Shock
• Grade IV - Profound shock with unrecordable blood pressure and / or pulse

N.B. Every DHF patient must have evidence of plasma leakage and thrombocytopenia.

Final grading of either non-shock DHF or DHF with shock (DSS) can be given only after the patient is afebrile
for 2 days.

Investigations in Acute Phase

 Platelet counts – low ( <100 x 109/l)
 Haematocrits – increased
 WBC count - leucopenia early in the illness, with atypical lymphocytosis (>15%)
Biochemical investigations (Optional)
 Coagulation profile – prolonged APTT, PT, raised FDP in DSS
 Serum electrolyte – Acidosis in DSS
 Liver enzymes – may be elevated
  Serum complement levels – Reduced
Every patient with altered consciousness, especially those with restlessness, confusion and irritability should
have his/her liver functions monitored.

Confirmatory Laboratory Tests

Case management depends on the clinical diagnosis. The following tests may be carried out
for confirmation and epidemiological studies.
Serological diagnosis
 Haemagglutination inhibition test – acute phase sample on admission, and second sample 2 weeks later.
Positive result shows four fold rise in antibody titer.
 Dengue IgM and IgG detection – positive from 4th to 7th day of fever. Ig M indicates primary infection
and IgG indicates secondary infection.
Virus isolation with mosquito cell line for epidemiological purposes

The major causes of death in DHF

• Prolonged shock leading to DIC and multi organ failure
• Massive bleeding
• Fluid overload leading to cardiac failure / pulmonary oedema
• Acute liver failure with encephalopathy
• Encephalitis
• Myocarditis

With good clinical care, case fatality rate (CFR) should be around 0.5 – 1.0%, but otherwise may vary up to 5%.

Management of DHF/DSS
Management of DHF G I & II
1. Daily monitoring
2. PCV and Platelet count daily (starting from 3rd day onwards )
3. Paracetamol and sponging for high fever
4. Avoid NSAIDs through all routes (oral, IM, PR)
5. Encourage oral fluids, ORS, fruit juice
6. Encourage feeding
7. Admit if one of the following is present:
a. Those from distant places and/or transport difficulty
b. Platelet count <100,000/[Link]
c. PCV increased ≥20% of baseline or ≥44%
d. Spontaneous haemorrhage (G II)
e. Those who are not tolerating oral fluids
8. Give intravenous fluid therapy (6 mL/kg/hr x 1-2 hr) if
a. not orally tolerated
b. PCV increased ≥20% of baseline or ≥44%
(See flow diagram 1 at Page 7.)
 Management of DSS

Admit

1. Give oxygen
2. Correct hypoglycaemia
3. Start immediate fluid replacement for 1-2 hour
- GIII - iv 10 ml/kg/hr
- GIV - iv 20 ml/kg/hr

Improvement

Yes No

GIII - Reduce fluid rate to 6 ml/kg/hr Colloid (Plasma/Plasma expander)

Improvement
10-20 ml/kg/hr
GIV - Reduce fluid rate to 10
ml/kg/hr, then 6 ml/kg/hr Reassess after 1 hour
No Improvement

Improvement ↑PCV ↓PCV

after 1 hour
(Consider bleeding)
continue plasma/plasma Fresh whole blood
Reduce fluid rate to 3 ml/kg/hr expander 10 ml/kg/hr (max.
total 30 ml/kg) - PCV>40% - 10 ml/kg/hr

Improvement Improvement - PCV<40% - 10-20 ml/kg/hr

until improved
No Improvement
Crystalloid 6 ml/kg/hr x 1 hour

Continue up to 24-48 hr Consider complications

and fluid overload
Then, stop iv fluid therapy Reduce fluid rate to 3 ml/kg/hr
Improvement

Continue up to 24-48 hr

Then, stop iv fluid therapy

 Management of DHF G I & G II with PCV ≥ 20% of baseline or PCV≥44%

Admit

Initial Fluid 6 ml/kg/hr for 1-2 hour

Monitor PCV, Vital signs & Urine Output

Improvement No Improvement

Reduce fluid rate to

3 ml/kg/hr

Improvement

Deterioration at any time

Continue fluid 3 ml/kg/hr Treat as DSS

Continue up to 24-48 hr

Then, stop iv fluid therapy

Management of DSS
1. Admit all cases
2. Give oxygen, correct hypoglycaemia
3. Start immediate rapid volume replacement
a. G III – IV DS 10 ml/kg/hr (RL or NS if DS is not available)
b. G IV – IV DS 20 ml/kg/hr (RL or NS if DS is not available) for 1-2 hour
Run fluid as rapidly as possible if necessary
4. Subsequent replacement
a. If improved after Step 3
i. G III - Reduce the fluid rate to 6 ml/kg/hr
ii. G IV- Reduce the fluid rate from 20 to 10, then 10 to 6 ml/kg/hr for 1 hour
iii. If improve, reduce the fluid rate to 3 ml/kg/hr
iv. If improve, continue up to 24-48 hr
v. Then, stop IV fluid therapy
b. If not improved after Step 3
Give colloid (plasma expander/plasma) 10-20 ml/kg/hr
1. If not improved after colloid and high PCV (still in shock), continue
plasma/plasma expander 10 ml/kg/hr
a. If not improved after plasma/plasma expander for at total of 30
ml/kg, consider complications and treat accordingly
2. If not improved after colloid, with declining PCV (20% decrease from the
initial value)*, it indicates significant internal bleeding, and give fresh
whole blood transfusion
10 ml/kg/hr if PCV ≥40%
10-20 ml/kg/hr if PCV <40 until improved
*Examples of 20% decrease from initial value
PCV from 53% to 42% = 20% decrease
from 50% to 40% = 20% decrease
from 46% to 37.8% = 20% decrease

3. If improved, go to Step 4.a.i or [Link] with crystalloid

5. Platelet concentrate transfusion
a. Platelet count <20,000/[Link] without bleeding
b. Platelet count 20,000 to 50,000/[Link] with bleeding
6. If features of fluid overload such as dyspnea, orthopnea, filling neck vein, rapidly enlarging liver,
HR>120/min, crepitation (pulmonary oedema), low PCV, present treat with intravenous furosamide 1
mg/kg stat.
7. If there is evidence of coagulopathy (prolonged PT & APTT) or Disseminated Intravascular
Coagulation present, use (Fresh Frozen Plasma and/or Platelet concentrate) OR Platelet-rich plasma
8. Correct electrolyte imbalance and metabolic acidosis in severe and prolonged shock
9. Antibiotics are usually not indicated unless there is massive GI bleeding or suspected bacterial
infection
 10. Steroids
a. not indicated for DSS
b. may be used in encephalopathy
In actual practice, some suspected DHF/DSS patients (possible prolonged shock at home) present with
shock and normal / low PCV. INTERNAL BLEEDING should be suspected in these patients.

N.B. Exercise caution when administering fluid therapy to children weighing more than 30 kg

Total maintenance fluid therapy for 24 hours

- 1st 10 kg = 100 ml/kg/day
- 2nd 10 kg = 1000 ml + 50 ml/kg/day for each excess of 10 kg
- more than 20 kg = 1500 ml + 20 ml/kg/day for each excess of 20 kg
- maximum for male = 2.5 L/day
- maximum for female = 2.0 L/day

Monitoring
1. Frequent monitoring of vital signs every hour during shock
2. PCV every 2 hour in first 6 hours of shock, then as required
3. Platelet count daily
a. 3rd day onwards
b. if shock present, up to 24 hour after recovery from shock
c. if bleeding present, as required
d. if complications present

Laboratory Investigations
1. PCV and Platelet count serially
2. Urea and Electrolytes in complicated cases
3. Coagulation screen (PT, APTT) if indicated
4. Liver function tests (ALT, AST) if indicated

Discharge criteria
All of the following must be present
1. Absence of fever for more than 24 hour without the use of antipyretics and return of appetite
2. Visible improvement in clinical picture
3. Stable PCV
4. If no complications for 48 hours after recovery from shock
5. No respiratory distress from ascites or pleural effusion
Prevention of DHF
1. Prevention of mosquito bite at day time – use of insecticide, wearing clothes that cover the
body, use of mosquito nets and screening of houses, screens in doors and windows
2. Removal of breeding places – use of larvicide (Abate), clearing of flower vases, removal of all
possible areas where water can collect

MEASLES
Causal orgnism
 Paramyxovirus (RNA virus)
Mode of transmission
 Droplet infection
Incubation period
 10-14 days

Measles rash

Clinical features
Prodromal stage (3-5 days before eruptive stage)
- Fever
- Conjunctivitis, catarrhal or coryza – characterized by consistently running nose, and dry cough

Koplik’s spots

- Koplik’s spots - pathognomonic sign: small grayish white dots as small as grains of sand
surrounded by reddish areola appear on the inner side of cheek opposite the lower molar teeth.
They usually disappear rapidly usually within 12 to 18 hour
Exanthematous stage (4th day onwards)
- Confluent maculopapular rashes.
- Start behind the ears and along the hair lines and on the posterior part of the cheek
- Spread rapidly to involve the face
- Then downward and become generalized. Blotchy appearance.
 - In severe measles – it may become haemorrhagic (usually fatal but occurrence rare)
Convalescent stage
- When the rashes fade, brown staining of the skin and desquamation.

Differential diagnoses of maculopapular rash

1. Rubella
2. Infectious mononucleosis
3. Enteroviral infection - Coxsackie A, B
4. Drug eruption
5. Meningococcaemia

Complications
1. Respiratory (due to reduced cell mediated immunity)
- Suppurative otitis media
- Tracheitis
- Laryngo tracheobronchitis
- Bronchitis
- Bronchopneumonia – secondary to bacteria infection e.g. - Staphylococcal pneumonia.
- Giant cell viral pneumonia (especially in immunocompromised child)
- Suppurative lung disease

2. Non-respiratory
 Opthalmic complication
- conjunctivitis
- keratitis
- corneal ulcer
 Gastro intestinal tract
- stomatitis
- cancrum oris
- Gangrenous form of stomatitis due to anaerobic bacteria, Treponema vincenti
- Rapidly spread to form sloughing of gums and jaws and perforation of cheek
- In extreme case - teeth may be shed
- Peculiar foul odour.
- Gastroenteritis
- Persistent diarrhoea
 Central nervous system – encephalitis, subacute sclerosing panencephalitis (SSPE)
 Others – malnutrition, leucopenia, thrombocytopenia

Investigations
 Serology – can detect measles IgM
 CXR (PA) view for respiratory complications
 EEG for encephalitis

Treatment
 Supportive treatment only
- Antipyretics
- Adequate fluid intake
- Vitamin A
 Antibiotics are only necessary for secondary bacterial infections

Preventive measures
 Active immunization
- According to UCI at 9 months of age
- MMR may be given (12 months to 15 months) if available.
POLIOMYELITIS
Causal organism
 Poliovirus (RNA) virus
Three distinct serotypes
- Type (I) - major epidemics (most common cause of paralytic polio)
- Type (II) - sporadic
- Type (III) - intermediate
Mode of transmission
 Faecal-oral route
 Direct contact with infected person
Incubation period
 7- 14 day ( 1-3 week)

Predisposing Factors
 Clinical severity is increased by age & pregnancy
 The following can precipitate paralysis:
- Intramuscular injection
- Minor traumatic procedure
- Tonsillectomy
- Strenuous physical activity
- Immune deficiency state
- High dose corticosteroid therapy

Clinical features
 95 % asymptomatic
Different phases
(1) Abortive type – asymptomatic
(2) Subclinical infection
(3) Clinical infection without paralysis
(4) Clinical infection with paralysis – paralytic polio
Initial symptoms-
 Pyrexia
 Headache, malaise, cough
 Slight neck stiffness
 Upper respiratory tract infection and sore throat
 GI upset
 Back pain & joint pain
May or may not progress to paralytic polio.

Paralytic polio
Spinal form
- Weakness of some of muscles of neck, abdomen, trunk & diaphragm, thorax or extremities
Bulbar form
- Weakness in motor distribution of one or more cranial nerve with or without dysfunction of vital
centers of respiration and circulation
Encephalitic form
- Irritability, disorientation, drowsiness and coarse tremors and sometimes inadequate ventilation

Investigations
Isolation of polio virus from the patient
 From stool
- Virus can be present up to 2 weeks after onset of paralysis (2 samples)
 From serum
 - Samples of serum from acute and convalescent cases
- Significant rise in antibody titre during the illness (Complement fixations antibodies, neutralizing
antibodies)
 From CSF - virus culture

Differential diagnoses of paralytic polio

 Infectious polyneuritis (Guillian-Barre Syndrome)
- Paralysis is characteristically symmetrical with or without associated sensory changes
 Peripheral neuritis
 Encephalitis
- Arthropod-born viral encephalitis, rabies, tetanus, botulism and demyelinating types of
encephalitis may be confused with bulbar poliomyelitis.

Treatment
 Supportive treatment
- Simple analgesic
- Bed rest until child’s temperature is normal for several days
- Application of hot pack for muscle spasm and pain
 Physiotherapy
 Nursing care – Bladder and bowel care
 For Respiratory failure – Ventilatory support

Preventive measure for eradication of polio

Polio eradication program
Strategies
 EPI (Extended Program of Immunization)
 NIDS (National Immunization Days)
 AFP (Acute Flaccid Paralysis) surveillance
 Mopping up door to door immunization
 Outbreak Response Immunization (ORI)

NIDS (National Immunization Days)

 Simultaneous mass OPV immunization all under 5s regardless of previous immunization status
 The advantages are to establish herd immunity in the community and eradicate polio

AFP Surveillance program

1. Immediate AFP reporting
2. Active surveillance

Acute flaccid paralysis - Any case of acute flaccid paralysis in children under 15 years of age including
Guillian-Barre syndrome for which no other cause is apparent.
Case investigation include
1. Verify AFP
2. History and examination
3. Investigations for detection of polio virus after collection of stool specimen
4. Outbreak response immunization
5. 60 days follow–up
Outbreak Response Immunization (ORI)
 One AFP case in 15 yr old which remain suspected polio case after verification - should trigger ORI
 Should start immediately within 24-48 hour after AFP case has been verified
 All children below 5 yr of age
 No child is missed
 House to house immunization is recommended
MUMPS (EPIDEMIC PAROTITIS)
Causal organism
 Mump virus
 One of myxoviruses (RNA virus)
 Occasionally epidemic

Incubation period
 14 to 21 days

Mode of transmission
 Droplet infection or from recently contaminated articles and close contact.

Clinical Feature
 Prodromal symptoms
- Malaise, fever, headache, and anorexia
 Salivary gland enlargement
- Occurs in 1 to 2 days later, parotid glands are the most frequently affected.
 Pain and swelling develop around the ear
- Swelling appears which extends forwards from the lobe of ear, downwards over the angle of jaw
and backward behind the pinna which is usually pushed outwards.
- Orifice of Stenson’s duct may be swollen
- The mouth rather dry

Complications
 CNS
- Aseptic Meningitis
- Post-infectious encephalitis
- Neurological sequalae and even death
 Orchitis
- 20% of post-pubertal male
- Occasionally occur in undescendent testis
- Usually unilateral
- Sterility (rare complication)
 Pancreatitis
- Intense abdominal pain and rigidity of abdominal wall
 Other complications
- Oophoritis
- Mastitis,
- Bartholintis
- Myocarditis
- Hepatitis
- Thyroiditis
- Thrombocytopenic Purpura.
Preventive measure
 MMR vaccine
 Live attenuated vaccine

RUBELLA
Causal organism
 RNA Virus
Mode of Transmission
 Droplet infection
Incubation period
 18 to 21 days

Clinical features
Prodromal stage
 Rare to have prodromal stage in children
 In female adult, there are malaise, headache, fever, and conjunctivitis and arthritis.

Appearance of rash
 Start over face (maculopapular rash)
 Soon spreads to cover the trunk and later the limbs
 Basic lesion appears as fine, pink macules which is originally discrete but can soon coalease over the
face and trunk

No desquamation of rashes
 Usually disappear 2 to 3 days

Lymph node enlargement

 Usually one week before the rash
 Cervical, post auricular and sub occipital glands are involved.
 Tender and sometime unassociated with any rash

Congenital rubella syndrome

Microcephaly in congenital rubella

syndrome

 Most serious complication of rubella

 May occur when a non-immune mother acquires rubella in early pregnancy.
 Result in uterofoetal infection
 Most dangerous during first 12 week of pregnancy
Clinical features of congenital rubella syndrome
 Abortion, IUGR, SGA.
 Microcephaly, mental retardation
 Heart defect - PDA, VSD, PS, TOF
 Deafness
 Occular defect – Cataract, glaucoma, micro-opthalmia, retinopathy

Differential diagnoses of Rubella

1. Measles
Main different from measles rash
- Subclinical or clinical infection
- Rash with no conjunctivitis, no desquamation
- No staining
- Associated with polyarthritis or arthralgia
2. Enteroviral infection e.g. Echo, Coxsackie virus
3. Infectious mononucleosis
4. Scarlet fever
5. Erythema infectiosum
6. Various drug eruption / rash (drug allergic rash)

Management
Conservative treatment
 No specific treatment in rubella infection.
 Conservative management or symptomatic management only

Preventive Measure & Importance of Prevention

 To prevent Congenital Rubella Syndrome especially for the girls before child bearing age
 Active immunization with MMR (Measles vaccine conjunction with mump and rubella)vaccine
 First dose at one year of age, second dose – preschool or 12 to 14 year old
 Contraindication - immune deficiency, symptomatic HIV Infection, anaphylactic egg allergy

CHICKEN POX
Causal organism
- Varicella Zoster virus (VZV)
- (Human herpes virus 3 (HHV3)
- DNA virus
Incubation period
- 2 to 3 weeks

Clinical Features
 Mild malaise, fever may or may not be present or absent
  Rash - The rash as a crop of macules which within hour pass through a papular stage to become
vesicular. The vesicular stage persists for 3 to 4 days becoming pustular and finally forming a crust.
- The spots are superficial and vesicle may be irregular in shape and they are often surrounded by
red areola.
- Lesions at different stages may be seen.
- The trunk is principally involved. Face, scalp and proximal part of limbs
- By the time there is vesiculation – there is intense pruritus
 Enantham
- Vesiculation over palate, tongue and buccal membrane, conjunctiva and vagina

Differential diagnoses
Differential diagnosis of vesicles and pustules
1. Impetigo
2. Scabies
3. Dermatitis hepatiformis
4. Ezema hepaticum or vaccinatum
5. Erythema multiforme

Differences between Chicken Pox and Small Pox

 Small Pox
Agent - Variola virus
Incubation period - 12- 14 days
Clinical features
1. Prodromal phase
2. Distribution of rashes
- start face and forearm
- spread to trunk
- macules  papules  vesicle (characteristic umbilication surrounded by red areola  pustules 
crusted lesion (serial sequence of stages)

 Chicken Pox
Clinical features
1. Prodromal phase usually absent
2. Distribution of rashes  One can see different stages at the same time

Common complications
 Secondary skin infection - cellulitis, erysipelas
 Pneumonitis
- Usually in adult and immunocompromised children.
- Present with acute respiratory distress syndrome or haemoptysis
- CXR – Diffuse nodular infiltration, Miliary calcification
- In a normal child – most likely to be bacterial due to Streptococcal pneumoniae and group A
streptococcus or Staphylococcus aureus
 Neurological
- Post infectious encephalitis
- Cerebella ataxia – excellent prognosis
- CSF – Mild lymphocytic pleocytosis , slight elevation of protein
- Reye syndrome (10%) secondary to chicken pox
- Transverse myelitis
- Acute infantile hemiplegia
- Guallian Barre syndrome
 Appendicitis
 Others
- Myocarditis
- Pericarditis
- Endocarditis
- Hepatitis
- Glomerulonephritis
HIV INFECTION IN CHILDREN
Causal organsim
 RNA virus (retrovirus)
 Types
- HIV-1 - More common and more pathogenic
- HIV-2 - Transmission is low and infection to disease interval is longer
Virus can be inactivated by
- Heat (56ºC for 30 min.)
- Ether, Acetone
- 20% ethanol
- 0.2% Sodium Hypochloride (Bleaching Powder)

Mode of transmission in children

HIV is transmitted in two main ways.
1. Vertical transmission
- From an infected pregnant mother to her child (over 90 % of pediatric HIV infections)
- The risk of a baby acquiring the virus from an infected mother ranges from 25% to 50% if there is no
intervention
2. Horizontal transmission
- From infected blood and blood products - via transfusion or via unsterile needles and syringes
- Sexual abuse

Clinical Features
WHO Case Definition
The diagnosis of paediatric HIV infection is made if at least two major and at least two minor signs are present.

Major signs
- Weight loss or abnormally slow growth
- Chronic diarrhea (>1 month)
- Prolonged fever (>1 month)

Minor signs
- Generalized lymph node enlargement
- Oro-pharyngeal candidiasis
- Recurrent common infections, such as ear infection and pharyngitis
- Persistent cough
- Generalized rash
- Confirmed HIV infection in the mother

Diagnosis
Clinical
In those without HIV testing in antenatal period, children infected with HIV are usually diagnosed clinically by
- having a high index of suspicion (use criteria for clinical recognition, WHO Criteria)
- and later on HIV Antibody test is done for the child as well as the mother

Laboratory diagnosis
 HIV Antibody Test - For children born to HIV infected mothers HIV antibody test should be done
every 3-6 monthly basis from 6 months of age up to 18 months. Persistence of antibodies beyond this
age indicates infection.
 To show the presence of virus in the blood
- HIV viral culture
- p24 antigen testing
- HIV PCR test
Management
Management of infants born to HIV infected mother
Anti retroviral prophylaxis (PMCT – prophylaxis of mother to child transmission)
 Administer Nevirapine 2mg/kg to the babies of HIV infected mother within 48 - 72 hours after birth.
OR
 Administer oral Zidovudine every 6 hourly up to 6 weeks after birth

Provide family education, counseling and support

 Good hygienic practice
 How to prevent horizontal spreading of HIV-infection.

Appropriate infant feeding

 Infant feeding counseling - Formula feeding if affordable

Appropriate immunizations
 All routine immunization can be given

Cotrimoxazole prophylaxis
 Trimethoprim 6 mg/kg /day once a day starting from 6 weeks of age until 12 months of age to prevent
Pneumocystic carinii pneumonia.

Prevention, diagnosis and treatment of opportunistic infections

Use of antiretroviral therapy

Pneumocystic carinii pneumonia

Bilateral interstitial infiltrates (frequently atypical pattern on CXR)
 High-dose TMP-SMZ (TMP 20 mg/kg/day every 6 hours IV or, in mild case PO) for 21 days
 Steroid reduces mortality in severe cases
 In case of TMP-SMZ intolerance, alternative treatments are Dapsone + Trimethoprim or Primaquine +
Clidamycin

Antiretroviral therapy for HIV infected children

 Should only be started after appropriate counseling
 Groups of Anti-Retro viral drugs
- NNRTI’s – Non-Nucleoside Reverse Transcriptase Inhibitors
e.g. Nevirapine (NVP), Efavirenz (EFV)
- NRTI’s – Nucleoside Reverse Transcriptase Inhibitors
e.g. Zidovudine (ZDV, AZT), Stavudine (d4T)
- PI’s – Protease Inhibitors
e.g. Indinavir (IDV), Ritonavir (RTV), Nelfinavir (NFV)

Prevention
Anti retroviral prophylaxis (PMCT)
- Nevirapine 200 mg to the mother at onset of normal labour or 4-6 hours before Elective Caesarean
Section
- Administer oral Nevirapine 2 mg /kg within 48- 72 hours after birth to the babies
Interventions to Reduce Mother to Child Transmissions of HIV
- Voluntary Confidential Counseling and HIV testing - Offers benefits for HIV-positive women, and
their sex partners even in the absence of therapeutic interventions.
- Behavioral Interventions - Reduction in the frequency of unprotected sexual intercourse during
pregnancy with consistent condom use.
- Therapeutic Interventions - Nutritional supplementation of iron, folate, multivitamins and vitamin A
and treatment of sexually transmitted diseases (STDs)
IMMUNIZATION
VACCINE-PREVENTABLE DISEASES
Infectious diseases can be prevented through immunization by-
1. Stimulating an active immunological defense mechanism through administration of antigens, usually
prior to natural exposure to infectious agent (active immunity); or
2. Temporarily supplying performed exogenous animal/human antibody to suppress disease, given soon
after or prior to exposure (passive immunity).
Active immunization agents are known as vaccines. An ideal vaccine should
(a) be easy to produce in a well standardized preparation
(b) be easy to administer
(c) not produce disease in the recipient
(d) induce permanent immunity
(e) be free of toxic substances and
(f) have minimal side effects
SPECIFIC PROTECTION AGAINST COMMON DISEASES
Tuberculosis
Bacillus Calmette Guerin (BCG) vaccination
 An attenuated strain of Mycobacterium tuberculosis var. bovis
 Supplied in freeze-dried (lypophilized) form
 Potency remains satisfactory for several months at 4°C
 Administered intradermally over deltoid muscle
 Dosage - 0.05 ml (newborn) or 0.1 ml (all other ages)
 May be given any time from birth since mother’s immunity is not transferred to the fetus
 After 2-3 weeks a papule develops at the site (indicating the multiplication of BCG) which gradually
heals leaving a scar
 Immunization of the infant appears to offer significant protection from progressive primary and
disseminated tuberculosis including meningitis.

Poliomyelitis
 Inactivated (killed) poliovirus vaccine (IPV) developed by Salk
 Live attenuated (oral) poliovirus vaccine (OPV) by Sabin
 Both vaccines are usually supplied as a trivalent antigen containing the three types of polioviruses
Oral Poliovirus Vaccine (OPV)
 OPV of the three types of attenuated poliovirus in its each liquid dose, two drops are preferred
 Three doses are necessary at interval of at least four weeks
 Frequency of vaccines failure rate can be reduced by increasing the number of doses for primary
immunization
 National Expended Program on Immunization, three doses of OPV during infancy along with DPT,
followed by a fourth dose during second year of life are recommended
 Potency of OPV is stable for 3-4 months at 4-8°C and for 1-2 years at -20°C
 Temperature fluctuations, particularly those above 8°C rapidly reduce the potency.
 Vaccine potency can be effectively monitored using vaccine vial monitors (VVM)
 Transient diarrhea following OPV has been noted
 One in a few million vaccinees may develop paralytic poliomyelitis due to vaccine virus infection
itself
Inactivated (killed) poliovirus vaccine (IPV)
 primary immunization requires three dose, given intramuscular or subcutaneous, at 4-8 weeks interval
 periodic booster doses of IPV are necessary to maintain high antibody level
 IPV should be used in immunocompromized children, those with AIDS, family members of
immunodeficient individual, particularly partially immunized or unimmunized adults and in some
tropical countries with poor facilities for cold chain
Diphtheria
 The toxoid vaccine, adsorbed with aluminum hydroxide is usually combined with pertussis and tetanus
toxoid vaccines as a triple antigen (DPT vaccine) or with tetanus toxoid (DT vaccine)
  Primary immunization requires three doses, at interval of 4, 6 or 8 weeks; the first booster is
recommended during the second year of life (e.g. at 18 months) and a second booster at five years
 Three doses of primary vaccination during first year and a booster dose at the end of 2 nd year of life
achieves protective antibody level of >1 IU/ml that lasts till the end of the first decade
Pertussis
 Usually given in the form of the DPT vaccine
 Each contains a required number of killed organisms of B. pertussis
 Three doses are recommended at 4-8 weeks of interval, commencing at 1-3 months of age so that
primary immunixation is completed by 4-6 months of age
 The protective efficacy is approximately 75%, occasional vaccine failure may be expected
 Common adverse reaction – local pain, swelling, mild to moderate fever and irritability
 Rarely convulsions may occur either due to the fever or due to an encephalopathy syndrome
 Some children may develop a hypotonic hypo-responsive state (pale, limb and unresponsiveness)
 An infant who develops prolonged screaming or convulsions following a dose of DPT should not be
given pertussis vaccine
 Static neurological disease (e.g. Cerebral palsy) and febrile convulsions are not contraindication
 It is generally recommended that pertussis vaccine should not be given to children over five to six years
old
Acellular pertussis vaccine (aP)
 Is relatively less reactogenic
 All aP vaccine contain inactivated pertussis toxin, which in most cases is combined with filamentous
haemaglutinin and sometimes additional B. pertussis components such as fimbrial antigens and
pertacitin
 Immunization of infants with DwPT or DaPT has shown a similar efficacy of 80% or more in
preventing typical pertussis and reducing related morbidity and mortality
 aP vaccine is also available in combination with diphtheria, tetanus toxoids, hepatitis B, Haemophilus
influenzae type b and killed poliovirus (IPV) vaccine
 Contraindications to DaPT are very rare
 Acellular vaccines are considered costlier

Tetanus
 Since there is no natural immunity to C. tetani toxin, unimmunized mothers do not transfer antibodies
to the infants, immunizing pregnant women or women of child-bearing age against tetanus is an
important public health policy to reduce incidence of neonatal tetanus in high risk countries
 This is achieved by using tetanus toxoid (TT) as the immunizing agent
 Tetanus toxin is very toxic, the lethal dose for human being less than 2.5 g/kg
 Toxin is inactivated by formaldehyde to yield TT
 It is adsorbed into aluminum salts (hydroxide or phosphate) to increase its antigenicity
 TT can withstand 37°C for a few weeks without a significant loss of potency
 Usually administered combined with toxoid of diphtheria and pertussis killed vaccine as DPT
 Combination of DT also available
  Single toxoid preparation of TT is used for older children, adults and pregnant weman
 Three doses of DPT vaccines are recommended (at 1 month interval each) for primary immunization
followed by boosters at approximately 18 months and 5 years of age
 Subsequent TT boosters are recommended at 5 to 10 years interval

Measles
 Live attenuated measles virus is used as the vaccines
 Several strains of attenuated viruses are used
 Grown in cell culture of human, canine or avian origin, harvested and lyophilized for preserving
potency
 Shelf life is at least one year at 4-8°C
 May be given subcutaneous or intramuscular
 After reconstitution its potency drops rapidly
 For these two reasons, reconstituted vaccine should be used the same day and left over must be
discarded
 Depending upon the strain of vaccine virus, between 10 and 20% of vaccinees may develop mild to
moderate fever abut 6-8 days after vaccination, between 1 and 5% may develop a few red spots on the
trunk
 Malignancies associated with immunosuppression and therapy with antimetabolites, alkylating agents
and corticosteroids are contraindication
 Residual maternal antibody in the infant’s serum neutralizes the immunogenic property of the vaccine,
it should be offered at an age when most infants would have lost this affect
 Therefore the recommended minimum age is 9 months

Hepatitis B
Plasma derived hepatitis B vaccine
 Is a subunit vaccine containing surface antigen (HBsAg) prepared from pooled plasma of HIV negative
HBV carriers
 HBV surface antigen particles are harvested, purified and residual virus is inactivated
Recombinant hepatitis B vacciney
 Genetically engineered vaccine prepared in a vector into which gene of HBsAg has been introduced
 Highly immunogenic with seroconversion rates of 96% reported after 3 doses
 Administered intramuscularly in the deltoid or in the antero-lateral thigh
 The response to gluteal injection is not optimal
 Three doses of 0.5 ml each are to be given at 0, 1 and 6 months
 To raise the immunity faster, the vaccination can also be done at 0,1 and 2 months
 In UCI, given at birth, 1.5 and 3.5 months of age
 Dose of 10 g is required for children less than 10 years and 20 g is required for adults and children
>10 years
 Immunocompromized patient should receive twice the recommended dose
  HBV not only prevents the vertical transmission at birth but also, and perhaps more importantly, the
horizontal child to child transmission in early childhood

Haemophilus influenzae vaccines

 Currently several Haemophilus inflyenzae type b (Hib) vaccines are available and listed on national
immunization programs of at least 20 countries
 Hib capsular polysaccharide induces production of antibodies in older children and adults
 This phenomenon is inadequate in infants and very young children less than 18 months old, who
response poorly to polysaccharide antigens
 Thus failing to achieve protective levels of antibodies or a long lasting immunological memory
 For these reasons, the Hib polysaccharide was conjugated to a T cell dependent protein antigen to
develop a new generation of vaccines
 These Hib vaccines not only induce protective circulating antibodies and immunological memory in
infants, but also result in decreased nasopharyngeal colonization of Hib
 Thus a herd immunity may also be achieved
 Routine vaccination is started at the age of 2 months of age
 A time lag of 8 weeks between any two doses is ideal. A booster is recommended at 12-18 months of
age
 Only 2 doses is given for those where Hib immunization has not been started by 7 months of age
 More than or equal to 15 months should be given only one dose
 For children more than 5 years, vaccination is only indicated if they are suffering from an underlying
immune disorder or asplenia
 All conjugate Hib vaccines are given intramuscularly
 No known adverse effects or absolute contraindications except for hypersensitivity to vaccine
components

Universal Childhood Immunization in Myanmar

 RESRIRATORY SYSTEM

ACUTE RESPIRATORY INFECTIONS (ARI)

Introduction
Respiratory tract infections – commonest cause of illness in children
ARI – 25-42% of OPD visits in developing countries (WHO 1995)
ARI - 1/3 of all hospital infections in developing countries (WHO 1995)
ARI – 4.3 millions deaths in < 5 (WHO 1990)
Overall incidence of ARI – same in developed and developing countries
AURI – 4 to 8 episodes in urban, 3-4 in rural
Pneumonia – 0-4 years
-- 7 – 18 per 100 / year (developing)
Pneumonia – 3/4 of all ARI deaths
Percent of total deaths – developing countries
-- 20-25% - < 2 months
-- 50-60% - under 1 year
-- Very few >1 year
Pneumonia- No. 1 killer (U5MR Survey 1995)

Definitions
RTI – infections in any area of respiratory tract including ears, nose & throat
ARI – all RTI of less than 30 days’ duration, except acute ear infections of less than 14 days duration
AURI – ear, nose & throat
ALRI – epiglottis - lungs

Risk factors for Pneumonia or death from ARI in developing countries

 Young age
 Lack of immunization
 Malnutrition – poor breast feeding practices
 Vitamin A deficiencies
 Low birth weight
 Cold weather or chilling
 Overcrowding
 High nasopharyngeal carriage of pathogenic bacteria
 Pollution – tobacco smoke, biomass smoke, air pollution(WHO – 1995)
Acute coryza (Common cold)
 Majority are due to viral infections
 Fever, sneezing, cough, poor feeding,
 Little or no systemic upset
 Not increase in respiratory rate
 Bacteria – Group A Streptococcus, Pneumoccous
 Purulent nasal discharge
 Treatment -- supportive – high fluid intake, paracetamol, home made safe remedy
 Antibiotics – marked purulent nasal discharge
 obvious toxicity
 persistent of signs and symptoms

Acute Tonsillitis
 May be viral, but significant number are due to bacterial cause- Group A beta-haemolytic
Streptococcus
 Exudative tonsillitis with white pustules
  Tender cervical lymphadenitis
 Antibiotics- Pen V, Erythromycin or Cephalexin for 7 to 10 days

Indications for tonsillectomy

Absolute indications
 Obstructive sleep apnoea
 Peri-tonsillar abscess
 Suspect of malignancy

Relative indications
 Recurrent tonsillitis – proven strep infections more than 3 times/year for two years
 Recurrent febrile convulsions due to acute tonsillitis

PNEUMONIA
Common at all ages, but most common in infants and young children
Developing countries – more common and more severe
Guidelines - WHO Guidelines
British Thoracic Society
Canadian Guidelines

Clinical diagnosis
WHO Guidelines – presence of tachypnoea

Under 2 months > 60 breaths / min

2 – 12 months > 50 breaths/ min
12 months > 40 breaths/ min
Presence of fever, acute respiratory symptoms, or both plus presence of parenchymal exudates on CXR

Aetiological diagnosis
Lung-puncture studies in developing world
 Strep pneumoniae
 Haemophilus influenzae type B
 Stap aureus
 S. pyrogenes
 Gram (-) enteric bacterias

Investigations
In community – no investigations is needed if clinical signs are present
Hospital
 Blood culture - < 10% positive
 Acute & convalescent serum
 Nasopharyngeal aspirate
 Pleural fluid – microscopy, culture
Preschool child + wheezing – Bacteria unlikely
Fever, tachypnoea, dyspnoea, >3years, >38.5.C – usually bacteria

Radiological diagnosis
If clinical signs are present – Radiological exam is not necessary
If clinical recovery is satisfactory – no repeat X-ray
(BTS Guideline)

Management
BTS Guideline
  Young children with mild symptoms of LRTI – no antibiotics
 Oral antibiotics for CAP
 < 5 Amoxcillin – first choice
 > 5 year- Mycoplasma – Macroloid are 1st choice
 IV Antibiotics – severe symptoms, not able to take orally

Acute Respiratory Infection (ARI)

Assess the severity of pneumonia in children between 2 months and 5 years

(WHO Classification)
 Simple
 Meant for basic health workers

In a child (2 months-5 yrs) with cough or difficult breathing

Very severe pneumonia or very severe disease
 Danger signs are present
 Central cyanosis
 Not able to drink or breast feed, or vomiting everything
 Convulsions, lethargy or unconsciousness
 Severe respiratory distress
 Drowsy or abnormally sleepy, or
 Severe malnutrition

In addition, some or all of the other signs of pneumonia or severe pneumonia may be present such as
 Fast breathing:
Age <2 month ≥ 60 / minute
Age 2-11 months ≥ 50 / minute
Age 1-5 years ≥ 40 / minute
 Nasal flaring
 Grunting (in young infants)
 Lower chest wall indrawing (lower chest wall goes in when the child breathes in: if only the soft tissues
between the ribs or above the clavicle goes in when the child breathes, this is not the lower chest wall
indrawing)
 Chest auscultation signs of pneumonia
 Decrease breath sounds
 Bronchial breath sounds
 Crackles
 Abnormal vocal resonance (decrease over a pleural effusion, increased over lobar consolidation)
 Pleural rubIf pulse oximetry is available, obtain an oxygen saturation measurement in all children
suspected to have severe or very severe pneumonia
 If possible, obtain a chest X- ray to identify pleural effusion, empyema, pneumothorax , pneumatocele ,
interstitial pneumonia and pericardial effusion.

Severe pneumonia
Cough or difficult breathing plus at least one of the following signs:
 Lower chest wall indrawing
 Nasal flaring
 Grunting ( in young infants )
 Check that there are no signs of very severe pneumonia such as
Central cyanosis
- Inability to breastfeed or drink
- vomiting everything
- Convulsions, lethargy or unconsciousness
 - Severe respiratory distress
In addition, some or all of the other signs of pneumonia may able to present
Fast breathing: Age < 2 months: ≥ 60/minutes
Age 2 – 11 months ≥ 50/minutes
Age 1 – 5 years ≥ 40/minutes
Chest auscultation signs of pneumonia:
 Decreased breath sounds
 Bronchial breath sounds
 Crackles
 Abnormal vocal resonance (decreased over a pleural effusion, increased over
lobar consolidation)
 Pleural rub.
A routine chest X-ray rarely gives information which will change the management of severe
pneumonia and is therefore not recommended.

Pneumonia
Diagnosis
On examination, the child has cough or difficult breathing or fast breathing
Age – 2 to 11 month ≥ 50/ min
1 to 5 years ≥ 40min
Check that the child has none of the sign or severe or very severe pneumonia
In addition other sign of pneumonia may be present, crackles, reduced breath sound or an area of bronchial
breathing

No pneumonia (cough or cold)

Common features:
 Cough
 Nasal discharge
 Mouth breathing
 Fever
 The followings are absent
- Fast breathing
- Lower chest wall indrawing
- Stridor when the child is calm
- General damger sigms

Assess the severity of pneumonia in children less than 2 months of age

(WHO Classification)

In an infant <2 months with cough or difficult breathing

Severe pneumonia or very severe disease

 Fast breathing (  60/min )
 Severe chest indrawing
 Danger signs –
- stopped feeding well
- abnormally sleepy or difficult to wake
- Convulsions
- stridor in calm child or wheezing
- grunting
- central cyanosis
- Apnoeic episode
- distended or tense abdomen
 - fever 38ْ C or more, or low body temperature <35 ْ C
No pneumonia
No above danger signs

Common causal organisms for pneumonia

Bacteria
2 months to 5 years – [Link]
[Link]
Staph aureus (common in <1yr)
Under 2 months – Group B strep
[Link]
Staph. Aureus

Viruses
Respiratory syncytial virus (RSV)
Influenza virus
Parainfluenza virus
Measles
Chickenpox
Others
Fungus
Protozoa

Physical signs of pneumonia (tables from SIO)

Fast breathing
age <2 months: > 60/minute
age 2-12 months: >50/minute
age 12 months to 5 years: >40/minute

Chest indrawing

Sign of consolidation
 decreased breath sounds
 bronchial breath sounds
 Crackles
 abnormal vocal resonance (decreased over a pleural effusion, increased over lobar consolidation)
 pleural rub

Signs of effusion
 Reduced air entry
 mediastinal shift to the opposite site
 stony dullness on percussion

Sign of pyopneumothorax
 reduced air entry
 mediastinal shift to the opposite site
 hyper-resonance on percussion
Investigations
Radiological features of
 Bronchopneumonia (patchy opacities)
 Pneumococcal pneumonia(lobar consolidation)
 Staph. Pneumonia (pneumatocoele, pyopneumothorax)
Other investigations
  Blood of CP – Neutrophil leucocytosis
 Blood for culture & sensitivity

Common complications of pneumonia

Extend to pleural cavity especially staphylococcal pneumonia
 Pneumothorax
 Empyema
 Pyopneumothorax
Persistent pneumonia (Failure to response with adequate treatment)
Septicemia and distant infections
Heart failure

Common causes of persistent pneumonia

 TB
 Chlamydia
 Aspiration/Foreign body
 Pneumocystis carinii pneumonia (PCP)- ( In cases of HIV infection )

Magement of pneumonia
(according to WHO Standard Management Guideline)
Management of very severe disease
Treatment
 Admit the child to hospital
 Antibiotic therapy
- Give ampicillin ( 50mg/kg IM every 6 hours ) and gentamicin (7.5 mg/ kg IM once a
day) 5 days; then, if child responds well, complete treatment at home or in hospital with
oral amoxicillin (15 mg/kg three times a day) plus IM gentamicin once daily for a further
5 days for less than 2 months old child.
- Give chloramphenicol (25mg/kg IM or IV every8 hours) until the child has improved.
Then continue orally 4 times a days for a total course of 10 days for children 2 month to 5
years of age. Or use ceftriaxone (80 mg/kg or IV once daily).
- If the child does not improved within 48 hours switch to gentamicin (7.5 mg/kg IM once a
day) and cloxacillin (50 mg/kg IM or IV every 6 hours), as described below for
staphyloccal pneumonia. When the child improves, continue cloxacillin (or dicloxacillin)
orally 4 times a day for a total course of 3 weeks.
 Oxygen therapy
- Give oxygen to all children with very severe pneumonia.
- Continue with oxygen until the sign of hypoxia (such as severe lower chest wall
indrawing or breathing rate ≥ 70/ minute.) are no longer present.
 Nurses should check every 3 hours that the catheter or prong are not blocked with mucus and
are in correct place and that all connection is secure.

Supportive care
 If the child has fever (≥39˚C or ≥102.2˚F) which appears to be causing distress, give
paracetamol.
 If wheeze is present, Nebulized salbutamol if available (2.5mg<5 year/5mg >5year) OR
 IV Aminophylline (5mg/kg /dose).
 Remove by gentle suction any thick secretions in the throat, which the child cannot clear.
 Ensure that the child receives daily maintenance fluids appropriate for the child's age, but
avoid over hydration.
- Encourage breastfeeding and oral fluid
- Nasogastric tube feeding - if unable to drink
- Encourage the child to eat as soon as food can be taken
 Reassess every 3 hours, minimum twice a day.
 Monitoring
The child should be checked by nurses at least every 3 hours and by a doctor at least twice a day. In the
absence of complications, within two days there should be sign of improvement (breathing not so fast, less
indrawing of the lower chest wall, less fever, and improved ability to eat and drink.

Complications
If the child has not improved after two days, or if the child's condition has worsened, look for complication
or other diagnoses If possible obtain a chest X-ray .The most common complications are given below.

Staphylococcal pneumonia
 There is rapid clinical deterioration despite treatment, a pneumatocele or pneumothorax with
effusion on chest X-ray, numerous gram positive cocci in a smear of sputum or heavy growth of S.
aureus in cultured sputum or empyema fluid. The presence of septic skin and pustules supports the
diagnosis.
 Treat with cloxacillin (50mg/kg IM or IV every 6 hours) and gentamicin (7.5mg/kg IM or IV once
a day). When the child improves, continue cloxacillin orally 4 times a day for a total course of 3
weeks.
Empyema
 Persistent fever, and
 Physical and chest X- ray signs of pleural effusion.

Tuberculosis
 Persistent fever for more than 2 weeks and signs of pneumonia should be evaluated for
tuberculosis.
 If another cause of the fever cannot be found, tuberclosi should be considered and treatment for
tuberculosis.

Management of severe pneumonia (2 months - 5 years)

 Admit
 Give oxygen until the sign of hypoxia (such as severe lower chest wall indrawing or breathing rate ≥
70/ minute.) are no longer present.
 Parentral antibiotics Give benzylpenicillin (50,000 units/kg IM or IV every 6 hours) for at least 3 days.
 When the child improves, switch to oral amoxicillin (25 mg/kg 2 times a day).
 The total course of treatment is 5 days.
 If the child does not improve within 48 hours, or deteriorates, look for complications and treat
accordingly. If there are no apparent complications, switch to chloramphenicol (25 mg/ kg every 8
hours IM or IV) until the child has improved. Then continue orally for a total course of 10 days.
 If wheeze is present, Nebulized salbutamol if available (2.5mg<5 year/5mg >5year) (or) IV
Aminophylline (5mg/kg /dose).
 Give supportive care
- If the child has fever (≥39˚C or ≥102.2˚F) which appears to be causing distress, give
paracetamol.
- If wheeze is present, Nebulized salbutamol if available (2.5mg<5 year/5mg >5year) (or) IV
Aminophylline (5mg/kg /dose) .
- Remove by gentle suction any thick secretions in the throat, which the child cannot clear.
- Ensure that the child receives daily maintenance fluids appropriate for the child's age, but
avoid over hydration.
- Encourage breastfeeding and oral fluid
- Nasogastric tube feeding - if unable to drink
- Encourage the child to eat as soon as food can be taken
- Reassess once daily

Management of pneumonia
  Antibiotics at home
- Cotrimoxazole: 4mg/kg trimethoprim or 20mg/kg sulfamethoxazole twice a day. (or)
- Amoxicillin - 15mg/kg 3 times a day- for 5 days
 advise mother
 Return after 2 days
 Home care
- feed the child
- more fluid
- soothe the throat and relieve cough with a safe remedy
 When to come back immediately:
< 2 months - Breathing becomes difficult or becomes fast
- Feeding becomes a problem
- The child becomes sicker
>2 months - Breathing becomes difficult or becomes fast
- Unable to drink
- The child becomes sicker
 When the child returns
- If the breathing has improved ( slower ) , there is less fever, and the child is eating better ,
complete three days of antibiotics treatment
- If breathing rate, fever and eating have not improved , change to the second line antibiotics
and advise the mother to return again in two days
- If there are signs of severe or very severe pneumonia, admit the child to the hospital and
treat accordingly to the guideline.

Management of no pneumonia (cough or cold)

 Treat at home
 Treat fever If the child ha fever (≥39 ْ C or ≥ 102.2 ˚ F) which appears to be causing distress, give
paracetamol.
 More fluid, breast feed frequently
 Encourage the child to eat as soon as food can be taken
 Keep young infant warm (<2 months)
 Clean nose if interfere with feeding
 Safe cough remedy

Prevention
 Breast feeding
 Immunization – BCG, DPT, Measles, pneumococcal, HiB
 Vitamin A Supplementation
 Avoid air pollution
 Good nutrition

BRONCHIOLITIS
 Common serious respiratory infection of infancy
 More in winter
 Common in aged 1-9 months
 Rare after 1 year of age

CAUSAL ORGANISMS
 Respiratory Syncitial virus – commonest
 Parainfluenza virus
 Adenovirus

Clinical features
  Coryzal symptoms precede a dry cough and increasing breathlessness
 Wheezing is often but not always present
 Feeding difficulty associated with increasing dyspnoea
 Recurrent apnoea – especially in 1st few months of life

More severe in - Prematurely born baby with bronchopulmonary dysplasia

- Infants with congenital heart disease.

Characteristic findings
 Dry cough (may be spasmodic)
 Tachypnoea
 Subcostal and intercostal recession
 Hyperinflation of the chest
o Sternum prominence
o Liver & spleen displaced downwards
 Fine crackles
 High pitched wheeze (Expiratory > inspiratory)
 Tachycardia
 Cyanosis or pallor.

Investigations
 IDENTIFICATION OF RSV
- Nasopharyngeal secretions by using fluorescent antibody test
(Rapid test)
 CXR
- Hyperinflation of the lung field due to air trapping
 BLOOD GAS ANALYSIS
- lower arterial O2 and raised CO2 tension in more severe cases

MANAGEMENT
SUPPORTIVE
 Humidified O2 by head box
 Alternatively O2 by nasal catheter
 Adequate hydration by nasal or IV if needed
 If possible, monitored by pulse oxymeter and adjust the O 2 concentration
 Cardiopulmonary monitoring – for apnoea, signs of respiratory failure, drowsiness, respiratory distress and
cyanosis, signs of heart failure

Use of Antibiotics:- if suspect secondary bacterial infection

Use of steroid, bronchodilator- controversial
Antiviral drug (ribavirin) - may try, may use in infants with underlying cardiopulmonary disorder or
immunodeficiency
Mechanical ventilation - require in 2% of patients

Prognosis
 Most recover in 2weeks
 50% will have recurrent episodes over the next 3-5 years
 Complication like bronchiolitic obliterans rarely
Difference between Bronchiolitis and Bronchopneumonia

Bronchiolitis Bronchopneumonia
Causal organism Mainly viruses Bacterial in origin
- RSV (75-80% ) - Strep. pneumoniae
- Influenza - H. influenzae
- Parainfluenza - Staph. aureus
- Adenovirus

Age Mainly under 2 years Any age

Season Cold season Any season

Clinical features Fever, cough, wheeze High fever, cough,

More of rhonchi, Fast breathing
crepts may be present More of crepitation
occasional rhonchi

Investigations Nasopharyngeal Aspirate for Blood Culture—Positive in 40%

RSV—Positive of cases
CXR—Overinflated lungs CXR—Patchy consolidation
CP—Neutrophil leucocytosis
CP—WBCs - normal

Appropriate antibiotic therapy

Treatment Supportive—Oxygen
Nursing care
Intubation and ventilation in
severe cases
Collapse, consolidation
Complications Rare Lung abscess
Respiratory failure Pleural effusion, Empyema
Heart failure
Septicaemia
Respiratory failure

Prognosis is good if there is no

Clinical Course Self-limiting complication
STRIDOR
COMMON DIFFERENTIAL DIAGNOSIS OF ACUTE STRIDOR
 Acute laryngotracheo-bronchitis
- Onset 1-2 days of coryza, barking cough, hoarseness, fever
- tachypnoea, respiratory difficulty, throat-clear
 Laryngeal diphtheria
- fever (+), DPT immunization status (-)
- toxic, Bull neck, grayish- white membrane on throat examination
 Acute epiglottitis
- Onset -hours, high fever, drooling of saliva
- toxic, sits leaning forward, neck extended, cherry red epiglottis (done with caution)
 Angioneurotic oedema
- sudden onset, h/o allergy
- non- pitting oedema on limbs, urticarial rash
 Retropharyngeal abscess
- bulging post pharyngeal wall, hyperextension of the neck
 Foreign body
- sudden onset, H/O choking +
- unequal air entry, reduced air entry, cyanosis + , fever (-)

Radiological findings
 In acute epiglottitis, thumb sign is seen in lateral neck X-ray
 In retropharyngeal abscess, widening of pre-vertebral space in neck X-ray
 In foreign body - radio-opaque shadow can be seen in lateral neck x ray
Management
 General care
 Indications for tracheostomy
- severe chest indrawing
- rising pulse
- agitation
- anxiety
- cyanosis

 Specific management
Epiglottitis
- Injection chloramphenicol 25mg/kg/6H, switch to oral after 3 days (total 10 days) OR
- Injection 3rd generation cephalosporin, ceftriaxone or cefotaxime
- Prophylaxis – Rifampicin 20mg/kg/day OD for 4 days to non-immunised contacts and index
case.
Foreign body
- for infant hold the child upside down and slap on the back
- Heimlich maneuver
- Oxygen
- Tracheostomy
- Bronchoscopic removal
Diphtheria
- [Link] penicillin is the drug of choice.(Dose – 0.5 L/kg/dose, 6 hourly x 7-10 days) or
Erythromycin 50mg/kg/day 6 hourly x 10 days for those who are sensitive to penicillin. plus
- IV/IM diphtheria antitoxin 40,000 IU.
- Tracheostomy
Acute laryngotracheobronchitis (ALTB)
- Hydration, close monitoring
- Dexamethasone IM or Oral 0.3 mg/kg/dose OD, maximum 3 days depending on response.
 - If severe, intubation and ventilation
Retropharyngeal abscess
- Antibiotic – [Link] 50,000U/kg/6h
[Link] 25mg/kg/6H,
- Refer for incision
Angioneurotic oedema
- S/C adrenaline 1:1000 0.5ml in older, 0.25ml in younger children
- [Link] chlorpheniramine 5-10mg
- IV- hydrocortisone 5mg/kg/dose

BRONCHIAL ASTHMA
Definition
Asthma is a chronic inflammatory disorder of the airway in which many cells and cellular elements play a role.
The chronic inflammation causes an associated increase in airway hyper-responsiveness that leads to recurrent
episodes of wheezing, breathlessness, chest tightness and coughing, particularly at night or in the early morning.
These episodes are usually associated with widespread but variable airflow obstruction that is often reversible
either spontaneously or with treatment.

Clinical features of asthma

 Episodic dyspnoea and wheeze
 Nocturnal cough
 Trigger factors e.g. dust, fumes, noxious smell.
 Family history of asthma
 Seasonality
 Relief spontaneously or with bronchodilators
 Other evidences of atopy e.g. rhinitis, eczema
 Hyper-inflated chest and other chest deformities e.g. Harrison's sulcus
 Widespread expiratory rhonchi

Signs of Acute Severe Asthma

o too breathlessness to talk
o too breathlessness to feed
o tachypnoea
o tachycardia
o pulsus paradoxus
o use of accessory muscle of breathing

Signs of Life threatening asthma

 cyanosis
 silent chest
 poor respiratory effort
 fatigue or exhaustion
 agitation or reduced level of consciousness

** Diagnosis of asthma is mainly on clinical features.

Complications of asthma
1. Emphysema and airway remodeling
2. Pneumothorax
- respiratory rate increased
- heart rate increased
- cyanosis 
 - trachea shift
- hyper-resonance
- reduced air entry
3. Respiratory failure
- respiratory rate increased or decreased
- heart rate decreased
- cyanosis +
- agitation
- suprasternal retraction & accessory muscles working
- wheezing
- silent chest
- inability to speak full sentences

Differential diagnosis of recurrent wheeze

 Gastro-oesophageal reflux
 Pulmonary eosinophilia (Loffler's syndrome)
 Tropical eosinophilia (Due to microfilaria)
 Viral induced wheeze
- 2 mths – 2 yrs, coryza, dry repetitive cough, low grade fever, cold season
- tahypnoea, respiratory distress, cyanosis, wheeze, hyper-resonance, fine crepitations,
expiratory rhonchi, hepatosplenomegaly
 Foreign body
- sudden onset, h/o chocking , cough,
- unequal air entry, reduced air entry, cyanosis , fever (-)
 Tuberculosis

INVESTIGATIONS
 CXR – for evidence of complications such as pneumothorax.
 Evidence of allergy may be present
- Eosinophilia (absolute count > 600/cumm)
- Increased IgE
- Skin tests
 lung function tests (can be done in children of > 6 years of age)
- PEFR – reduced
- FEV1 – reduced varies with age and height of the child
- FVC – reduced
- FEV1 / FVC – reduced
 Arterial blood gas – reduced Pa O2, increased Pa C O2, and reduced pH in
severe case
 Pulse oximetry – reduced Sa O2

Management of acute severe asthma

 High flow O2 (5 L/min)
 Prednisolone (short course)
1-2 mg/kg once a day for 3-5 days
 Nebulized salbutamol – 2.5 mg/ dose for under 5 years, 5 mg/dose for >5 years, or salbutamol
inhalation via spacer 10-20 puffs, can be repeated every 30 minutes to 2 hours (maximum 3 doses), if
not improve – refer to ICU

Management of life threatening asthma

 High flow O2 (5 L/min)
 Nebulized salbutamol – 2.5 mg/dose for <5 years, 5 mg/dose for >5 years (should not be given without
O2; High risk of bronchospasm is present under 1 year)
 Infusion of aminophylline
 - Initial dose: 5 mg / kg (max. 300mg) over 20 min if the child has not taken Aminophylline or
Theophylline within 24 hours followed by continuous infusion 0.9 mg/kg/hr
 IV hydrocortisone 4 mg/kg/ 6 hours
 Reassess for progress

CRITERIA FOR TRANSFER TO ICU

- Becomes worse or there is persisting hypoxia or hypercapnoea
- Exhaustion, feeble respiration, confusion or drowsiness
- Coma or respiratory arrest

Long-term management of asthma

There are 4 interrelated components of asthma therapy to achieve and maintain control of the clinical
manifestations of the disease for prolonged period.
Component 1. Develop patient/family/doctor partnership
Component 2. Identify and reduce exposure to risk factors
Component 3. Assess, treat, and monitor asthma
Component 4. Manage asthma exacerbations

Component 1: Develop Patient/Family/Doctor Partnership

Children and their families can be actively involved in managing asthma to prevent problems and enable
children to live productive, physically active lives. They can learn to:
• Avoid risk factors
• Take medications correctly
• Understand the difference between “controller” and “reliever” medications
• Monitor asthma control status using symptoms and, if available, PEF in children older than 5 years of age
• Recognize signs that asthma is worsening and take action
• Seek medical help as appropriate

Health education is the essential part of asthma care. A variety of methods – discussion, demonstrations, written
materials, group classes, video or audio tapes, drama and patient support groups – can reinforce educational
message.

Component 2: Identify and Reduce Exposure to Risk Factors

TO IMPROVE CONTROL OF ASTHMA AND REDUCE MEDICATION NEEDS, RISK FACTORS
SHOULD BE IDENTIFIED AND EXPOSURE TO RISK FACTORS SHOULD BE REDUCED OR, IF
POSSIBLE, AVOIDED.
COMMON ALLERGENS AND RISK FACTORS INCLUDE:

- TOBACCO SMOKE
- DRUGS, ALLERGENS AND ADDITIVES
- HOUSE DUST MITES
- ANIMALS WITH FUR
- COCKROACHES
- OUTDOOR POLLENS AND MOLD
- INDOOR MOLD

Component 3: Assess, Treat, and Monitor Asthma

Assessing Asthma Control
- Level of asthma control is assessed by reviewing the day and night time symptom, limitation of
activities, need for reliever/rescue treatment, lung function assessment and presence of exacerbations.
TREATING TO ACHIEVE CONTROL
- Based on control of asthma, step-wise management approach is considered.
 Management Approach Based On Control: Children 5 Years and Younger
The available literature on treatment of asthma in children 5 years and younger precludes detailed treatment
recommendations. The best documented treatment to control asthma in these age groups is inhaled
glucocorticosteroids and at Step 2, a low-dose inhaled glucocorticosteroid is recommended as the initial
controller treatment.

Monitoring to Maintain Control

- to maintain control and establish the lowest step and dose of tratement to minimize cost and maximize safety,
ongoing monitoring is essential.
- 1 – 3 month after initial visit and every 3 months thereafter
- After exacerbation, follow-up should be offered within 2 weeks to one month.
Component 4: Manage Exacerbations
- ASSESS THE SEVERITY OF EXACERBATION
- TREAT THE CHILD ACCORDING TO SEVERITY
- MONITOR RESPONSE TO TREATMENT
- FOLLOW-UP
- IDENTIFY FEATURES THAT PRECIPITATED THE EXACERBATIONS
- Implement the strategies for the avoidance of precipating factors
- Review of the patient's medication
SUPPURATIVE LUNG DISEASE
LUNG ABSCESS
DEFINITION
It is a suppurative process resulting in destruction of pulmonary parenchyma and formation of a cavity
containing purulent material.

PREDISPOSING CONDITIONS
1. Following any specific pneumonia
(Staphylococcus aureus, Klebsiella )
2. Aspiration of infected material
3. Aspiration of foreign body
4. Obstruction followed by infection e.g. thick mucus obstruction such as whooping cough, measles
5. Immune deficiency

CLINICAL FEATURES
 Insidious onset
 Intermittent or recurrent fever (spiking fever)
 Cough with expectoration of purulent sputum
 Clubbing of fingers
 Coarse crepitations and bronchial breath sound may be heard.

RELEVANT INVESTIGATIONS
1. Blood for complete picture –neutrophil leucocytosis
2. CXR – a cavity with or without a fluid level surrounded by alveolar infiltration.
3. Sputum examination
Gram stain – Gram positive/Gram negative bacilli or cocci
Sputum culture and sensitivity – a mixture of aerobic and anaerobic bacteria

COMPLICATIONS
1. Pyopneumothorax
2. Empyema
3. Brain abscess
4. Haemoptysis
5. Septicaemia

TREATMENT
 Antibiotics
Inj: Cloxacillin 25mg/kg/dose 6 hourly + inj: Genta 2.5mg/kg/dose 8 hourly + inj: Metronidazole
7mg/kg/dose 8 hourly to cover Staph, anaerobic, and Gram negative bacilli, then according to C&S for 2
weeks then followed by oral administration for 3-4 weeks.
 Postural drainage and chest physiotherapy
 Treatment of underlying cause (e.g. removal of foreign body by bronchoscopy)
 Surgery
Indication for surgery
o Localized abscess not responding to medical treatment
o Abscess in sequestrated lobe
o Bronchopleural fistula
o Recurrent haemoptysis

BRONCHIECTASIS
DEFINITION
It is a chronic suppurative disease characterized by destruction of the bronchial and peribronchial tissues,
dilation of bronchi and accumulation of infected material in the dependent bronchi.
Diseases which commonly give rise to bronchiectasis
1. Post-measles
2. Post-pertussis
3. Recurrent episodes of respiratory infections such as bronchitis, bronchiolitis
4. Cystic fibrosis
5. Other predisposing factors
- Aspiration of foreign body, food or mucous plug in the bronchus.
- Congenital disorders of bronchi such as bronchomalacia, communicating type of bronchial
cyst or sequestrated lungs.
- Immunodeficiency syndrome - cause recurrent pulmonary infections

CLINICAL FEATURES
 Insidious onset
 Cough with copious purulent foul smelling sputum
 Haemoptysis
 Poor general health with recurrent infection, loss
of appetite and poor weight gain.
 Crepitations and rhonchi
 Clubbing of fingers and toes. Clubbing of Toes

INVESTIGATIONS
1. Sputum for C&S
2. CXR – honeycomb appearance of the involved area
indicating multiple small abscess cavities.
3. Bronchoscopy – where there is a possibility of surgical intervention.
4. CT Chest – has replaced bronchography

TREATMENT
 Antibiotics
- Antistaph, aminoglycoside, quinolone and or broad-spectrum antibiotics such as amoxycillin and
potassium clavulunate or ampicillin and sulbactam sodium or oral cephalosporin etc, and then
according to C&S for 2-3 weeks
 Postural drainage for effective mucous clearance
 Surgery – resection of the involved area of the lung
Indication for surgery
o Bronchiectasis localized to one segment of the lung
o Condition progresses despite adequate medical treatment.
o Bronchiectasis following aspiration of foreign body
o Bronchopleural fistula
o Lobar bronchiectasis
o Intrinsic obstruction of the bronchus
EMPYEMA
DEFINITION
IT IS AN ACCUMULATION OF PUS IN THE PLEURAL SPACE.

CAUSAL ORGANISMS
1. Most often associated with Staphylococcus aureus
2. Others- Pneumococci, Haemophilus influenzae, Anaerobic and Microaerophilic infections, Mycotic
infections

CLINICAL FEATURES
 Initial signs and symptoms of bacterial pneumonia.
 Prolongation of fever with respiratory difficulty
 Clubbing
 Signs of fluid in affected side.

COMPLICATIONS
1. Empyema necessitates – the pus may dissect through the chest wall.
2. Pyopneumothorax
3. Bronchopleural fistula
4. Organization and pleural thickening (frozen chest)

INVESTIGATIONS
1. Blood for complete picture – neutrophil leucocytosis
- anaemia due to chronic infections
2. Blood for ESR - raised
3. CXR
- To confirm the diagnosis and to find out associated pulmonary
pathology.
- More or less homogenous opacity obliterating the normal marking of
the lung.
- Obliteration of the costophrenic or cardiophrenic angles.
- For estimation of amount of fluid and to detect
any mediastinal shift.
Pleural effusion/empyema (L)
4. Aspirated fluid for culture and sensitivity - before antibiotics to detect causal organism
5. Blood culture - can detect causal organism in 62% of cases

Treatment
 Systemic antibiotic therapy
- inj: penicillinase resistant penicillin for Staph. infection (cloxacillin, methicillin , vancomycin)
and
- inj: penicillin, inj: cefotaxime, or ceftriaxone for pneumococcal infection
or inj. chloramphenicol for H. influenza infection
- then according to culture and sensitivity for 3-4 weeks
 Surgical procedures
- Underwater-sealed drainage
In infants – should be kept till nearly all the fluids are drained.
Chest tube that is no longer draining should be removed.
- Thoracotomy – loculated empyema
- Decortication – thick wall empyema cavity with inadequate treatment, extensive fibrinous
changes. (very rare)
 Physiotherapy
 Long term follow-up: to detect pulmonary function
 CARDIOVASCULAR SYSTEM

CONGENITAL HEART DISEASES

Classification of the common congenital heart disease (CHD) with examples
1. Acyanotic congenital heart disease
 Ventricular Septal Defect - VSD (most common congenital heart disease)
 Atrial Septal Defect - ASD
 Patent Ductus Arteriosus - PDA
2. Cyanotic congenital heart disease
 Tetralogy of Fallot - TOF (commonest cyanotic congenital heart disease)
 Transposition of Great Vessels - TGA

Clinical features
 Common clinical features of acyanotic cases
- Asymptomatic throughout life e.g. small VSD
- Asymptomatic in early life but development of symptoms later, as feeding difficulties, profuse
perspiration, dyspnoea e.g. VSD, ASD
 Cyanosis
- At birth – e.g. TGA
- Later – e.g. TOF
 Growth stunting
 Repeated chest infection especially those with Left to Right shunt (e.g. VSD)
 Heart failure
 Infective endocarditis

VENTRICULAR SEPTAL DEFECT

Clinical features
Depend on size of defect
Small VSD (<0.5 cm2)
- Asymptomatic,
- Loud pansystolic murmur best heard at lower left sternal edge frequently with thrill.
Large (>1 cm2)

Symptoms - usually present in early infancy around 6 – 10 weeks of age

- Dyspnoea
- Feeding difficulties
- Poor growth / failure to thrive
- Repeated chest infection
- Can develop congestive heart failure at this time
Signs
- Prominence of precordium (common)
- Cardiomegaly (down and out displacement of apex beat)
- Heaving apical impulse (left ventricular hypertrophy)
- Systolic thrill and less harsh, more blowing PSM best over the lower left sternal border
- Pulmonic component of 2nd heart sound may be increased as a result of pulmonary hypertension
- Presence of MDM at the apex is caused by the increased mitral valve flow and indicates
pulmonary:systemic flow ratio ≥ 2:1

Investigations
 CXR
- Small VSD – normal heart size and normal pulmonary vascularity
- Large VSD – gross cardiomegaly (left ventricle + later right ventricle), increased pulmonary
vascular markings (plethoric lung field)

Fig. Cardiomegaly with plethoric lung field

 ECG
- Small VSD – Normal
- Large VSD – LVH, Biventricular hypertrophy later, Peak ‘’P’’ wave
 Echocardiogram
- Two dimension to detect structural defects - site, size, vegetations, chamber enlargement
- Doppler – to detect pressure gradient across defect, to visualized small defect of muscular septum
 Cardiac catheterization
- Increased oxygen saturation and pressure in the RV and pulmonary artery
- Pulmonary artery pressure is measured to calculate pulmonary blood flow and vascular resistance

Natural Course and Complications

- Spontaneous closure (30-50%) in small defect, majority during the first 2-4 years of life. Small
muscular VSDs are more likely than membraneous VSDs
- Congestive heart failure
- Infective endocarditis
- Acquired infundibular pulmonary stenosis
- Pulmonary vascular disease (pulmonary arterial hypertension)
- Eisenmenger Syndrome (when blood is shunted partially or totally from right to left as a result of
development of pulmonary vascular disease)

Treatment
Small VSD
- Reassurance
- No restriction on physical activity
- prophylaxis of infective endocarditis
- Long term follow up until spontaneous closure occurs
Large VSD
 Medical treatment
- prevention and treatment of respiratory infections
- control of congestive heart failure
- prophylaxis of infective endocarditis
- nutritional support
 Surgical treatment
 Closure of the defect (primary repair), using Dacron patch
Indication
- Patient at any age in which congestive heart failure which cannot be controlled
- Pulmonary hypertension
- Pulmonary systemic blood flow > 2 : 1
Contraindication
- Reversed shunt (right to left)
- Severe pulmonary vascular disease
 Others
- Pulmonary palliative banding with repair
- Catheter occlusion devices are also being tested for closuring the defect

TETRALOGY OF FALLOT
Consists of
 Pulmonic stenosis
 Ventricular septal defect
 Over-riding of aorta and
 Right ventricular hypertrophy

Clinical Features
Cyanosis – occurs later in the 1st year of life with increasing hypertrophy of the right ventricle infundibulum and
patient growth. It is the most prominent in the lips, mouth and nail beds
Paroxysmal hypercyanotic attacks / blue spells – a problem during the first two years of life. The infant starts
crying, dyspnoeic, restless, cyanosis increases, convulsion may occur and may lose consciousness. It occurs
predominantly after waking up or following exertion
Dysponea – occurs on exertion. Toddlers play for a short time and then sit or lie down. Older children
characteristically assume a squatting position for the relief of dyspnoea

Examination
 Retarded growth
 Central cyanosis and digital clubbing
 Older children may have dusky blue skin, gray sclerae with engorged blood vessels
 Pulse and arterial pulse pressure usually normal
 Left hemithorax may bulge anteriorly because of RVH
 Heart size is generally normal
 Left parasternal heave (right ventricular impulse) can be detected
 Systolic thrill along the left strenal border in the third and fourth parasternal spaces (about 50%)
 Ejection systolic murmur is most intense at the upper sternal border (2 nd left intercostal space)
 2nd heart sound is single or the pulmonary component is soft
Investigations
 CXR
- Oligaemic lung field (reduced pulmonary blood flow)
- Heart size normal
- Boot shape (concavity at the pulmonary conus and rounded tilted apex)

Fig. Boot-shaped heart with oligaemic lung fields

 ECG
- Right axis deviation, RVH
 Echocardiogram – establishes the diagnosis
- VSD
- PS
- RVH
- Over-riding of the aorta
 Cardiac catheterization
- Morphological defect
- Systolic Pressure in RV almost equal to LV pressure
- Pulmonary artery pressure –
- Oxygen saturation – depends on right to left shunt

Treatment
Medical treatment
 Hypercyanotic spells
One or more of the followings in sequence
- Calming and placement of infant on the abdomen in knee-chest position
- 100% oxygen (mask)
- IV Propranolol 0.1-0.2 mg/kg and then prophylactic dose 0.5-1 mg/kg/dose 2-3 times a day orally
- SC morphine 0.1 mg/kg (not more than 0.2 mg/kg)
- IV Sodium bicarbonate (in unusually severe spell)
- Vasopressors - IV phenylephadrine/methoxamine (if resistant to above therapy)

 General
- Maintenance of nutrition
- Prevention and treatment of infective endocarditis
- Prevention and prompt treatment of dehydration – adequate hydration, monitoring and
maintenance of hematocrit around 60% (viscosity increases if >60%)

 Extreme polycythemia and symptomatic patients

- Venesection and volume replacement with albumin or saline transfusion

Surgical treatment
 Palliative - systemic to pulmonary artery shunt
- Blalock-Taussig shunt (modified) – between subclavian artery and pulmonary artery (most
commonly used)
- Waterson shunt – between ascending aorta and right pulmonary artery
- Potts – between descending aorta and left pulmonary artery
  Corrective open heart surgery and repair (Curative)
- Relieve right ventricular outflow obstruction and closure of VSD

Complications
1. Cerebral thrombosis and embolization—due to polycythemia precipitated by dehydration. Thrombosis occurs
most often in patients younger than two years
2. Brain abscess less common. Patients are usually older than two years
3. Infective endocarditis
4. Hypercyanotic attacks
5. Delay of growth, development and puberty
6. Iron deficiency anaemia frequently with haematocrit levels in normal range (but too low for cyanotic heart
disease)

PATENT DUCTUS ARTERIOSUS

 Communication between aorta, distal to the origin of the left subclavian artery and the pulmonary at its
bifurcation
 Functional and anatomical closure normally occurs soon after birth.
 It is the most common in preterm infants.

Clinical Features
Small PDA
 may be asymptomatic
 Continuous murmur, loudest at 2nd left intercostal space

Large PDA
Symptoms
 May become symptomatic in early life and develop congestive heart failure around 6-12 weeks of age.
Older children give history of effort intolerance, palpitation (related to large stroke volume) and
frequent chest infections
Signs
 Pulse volume is increased, collapsing type (sharp rise and abrupt fall)
 Wide pulse pressure
 Prominent carotid pulsations (Corrigans Sign)
 Precordium
- Enlarged heart (apex beat displaced downward and outward)
- Prominent heaving apical impulse (left ventricular hypertrophy)
- Thrill (usually systolic) – maximal at 2nd left intercostal space and radiate toward the left clavicle,
left sternal border or apex
- Continuous machinery murmur (classic) – best heard at the 2nd left intercostal space, radiating to
the left clavicle and back
Investigations
Large PDA
 CXR
- Heart enlarged (LV + later RV)
- Increased pulmonary vascular markings (plethoric lung field)
 ECG
- LVH, biventricular hypertrophy later
 Echocardiogram
- Suprasternal notch scan allows direct visualization of the ductus
- Colour and pulsed Doppler - retrograde turbulent flow in the pulmonary artery during systole and
aortic retrograde flow in diastole

 Cardiac catheterization
- Increased oxygen and pressure in the pulmonary artery and the catheter can be passed from the
pulmonary artery across the ductus into the descending aorta.

Complications
 Heart failure, most often in early infancy (large PDA)
 Infective endocarditis, at any age
 Pulmonary / systemic embolism
 Rarely- Eisenmenger syndrome
 Non-infective thrombosis of the ductus with embolization and paradoxical emboli
 Ductus calcification
 Ductus / Pulmonary artery aneurysm

Treatment
Medical treatment
 In preterm infant
- No symptoms - wait for spontaneous closure
- Symptomatic preterm infants – IV indomethacin 0.1mg/ kg/ day for 3 doses
 Prevention and treatment of respiratory infection
 Control of congestive heart failure
 Prevention and treatment of infective endocarditis
 Nutritional support

Surgical treatment
 Indications
- As soon as diagnosis is made irrespective of age (preferably before 1 year of age)
 Method
- Surgical closure (ligation and division of the ductus by a standard left thoracotomy)
- Transcatheter closure using umbrella-like devices
RHEUMATIC FEVER
Aetiology
Immunological disorder initiated by group A β haemolytic streptococcal pharyngitis/tonsillitis

Diagnose initial attack of acute rheumatic fever using Jones Criteria (Modified)
Major criteria
 Migratory polyarthritis (about 75%)
- large joints (elbows, wrists, knees, ankles) does not result in chronic joint disease
- inflammatory signs (pain, redness, warmth, swelling, exquisitely tenderness)
 Carditis
- Pancarditis that involves the pericardium, myocardium and endocardium; major consequence of
chronic progressive valvular disease
- Endocarditis (valvulitis) – universal finding
- Mitral regurgitation – Apical PSM radiating to axilla, In significant mitral regurgitation may be
associated with apical MDM (Carey Coombs murmur) of relative mitral stenosis
- Aortic insufficiency – high pitched early diastolic murmur at the upper left sternal border
- Myocarditis - Cardiomegaly, soft 1st sound, tachycardia, gallop rhythm, congestive heart failure
- Pericarditis - Precordial pain, friction rub (superficial scratchy sound)
 Chorea
- Sydenham’s chorea – purposeless, non-repetitive, jerky involuntary movements of proximal part of
limbs, occurs much later than other manifestations. Emotional liability, incoordination, poor school
performance, uncontrollable movements and facial grimacing, exacerbated by stress and
disappearing with sleep are characteristics
- It is 3-4 times more common in females. It has a self limiting course of 2-6 weeks.
- It rarely leads to permanent neurological sequelae
 Erythema marginatum: rare (<3%)
- Characteristic rash consists of erythematous, serpiginous, macular lesions with pale centers that are
not pruritic. It occurs primarily on the trunk and extremities, but not on the face
 Subcutaneous nodules: rare (<1%)
- are most commonly observed in patients with severe carditis. These pea-sized nodules are firm and
non-tender, characteristically seen on the extensor surfaces of the tendons near bony prominences
such as elbows, knees, shins, occiput and spine.
-
Minor criteria
 2 clinical manifestations
- Fever – usually not more than 101-102 F
- Arthralgia – discomfort or pain, no inflammation
 2 laboratory manifestations
- Acute phase reactants – increased ESR, increased CRP
- Prolong PR interval on ECG
 Evidence of recent Group A streptococcal infection (microbiologic or serologic) :
- Raised ASO titre (>333 Todd’s units) or rising titre
- Positive throat swab culture
- Rapid streptococcal antigen test
N.B: to make diagnosis, patient must have 2 major criteria, or 1 major and 2 minor criteria and evidence of GAS
recent infection

Investigations
1. Throat swab culture
2. ASO titre
3. Acute phase reaction – ESR, CRP
4. ECG – prolonged PR interval
5. CXR – cardiomegaly in significant carditis
6. Echocardiogram – Valvular regurgitation in Doppler, mitral & aortic valve may be affected
Complications
 Chronic valvular heart disease
 Acute heart failure

Investigations
1. Throat swab and culture
2. ASO titre
3. Acute phase reaction – ESR, CRP
4. ECG – prolonged PR interval
5. CXR – cardiomegaly in significant carditis
6. Echocardiogram – valvular regurgitation in Doppler, mitral and aortic valve may be affected

Treatment
 No specific treatment
 Symptomatic combined with suppressive therapy

General
- Bed rest during the acute phase, until disease activity ceases (normal temperature and pulse rate).
Patient without carditis can be ambulatory in 2-3 weeks. It may be continued for 2-3 months if
carditis is present.

Treatment of Arthritis
 NSAIDs – Salicylates (Aspirin) – Anti-inflammatory action, 100 mg/kg/day in 4 divided doses PO,
reduced to 1/3 with clinical response, taper over 2 weeks when CRP/ESR normalizes
Treatment of carditis
 Steroid
- Prednisolone: 2mg/kg/day in 4 divided doses PO over 2-3 weeks followed by tapering dose
(reduce 5 mg/24 hour every 2-3 days).
Indication
- Moderate to severe carditis or cardiac failure
- Anti-inflammatory action
- Treatment of heart failure if present
Treatment of chorea
 Sedation – Diazepam (mild cases), Haloperidol (severe cases), or Sodium Valproate
 Prevent trauma
 Reassurance
Treatment of sore throat
 Eradication of GAS from upper respiratory tract
- IM procaine penicillin 400,000 units BD x 10 days or oral penicillin V 250 mg QID x 10 days or
- Erythromycin 250 mg QID x 10 days (for Penicillin hypersensitivity)

After this, long term secondary prevention should be started.

Prevention
 Rheumatic fever occurs following Streptococcal infection of the throat.
 Recurrence of rheumatic fever can damage heart
 Patient with rheumatic fever disease needs prevention from infective endocarditis and further damage.

Primary prevention
 General
- Avoid the overcrowded areas and good nutrition
 Antibiotic treatment of GAS, URTI to prevent initial attack
 Acute rheumatic fever
 - Injection Procaine Penicillin 0.5 L Unit/kg 12 hourly for 7-10 days or
- Oral Penicillin V 250 mg 6 hourly for 10 days or
- Oral Erythromycin 40 mg/kg/day 3 divided dose for 10 days (if hypersensitive to penicillin)
Secondary prevention
 Long term antibiotic prophylaxis to prevent recurrences; prevent colonization of URT with GAS, in
those who have had an attack of acute rheumatic fever.
- IM benzathine penicillin 1.2 Mega Units once every 3-4 weeks (< 2yr – 0.6 MU)
- Alternative: oral Penicillin V 250 mg BD or oral Sulphadiazine 500 mg BD
- or oral Erythromycin 250 mg BD (if hypersensitive to penicillin or sulphur)

Category Duration
ARF without carditis - 5 years or until 21 years of age whichever
is longer

ARF with carditis without residual - 10 years or adulthood whichever is longer

valvular disease (clinical/echo)

ARF with carditis and residual - At least 10 years since last episode and at
valvular disease (clinical/echo) least until 40 years of age. Sometimes, life
long prophylaxis

Tertiary prevention
 Prevention of infective endocarditis
- Tooth extraction - Amoxycillin 50mg/kg 1 hour before, 25 mg/kg 6 hours after 1 st dose
- Genitourinary procedures – Inj: Ampicillin 50mg/kg ½ hour before procedure, then 8 hr later, Inj:
Gentamycin 2mg/kg ½ hour before procedure, then 8 hr later

RHEUMATIC HEART DISEASES

Differences between acute carditis and established valvular heart disease
Acute carditis
(Varies between severe fulminant and fatal to mild transient cardiac involvement)
Endocarditis/Valvulitis (mitral +/- aortic valve)
 One or more cardiac murmurs, such as apical systolic / PSM and MDM
Myocarditis
 Acute heart failure
 Soft heart sounds with tachycardia
 ECG – prolong PR – more than 0.18 sec, Flattened T waves, Prolong QT interval can also occur
Established valvular heart disease
Mitral stenosis
 Right ventricular hypertrophy
 Loud 1st sound MDM +/- presystolic murmur in mitral area
 Loud P2 (if pulmonary hypertension is present)
Mitral regurgitation
 Systolic thrill, PSM in mitral area and radiation to the axilla
 Left ventricular hypertrophy

Aortic incompetence
 Collapsing pulse, wide pulse pressure
 EDM in upper and middle left sternal border with radiation to apex and to aortic area.
 Left ventricular hypertrophy
Mitral Insufficiency
Clinical features depends on severity
Mild
 No symptoms, high pitched PSM (apex) radiates to axilla
 Signs and symptoms of chronic heart failure may be present
Severe
 Fatigue, easily tired
 Exertional dyspnoea, palpitation, paroxysmal nocturnal dyspnoea, orthopnoea, oedema
 Heart enlargement
 Heaving apical left ventricular impulse (LVH)
 Apical systolic thrill
 Apical PSM radiating to axilla

Investigations
Severe MR
 CXR
- Heart enlarged (LA & LV prominence),
- Perihilar congestion (pulmonary venous hypertension)
 ECG
- LAH & RAH (bifid P waves)
- LVH, LAD
 Echocardiogram
- LA and LV
- Doppler studies – demonstrate MR severity
Treatment
1. Early detection, prompt and adequate treatment of infection
2. Medical treatment of heart failure if present
3. Treatment of carditis if present (See Rheumatic Fever)
4. Prevention of Rheumatic fever (secondary prevention)
5. Prevention of infective endocarditis (tertiary prevention)
6. Surgery: valve repair (annuloplasty), valve replacement in some children
Indications
 Recurrent heart failure, despite adequate medical treatment
 Dyspnoea with moderate activity
 Progressive cardiomegaly with pulmonary hypertension

Mitral Stenosis
Clinical Features correlates with severity of obstruction
Mild
 No symptoms initially
Severe
 Exercise intolerance and dyspnoea
 Orthopnoea
 Paroxysmal nocturnal dyspnoea
 Haemoptysis
 Hepatomegaly, ascites, oedema (from pulmonary hypertension and enlargement RV dilatation and
functional TR)
 Moderate cardiomegaly
 Apical impulse is tapping
 Left parasternal heave or epigastric pulsation (RVH)
 Loud S1, opening snap, MDM with presystolic accentuation at the apex, long, low pitched
 Loud pulmonary 2nd sound (if pulmonary hypertension is present)
Investigations
Severe MS
 CXR
Heart
- Mitralization – straightening of left heart border
- Left atrial enlargement (elevated left bronchus and double right border of the heart)
- Prominent pulmonary artery and prominent right-sided heart chambers
Lungs
- Greater perfusion in upper lobes
- Kerley B lines (horizontal, at costophrenic angle)
- Bat’s wing hilum (alveolar oedema)
- Pulmonary hypertension - prominent pulmonary conus, translucent peripheral lung fields
 ECG
- LAH
- RVH … RAD
 Echocardiogram
- Shows distinct narrowing of the mitral orifice during diastole
- LA enlargement and RVH/enlargement
Treatment
Medical
1. Early detection, prompt and adequate treatment of infection
2. Medical treatment of heart failure if present
3. Treatment of carditis if present (See Rheumatic Fever)
4. Prevention of rheumatic fever (secondary prevention)
5. Prevention of infective endocarditis (tertiary prevention)
Surgical
 MV replacement is avoided unless absolutely necessary
 Mitral valvotomy or balloon catheter mitral valvuloplasty
Indications – Symptomatic, stenotic, pliable, non-calcified valves without atrial arrhythmia or thrombi

Aortic Insufficiency
Combined mitral and aortic insufficiency is more common than aortic involvement alone

Clinical Features
Mild
 Symptoms unusual

Severe
 Palpitations
 Exertional dyspnoea, orthopnoea and PND
 Collapsing water-hammer pulse
 Bounding carotic pulsations (Corrigan sign) or peripheral pulses
 Wide pulse pressure (elevated systolic blood pressure and lowered diastolic pressure)
 Enlarged heart
 Left ventricular apical heave (LVH). A diastolic thrill may be present
 EDM best over upper left sternal border with radiation to the apex and to aortic area. Easily audible
with the diaphragm, in full expiration and the patient leaning forward

Investigations
 CXR - Left ventricle & aortic knuckle enlargement
 ECG – LVH signs
 Echocardiogram – shows a large LV. Doppler studies demonstrate degree of aortic insufficiency
Treatment
Medical
1. Early detection, prompt and adequate treatment of infection
2. Medical treatment of heart failure if present
3. Treatment of carditis if present (See Rheumatic Fever)
4. Prevention of Rheumatic fever (secondary prevention)
5. Prevention of infective endocarditis (tertiary prevention)

Surgery - valve replacement

Indication:
Signs of decreasing myocardial function manifested by
 Increasing left ventricular dimensions (echo)
 Decreasing left ventricular ejection fraction

Infective Endocarditis
Common causal organisms
 Streptococcus viridan group (leading cause in child)
 Staphylococcus aureus (leading cause in child)
 Streptococcus fecalis (enterococcus)

Clinical features
History
 Prior CHD/RHD
 Preceding dental/other surgical procedure, Central venous catheter, Prosthetic heart valve

Features of bacteraemia
 Fever (usually low grade), rigor, malaise, weakness, loss of appetite, weight loss, night sweats,
splenomegaly, anaemia, tinge of jaundice, myalgia, arthralgia

Haemodynamic changes due to underlying heart disease

 Changing murmur, heart failure, arrhythmia

Systemic embolization
 Neurologic complications (embolic strokes, cerebral abscesses, mycotic aneurysms, sudden blindness)
often associated with staphylococcal disease
 Splenic or myocardial infarct, ischemic limbs, mycotic arterial aneurysm and metastatic abscesses
(meninges, pericardium, bone and joint)

Immune Complex disease / Vasculitis

 Classic skin findings include splinter haemorrhage (linear lesions beneath nails), Osler’s nodes (tender
nodules in digit pads), Janeway lesions (painless erythema/hemorrhage, palms and soles), petechiae
and clubbing.
 Other manifestations are splenomegaly, glomerulonephritis and arthritis

Investigations
1. Blood culture 3 times – within 24 hours at different sites, after careful preparation
2. Blood for CP – normochromic normocytic anaemia, polymorphonuclear leucocytosis
3. ESR and CRP – increased
4. Urine RE – microscopic haematuria and albuminuria may be seen
5. Echocardiogram for presence of vegetations, reduced LV function, absence of vegetation does not
exclude infective endocarditis
6. Immunological changes – increase in gamma globulin, false positive STS, Rheumatoid Factor
Differential diagnosis
1. PUO
2. Nephritis
3. Anaemia – malaria
4. Autoimmune disease

Complications
1. Heart failure (from mitral and aortic valve vegetations)
2. Embolization (systemic + pulmonary)
3. Effects of anaemia
4. Endotoxaemic shock

Management
Treatment of the current episode
Main principles consist of -
1. Starting the empirical treatment as early as possible
2. Identification of the organism
3. Finding out the antibiotic sensitivity
4. Using high doses of bactericidal antimicrobial agents for a long period to eradicate organisms in
inaccessible avascular vegetation and prevent relapse

Antibiotics
 High dose, IV Crystalline Penicillin 1Lakh /kg/dose 6 hourly for 4-6 weeks and Gentamycin
2.5mg/kg/dose 8 hourly for 2 weeks
 For Staphylococcus aureus, IV Cloxacillin 25mg/kg/dose 6 hourly for 4-6 weeks
Prophylactic Measures (prevention of endocarditis)
 Dental hygiene and antibiotic prophylaxis before tooth extraction, surgical procedures
 Dental procedure - Amoxycillin 50mg/kg 1 hour before, 25 mg/kg 6 hours after 1 st dose
 Genitourinary procedures - Inj: Ampicillin 50mg/kg ½ hour before procedure, then 8 hr later, Inj:
Gentamycin 2.5mg/kg ½ hour before procedure then 8 hr later

Pen allergic or on continuous penicillin prophylaxis

 Minor procedure – PO Clindamycin 20 mg/kg (600 mg max) 1 hour before, not to repeat or
Azithromycin PO 15 mg/kg 1 hour before
 Major procedure - Clindamycin IV 10 mg/kg (300 mg max) within 30 min before, no repeat +
Gentamycin IV/IM 2 mg/kg (100 mg max) within 30 min before and 8 hr later
 Prompt treatment of any infections in patient with heart disease.
HEART FAILURE
Causes
1. Congenital heart diseases
2. Acute rheumatic carditis
3. Established rheumatic heart disease
4. Beri beri
5. Complication of pneumonia
6. Severe anaemia
7. Acute hypertension due to acute glomerulonephritis
8. Viral myocarditis
9. Supraventricular tachycardia (SVT)
10. Cardiomyopathies

Clinical Features
In infants
Symptoms:
 Feeding difficulties
 Breathlessness and excessive perspiration while sucking breast
 Persistent cough and wheeze
 Irritability, poor weight gain
Signs:
 Tachypnoea, sweating
 Prolonged tachycardia (>160/min)
 Cardiomegaly (invariable)
 Failure to thrive
 Hepatomegaly
 Oedema – may be generalized, usually the eyelids as well as the sacrum and less often the legs and feet

In Older children
Symptoms:
 Fatigue
 Effort intolerance
 Anorexia
 Abdominal pain
 Dyspnoea on exertion
 Orthopnoea
 Cough
Signs:
 Tachypnoea
 Tachycardia
 Cardiomegaly (invariable)
 Raised JVP
 Triple rhythm
 Bilateral basal crepitation
 Tender enlarge liver
 Dependent oedema or anasarca may be present

Investigations
1. CXR
 Cardiac enlargement
 Fluffy perihilar pulmonary marking
2. ECG
  Rhythm abnormalities
 Chamber hypertrophy/enlargement
 low voltage
3. Biochemical tests
 Urea and electrolytes
 Creatine
4. Investigations for underlying cardiac lesions e.g. Echocardiogram

Treatment
General
 Bed rest
 Oxygen
 Diet
 Fluid and electrolytes
 Relieved fever if temperature > 38°C

Drugs
 Digoxin 0.02 – 0.04 mg/kg/day PO (1/2 stat, 1/4 and 1/4 at 6-8 hours interval) Maintenance 1/4 - 1/3
of total digitalizing dose OD – BD
 Diuretics – Frusemide 1 mg/kg/dose IV or 2-3 mg/kg/day PO
 Vasodilators – e.g. ACE inhibitors – Enalapril 0.1 mg/kg OD-BD
- Captopril 0.05 – 0.1 mg/kg BD – TDS PO
 Others – Inotropes – e.g. Dopamine, Dobutamine

Treatment of underlying cause

Surgery
 Valve replacement
 Valvoplasty
 Heart transplant (lesion not amenable to surgical repair and end stage cardiomyopathy)
 GASTROINTESTINAL SYSTEM

Diarrhoeal Diseases
Definition
The passage of unusually loose or watery stools, usually at least three times in a 24 hour period.
However, it is the consistency of the stools rather than the number that is most important. Frequent passing of
formed stools is not diarrhoea.

EPIDEMIOLOGY OF DIARRHOEAL DISEASES

 Mode of transmission: - faecal-oral route
 Susceptible hosts – Failure to breastfeed until at least 2yrs of life
Malnutrition
Measles
Immunodeficiency or immunosuppression
Age (1st 2yrs of life) – due to combined effects of declining maternal acquired
antibodies and lack of active immunity in infants

Aetiology
 Bacteria - e.g. E. coli, Proteus, Shigella, Salmonella, Vibrio Cholerae
 Viruses - e.g. Rota virus
 Parasites - e.g. G. lamblia, E. histolytica
 Fungi - e.g. Candida
 Disaccharidase deficiency
 Systemic infections - e.g. Algid malaria

MAJOR CONTRIBUTORY FACTORS

 Mismanaged feeding:
- Failure to take exclusive breast feeding for first 4-6 months of life
- Using feeding bottles for infant
- Storing cooked food at room temperature
 Poor sanitation:
- Using contaminated drinking water
- Failure to wash hands after defecation, after disposing of faeces or before handling food
- Failure to dispose faeces hygienically
 Malnutrition
 Immunosuppression, immune deficiency

TYPES OF DIARRHOEAL DISEASES

Four clinical types
1. acute watery diarrhoea (including cholera), which lasts several hours or days
2. acute bloody diarrhoea, which is also called dysentery
3. persistent diarrhoea, which lasts 14 days or longer
4. diarrhoea with severe malnutrition (marasmus or kwashiorkor)

COMPLICATIONS OF ACUTE WATERY DIARRHOEA

 Malnutrition
 Fluid and electrolytes imbalance:
o dehydration, shock
o hypokalaemia
o metabolic acidosis
o isotonic dehydration
 o hypertonic (hypernatraemic) dehydration
o hypotonic (hyponatraemic) dehydration
o hypocalcemia and
o hypomagnesemia
 Seizures due to hypoglycaemia, hyperthermia, hyper/hyponatraemia
 Septicaemia
 Secondary lactose intolerance
 Haemolytic uraemic syndrome

PATHOPHYSIOLOGY OF DIARRHOEAL DISEASES

Intestinal physiology
- Caused by disturbance in mechanism of transport of water and electrolytes in the small intestine
- Water and electrolytes are simultaneously absorbed by villi and secreted by crypts of bowel epithelium
which cause two directional flows between intestinal lumen and blood
- Any change in two directional flow results in reduced net absorption or increased secretion causing
diarrhoea

Mechanism of watery diarrhoea

- Secretory mechanism
 when absorption of sodium by villi is impaired and secretion of the chloride in crypts is
increased; loss of water and salts from body as watery stool (may result from action on the
bowel mucosa by bacterial toxins such as [Link], Vibrio cholerae or virus)
- Osmotic mechanism
 osmotically active substance is ingested, when poorly absorbed – diarrhoea occurs. E.g. in
lactase deficiency – the ingested lactose can cause diarrhoea.

Assessment of a child with diarrhoea

History
Ask the mother or other caretaker about:
 presence of blood in the stool
 duration of diarrhoea
 number of watery stools per day
 number of episodes of vomiting
 presence of fever, cough, or other important problems (e.g. convulsions, recent measles)
 pre-illness feeding practices
 type and amount of fluids (including breastmilk) and food taken during the illness
 drugs or other remedies taken
 immunization history

Physical examination
First, check for signs and symptoms of dehydration.
Look for these signs:
 General condition: is the child alert; restless or irritable; lethargic or unconscious?
 Are the eyes normal or sunken?
 When water or ORS solution is offered to drink, is it taken normally or refused, taken eagerly, or is the
child unable to drink owing to lethargy or coma?

Feel the child to assess:

Skin turgor - When the skin over the abdomen is pinched and released, does it flatten immediately, slowly, or
very slowly (more than 2 seconds)?

Then, check for signs of other important problems.

Look for these signs:
 Does the child's stool contain red blood?
  Is the child malnourished?
 Is the child coughing? If so, count the respiratory rate to determine whether breathing is abnormally
rapid and look for chest indrawing.

Take the child's temperature:

 Fever may be caused by severe dehydration, or by a non-intestinal infection such as malaria or
pneumonia.

Management
Determine the degree of dehydration and select a treatment plan
A B C
LOOK AT:
CONDITION Well, alert Restless, irritable Lethargic or
unconscious
EYES Normal Sunken Sunken
THIRST Drinks normally, not Thirsty, drinks eagerly Drinks poorly, or not
Thirsty able to drink
FEEL: SKIN PINCH Goes back quickly Goes back slowly Goes back very slowly
DECIDE The patient has If the patient has two or If the patients has two or
NO SIGNS OF more signs in B, there is more signs in C, there is
DEHYDRATION SOME SEVERE
DEHYDRATION DEHYDRATION
TREAT Use Treatment Pan A Weigh the patient, if Weigh the patient and
possible, and use use
Treatment Plan B Treatment Plan C
URGENTLY

Objectives
The objectives of treatment are to:
• prevent dehydration, if there are no signs of dehydration
• treat dehydration, when it is present
• prevent nutritional damage, by feeding during and after diarrhoea and
• reduce the duration and severity of diarrhoea, and the occurrence of future episodes, by giving supplemental
zinc.

Treatment Plan A: home therapy to prevent dehydration and malnutrition

Rule 1: Give the child more fluids than usual, to prevent dehydration
What fluids to give - Wherever possible, these should include at least one fluid that normally contains salt. Plain
clean water should also be given.
Suitable fluids
Most fluids that a child normally takes can be used. It is helpful to divide suitable fluids into two groups:
Fluids that normally contain salt, such as:
• ORS solution
• salted drinks (e.g. salted rice water or a salted yoghurt drink)
• vegetable or chicken soup with salt

ORS solution
Composition of reduced (low) osmolarity ORS solution
Reduced osmolarity ORS grams/litre mmol/litre
Sodium chloride 2.6 Sodium 75
Glucose, anhydrous 13.5 Chloride 65
Potassium chloride 1.5 Glucose, anhydrous 75
Trisodium citrate, dihydrate 2.9 Potassium 20
Citrate 10
Total Osmolarity 245
Fluids that do not contain salt, such as:
• plain water
• water in which a cereal has been cooked (e.g. unsalted rice water)
• unsalted soup
• yoghurt drinks without salt
• green coconut water
• weak tea (unsweetened)
• unsweetened fresh fruit juice.

Unsuitable fluids
A few fluids are potentially dangerous and should be avoided during diarrhoea.
Some examples are:
• commercial carbonated beverages
• commercial fruit juices
• sweetened tea.

Other fluids to avoid are those with stimulant, diuretic or purgative effects, for example:
• coffee
• some medicinal teas or infusions.

How much fluid to give

The general rule is: give as much fluid as the child or adult wants until diarrhoea stops.
As a guide, after each loose stool, give:
 children under 2 years of age: 50-100 ml (a quarter to half a large cup) of fluid
 children aged 2 up to 10 years: 100-200 ml (a half to one large cup)
 older children and adults: as much fluid as they want

Rule 2: Give supplemental zinc (10 - 20 mg) to the child, every day for 10 to 14 days
By giving zinc as soon as diarrhoea starts, the duration and severity of the episode as well as the risk of
dehydration will be reduced. By continuing zinc supplementation for 10 to 14 days, the zinc lost during
diarrhoea is fully replaced and the risk of the child having new episodes of diarrhoea in the following 2 to 3
months is reduced.

Rule 3: Continue to feed the child, to prevent malnutrition

The infant usual diet should be continued during diarrhoea and increased afterwards. Food should never be
withheld and the child's usual foods should not be diluted. Breastfeeding should always be continued.

What foods to give - depends on the child's age, food preferences and pre-illness feeding pattern; cultural
practices are also important. In general, foods suitable for a child with diarrhoea are the same as those required
by healthy children.

How much food and how often - Offer the child food every three or four hours (six times a day). Frequent, small
feedings are tolerated better than less frequent, large ones.
After the diarrhoea stops, continue giving the same energy-rich foods and provide one more meal than usual
each day for at least two weeks. If the child is malnourished, extra meals should be given until the child has
regained normal weight-for-height.

Rule 4: Take the child to a health worker if there are signs of dehydration or other problems

The mother should take her child to a health worker if the child:
• starts to pass many watery stools;
• has repeated vomiting;
• becomes very thirsty;
• is eating or drinking poorly;
• develops a fever;
• has blood in the stool; or
• the child does not get better in three days.

Treatment Plan B: oral rehydration therapy for children with some dehydration
Children with some dehydration should receive oral rehydration therapy (ORT) with ORS solution in a health
facility following Treatment Plan B
Children with some dehydration should also receive zinc supplementation as described above.

How much ORS solution is needed?

Approximate amount of ORS to give in the first 4 hours
Age < 4 months 4-11 months 12-23 2-4 years 5-14 years 15 years or
months older
Weight < 5 kg 5-7.9 kg 8-10.9 kg 11-15.9 kg 16-29.9 kg 30 kg or
more
In ml 200-400 400-600 600-800 800-1200 1200-2200 2200-4000

If the child's weight is known, this should be used to determine the approximate amount of solution needed. The
amount may also be estimated by multiplying the child's weight in kg times 75 ml.
If the child's weight is not known, select the approximate amount according to the child's age.

The exact amount of solution required will depend on the child's dehydration status.
If a child wants more than the estimated amount of ORS solution, and there are no signs of over-hydration, give
more.
Oedematous (puffy) eyelids are a sign of over-hydration. If this occurs, stop giving ORS solution, but give
breastmilk or plain water, and food. Do not give a diuretic. When the oedema has gone, resume giving ORS
solution or home fluids according to Treatment Plan A.

How to give ORS solution

A family member should be taught to prepare and give ORS solution. The solution should be given to infants
and young children using a clean spoon or cup.
Feeding bottles should not be used. For babies, a dropper or syringe (without the needle) can be used to put
small amounts of solution into the mouth.
Children under 2 years of age should be offered a teaspoonful every 1-2 minutes; older children (and adults)
may take frequent sips directly from the cup.
Vomiting often occurs during the first hour or two of treatment, especially when children drink the solution too
quickly, but this rarely prevents successful oral rehydration since most of the fluid is absorbed. After this time
vomiting usually stops. If the child vomits, wait 5-10 minutes and then start giving ORS solution again, but
more slowly (e.g. a spoonful every 2-3 minutes).

Monitoring the progress of oral rehydration therapy

Check the child from time to time during rehydration to ensure that ORS solution is being taken satisfactorily
and that signs of dehydration are not worsening.
If at any time the child develops signs of severe dehydration, shift to Treatment Plan C.
After four hours, reassess the child fully, following the guidelines in Table 1. Then decide what treatment to
give next:
If signs of severe dehydration have appeared, intravenous (IV) therapy should be started following Treatment
Plan C.
• If the child still has signs indicating some dehydration, continue oral rehydration therapy by repeating
Treatment Plan B. At the same time start to offer food, milk and other fluids, as described in Treatment Plan A,
and continue to reassess the child frequently.
• If there are no signs of dehydration, the child should be considered fully rehydrated. When rehydration is
complete:
- the skin pinch is normal;
- thirst has subsided;
- urine is passed;
- the child becomes quiet, is no longer irritable and often falls asleep.
Teach the mother how to treat her child at home with ORS solution and food following Treatment Plan A. Give
her enough ORS packets for two days. Also teach her the signs that mean she should bring her child back.

Giving Zinc
Begin to give supplemental zinc, as in Treatment Plan A, as soon the child is able to eat following the initial
four hour rehydration period.

Giving food
Except for breastmilk, food should not be given during the initial four-hour rehydration period. However,
children continued on Treatment Plan B longer than four hours should be given some food every 3-4 hours as
described in Treatment Plan A.
All children older than 6 months should be given some food before being sent home.

Treatment Plan C: for patients with severe dehydration

Guidelines for intravenous rehydration
The preferred treatment for children with severe dehydration is rapid intravenous rehydration, following
Treatment Plan C.
If possible, the child should be admitted to hospital.

Guidelines for intravenous treatment of children and adults with severe dehydration
Start IV fluids immediately. If the patient can drink, give ORS by mouth until the drip is set up. Give 100 ml/kg
Ringer's Lactate Solution divided as follows:

Age First give 30 ml/kg in Then give 70 ml/kg in

Under 12 months (infants) 1 hour 5 hours
Older 30 minutes 2 ½ hours

 Reassess the patient every 1-2 hours. If hydration is not improving, give the IV drip more rapidly.
 After six hours (infants) or three hours (older patients), evaluate the patient using the assessment chart.
Then choose the appropriate Treatment Plan (A, B or C) to continue treatment.
 If Ringer's Lactate Solution is not available, normal saline may be used.
 Repeat once if radial pulse is still very weak or not detectable.

Prevention
1. Breastfeeding
- During the first 6 months of life, infants should be exclusively breastfed. Exclusively breastfed babies are
much less likely to get diarrhoea or to die from it than are babies who are not breastfed or are partially breastfed.
Breastfeeding should ontinue until at least 2 years of age.
2. Improve feeding practices
- Complementary foods should normally be started when a child is 6 months old. Good feeding practices
involve selecting nutritious foods and using hygienic practices when preparing them.
3. Use of safe water
- The risk of diarrhoea can be reduced by using the cleanest available water and protecting it from
contamination.
4. Handwashing
- The risk of diarrhoea is substantially reduced when family members practice regular handwashing. All family
members should wash their hands thoroughly after defecation, after cleaning a child who has defecated, after
disposing of a child's stool, before preparing food, and before eating. Good handwashing requires the use of
soap or a local substitute, such as ashes or soil, and enough water to rinse the hands thoroughly.
5. Food safety - key messages concerning the preparation and consumption of food:
• Do not eat raw food, except undamaged fruits and vegetables that are peeled and eaten immediately;
• Wash hands thoroughly with soap after defecation and before preparing or eating food;
• Cook food until it is hot throughout;
• Eat food while it is still hot, or reheat it thoroughly before eating;
• Wash and thoroughly dry all cooking and serving utensils after use;
• Keep cooked food and clean utensils separately from uncooked food and potentially contaminated utensils; and
• Protect food from flies by means of fly screens.
6. Use of latrines and safe disposal of stools
7. Measles immunization
Dysentery
Definition
Diarrhoea with visible blood in the stool.

Clinical features
 Visible blood in diarrhoeal stool
 Fever
 Cramping abdominal pain, tenesmus
 Weight loss and worsening of nutritional status
 Severe complications ( toxic megacolon , intestinal perforation, rectal prolapse, convulsion ,
septicaemia, haemolytic uraemic syndrome)

Diagnosis
o Stool R.E- RBC and pus cells in the stool, trophozoites of E. histolytica (rare in children under 5 yrs)
o Stool for culture and sensitivity – to detect pathogenic bacteria

Management

 Antimicrobial therapy
 Trimethoprim-sulphamethoxazole – dose TMP 4 mg/kg/dose and SMX 20 mg/kg/dose for 2 days or
 Norfloxacin – 10mg/kg/dose b.d. for 2 days
 if not improved or presence of trophozoites form of [Link] in stool examination add
Metronidazole (oral) – 10 mg/kg/dose t.d.s. for 5 days

 Fluids – Evaluate signs of dehydration and treated accordingly.

 Feeding – Continue feeding in order to prevent nutritional damage.
 Follow up – who not showing clear improvement within 2 days and high risks (infants,
 malnourished child, dehydrated patients) should be closely followed up.
Persistent diarrhoea
Definition
 Diarrhoea episode lasts for 14 days or longer.

Risk factors
 Malnutrition
 Recent introduction of animal milk or formula milk
 Young age(under 18 months of age)
 Immunological impairment
 Recent diarrhoea

Investigations
 Stool R.E
 Stool for culture and sensitivity
 Stool for reducing substance.
 Stool pH
Treatment
 Fluid and electrolytes replacement
 Assess hydration status and treat accordingly.
 Nutritional therapy(important aspect of treatment )
o Ensure full energy intake i.e.110kcal/kg/day by giving thick cereal with vegetable oil.
o Give frequent small meals, at least 6 times a day.
o provide supplementary vitamins and minerals
o Give extra meal each day for at least one month.
 Anti-diarrhoeal drugs should not be given.
 A course of appropriate antimicrobial and antiprotozoal therapy for enteropathogenic E. coli,
Giardiasis, E. histolytica.

Preventive strategies of diarrhoeal diseases

 Breast feeding
Exclusive breast feeding – during 1st 6 months and continued at least to 2 years of age (to reduce risk of
severe diarrhoea and other serious infection.)
 Weaning practices should begin at 6 months.
 Proper use of water for hygiene and drinking
 Hand washing
 Use of sanitary latrines
 Safe disposal of stool of young children
 Measles immunization
 LIVER DISORDERS
VIRAL HEPATITIS
Causal organisms of viral hepatitis
1. Hepatitis A virus
2. Hepatitis B virus
3. Hepatitis C virus
4. Hepatitis D virus
5. Hepatitis E virus
6. Non A-E viral hepatitis
7. Cytomegalovirus
8. Epstein-Barr virus
9. Herpes simplex virus

Incubation period, mode of spread, nature of disease and prevention of hepatitis A, B, C, D, and E

Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E

Incubation 2-4 wk 4-20 wk 2-26 wk 6-9 wk 3-8 wk
Spread
Faeces Yes No No No Yes
Blood Uncommon Yes Yes Yes No
Saliva Yes Yes Yes ? ?
Sexual Uncommon Yes Uncommon Yes ?
Vertical No Yes Uncommon Yes No
Chronic No Yes Yes Yes No
infection
Prevention
Active Vaccine Vaccine No Prevented by No
Passive Immune serum Hyperimmune No Hepatitis B No
globulin serum globulin vaccination

Phases of the clinical course of Hepatitis

1. The pre-icteric phase – prodromal symptoms usually precede the development of jaundice by few days to 2
weeks.
 Chills, malaise, and headache
 GI symptoms – anorexia and nausea may be prominent and vomiting and diarrhoea may follow.
 A steady upper abdominal pain
 Splenomegaly may occur
 Arthralgia, arthritis and skin rashes may occur in HBV infection
2. The icteric phase – dark urine and yellow tint to the sclera herald the onset of jaundice.
 As obstruction to the biliary canaliculi develops, the jaundice deepens, the stools become paler, the
urine darker and the liver more easily palpable.
3. The convalescent phase – appetite improves and GI symptoms diminish in intensity.
 The jaundice recedes, the stools and urine regain their normal colour, the liver enlargement
regresses.
 In the course of 3-6 weeks the majority of cases recover.

 Mild cases may run an anicteric course recognized only because of known contact with a definite case or by
association with vague GI complaints or malaise with bilirubinuria and biochemical evidence of hepatic
dysfunction.
Signs and symptoms of hepatocellular failure
Signs
 Increasingly severe jaundice, anorexia, vomiting
 Change in sleep rhythm,
 Spontaneous bleeding into skin or GI tract may occur.
 Ascites may develop
 Flapping tremor
 Tendon reflexes become increased, bilateral extensor planter responses
 Change in behavior
 Deterioration in hand writing, inability to perform the simple mental arithmetic tasks, constructional apraxia
 Fetor hepaticus – sweet musty odour to the breath
 Eventually decerebrate or decorticate posture, and become unconscious.
 Hypotonia and areflexia occur terminally

Symptoms
 Lethargy, verbal confusion
 Irrational hyperactivity
 Restlessness, disorientation
 Repeated yawning, and sucking movement
 Apathy, stupor, and coma

Investigations
1. Liver function test including transaminases
  plasma aminotransferase activity exceeding 400U/l – most striking abnormality.
  plasma bilirubin – reflects the severity of the jaundice.
  alkaline phosphatase activity – marked cholestasis develops.
 Normal albumin concentration
2. Bilirubinuria is an early finding, usually continuing into the convalescent period. Mild proteinuria may
occur.
3. Prolongation of prothrombin time is a reliable indication of severe liver damage.
4. The white cell count is normal or low in uncomplicated cases.
5. Hepatitis serology for A, B, E, CMV and EB virus infection
6. Detection of HBs Ag

Differential diagnosis
1. Hepatitis due to toxin and drugs
2. Weil’s disease (Leptospirosis)

Complications
1. Acute hepatic failure
2. Renal failure
3. Aplastic anaemia
4. Chronic hepatitis
5. Cirrhosis (with Hepatitis B, C)
6. Hepatocellular carcinoma

Management
Only the more severely affected patients require care in hospital, principally to allow early detection of
developing acute hepatic failure.
1. No specific treatment
2. General supportive measure – diet, liver support, fluid, drugs to avoid
Diet:
- High calorie diet
- Initially due to nausea and anorexia, a light diet with fruit drinks and glucose should be given.
- Good protein intake should be encouraged.
- If vomiting is severe, IV fluid and glucose may be required.

Avoid taking drugs

Drugs should be avoided if possible, especially in severe hepatitis, because many are metabolized in the liver.
This applies especially to sedatives and hypnotics.

3. Management of hepatocellular failure – refer to cirrhosis of liver

Prevention
1. Environmental sanitation
2. Personal hygiene
3. Safe water supply
4. Proper sterilization of syringes and needles. Use of disposable syringes and needles is the best method.
5. Screening of blood donors
6. Active immunization
 Routine immunization: with 3 doses at 0, 1, and 6 months interval or at birth, one and six months
of age in neonate. Booster dose is followed every 5 years.
 Management of babies born to HBsAg positive mothers
1. All the babies born to mothers carrying hepatitis B (HBsAg +ve) must be immunized four
doses: at birth, one, two, and twelve months with a blood sample at 14 months to check
antibody levels.
2. Babies born to mothers with high infectivity (are defined as those who are e antigen
positive, e antibody negative or both e antigen and e antibody negative) must be given 2
ml (200 IU) immunoglobulin as well as vaccine, ideally within the first 12 hours of life.
7. Health education

Prognosis
Viral hepatitis A
 Acute hepatic failure
 Chronic infection does not occur.

Viral hepatitis B
 90-95% has full recovery.
 5-10% will develop chronic infection. Chronic hepatitis B is asymptomatic and develops complications
such as cirrhosis (15-20%) and hepatocellular carcinoma.
 Chronic infection also common in immunodeficient individual such as Down's syndrome and HIV
infection.
 At /after delivery;
- if mother is HBe antigen positive - 85%
- if Hbe antibodies are present – 25% infants become carriers
- if HBs antigen positive alone – 10-20%.

Viral hepatitis C
 80% develop chronic infection.
 Chronic hepatitis C infections are usually asymptomatic. Most develop cirrhosis and hepatocellular
carcinoma.
CIRRHOSIS OF THE LIVER
Definition
Cirrhosis is characterized by hepatic parenchymal damage with fibrosis and nodular regeneration throughout the
liver, accompanied by distortion of normal lobular pattern.

Common causes in children

1. Idiopathic (cryptogenic)
2. Obstructive biliary diseases - Congenital extrahepatic biliary atresia, Neonatal hepatitis syndrome,
Choledochal cyst
3. Infection of the liver - Viral hepatitis B, C, or D
4. Cardiac causes – any congenital heart disease with heart failure
5. Drugs – Methotrexate
6. Metabolic disorders - Haemochromatosis (primary or secondary), Wilson's disease (hepatolenticular
degeneration), Alpha-1-antitrypsin deficiency
7. Persistent blockage of the venous return from the liver: e.g. veno-occlusive disease, Budd-Chiari syndrome

Clinical features of hepatic cirrhosis

1. Hepatomegaly (although liver may be small)
2. Jaundice
3. Ascites
4. Circulatory changes - Spider telangiectasia, palmar erythema, cyanosis
5. Endocrine changes: (In adolescent) - Loss of libido, hair loss, Male: gynaecomastia, testicular atrophy,
impotence, Female: breast atrophy, irregular menses, amenorrhoea
6. Haemorrhagic tendency - Bruises, purpura, epistaxis, menorrhagia
7. Portal hypertension - Splenomegaly, collateral vessels, variceal bleeding, fetor hepaticus
8. Hepatic (portosystemic) encephalopathy
9. Other features - Pigmentation, digital clubbing, low-grade fever

Palmar erythema Spider telangiectasia

Clinical features of different stages of hepatic failure:

1. Pre-hepatic coma
 Apathy, inability to concentrate, confusion, disorientation, dementia
 Slow slurred speech
 Reversal of sleep pattern
 Constructional apraxia, inability to perform simple arithmetic tasks
 Flapping tremor
 Bleeding tendency (decreased coagulation factors)

2. Hepatic coma
 Precoma progressing to delirium and coma
 Hyper-reflexia, extensor planter response
 Fetor hepaticus

Investigations
1. Liver function test
 May be normal
 With the progression of cirrhosis – increasing bilirubin, and enzymes aminotransferase level
2. Total and differential protein – a low albumin level with normal or increased gamma globulin
3. Prothrombin time
 Increased prothrombin time and could not be corrected by giving vitamin K.
 It provides the valuable prognostic information in patients with acute and chronic liver failure.
4. USG abdomen – increased echogenicity, and variable liver size.
5. Liver biopsy
6. Viral markers of hepatitis B and C
7. Upper GI endoscopy to detect varicies

Management of cirrhosis
1. Removal of the cause
2. Maintenance of nutrition and water and electrolyte balance
 High protein diet
 Low sodium
3. Supportive treatment
 For ascites – frusemide alone or in combination with aldosterone antagonist (spironolactone)
 If marked ascites – abdominal paracentesis

Management of Hepatocellular failure

Mainly supportive
1. Diet - protein restriction to 0.5 gram/kg/day or less
 Fluid restriction
2. Gut sterilization
 Bowel wash out
 Lactulose oral/enema
 Oral neomycin – to decrease the enteric bacteria that produces ammonia
3. Avoid hepatotoxic agents, nephrotoxic agents, benzodiazepines and sedatives e.g. morphine
4. General measures
 IV infusion of electrolytes & 10-20% of glucose solutions – to maintain normal potassium
concentration and blood glucose.
 A parenteral H2 receptor blocker is administered prophylactically to prevent potential GI bleeding.
 Vitamins supplement – especially vitamin B and K
 For cerebral oedema – endotracheal intubation and hyperventilation
5. Orthotopic liver transplant

COMPLICATIONS OF CIRRHOSIS
1. Portal hypertension
2. Increased susceptibility to infection
3. Hepatoma
4. Malnutrition
5. Bleeding diathesis
6. Spontaneous bacterial peritonitis
7. Renal failure
8. Hepatic encephalopathy
 RENAL SYSTEM

ACUTE POST STREPTOCOCCAL GLOMERULONEPHRITIS

Common in children, rare before the age of 3 years
Post infectious GN - Sterptococcal – group A type 12, 4 (tonsillitis)
- Group A type 49 (skin infection)
- staphylococcal infection
Acute glomrulonephritis following streptococcal infection is the commonest type in children.

Criteria for diagnosis

Characterized by abrupt onset of
 haematuria,
 Oliguria
 Edema
 Hypertension and
 Proteinuria (mild)

Pathogenesis
Immune - complex disease probably due to cross reaction of antibodies produced in response to exogenous
antigen (Streptococcal antigen) with endogenous basement membrane (Renal)
Formation of antigen-antibody complexes which transverse the glomerular basement membrane.
Activation of complement system leads to release of substances which attract neutrophils.
Lysosomal enzymes released by neutrophils are responsible for the damage to the glomerulus.

Pathology
 Proliferation of mesangial cells and infiltration with neutrophils in glomerular tufts (Light
micorscopy)
 Lumpy deposit on subepithelial side of capillary basement membrane. (Electron microscopy)
 Immune fluorescent - granular deposit of Ig G and complement along the capillary wall

Clinical features
History of upper respiratory tract infection or skin infection approximately 2 weeks prior to the onset
 Rapid onset of -
- Puffiness around the eyes and pedal oedema (first symptom)
- Urine coloured is characteristically coca coloured (Smoky red urine)
- Oliguria usually correlates with severity of disease.
 Features of hypertension – head ache, vomiting, photophobia

Complications of AGN
 Acute renal failure
 Hypertensive heart failure
 Hypertensive encephalopathy

Course of the disease

Oliguria - Diuresis - Recovery
Gross haematuria & significant proteinuria disappeared within 2 weeks
Microscopic haematuria & mild proteinuria – several months
Investigations
 Urine RE
 Macroscopy
- Smoky red urine
- 1+ or 2++ proteins
Microscopy
- Red cell casts
- Granular casts
 Blood examination
 Blood Urea - raised (Normal range - 4 to 18 mg/dl)
 Serum creatinine - raised (Normal range - 27 to 72 micromole/l)
 Blood for CP – Normocytic anaemia
 Blood electrolytes – Hyperkalaemia (upper limit of normal or raised)
 Acidosis, Hyperkalaemia if renal failure present
 Complement level – hypocomplementaemia (C3, C4)
 ASO titre may be raised (>300 IU)
 Throat swab C&S – may be positive for streptococcal infection

Differential diagnosis
Causes of haematuria in children
Glomerular diseases
Various types of glomerulonephritis
Ig A nephropathy
Mesangiocapillary glomerulonephritis
Glomerulonephritis due to viral, malaria, fungal and rickettsial
Associated with Systemic diseases
- Henoch-Schonlein purpura nephritis
- Haemolytic uremic syndrome
- SLE nephritis
- HIV nephropathy
- Blood dyscrasia
- UTI

Management of AGN
Nonspecific treatment
 Antimicrobial therapies to eradicate the streptococci
- Inj IM Procain Penicillin 25,000 to 50,000 unit/ kg x 7-10 days or
- Erythromycin (if sensitive to Penicillin) 30 to 50 mg/kg/day in 4 divided doses x 7-10 days
 Monitoring
- Intake and output chart OD
- BP chart depend on severity – BD/4 hourly/6 hourly
- Weight chart daily
- Urine albumin chart daily
 Dietary management
- Restriction of protein if blood urea is elevated >75 mg%
- Restriction of potassium and sodium
 Fluid restriction
- 1/2 or 1/3 of the previous day out-put + insensible loss (400 - 500ml/m2 body surface areas) or
Insensible loss –
- 1 -10 kg – 25 ml/kg
- 10 – 20 kg – 12.5 ml/kg
- >20 kg – 5 ml/kg
Increases Decreased
Abnormal fluid loss Oedema or antidiuretic state
By 12% for every 1°C >37°C
10-20% if sweating
25-75% if hypermetabolic
25% for radiant heater or phototherapy

Treatment of Hypertension /Hypertensive encephalopathy

Mild/Moderate hypertension
- Nifedipine - 0.25mg/kg/dose (oral or sublingual)
(Action within 30 to 40 min) can be repeated in 2 to 4 hours if necessary
- IV/Oral Hydralazine (IV – 0.5 mg/kg stat followed by 0.1-0.2 mg/kg/Hour IV infusion Oral - 1-2
mg/kg/day
Gradual reduction in blood pressure is important

Hypertensive encephalopathy
Clinical presentation
 Headache/ projectile vomiting, confusion, seizures and convulsion.
Treatment
To reduce BP to the upper limit of normal range over 48- 72 hours
 sublingual Nifedipine is first line of treatment
 IV Frusemide 1-2 mg/kg/dose
 Sodium nitroprusside or Labetalol IV infusion 1-3 ml/kg/hour
 IV frusemide 1-2mg/kg/dose
Gradual reduction in blood pressure is important

The followings should be regarded as severe hypertension-

Systolic BP Diastolic BP
1-2 years >118 mmHg >82 mmHg
3-5 years >124 mmHg >84 mmHg
6-9 years >130 mmHg >86 mmHg
10-12 years >134 mmHg >90 mmHg

Other support treatments

 Dialysis for acute renal failure with severe hypertension
 Control of seizures by anticonvulsant drugs.
 Treat cerebral oedema with diuretics or mannitol.

Prognosis of ASGN
- Excellent – Complete recovery >95%
- Recurrence – extremely rare
NEPHROTIC SYNDROME
Nephrotic syndrome is a common renal problem in preschool children. The most common cause of
nephrotic syndrome is idiopathic minimal change nephrotic syndrome. Boys are more affected than girls.

Diagnostic Criteira
Characterized by massive proteinuria, hypoalbuminaemia and generalized oedema and hypercholesterolaemia.

Proteinuria > 40 mg/m2/Hr

Hopoalburminaemia < 2.5 gm/dl

Classification of nephrotic syndrome

1. Minimal change nephrotic syndrome (MCNS)
2. Other histological types

Aetiology
 90% - idiopathic.
 Other causes, e.g. - Post Streptococcal Glomerulonephritis
- Hepatitis B

Pathophysiology of Nephrotic Syndrome

Increased Glomerular Permeability

Proteinuria

Hypoalbuminaemia Hypogamma-globulinaemia

Plasma oncotic pressure  Interstitial oedema

Intravascular volume Oedema

Sodium retension Hypovolemia

Acute tubular necrosis PCV

Death Thrombosis
Pathology
Idiopathic nephrotic syndrome – morphologic pattern
1. Minimal change (85%) – normal in light microscopy
EM (electron microscopy) – fusion of epithelial foot processes
2. Focal segmental sclerosis (10%)
3. Mesangial proliferative groups (5%) – diffuse increase in mesangial cells and matrix
4. Membranous glomerulonephritis – thickened glomerular basement membrane

Clinical features
 M>F (2:1)
 Age - peak incidence in preschool children
 Medium age - 2.5 years
 Initial episode and subsequent relapses may followed an apparent viral (URTI)
 Generalized edema developed over a course of several weeks
- Initially noted around the eyes
- Lower extremities (pitting oedema)
- Associated with weight gain
- Ascites
- Pleural effusion
Course of the disease
 Most children –respond well to steroid therapy
 No residual renal dysfunction

Management
Monitoring
 Daily intake- output chart
 Daily Urine albumin chart
 Daily Body weight chart
 Blood pressure chart
Investigations
 Urine examination - macroscopic - clear and colourless
 Urinalysis - heavy proteinuria, hyaline casts
 Urine for culture & sensitivity
 Blood total and differential protein - low serum albumin (normal –3.9 to 5gm/l)
 Blood urea and electrolyte - usually normal
 Blood cholesterol - increased (>200 mg/dl)
 Complement level – normal
 Renal biopsy
Indications for renal biopsy
 Age of onset - below 6 months or > 12 years
 Persistent microscopic haematuria
 Initial macroscopic haematuria at any age (absence of infection)
 Persistent hypertension
 Persistently low serum complement C3
 Proteinuria despite 4 weeks daily steroid therapy

Management of Nephrotic syndrome

Management of steroid responsive nephrotic syndrome
Initial episode
 Diet
- Low salt diet, low sodium, to prevent fluid retention and oedema
- Recommended daily allowance of protein (1.5-2 G/kg/day + adequate calorie for age)
 - Normal protein diet with adequate calories for age
- Fluid restriction – Previous day out put + Insensible loss
 Steroid
- 60 mg/m2/day (maximum 80 mg/day) single dose or 4 divided doses for at least 4 consecutive
weeks followed by
- 40 mg/m2 (maximum 60 mg) single morning dose, alternate day for 28 days and then slowly
tapered and discontinued over the next 2-3 months
 Albumin
Clinical indications
- Clinical hypovolemia - 20% albumin 1gm/kg (5 ml/kg) over 4 to 6 hours
- Symptomatic oedema
- Low serum albumin alone is not an indication
 Diuretic is indicated if there is severe oedema.
- Furosemide 1mg/kg/day in 2 divided dose
 Penicillin prophylaxis should be given to prevent pneumococcal infection
- Penicillin V 125 mg bd (<5 years) and 250 mg bd (> 5 years) until remission occurs.
Management of relapse
Characteristic feature of Steroid responsive nephrotic syndrome
 Tendency to relapse triggered by infection, allergic events
 Relapse rate 60%
 Management of first 2 relapse
- Prednisolone- 60 mg/m2 daily divided dose until remission. (Urine albumin clear/trace for 3
consecutive days)
- Followed by 40mg/m2 alternate day and tapered over 1-2 months.
 Frequent Relapse
- Prednisolone - maintenance 0.5 mg/kg alternate day for up to 12 months
Steroid dependent
Other immnosuppressive drugs
- Levamisole - 2.5 mg/kg alternate day for 4 to 12 months.
- Oral cyclophosphamide 2-3mg/kg/day single dose for 8- 12 weeks
- High dose pulse methylprednisolone
- Cyclosporin
- Mycophenolatemofitil (MMF)

Indications for immunosuppressive therapy

 Steroid dependent patients,
 Frequent relapsers, and
 particularly if the children suffers severe corticosteroid toixicity

Should get cyclophosphamide 2-3 mg/kg/day single dose for 8-12 weeks. Alternate day prednisalone
therapy is often continued during the course of cyclophosphamide. Cyclophosphamide has been shown to
prolong the duration of remission and to reduce the number of relapses. The potential side effects of the
cyclophosphamide (neutropaenia, disseminated varicella, haemorrhagic cystitis, alopecia, sterility and
increased risk of future malignancy) should be carefully reviewed.

Complications
 Infection
- Pneumococcal infection – peritonitis and pneumonia
- Flare up of TB
- Urinary tract infection (UTI)
Parents and children should be advised and cautioned about contact with chickenpox and measles.
 Thrombosis
 Complications of steroid therapy such as
 - Hypertension
- Growth retardation
- Cataract
 Hypovolemic shock
- Abdominal pain, cold clammy extremities, weak pulse volume, hypotension

Immunization
While the child is on steroid therapy, within 6 weeks after cessation, only killed vaccine may

safely be administered. Live vaccine can be administered 6 weeks after cessation of steroid therapy

Definitions in Nephrotic syndrome

Remission
Urinary protein occurrences - trace or negative for 3 consecutive days

Steroid responsive
Remission achieved by steroid therapy alone

Relapse
Urine – 3 - 4 + proteinuria and oedema
Frequent relapse
4 or more relapses in a 12 month period after responding well to prednisolone
Steroid dependent
Relapse occurs while on alternate-day steroid therapy or within 28 days of stopping prednisolone
therapy.
Steroid resistance
Failure of achieve response in spite of 4 weeks prednisolone therapy
 FLOW DIAGRAM FOR THE MANAGEMENT OF STEROID SENSITIVE NEPHROTIC SYNDROME

Initial presentation
Prednisolonen 60 mg/m 2/day divided doses x 4 weeks followed
by 40 mg/m2 single dose alternate day tail off over the next 2-3
months

Relapse
Prednisolonen 60 mg/m 2/day daily divided doses until proteinuria
2
free x 3 consecutive days followed by 40 mg/m /day single dose
alternate day and tapered over the next 1-2 months

Frequent relapse,

Steroid dependence

Refer for evaluation

Alternate day prednisolone
To maintain remission
Assess steroid threshold

Threshold <0.5 mg/kg Threshold >0.5 mg/kg

on alternate days on alternate days, or steroid toxicity

Alternate prednisolone - levamisole

- Cyclophosmide
for 8-9 months - Cyclosporin A
ACUTE RENAL FAILURE
Definition
Rapid deterioration in renal function (significant >50% decrease in glomerular filtration rate) over a
period of hours to days, leading to fall in urine output (<0.5-1 ml/kg/hr) with an accompanying
accumulation of nitrogenous wastes in the body.

Treatment
 Fluid restriction (insensible loss + urine output)
 Diuretic should be used as initial therapy to mobilize retained fluids
- IV frusemide 1-5 mg/kg
 Correction of electrolyte imbalances
- Treatment of acidosis with 8.4% sodium bicarbonate 1-2 ml/kg/dose
 Treatment of hyperkalaemia
- Stop all potassium input
- Monitor with ECG.
- IV10% Calcium gluconate (0.2 to 0.5 ml/kg)
- IV 8.4% NaHCO3 1-2 ml/kg
- IV 50% glucose with insulin infusion
- Nebulised Salbutamol
- Ion exchange resins
- Dialysis/Haemofiltration
Dialysis may be required if:
- Pulmonary oedema refractory to diuretics
- Persistent hyperkalemia
- Severe acidosis unresponsive to medical management
- Neurological symptoms due to uraemia or hyponatremia
- Uraemia >100-150 mg%
Treatment of left ventricular failure and pulmonary oedema
- Diuretics – IV Frusemide 2mg/kg/dose
- Venesection immediately if required removal of 100 – 200 ml of blood (life saving)
- Inotropic agents – Dopamine / Dobutamine
- Dopamine may improve renal blood flow in low dose
- Dobutamine may improve renal perfusion by enhancing myocardial contractility.
- Respiratory support (intubate and ventilate)
- Dialysis
URINARY TRACTINFECTION IN CHILDREN

Urinary tract infection is common in infants and children and may cause permanent
kidney damage.

DEFINITION
INFECTION OF THE URINARY TRACT IS IDENTIFIED BY GROWTH OF A SIGNIFICANT
NUMBER OF ORGANISMS OF A SINGLE SPECIMEN OF URINE, IN THE PRESENCE OF SYMPTOMS.
INCIDENCE
- DURING THE FIRST FEW MONTHS OF LIFE – MALES MORE THAN FEMALES
- AFTER1YEAR - UTI IS MORE COMMON IN FEMALES.

Causal organisms
- Escherichia coli (> 90% of first infection)
- Klebsiella
- Pseudomonas aeroginosa
- Proteus mirabilis
- Staphylococcus saprophyticus

Factors that predispose to UTI

Urine is excellent media for bacterial growth
Urinary stasis (due to out flow obstruction in renal tract)
- Constipation
- Infrequent voiding
- Stone/ posterior urethral valves/ congenital malformations
Perineal & uritheral factors
- Per urethral area often contains bacteria from the bowel lead ascending infection.
- Short female urethra provides an easy access to the bladder
- Further ascent of bacteria to the kidney is facilitated through vesicoureteric reflux.
Parasites
- Antibacterial resistance pattern
- Invasive qualities of bacteria (e.g. bacteria adhesion to uro- epithelium (Ecoli))

Diagnosis
Diagnosis based on the clinical sign and symptoms as well as confirmed urine culture result.
Clinical features
The 2 broad clinical categories of UTI are (1) acute pyelonephritis, or upper UTI (complicated UTI),
and (2) acute cystitis (simple) or lower UTI.

Upper tract sign (pyelonephritis) Lower tract sign (cystitis)

(Parenchymal involvement & risk of renal scar) (No involvement of renal
parenchyma/ no risk of scar)
Fever - Nonspecific abdominal pain/pain
in SPA
Lethargy - Urgency
General malaise / irritability - Frequency
Vomiting - Wetting
Loin pain/abdominal pain - Hematuria

In Neonate and very young children – no classic signs and symptoms

- Non specific symptoms – irritability, poor feeding, failure to gain weight, vomiting and diarrhoea,
prolonged jaundice.
 - Fever is often present or may be absent
- These patients are at higher risk for renal injury than older children ***

Investigations
 Collection of urine
- Mid stream clean catch urine is the ideal sample.
- Suprapubic puncture approach is the gold standard for urine specimen collection in neonates
and infants.
 URINALYSIS
- NORMAL PH / ALKALINE URINE
- URINE MICROSCOPY SHOULD BE UNDERTAKEN WITH FRESH UNSPUN URINE.
- SIGNIFICANT PYURIA IS DEFINED AS >10 WBC/ L IN BOYS AND > 50 WBC/L IN
GIRLS.
- WBC PRESENT. RBC PRESENT.
- MOTILE BACTERIA (ANY AMOUNT) PER HIGH POWER FIELD
Dipstick analysis
Nitrite Test
Nitrates are reduced to nitrite by certain bacteria. . Positive test implies the presences of bacteria in the bladder.
Leukocyte Esterase test
This test demonstrates presence of pyuria by histochemical methods that detect esterase in neutrophils.
 Urine Culture
PROPERLY COLLECTED POSITIVE URINE CULTURE IS THE GOLD STANDARD FOR
DIAGNOSING UTI.
SIGNIFICANT BACTERIURIA
- 5 MICROORGANISMS/ ML OF CLEAR FRESHLY PASSED
URINE OR
- ANY GROWTH FROM URINE OBTAINED BY CORRECTLY PERFORMED SUPRA-PUBIC
PUNCTURE.
Imaging
The following investigations should be done in child with recurrent UTI or first UTI in <1year or Child
with suspected urinary tract anomalies or family history of vesico ureteric reflux.
1. Renal ultrasound scan – detect hydronephrosis, renal pelvic dilatation.
2. Plain X Ray Abdomen – to detect renal stone
3. IVP (Intravenous urogram) – detect renal anatomy and function. Careful in patient with renal failure.
High risk of radiation.
4. DMSA Scan (dimercaptosuccinic acid) – method of choice for identifying renal scarring.
5. MCUG (MICTURATING CYSTO-URETHRO GRAM) – USEFUL FOR THE DIAGNOSIS AND
GRADING OF VUR
6. DTPA (DIETHYLENE TRIAMINEPENTA ACETIC ACID)- EVALUATION OF OBSTRUCTIVE
UROPATHY

TREATMENT OF ACUTE URINARY TRACT INFECTION

Main objectives are
 To eradicate organism
 To relieve symptoms
 To prevent both further UTI and new or progressive renal damage.

Antibiotic treatment
 Oral medication is used in child with cystitis
- Cotrimoxazole (Trimethoprim/sulfamethoxazole) - 6-12 mg/kg TMP, 30-60 mg/kg SMX, divided
12 hourly or
 - Amoxicillin - 20-40 mg/kg/day, divided 8 hourly or
- Augmentin - 7.5-15 mg/ kg/dose 8 hourly (based on Amox) or
 The usual duration of therapy is 5-7 days for simple cystitis.
 Broad-spectrum parenteral antibiotics for children with pyelonephritis (complicated UTI)
- Combination of Amino glycoside and
- Ampicillin or Augmentin or Third generation cephalosporin group
Supportive therapy
- A liberal fluid intake is encouraged and helps to alleviate dysuria.
- Antipyretics are used to relieve fever.
- Analgesics may be needed for dysuria or severe bladder spasms

Complications
1. Pyelonephritis or renal abscess
2. Recurrent UTI
3. Renal parenchymal scar formation.
4. Hypertension
5. Impaired renal function, and End Stage Renal Disease (ESRD)

Prevention
1. Avoid constipation.
2. Wiping should be done in a front to back direction
3. Emptying the bladder properly is very important. (Double voiding)
4. Encourage the child to drink as much as possible
5. Avoid tight underwear or pants and changed daily.
 HAMATOLOGY & ONCOLOGY

IRON DEFICIENCY ANAEMIA

Anaemia resulting from lack of sufficient iron for synthesis of haemoglobin
Most common haemotologic disorder of infancy and childhood

Iron requirement of children among different age groups

• 6 months-2 years 15mg/day
• 4-10years l0mg/day
• ll-18years 18mg/day

Iron deficiency anaemia

 common causes (30 % of global population)
1. Low iron stores
The iron stores of the infants are low in the following conditions.
 Preterm and small for date babies
 Twins
 Early clamping of the cord
 Haemorrhage from the cord and placenta
 Feto-fetal or feto-maternal transfusion
 Increased losses (e.g., parasitic infestations)
 Rapid growth (e.g. preterm babies)
2. Diminished iron intake
Cow's milk is a poor source of iron. Cow's milk allergy may cause occult
gastrointestinal bleeding. Breast milk is a relatively better source of iron.
Haemoglobin level may remain normal in babies fed exclusively on breast for 5-6
months.
3. Excessive losses of iron from the body.
Occurs through apparent or occult bleeding
Common causes are:
 Hookworm infestation
 Polyposis
 Prolapsed rectum
 Portal hypertension
 Ulcerative colitis
 Meckel's diverticulum
 Hiatus hernia
 Enteropathies of diverse types
 Dysentery
 Cephalhaematoma during the newborn period.
4. Diminished iron absorption
 Iron absorption is reduced in coeliac disease and in other causes of malabsorption
syndrome.
 High concentration of phytates/ calcium salt and rich fibre in the vegetarian diet
impair iron absorption.
5. Increased demand.
Premature and LBW infants grow rapidly after birth to catch up with the growth
requirements. They need to increase their body mass more rapidly. If the supply of iron is
in marginal, they develop iron deficiency anaemia. Similarly, during the period of rapid
growth (infancy and puberty), daily iron requirement is more.
6. Errors of iron metabolism
In some rare disorders such as idiopathic pulmonary hemosiderosis, sideroblastic anaemia
and congenital transferrin deficiency, iron is not utilized for erythropoiesis but is stored in
the tissues.

Common clinical manifestations

1. Signs and symptoms of anaemia
Pallor is the major symptom
 Onset is insidious
 There may be failure to thrive
 Easily fatigued.
 Suffer from frequent infections
 Spleen is enlarged in 15% of cases
 Severe anaemia leads to cardiac enlargement, systolic and even diastolic flow
murmurs
 Tongue papillae are atrophied
 Structural changes in the intestines may lead to malabsorption and even protein
losing enteropathy.
 Nails become thin, brittle and flat.
 Longitudinal ridges appear on nails, which may become
spoon shapedand concave. (Koilonychia)
 Some children develop a habit of eating mud, scraping of
the wall, ash etc.(pica)
 Persistent iron deficiency may result in growth
retardation and reduced mental performance.
 Attention span, school performance and general activity of children
may get adversely affected.
 When hemoglobin level falls to <5 g/dl, irritability and anorexia are prominent.
Tachycardia and cardiac dilatation occur and systolic murmurs are often present.
2. Signs and symptoms of underlying causes.
E.g. Clinical features of chronic infection- TB, Malaria, etc.
3. Signs and symptoms of complications
 Anaemic heart failure (cardiomegaly, haemic murmur)
 Splenomegaly
 Repeated Upper Respiratory Tract Infection
Investigations
For the diagnosis of iron deficiency anemia and to find out the underlying causes
1. Blood for complete picture (CP)
 Blood film - Hypochromic microcytic anaemia.
 Anisocytosis and poikilocytosis (+)
 Total and Differential Count -normal
 MCV, MCH and MCHC are reduced
2. Serum iron level is usually less than 30 µg/dl
3. Total iron binding capacity (TIBC) is increased
4. Reticulocyte count is decreased.
5. Bone marrow Hypercellular with erythroid hyperplasia
6. Stool RE Hook worms and Trichuriasis
7. Stool for occult bloodPresent - hiatus hernia
8. Blood for MP
9. Urine RE
10. Radiological Investigations
 CXR for evidence of Tuberculosis

Treatment
1. The underlying cause of iron deficiency should be treated
 Deworming the patient, change in dietary habits, wearing shoes
 Treating causes of persistent blood loss if any (polyps, chronic dysentery,
ulcerative colitis etc).
2. Iron therapy
 Oral: ferrous sulphate/ ferrous gluconate/ ferrous succinate
- Elemental iron 3-6mg/kg orally in three divided doses
- Iron should not be given just after the milk feeds or after food.
- Oral iron therapy should be continued for at least 6-8week after the
haemoglobin has reached normal level, to replace the iron stores.
 Parenteral (Iron dextran)
- Iron requirements are determined from the equation.
Iron (mg) = wt (kg) x Hb deficit (g/dl) x 80/100 x 3.4 x 15 (OR)
Wt (kg) x Hb deficit (g/dl) x 4
- Within 72-96 hour after administration of iron to an anemic child, peripheral
reticulocytosis is noted.
Prevention
 Avoid diet restriction
 Daily iron requirement in the first year of life is 5-7 mg.
 Children fed purely on milk diet are prone to develop anaemia.
 To prevent anaemia, supplementary foods rich in iron should be given
to the child from 4 months of age. Pulses, beans, peas, and green leafy
vegetables are fairly good sources of iron.
 Preterm and L.B.W infants who usually have low iron stores should
receive 10-15 kg of elemental iron daily.
 Iron supplements are necessary during adolescence for preventing anaemia
of puberty.
 Iron availability in the diet can be improved by:
 Increasing the ascorbic acid in the diet to increase iron absorption.
 Increasing the iron intake
 By reducing the inhibitors in the diet.
 Fortification of food products
 Hookworm infestation should be managed with anthelmintics
 Children should be encouraged to wear shoes while going to the field, to prevent
infestations with the infective form of hookworm larvae.
THALASSAEMIA SYNDROMES
Thalassaemia – Genetically determined defects in globin chain synthesis causing disorder of
hemoglobin production and abnormal erythropoiesis.
Normal α : β - 1:1
α Thalassaemia - 0:1
β Thalassaemia - 1:0
Different types of Hb among normal adult, children and foetuses
 Adult - Hb A (α 2 β2), Hb A2 (α 2 δ2)
 Children - Hb A(α 2 β2), Hb A2 (α 2 δ2)
 Foetus - Hb F (α 2 γ2), Hb Barts (γ4)
Types of Thalassaemia syndrome in Myanmar
 Thalassaemia Major
 Thalassaemia E (Hb E + β Thalassaemia)

Clinical features of Thalassaemia syndrome

Clinical features of β thalassaemia major
Failure to thrive in early childhood is a common presentation .Because of the variability in
the severity of the fundamental defects, there is a spectrum of clinical severity which
considerably influences the management.
The infants are born normally, but later develop
 Anaemia and jaundice
 Hepato-splenomegaly
 The children usually have thalassaemic facies characterized by:
- bossing of skull
- prominent frontal and parietal eminence with flattened vault
- straight forehead
- hypertrophy of mandible
- prominent malar eminence
- depressed bridge of the nose
 Teeth are malformed.
 Reduced activity and physical growth.
 Irregular fever and intercurrent infections
 Pathological fracture of long bones in the untreated cases.
 The course of the disease depends on the severity of the disease
Death may be due to severe anaemia, cardiac or liver failure.

Fig. Thalassaemic facies

Clinical features of Thalassaemia intermedia
 The clinical manifestations are in between Thalassaemia major and minor

Clinical features of Thalassaemia minor

 Mildest form of illness
 Very mild anaemia
 Mild jaundice
 Abdominal pain
 Often confused with iron deficiency anaemia.

Clinical feature of Thalassaemia E

Presentation of Thalassaemia E is similar to clinical features of β Thalassaemia major.

Laboratory investigations
1. Haemoglobin
 Reduced (2-6 g/dl)
 Foetal haemoglobin level is increased while Hb A2 is normal or increased
2. Cells
 Total erythrocyte counts - reduced (2-3 million/mm3);
 Haematocrit is reduced
 MCV and MCH are low
 Reticulocyte count appears to be elevated
 Mild leucocytosis and thrombocytosis are present due to prolonged
stimulation of the bone marrow.
3. Peripheral smear
 Red cells show hypochromia, microcytosis, anisopoikilocytosis and target
cells
 Marked basophilic stippling and variable polychromasia
 Nucleated red cells are present.
4. Haemoglobin electrophoresis
 To detect different types of haemoglobin such as Hb A (absent or reduced), A2
(normal or increased), and F (increased)
5. Singers test (alkaline denaturation test)
 Hb F resists denaturing by alkali.
6. Osmotic fragility
 The fragility of the cells on exposure to hypotonic saline is decreased.
7. Serum bilirubin level
 Moderately elevated (unconjugated)
8. Serum Iron level
 High as a result of increased iron absorption, ineffective utilization, and
release of iron from continuous haemolysis of red cells.
9. Iron binding capacity - reduced.
10. Bone marrow – Hyperplasia
11. PCR – DNA can be amplified
12. Restriction fragment length polymorphism
Antenatal Diagnosis
 Fetal blood sampling for globin chain synthesis
 Amniotic fluid cell culture for DNA analysis
 Chorionic villus sampling

Radiological changes in Thalassaemia

 Small bones of the hands - lace like pattern (Thinned cortex with widened medulla,
increased trabeculations)
 Skull bones - widening of diploic space, separation of tables, thickening of vault
(hair on end appearance)

Management of thalassaemia
 Blood transfusion
- The mainstay of managing these cases is repeated blood transfusion
- Blood products that are leuko-reduced for blood transfusion
- Transfusion therapy promotes general health & well being and avoids the
consequences of ineffective erythropoiesis.

Low transfusion regime

 Haemoglobin level is maintained between 6-8 g/dl
High transfusion regime
 Haemoglobin level is maintained between 8-10 g/dl to ensure an active life, adequate
growth and to prevent the ill effects of chronic anaemia.
 Packed cell transfusion should be given; 10-15 ml/kg every 2-3 weeks
SUPER TRANSFUSION REGIME
 Haemoglobin level is maintained between 10-12 g/dl.

All thalassaemia patients should be vaccinated with hepatitis B vaccine before starting
transfusion.

Chelation therapy (1 unit of blood = 200 mg of elemental iron)

Desferrioxamine - continuous subcutaneous infusion in a dose of 25-50 mg/kg/day
over a period of 8-12 hours, during the night using micro infusion pump (at least 5-6
nights/ week). Deferiprone (Oral form) - also available
Treatment should start serum iron ~ 2000 µg/l

Splenectomy
Indications
 Hypersplenism
  When the transfusion requirement exceeds 250 ml/kg/year of packed red cells.
 Abdominal discomfort
- It should be done in children older than 6 years to prevent post splenectomy sepsis.
- Children undergoing splenectomy should be immunized with pneumococcal,
[Link] and meningococcal vaccines.
- Life long penicillin prophylaxis is desirable after splenectomy.
- Treatment of thrombosis after splenectomy, with aspirin

Haematinics
 Avoid iron to prevent iron overload.
 Folic acid supplement = 1-5 mg/d

Diet - Avoid iron supplement, cereals, tea helps iron excretion

New Therapeutic approaches

Bone marrow transplantation
Defective stem cells are replaced with normal stem cells, thereby preventing the
imbalance between δ and β chains and ill effects of thalassaemia. This bone
marrow transplantation offers a cure. It is only possible if HLA matched sibling
donor is available.
Gene manipulation
 To decrease the excess of alpha chains by increasing the gamma chains which
combine with alpha chain to form foetal haemoglobin.
 Various chemotherapeutic drugs like azacytidine, myleran, hydroxyurea have
been used.
Gene therapy
 Transfer of normal gene in stem cells to correct the underlying defect

Prenatal diagnosis of thalassaemia syndromes

Foetal blood sampling
 To determine the beta versus alpha chain ratio from foetal blood.
Chorionic villus sampling
 Can be done between 10-12 weeks of pregnancy.

Complications
 Complication due to intramedullary erythropoiesis
E.g. frontal bossing, prominent malar bones (cosmetic effects), etc
 Complications due to haemosiderosis
Iron deposits in major organs - liver, heart, pancreas etc. lead to cirrhosis of
liver, cardiac cirrhosis, diabetes mellitus respectively and heart failure
 Anaemic heart failure
 Stunted growth
 Fracture of long bones.
 Complications due to repeated blood transfusions and splenectomy
- Risk of transmission of viral infections like (HIV, hepatitis B
 &C, cytomegalovirus)
- Post splenectomy sepsis is common below 6 years of age.

Genetic counseling
Refer to Genetics section

G6PD DEFICIENCY
(Acute Intravascular Haemolysis)
The agents causing acute intravascular haemolysis (in G6PD deficient patients)
1. Antimalarial drugs
e.g. Primaquine, Pamaquine, Chloroquine, Quinacrine
2. Antibacterials
e.g., Nalidixic acid, Sulphonamides (e.g. Trimethoprim, sulfamethoxazole ),
sulphones (dapsone), Nitrofurans (e.g. Nitrofurantoin), Quinolones
3. Analgesics, antipyretics
e.g., NSAIDs, Salicylates
4. Chemicals
e.g. Phenylhydrazine, Benzene, Napthalene mothballs
5. Illness
e.g. Diabetic ketoacidosis, Hepatitis
6. Miscellaneous
e.g. Synthetic Vitamin K, Fava beans, Methylene blue.

Clinical features of acute intravascular haemolysis

 Passing high coloured urine (haemoglobinuria)
 Fever, chill, tachycardia, backache
 JaundicePallor

Haemoglobiu
Diagnosis ria
 The diagnosis is based on the clinical profile
 Supravital staining of the red cells may show Heinz bodies
 During the phase of haemolysis, plasma haemoglobin is raised and
haemoglobinuria may be positive.
 After an attack of haemolysis, the reticulocyte count is elevated. Haemoglobin level is
low, with normocytic normochromic picture, along with polychromasia
 Unconjugated bilirubin level is raised with normal liver functions.
 Enzyme assay: G6PD enzyme should be estimated 6 weeks after the haemolytic
episode. Sub-normal levels of the enzyme activity (may be normal in acute stage)
 Direct Coomb's test is negative.
 Children who develop haemolysis following viral hepatitis develop severe jaundice
and have severe course with high mortality.
The genetic inheritance
 Sex- linked recessive (X-linked recessive)

Management
 There is no specific therapy
 Remove the precipitating agents
 Supportive measures should be given such as - Intravenous fluid, blood
transfusion to correct severe anaemia

Preventive measure
 Known oxidants should be used with caution in male patients in geographic
areas having high prevalence rate of G6PD deficiency.
 Known oxidants should be used only after screening for G6PD deficiency.
IMMUNE THROMBOCYTOPENIC PURPURA (ITP)
Types of ITP
Acute ITP
 It is characterized by petechial haemorrhage, ecchymosis, thrombocytopenia, reduced
platelet survival, presence of platelet antibodies and normal or increased number of
megakaryocytes in the bone narrow. In most cases no cause is identifiable.
Chronic ITP
 Persistent thrombocytopenia for more than six months

Clinical features
 Easily bruised and subcutaneous haemorrhages occur spontaneously or following
minor trauma.
 Skin bleeding - Petechiae, purpura, Ecchymosis.
 Bleeding from the mucosal surfaces - Hematemesis, malena and haemorrhages in the
brain may occur
 Anaemia is proportionate to the degree of bleeding.
 Spleen is palpable in only 10% of cases.

Investigations
 Isolated thrombocytopenia < 100,000/ mm3 in a complete blood count.
 Bleeding time is prolonged
 Platelet antibodies can be demonstrated in 70-90 % of children
 Bone marrow reveals normal or increased number of megakaryocytes.
Megakaryocytes show diminished budding

Treatment
Treatment of Acute ITP
 No specific therapy in children with platelet counts above 40,000/mm3
 The disease is usually self-limiting in nature (skin bleeding only, no mucosal
bleeding.)
 Supportive
- To avoid aspirin and related drugs
- Intramuscular injections should be avoided during the acute phase.
- Platelet count < 20,000/mm3 should be admitted as they have a higher
risk of serious bleeding.
- Fresh blood/ platelet transfusions may be given in life threatening situation or
prior to surgery, if there is severe thrombocytopenia
  Corticosteroids
Immediate steroid therapy is indicated when there is widespread bleeding
manifestation, with a low platelet count -below 25,000/mm3. They inhibit platelet
antibody production, interaction between platelet and antibodies, prolong platelet
survival, and improve vascular stability.
 Prednisolone - 1-2 mg/kg/day for 2-3 weeks, followed by tapering the doses
over the next 1-2 weeks, regardless of the response.
 Intravenous immunoglobulin (IV- Ig G)
It increases the platelet count by blocking the Fc receptor and protects the platelets
from antibodies.
A total dose of 2g/kg is given, using either one of the two protocols.
(1) 0.4g/ kg daily for 5 days
(2) 1 g/ kg of I V-Ig G for 2 consecutive days.
It can be used effectively to control the acute bleeding episodes, or to increase the
platelet count prior to surgery. Platelet count rises within 48 hours of infusion.
 Intravenous anti- D therapy
- for life threatening haemorrhage
- Useful only in D positive individuals
 Splenectomy
Indications:
- Patients having chronic ITP
- Uncontrolled bleeding or
- Those not responding to steroids or IV IgG therapy.
 Splenectomy should be undertaken after 6 years of age.
 Prophylactic penicillin is given to prevent gram positive infections
 All children should receive meningococcal, H. influenzae and pneumococcal
vaccine 3 weeks prior to splenectomy.
 Intracranial Haemorrhage (ICH)
- ICH is more common where platelets are below 20,000/mm3.
- To decrease the mortality, the platelet count should be increased rapidly either
by IV IgG, Methylprednisolone or platelet transfusion
- Splenectomy - if above measures fail.

Treatment of Chronic ITP

Goal of therapy is to decrease the risk of serious haemorrhage, rather than to achieve
normal platelet count.
- Corticosteroid: In acute ITP initiate therapy with corticosteroid and
subsequently
small doses are given either daily or preferably on alternate days for 4-6
months.
 - Immunoglobulins, IV anti- D, Rituximab (anti CD20 monoclonal antibody)
- Immunosuppressives - cyclophosphamide, azathioprine, cyclosporin
- Splenectomy

HYPOPLASTIC ANAEMIA
Definition
It is a condition resulting from marked reduction in precursor cells. Disturbance in these
precursor cells lead to aplasia of single line of cells in the marrow, or all cell lines.

Severe hypoplastic anaemia

 granulocyte count less than 500/ cu mm
 platelet count less than 20,000/cumm
 reticulocyte count less than 1%
 bone marrow is left with < 25% of haematopoietic cells

Very severe hypoplastic anemia – granulocyte count < 200

Causes
1. Idiopathic
2. Secondary
 Drugs-
- chloramphenicol
- dipyrones
- sulphonamides
- quinacrine
- phenytoin
- carbamazepine Chemicals- DDT
- Benzene
- Aromatic hydrocarbon
- Heavy metals
- Gold
- Arsenicals
- Exposure to ionizing radiation
 Infections - parvo virus, Hepatitis viruses, EB virus
 Paroxysmal nocturnal haemoglobinuria (25% of the cases associated with
aplastic anaemia)

Clinical features
 Anaemia
- progressive and persistent anaemia
- insidious onset of anaemia associated with progressive weakness and fatigue
 Bleeding
- Cutaneous bleeding - Petechiae, purpura, and ecchymoses are common
- Mucosal bleeding - Bleeding from gut or haematuria
 - Haemorrhage into tissues and viscera are less common
- Life threatening bleeding episodes are not uncommon
- Intracranial bleeding - headache, irritability, excessive drowsiness and
neurological deficit
 Infection
- Common as a result of leucopenia and neutropenia
- Recurrent respiratory infection and gastrointestinal tract infection which
may be fatal
Investigations
 Bleeding time-prolonged
 Clotting time-normal
 Complete blood picture (CBP) - pancytopenia
 Recticulocyte count- low
 Bone marrow aspiration and biopsy - may be dry
tap
 Hypocellular and cell trail are replaced by fat
 Ham test – to exclude PNH

Management
General
 Replacement therapy
- Correct anaemia - maintain Hb 7-8 gm/dl
- Platelet for bleeding episodes
- One unit of platelet increases platelet count by 10,000/10 kg Body weight
 Prevent / treat infection
- If patient is febrile, empirical antibiotic treatment i.e. combination of ampicillin,
aminoglycosides and metronidazole.
- Antifungal is considered in patients receiving several courses of antibiotics and
not responding to these in 10 days.
Specific
 Remove aetiological cause for secondary anaemia
 Androgens / anabolic steroids (Danazol) Daily dose of 2mg/kg/day Often need 3-5
months
 Steroids are not useful if given alone.
- Methyl prednisolone 10-20mg/kg/day for 10-15 days can induce remission
 Immunotherapy
- ATG (antithymocyte globulin), ALG (antilymphocyte globulin) and Cyclosporine
- Modify the T cell suppression and restore bone marrow stem cell function.
- Can be used either alone or in combination with methyl prednisolone.
- Haemopoietic growth factors (e.g. GMCSF) may be useful.
 Bone marrow transplant
- Need HLA matched donor
- 60-80% survival rate

Prognosis - depends on severity

Differential Diagnosis of purpura
I. Decreased production
1. Primary bone marrow disorder
 Acquired aplastic anaemia
 Fanconi anaemia
 Leukemia
 Myelodysplasia
 Congenital intrauterine rubella infection
2. Bone marrow invasion
 Metastatic cancer
 Myelofibrosis
 Infectious diseases (e.g. tuberculosis)
3. Bone marrow injury
 Drugs
 Chemical
 Radiation
 Infection
4. Nutritional disorders
 Vitamin B12 deficiency
 Folate deficiency
 Copper deficiency
5. Hereditary thrombocytopenic syndrome
 Hypomegakaryocytic thrombocytopenia
 Ineffective platelet production

II. Increased destruction

 Immune mediated thrombocytopenia
- Auto immune thrombocytopenia- ITP, SLE
- Alloimmune thrombocytopenia
 Post transfusion purpura
 Neonatal isoimmune thrombocytopenia
 Drug induced immune thrombocytopenia
 Heparin induced immune thrombocytopenia
 Disseminated intravascular coagulation (DIC)

III. Abnormal distribution of platelet

 Splenomegaly
 Hypersplenism
IV. Dilutional loss
 Massive transfusion of stored blood to bleeding patient

HAEMOPHILLIA
Types
1. Haemophilia A (factor VIII deficiency)
 2. Haemophilia B (factor IX deficiency)

The haemostatic mechanism

Inheritance pattern and the family tree

Sex linked recessive (see genetic section)

Family history - May present with history of similar disease in a male patient on the maternal
side.
Clinical features
Mild to moderate haemophilia
 Asymptomatic
 Prolonged bleeding following tooth extraction, severe trauma or
following surgery
Severe haemophilia
 Prolonged bleeding
 Muscle haematoma
 Bleeding in joints (haemarthrosis)
 Severe mucosal bleeding, usually occurring following trauma or tooth extraction
 Spontaneous bleeding episodes
 Excessive bleeding from umbilical cord in the newborn period
 Repeated episodes of haemarthrosis in weight bearing joints more in the knees,
ankles.
 Recurrent haemarthrosis leads to chronic arthropathy and there is higher risk for
bleeding in the joints.
 Retroperitoneal bleeding presents with severe abdominal pain, anaemia and shock
  Haematuria
 GI bleeding
 Intracranial bleed - cause of death

Haemarthrosi
s

Investigations
 Normal bleeding time
 Prolong clotting time,
 Normal PT
 Prolong APTT
 Factor VIII/IX assay
 Platelet count is normal or elevated
Treatment
Principles of management
 Control and prevention of bleeding episodes
 Treatment of complications and carry out rehabilitation measures
 Educate parents and children for early detection
 Benefits of prophylaxis, rehabilitation and prolonged management.
 Comprehensive care by a team including Paediatrician, Haematologist, Orthopaedic
Surgeon, Physiotherapist and Dentist etc.

Replacement therapy
 Fresh blood (<8hours old)
 Fresh plasma
 Fresh frozen plasma (contains factor VIII and IX) should be given in 3 0 min.
o Each unit contains nearly 200 units of factor VIII and XI
 Cryoprecipitate (factor VIII, von Willebrand factor and fibrinogen) should be given in
30 min.
o One unit contains nearly 100 units of factor VIII
o Half life of factor VIII - 8 hours
o Half life of factor IX -18-20 hours
 Factor VIII concentrate (pooled, increased risk of infection)
Drug therapy
 DDAVP for mild case, increase factor VIII by releasing it from body store
Epsilon-aminocaproic acid (EACA) and Tranexamic acid (inhibitor of fibrinolytic
enzyme) promote the haemostasis in oral bleeds but is contraindicated in haematuria as it
may precipitate renal failure.

Treatment of haemarthrosis
  General (R.I.C.E)
R. Rest
I. Ice compression
C. Compression (gentle) (bandaging)
E. Elevation of dependent joint to a comfortable position
Never aspirate the haemarthrosis.
 Analgesics
 Physiotherapy as soon as pain is relieved.

Surgical procedures
 Major surgery - raised up to 100% of factor VIII units and maintain at 30-50% up to 2
weeks
 Minor surgery or tooth extraction - raised up to 5 0% of factor VIII units
ACUTE LYMPHOBLASTIC LEUKEMIA
Definition
The leukaemias are a group of disorders characterized by the accumulation of malignant white cells in the bone
marrow and blood. These abnormal cells cause symptoms because of: (a) bone marrow failure, and (b) infiltration
of organs. (AV Hoffbrand)

AETIOLOGICAL FACTORS OF CANCER

 Infectious aetiology: oncogenic viruses – EBV, HIV, HTLV1
 Radiation – accidental, therapeutic
 Genetic factors – Chromosomal anomalies
 Immunodeficiency – congenital or acquired
 Drugs – antineoplastic drugs, hormones
 Chemicals – Hydrocarbons
 Others

Classification of Leukaemia
Acute
 Acute Lymphoblastic Leukaemia (ALL)
 Acute Myeloid Leukaemia (AML)
Chronic
 Chronic Myeloid Leukaemia (CML)
 Chronic Lymphocytic Leukaemia (CLL)

Types of Leukaemia seen in Children

 Acute Lymphoblastic Leukaemia (L1 – L3)
 Acute Myeloid Leukaemia (M0 – M7)
 Chronic Myeloid Leukaemia

Acute Lymphoblastic Leukaemia

It is the most common type of leukaemia in childhood as well as the most common childhood
malignancy. It has the best prognosis with current treatment modalities
Common clinical features
 Bleeding manifestations
 Anaemia
 Infection (fever, PUO)
 Lymphadenopathy
 Hepatosplenomegaly
 Bone and Joint pains
 CNS manifestations
 Others – testes, eyesLaboratory Investigations
Blood for Complete Picture
 Anaemia
 Thrombocytopenia
 High white cell count (in most cases)
 Presence of atypical cells and blast cells
Bone Marrow Aspiration
 Diagnostic, if blast cells are > 25 % (30%)
Cytochemistry
 PAS positive
 Sudan Black and Non-specific esterase negative
Immunophenotyping
 T or B lineage
 useful for risk stratification
Cytogenetics
 To detect abnormalities in chromosome number and structure e.g. TEL-AML1 and
Hyperdiploidy - good prognosis, t (4:11) – bad prognosis
Biochemistry
 urea and electrolytes
 uric acid
 renal and liver function tests as required
 calcium and phosphate
 LDH
 Others
Infection screen
 ESR
 CRP
 Cultures (blood, urine, stool, CSF)
 Swabs (ENT, any septic lesion)
Serological tests
 HIV
 Hepatitis B and C
 EBV
 CMV status

Imaging Procedures
 Chest X-Ray
 Ultrasound Abdomen
 Other imaging studies such as special X-Rays, Contrast studies, CT, MRI, Isotope scan
etc. should be done as indicated

Others Tests
 e.g., ECG and ECHO should be done if cardiotoxic drugs (like adriamycin) are included
in cytotoxic therapy.

Types of ALL (FAB classification)

 L 1 – monomorphic, small blast cells with high nuclear-cytoplasmic ratio
 L 2 – pleomorphic, larger blast cells, lower nuclear-cytoplasmic ratio
 L 3 – also known as Burkitt’s type ( basophillic cytoplasm with vacuolations)
 L1 L2 L3

Types of ALL (Immunophenotyping)

 Precursor B – ALL
 T- ALL
 B – ALL
* Common –ALL is a sub type of Precursor B – ALL, CD 10 (+)

Management
 Chemotherapy – mainstay of treatment
 Radiotherapy – in high risk and CNS leukaemia
 Surgery – Only for Diagnosis (Biopsies) and treatment of some complications
 Others – Bone Marrow Transplant and Immunotherapy

Emergency treatment
 Bleeding
 Febrile neutropenia
 Tumour lysis syndrome
 Mediastinal obstruction
 Others

Supportive treatment
 Replacement of blood and blood products
 Prevention and control of infection
 Nursing Care
 Fluid and electrolytes
 Food and nutrition
 Symptom control – pain, vomiting, insomnia, anorexia, etc
 Play and occupational therapy
 Vascular access
 Counselling and support
 Management of terminally ill child
 Others

Specific Treatment
Chemotherapy
 Induction of remission
 To induce remission (absence of any clinical or conventional laboratory evidence of
the disease) by using a combination of anticancer drugs +/- Radiotherapy
 Consolidation
To eliminate or reduce hidden leukaemic cell population with intensive chemotherapy
 Maintenance
To reduce the risk of relapse
* CNS directed therapy is included in each phase

Management of Complications
 Complications of leukaemia - sepsis, bleeding, others
 Complications of therapy - adverse effects of steroids, specific anticancer drugs
Types of Relapse
 Bone marrow relapse
 CNS relapse
 Testicular relapse

Poor Prognostic Factors

 Age - <1 year and > 10 years
 Gender – Male (some recent studies do not support this)
 Race – Black (recent studies do not support this)
 White cell count at diagnosis - >50,000/cumm
 FAB classification – L3
 CNS disease at diagnosis
 Immunophenotyping – B cells
 Cytogenetics – Hypodiploidy, BCR-ABL
 Bulky organomegaly and mediastinum mass
 Response to therapy

MALIGNANT LYMPHOMA
1. Hodgkin’s Disease
2. Non Hodgkin Lymphoma

Non Hodgkin Lymphoma

Definition
Non-Hodgkin lymphoma (NHL) is a malignant proliferation of cells of lymphocytic or
histiocytic lineage that spread in a pattern similar to the migration of normal lymphoid cells.

Clinical features
 Can arise in any lymphoid tissue
 Very rapidly progressive
Earlier symptoms
  Cough
 sore throat
 abdominal pain
 Vomiting and
 lymphadenopathy
 Fever and weight loss

Common presenting symptoms

 Mainly involving cervical and supraclavicular areas
 Neck and thoracic
- Anterior mediastinal widening
- Pleural effusion
- Respiratory embarrassment
- Superior vena cava obstruction
 Abdomen
- 30-40% of patients
- Ileum, caecum and appendix
- May present with intussusception or lower quadrant mass, Malignant
ascites and tumour lysis in rapidly progressive tumour

Lymphoblastic lymphoma
 Bone marrow is diffusely involved
 Similar to ALL.

Complications
 Tumor lysis syndrome-Combination of hyperuricemia, hyperkalemia, and
hyperphosphatemia with hypocalcemia, resulting in uric acid nephropathy that leads to
renal failure
 Gastrointestinal obstruction, perforation, bleeding, intussuception
 Inferior vena cava obstruction and venous thromboembolism
 Neurologic (e.g., paraplegia, increased intracranial pressure)
 Superior vena cava (SVC) and superior mediastinum syndrome (SMS)
 Massive pleural effusion
 Cardiac tamponade or arrhythmia

Staging of the disease

 Stage I – Confined to one lymph area
 Stage II – Confined to one side of the diaphragm
 Stage III – Confined to both sides of the diaphragm
 Stage IV – Bone marrow, liver and extra nodal sites

Investigations
 Complete blood picture
 Bleeding time & Clotting time
  Lymph node / Tissue biopsy
 Chest X-Ray
 Bone marrow biopsy
 CSF examination
 Infection screening
 Urea, Electrolytes
 Imaging-USG
 Computed Tomography

Management
Emergency Care
Treatment
A multidisciplinary approach is imperative to ensure the best therapy.
 Radiotherapy
Radiation adds no therapeutic benefit in children with limited disease. It increases both
short- and long-term toxicity. It can be used as emergent treatment for superior vena
caval obstruction, CNS, or testicular involvement.
 Surgery
- Performed if total resection can be achieved
- Additional indications include intussusception, intestinal perforation, suspected
appendicitis, or serious GI bleeding
 Pre-chemo management
- Allopurinol, hydration, and urinary alkalinization to prevent tumor lysis syndrome.
Monitor uric acid, BUN, creatinine, K+, Ca++, and PO4-.
 Chemotherapy
- Choice of a particular protocol is determined by histology and stage
- Drugs used: cyclophosphamide, vincristine, methotrexate (IV+IT), prednisolone,
daunorubicin, asparaginase, cytarabine, thioguanine, carmustine, hydroxyurea,
hydrocortisone, doxorubicin, mercaptopurine, etoposide
- Duration: 6 to 18 months
 Management of Relapse
- It indicates extremely poor prognosis.
- No uniform approach to rescue therapy
- Induce second remission with different/previously unused chemotherapy regimen
- Allogeneic or autologous bone marrow transplant should be considered.

Prognosis
 Important prognostic factors for outcome include tumor burden at presentation and
treatment administered.
 Disease free survival for 2 years
- Nearly 90% in limited stage disease
- 70% in stage III and IV diseases.
 CENTRAL NERVOUS SYSTEM

FEBRILE CONVULSIONS

This is a common group of childhood seizure and about 3-5% of children can have febrile
convulsion. However, if a child, especially under 1 ½ year, presents with first episode of fever
with fits, febrile convulsion should be considered only after exclusion of other important and
treatable causes like meningitis, cerebral malaria, encephalitis.

Following are typical features of simple febrile convulsion:

 Age between 6 months and 5 years (peak - 1-2 years)
 Sex – Boys affect more than girls
 Occurs within 24 hours of onset of fever, especially with the rising phase of a fever
 Generalized tonic or clonic or tonic clonic fits, no focal features
 Occurs with temperature 39˚C and more
 Less then 15 minutes duration.
 No residual neurological deficit like drowsiness or paresis after fits.
 Positive family history of febrile convulsion

Management of febrile convulsion

1. First aid measures for seizure
 Semi prone position
 Check Airway, Breathing and Circulation.
 Adequate airway and suction, O2
 Clothing must be loosened. Excess clothing removed.
 Don’t put anything into mouth
 To control fits if more than 4 minutes - PR Diazepam – 0.3 – 0.5 mg/kg
- Inj. IM Phenobarbitone - 10-20 mg/kg

2. Control fever
 Take off clothing and give tepid sponging.
 Antipyretic e.g. oral or rectal Paracetamol 15 mg/kg 4-6 hourly.

3. Not all children need to be admitted. The main reasons for admission are: -
 To exclude intracranial pathology especially infection
 Fear of recurrent fits
 To investigate and treat the cause of fever
 To allay parental anxiety, especially if they are staying far from the hospital.

4. Exclusion of other intracranial causes of fits

 Meningitis – signs of meningism, tense or bulging anterior fontanelle, prolonged or
frequent fits (check Full blood count, Lumber puncture)
 Encephalitis – change in sensorium, neurological signs may be present
  Cerebral malaria – came from or traveled to malaria endemic area, change in sensorium,
(check Malaria parasites)
Lumbar puncture should be considered in following conditions:
 Any signs suspicious of meningitis
 < 12 months old with first febrile seizure

5. Parents should be counseled on the benign nature of this condition.

6. Parents should also be advised on first aid measures during a convulsion:
7. Prophylaxis
Long term prophylaxis with daily anticonvulsants is not routinely used even if episodes are
frequent. However intermittent prophylaxis (like oral diazepam at the start of temperature and
every 8 hours for 24 hours only) can be considered for such children with frequent episodes.

COMA
Causes of coma in Children
1. Infection
 meningitis
 encephalitis
 cerebral malaria
 brain abscess
2. Vascular
 stroke - haemorrhage or large infarct
 hypertensive encephalopathy
3. Metabolic
 hypoglycaemia
 hyperglycaemia
 hypo/hypernatraemia
 liver failure
 renal failure
 adrenal failure
4. Toxic
 lead poisoning
 accidental ingestion of opiates
 anticonvulsants
5. Head injury
6. Increased ICP
 hydrocephalus
 space occupying lesion
7. Epilepsy - post ictal stage
Differential diagnosis of common causes of coma
Pyogenic Meningitis
 Preceding history of ear discharge, head injury, sinusitis may be present.
 Signs/Symptoms - Acute onset, fever, neurological Signs/Symptoms (irritability,
restlessness, vomiting, headache, photophobia, drowsiness, convulsions, coma),
bulging and tense fontanelle.
 Signs of meningeal irritation – Neck stiffness, Kernig’s sign, Brudzinski’s sign
 In meningococcal meningitis, petaechiae, and/or purpura, or maculopapular rashes
with signs of shock may be present.
 LP reveals turbid CSF with neutrophil leucocytes

TB Meningitis – See TB section

Encephalitis
 Signs/Symptoms- Headache–frontal or generalized, signs of increased ICP, signs of
meningism usually absent, rash may be present
 Lumbar Puncture – reveals increased pressure, moderate increase in cell count
 EEG – usually abnormal
 Viral serology – Japanese B encephalitis, Dengue
Cerebral malaria
 Acute onset of fever with history of travel to/ living in malaria endemic area within
one month.
 Hepatosplenomegaly may be present
 Blood MP may be (+), ICT for malaria, CSF – no leucocytosis
Brain abscess
 Fever, severe headache
 Focal fit or focal neurological signs
 Source of infection or predisposing factor such as TOF may be present
 CP shows neutrophil leucocytosis
 CT scan head confirms the diagnosis
Hypertensive encephalopathy
 History of sudden onset of neurological signs with increasing severity of headache
associated with scanty micturation and haematuria
 Puffy face, High BP
 Urine analysis shows-WBC, RBCs, RBC casts, granular casts and high blood urea
Lead encephalopathy
 History of lead contact (e.g. battery workshop), Unexplained anaemia may be
present.
 Behavioral changes, mental retardation may be present.
 X-ray long bones will show dense lead line, Blood lead level will be raised.
PYOGENIC MENINGITIS
Common causal organisms according to age
Neonatal period
Gram (-)ve
 Escherichia coli
 Pseudomonas
 Proteus
Gram (+)ve
 Group B Streptococcus
 Staphylococcal aureus
 Listeria monocytogenes
Infant & childhood
Gram (-)ve
 Haemophilus influenzae
 Neisseria meningitidis
Gram (+)ve
 Streptococcal pneumoniae
 Staphylococcal aureus
Clinical features
Newborn – 2 months
Signs and symptoms are not typical as in older children. Poor sucking, poor tone, staring
eyes, poor cry, irritability, drowsiness, and convulsions. There may be history of prematurity,
LBW, complicated labour, Prolonged Rupture of Membrane, maternal sepsis.
Older children
 Preceding history of ear discharge, head injury, sinusitis may be present.
 Signs/Symptoms – Acute onset fever, irritability, restlessness, vomiting, headache,
photophobia, drowsiness, convulsions, coma, bulging and tense fontanelle.
 Signs of meningeal irritation – Neck stiffness, Kernig’s sign, Brudzinski’s Sign
 In meningococcal meningitis- petaechiae, and/or purpura, or maculopapular rashes with
signs of shock may be present.

Investigations
For confirmation of diagnosis
CSF examination, including Gram stain and culture
 RE - Raised CSF pressure, Appearance – turbid or opalescent
- Raised protein (normal – 20 to 40mg %)
- Increased cell count, may be numerous, mainly neutrophils
- (Normal – 0 to 5 lymphocytes)
- Reduced sugar (normal – two thirds of blood sugar)
 Gram Stain (results within hours)
- Gram (+) cocci, Gram (-) cocci, Gram (-) coccobacilli or bacilli
 Culture and Sensitivity – Organisms identified (3 to 7 days to get the results)
 Antigen – Latex agglutination test
 Blood culture – may identify organisms
  Blood CP – Neutrophil leucocytosis
 Latex agglutination test of blood for antigen
For detection of complications
 CXR to detect aspiration and hypostatic pneumonia
 Ultrasound head and CT head for hydrocephalus, subdural effusion and brain abscess
 U&E for SIADH
Treatment
Antibiotics
 IV Crystalline Penicillin (0.5 -1 L/kg/ 6/H) & Chloramphenicol (25 mg/kg/dose, 6/H) for
10 - 14 days or
 3rd generation Cephalosporin for 10 – 14 days
 For neonatal meningitis – see Neonatal infection
Fluid
 Fluid restriction (2/3 of maintenance) if features of SIADH present
 Fluid replacement if shock is present in cases of meningococcal meningitis.
Steroid
 Dexamethazone (0.15 mg/kg/dose 6/H) for first 4 days
Monitoring with Neuro Observation Chart
Supportive treatment
 Care of unconscious patient - Nursing, bladder, bowel, skin care
Treatment of complications
 Cerebral oedema – IV mannitol 20% 7 to 10 ml/kg within 20 mins, can be repeated 8
hourly
 Seizure – anticonvulsants
 Apnoea – mechanical ventilation
Rehabilitation and Follow Up - including physiotherapy, occupation therapy, developmental
monitoring

Preventions
 Rifampicin 20 mg/kg OD for 4 days in H. influenzae and 10 mg/kg bd for 2 days in
meningococcal infection.
 Alternative – Ciprofloxacin (for adult contacts)
 Vaccination – Hib, meningococcal vaccine, pneumococcal vaccine.
 Adequate treatment of pyogenic infection elsewhere in the body.

Complications
Immediate
 Seizures
 Cerebral or cerebellar herniation
 Increase ICP
 Cranial nerve palsies
 Thrombosis of subdural sinuses
 Subdural effusion, ventriculitis, brain abscess
 SIADH
 Waterhouse-Friderichsen syndrome
Remote
 Neurological deficit – e.g. hemiplegia, aphasia, ocular palsies, deafness,
blindness, cerebral palsy
 Mental retardation
 Hydrocephalus
 Diabetes insipidus
 Epilepsy
CEREBRAL PALSY
Definition
Disorder of movement and posture, resulting from permanent non-progressive defect or
lesion of the immature brain

Causes of cerebral palsy

Antenatal
 Congenital malformation of the brain
 Intrauterine TORCH infection
 Radiation, trauma,
 Drugs (eg. Antiepileptic)
 APH, causing foetal anoxia,
 Hypertensive disease of pregnancy

Perinatal
 Prematurity, low birth weight
 Birth asphyxia
 Birth injuries

Postnatal
 Kernicterus
 Hypoglycaemia
 Meningitis
 Encephalitis
 Head injury
 Lead encephalopathy

Classification
Anatomical
Monoplegia, Paraplegia, Hemiplegia, Triplegia, Quadriplegia, Diplegia (4 limbs
affected, Lower Limbs>Upper Limbs), Double hemiplegia (4 limbs affected, Upper
Limb affected > Lower Limb)
Functional
Spastic, Dyskinetic (athetosis, chorea, rigidity, dystonia), Ataxic, hypotonic,
Mixed
Severity
Class I – No limitation of activity
Class II – Slight to moderate limitation
Class III – Moderate to great limitation
Class IV – No useful physical activity
Diagnosis
Mainly on clinical features
Risk factors - During antenatal, perinatal and postnatal periods
Usually presents with –
 Abnormal tone and posture in early infancy
 Delayed motor mile stones
 Abnormal gait, once walking is achieved
 Feeding difficulties with oromotor incoordination, slow feeding, gagging and
vomiting
 Developmental delay in language and social skills
 Persistence of primitive reflexes (eg. Moro’s Reflex, Stepping Reflex)
 Hand preference in those less than 12 months old in hemiplegic CP

Clinical examination
Particular attention is given to assessment of pattern of tone, posture, and observation of gait.
Spastic Type
 Due to damage to pyramidal tract,
 There will be increased tone (clasp knife)
 Increased deep tendon reflexes (DTR)
 Extensor plantar response
 Ankle clonus on affected limb.
Spastic Hemiplegia
- Unilateral involvement of arm and leg., arm affected more than leg.
- Fisting of the affected hand (usually present at the age of 4-12 months)
- A pronated flexed forearm and tiptoe walk on affected side.
- Intelligence is usually good
- Likelihood of epilepsy is minimal.
Spastic Quadriplegia
- Involves head, neck and 4 limbs
- High association with mental retardation and seizures, speech and visual problems
- Swallowing difficulties are common (pseudobulbar palsy)

Dyskinetic type
 Due to damage to extrapyamidal tract, there is fluctuating muscle tone and involuntary
movements (athetoid – slow writhing , chorea – sudden jerky)
 Hypotonia and delayed motor development in infancy
 Abnormal movements usually not evident before 1 year of age
 Intelligence is relatively unimpaired
 Seizures uncommon
 Speech problem due to oropharyngeal muscle involvement.

Ataxic type
 Due to cerebellar lesion, cerebellar signs may be present
Hypotonic type
 Early manifestation of choreo-athetoid or ataxic type

Association or complication
Neurological
Mental retardation, epilepsy, visual and hearing impairment, sleep problem
GI
Feeding intolerance, choking, gasteroesophageal reflux, constipation
Respiratory
Frequent chest infection, aspiration pneumonia
Musculoskeletal
Deformity, contracture
Social
Family burden

Treatment
Aim
 For child to be able to lead as near normal life as possible
 For independent life as much as possible
Management
 Multidisciplinary approach
 Identify associations or complications - mentioned above
 Manage accordingly
 Physiotherapy – mainstay of treatment for better function and prevention of contracture
 Occupational therapy for daily functioning and hand skills
 Speech therapy
 Orthopaedic treatment for contractures
 Medication for epilepsy, abnormal movement,
 Treatment of spasticity – diazepam, baclofen (oral, intrathecal), botulinum toxin
injection, Dorsal rhizotomy
 ENT referral for hearing and language problems
 Ophthalmologist referral for eye problem
 Psychological and intellectual assessment
 Schooling – depends on intelligence and degree of physical handicap
 Counseling
- Explain the diagnosis and prognosis
- Importance of physiotherapy treatment
- To avoid overprotection or rejection
HYDROCEPHALUS
Definition
Increase in size of the CSF spaces, associated with increase in intracranial pressure
secondary to pathophysiological processes.
Hydrocephalus is not a specific disease; rather, it represents a diverse group of
conditions that result from impaired circulation and absorption of CSF or, in rare circumstances,
from increased production by a choroids plexus papilloma. Ventricles are dilated.

Common causes
Congenital causes
 Intrauterine infection (TORCH)
 Congenital malformation
 Aqeductal stenosis
 Arnold Chiari malformation (Downward displacement of portion of cerebellum and
brain stem)
 Dandy Walker syndrome (Dilatation of 4th ventricle due to absence or deficiency of
cerebellar vermis and 4th ventricle outlet)
 Intracranial bleeds
Acquired causes
 Meningitis (TBM, Pyogenic)
 Intraventricular haemorrhage
 Trauma
 Tumour (Posterior fossa)

Diagnosis
Clinical features
Symptoms
- Headache, irritability, vomiting, nausea, anorexia, drowsiness or lethargy
Signs
- Inappropriately increasing OFC
- Tense anterior fontanelle
- Widened suture
- Distended scalp veins
- Setting-sun eyes (loss of upward gaze)
- Cracked pot sign
- Neck retraction or rigidity
- Signs of raised ICP - bradycardia, hypertension, papilloedema, and optic atrophy
can be present.
- Transillumination test - positive
Investigations
 USG head – Ventricular dilatation
 CT scan – Ventricular dilatation, identification of some causes
 Skull X-ray - Separation of sutures, erosion of the posterior clinoids, increase in
convolutional markings (beaten-silver appearance)
Differential diagnosis of large head
 Familial
 Achondroplasia, thalassaemia
 Rickets
 Hydrencephaly
 Megalencephaly
 Subdural effusion
 Hydrocephalus

Management
 Serial measurement of OFC
 Gradual slowing in progress of head size and becomes arrested - No treatment
 If head size is progressing at fast rate - Ventriculoperitoneal shunt
 Acetazolamide can be used in mild slowly progressive hydrocephalus
 CONGENITAL HYPOTHYROIDISM

Causes
Dysgenesis – aplasia, hypoplasia, ectopic thyroid
Maternal medication – antithyroid drugs

Clinical features
 Lethargic, less active, sleepy all the time, cries only occasionally, coarse cry
 Hypothermia, bradycardia, oedema
 Open posterior fontanel more than 1cm, wide open cranial sutures(earliest)
 Coarse facial features; puffy swollen eyelids, open mouth with tongue protrusion
(macroglossia)
 Feeding difficulties-choking spells, poor feeding
 Constipation
 Skin is dry, mottled and cool
 Large abdomen, and umbilical hernia
 Growth retardation (short stature, upper segment: lower segment ratio is infantile)
 Delayed skeletal maturation
 Delayed dental development
 Delayed puberty
 Poor school performance

The radiological changes of bones in congenital hypothyroidism

 Delayed bone age
 Epiphyseal dysgenesis

Laboratory investigations
 Reduced serum T3 and T4 and increased TSH

Treatment of congenital hypothyroidism

 Replacement therapy with thyroid hormone as early as possible and continue for life.
Synthetic sodium levothyroxine is mandatory to prevent mental retardation
 Start with small dose and increase every two weeks until subtoxic level is reached

Preventive measure
 Neonatal screening of at risk babies for hypothyroidism from the cord blood.
 Iodization of salt (IDD) program.
Fig. Coarse facial features and protruding tongue in congenital hypothyroid
 DERMATOLOGY

ECZEMA
Introduction
 Ectopic eczema has a genetic component and a dietary component (e.g. milk, eggs).
(If both parents were affected, there is a 60% risk that child will be)
 Exacerbating factors
- Contact with woolen clothing
- Humidify and excessive drying of the skin.
 Affects 3% children under 5 years old.
 Most common from 3 months to 2 years.
 Up to 80% of these children have positive family history of atopic conditions

Clinical features
 Affected areas - Scalp, face and trunk
Extensor surfaces of the limbs
Dorsal areas of hands and feet
 Skin changes - Erythema, vesicles, lichenification or crusting
Inflammation and intense itching of skin
 Painless lymphadenopathy
 Secondary infection can occur in broken skin

Investigations
 IgE-Increased in 80% of cases
 CP-Eosinophilia

Treatment
It is usually self-limiting with 50%and 90% of patients symptoms free at 13 and 18 years
respectively.
 Preventing of itching and scratching
Keep nails short and clean
Mittens
Night time sedation
 Emollients to keep the skin moist
 Avoidance of irritants such as soap
 Topical ointments/ creams containing steroids if inflammation is severe
 Antibiotics for secondary infection
 Avoidance of trigger factor
 Fig. Infantile eczema

ERYTHEMA MULTIFORME
 Uncommon condition in childhood
 Symmetrical target lesions (pale centre and red surrounding) most commonly on the
hands and feet and extensor surfaces of the limbs.
 They are non-pruritus.
 Follows Herpes simplex infection, mycoplasma pneumonia,Sulphonamide ingestion
 Characterized by formation of circular target lesion on limbs, with a red periphery and
blue (often bullous) centre Stoma and genital involvement are common.
 If widespread and extensive at 2 or more mucosal sites— Stevens Johnson Syndrome
 Rashes fade within 10 days but may recur
Treatment
 Care of eye and conjuntiva
 Steroids for Erythema multiforme major
 Acyclovir for Herpes

Steven-Johnson Syndrome- Antibiotics to prevent secondary infection, careful fluid &

electrolyte balance

Fig Stevens-Johnson syndrome

NAPPY DERMATITIS

 It is commonly caused by inadequate frequency of nappy changing. This causes bacterial

conversion of urine to ammonia which is an alkaline irritant leading to erythema and
ulceration.
 Combination elements of moisture , candidiasis and dermatitis (either sebarrhoeic or
primary irritants from urine and faeces)
Treatment
 Frequent changing
 Combination cream of 1% hydrocortisone and antimonilial agent
 Silicone or zinc barrier cream to protect the skin against moisture

Fig. Nappy dermatitis

Response – quick but recurrence is common

SCABIES
Causal organism - Sarcoptes scabiei
Mode of transmission-can be spread buy close direct contact
Clinical features
 Areas usually involved areas-wrist, back of elbows, axillary folds, nipple area, buttocks,
genital areas, legs and feet and between the fingers.
 Vesicle lesions associated with papules when scratched.
 Itchiness especially at night
 Burrow (black wavy line especially at interdigital spaces)-is diagnostic.
 Usually other members of family are also affected.
 Mite burrows in the skin depositing the eggs in the stratum corneum of the skin and
cause inflammation.

Investigation
 Skin scraping –demonstration of parasites
Treatment
Specific
 A single application of 1% lindane lotion below the face, to be left on for 12 hours.
 Gamma benzene hydrochloride.25% benzoate application.
 Oral-Ivermactin(single dose)
 Permethrin –topical application

Supportive
 Treat all the members of the family simultaneously.
 Bed linen and under wear should be changed and washed after treatment.
 Menthol calamine cream or 10% crotamitone to prevent pruritus.

Fig. Scabies
Prevention
 Personal hygiene
 Health education to the family and public regarding the spread of the disease.
 ACCIDENTS ANG POISONING

DROWNING
Definitions
Drowning – used when the victim dies
Near drowning – used when submersion victim survives

The places where drowning occurs:

 Small infants may drown in – bathtubs, home pool and ponds
 Older children - Drowning may occur in swimming pools, lakes or river

Common clinical features

Patient with near drowning can be grouped into three categories
1. Category A – Patients are awake and conscious
2. Category B - Victims are in stupor, have respiratory distress and cyanosis and
hypothermia
3. Category C – Patients are comatose, have central cyanosis and may be in a decorticate,
decerebrate or flaccid state

Treatment
 Immediate resuscitation for basic life support
Category A and B require supportive care
Category C requires advanced life support care
 Diuretics – for pulmonary oedema (IV Frusemide 1-2 mg/kg)
 Sodium bicarbonate – for metabolic acidosis ( IV NaHCO3 1-2 ml/kg)
 Convulsions – Diazepam 0.3-0.5 mg/kg per rectum or a loading dose of Phenobarbitone
15 mg/kg IM can be used
 Hypothermia – Adequate warming

POISONING
General management
1. Emergency stabilization measures
 The unconscious patient should be transported in a head down semi-prone
position
 To establish clear air way and maintain ventilation
 Urgent correction of potentially serious abnormalities such as metabolic acidosis,
hyperkalaemia and hypoglycaemia
 Neurological assessment is made by Glasgow Coma Scale (GCS)
 Convulsions - Control with diazepam
 Correction of hypotension and peripheral circulatory failure
 Regulation of body temperature
2. Identification of poison
 History, supportive evidence and laboratory analysis
 3. Removal of poison
 Eye decontamination – by copious irrigation with neutralizing solution (e.g. water or
normal saline) at least 30 minutes
 Dermal decontamination – removal all decontaminated clothes and irrigate the whole
body with water and saline as soon as possible after exposure
 Gut contamination – Emesis and gastric lavage
4. Administration of antidotes
The appropriate antidotes for 6 common poisoning
1. Milk and egg albumin for acid and corrosive poisoning
2. Vinegar and water for alkali poisoning
3. Naloxone for opiate poisoning
4. Ca EDTA and penicillamine for lead poisoning
5. Desferrioxamine for iron poisoning
6. Atropine and pralidoxime for insecticide poisoning
Poisons Antidotes
 methanol Ethanol
 Mushroom Atropine
 Iodine Sodium thiosulphate
 Atropine Physostigmine
 Digoxin Antidigoxin Fab
5. Promotion of excretion of toxin
 Forced alkaline diuresis - with 1.4% sodium bicarbonate
 Forced acid diuresis – with ammonium chloride 4 gm, give every 2 hours through
Ryle tube
 Haemodialysis – method of choice for removal of methanol and lithium
Haemoperfusion – with coated charcoal or exchange resin
 Peritoneal dialysis – less effective, advantages – no special facilities required
6. Other supportive therapy
 Anaemia – Packed cell transfusion
 Infection – Antibiotics

Brief diagnostic clinical features and management of common childhood poisoning

Bacterial food poisoning
Diagnostic clinical features
 When two or more persons who have ingested a common food develop similar signs of
acute illness characterized by nausea, emesis, diarrhea or neurologic symptoms
Management
Mostly supportive therapy –
 Adequate rehydration by parental fluid
 Antibiotics
- Chloramphenicol for salmonella food poisoning
- No antibiotics for staphylococcal food poisoning
 Preventive measures
- Proper refrigeration of food
- Proper hygienic technique in food preparation
Kerosene poisoning
Diagnostic clinical features
 History of accidental ingestion, history of coughing, chocking or vomiting
 Characteristic smell gives the clue
 Respiratory difficulties, cyanosis, tachycardia and fever
 Features of pneumonia, pulmonary oedema and haemorrhage with cardiac arrythemias
 Hepatopmegaly, proteinuria, haematuria occurs following large overdose
Management
 Mainly symptomatic and supportive
 Induction of emesis or gastric lavage is contraindicated
 Oxygen and physiotherapy and if necessary, positive airway pressure and other
ventilatory assistance
 Observation for at least 24 hours, even in asymptomatic child

Lead poisoning
Diagnostic clinical features
 History of inhalation of lead fumes, history of ingestion of lead paint chips or repetitive
ingestion of inorganic lead compound, from battery shops and domestic use, history of
pica
 May be asymptomatic and detected only on screening
 Older children may manifest as pain in abdomen and resistant anaemia
 Younger children manifest as acute lead encephalopathy

Investigations
 Blood CP – Microcytic hypochromic anaemia with punctuate basophilia
 Lead lines at growing ends of long bones in radiological examination
 Blood lead level – increased (between 50-99 μg/100ml in asymptomatic patients and
>100 μg/100ml in patient with definite lead poisoning)
 Urinary corprophyrin level – Increased (Normal – 100-200 μg/day)
Management
 Remove from exposure
 Specific Antidote – Calcium EDTA
 D- penicillimine
 Treatment of cerebral oedema
 Anticonvulsants for seizures
 Fluid and electrolytes replacement
 Follow up regularly at least until school age to prevent recurrence and to assess the
degree of recidual brain damage

Insecticide (Organophosphate) poisoning

Diagnostic clinical features
 Excessive parasympathetic activities, weakness, blurred vision, headache, giddiness,
nausea and chest pain
  Excessive secretions in the lungs, profuse sweating and marked salivation
 Constricted pupil, papiloedema, muscle twitching convulsion and coma in severe cases
 Reflexes are absent and sphincter control is lost

Management
 If there has been contact with insecticide, skin or eyes, these are thoroughly washed with
normal saline
 Gastric lavage
 IV Atropine sulphate 0.05 mg/kg. May need to repeat dose if unresponsive
 IV Pralidoixime 25 mg/kg given over 30 minutes every 8-12 hours in young children. In
older children, maximum dose (1G/dose) may be given
 Artificial respiration may be necessary to sustain life

Tapioca poisoning
Diagnostic clinical features
 History of eating tapioca (Pa-Law-Pe-Nan)
 Poisoning is due to cyanide that is contained in the root
 Blue lips (Cyanosis), shock, respiratory difficulties and nausea or vomiting
Management
 Severe case should be hospitalized
 Keep airway clear
 Give oxygen if cyanosis is present
 Gastric lavage
 Treat shock by intravenous fluid
 Antidote – IV Sodium nitrite, 10 ml of 3% solution (300 mg) followed by Sodium
Thiosulphate, 50 ml of 25% solution

Paracetamol poisoning
Diagnostic clinical features
 History of ingestion or high index of suspicion
 Anorexia, nausea, vomiting, malaise, pallor, right upper quadrant abdominal pain and
tenderness
 Peak liver function abnormality, resolution of hepatic dysfunction or complete liver
failure
Investigations
 Measure plasma level of hepatic enzymes and bilirubin
 Prothrombin time should be measured daily in patient with toxic level
 Renal function should be monitored
Management
 Used of activated charcoal - if present within 2 hours of ingestion
 Antidote – N-acetylcysteine to be given if the blood level is above the toxic range
compared with normograph

Prevention of accidental poisoning

1. Protection of the child
2. Clear labeling
3. Keep household chemicals and poisons out of sight and reach of children
4. Dangerous drugs should be stored in bottles with safety cap
5. Education of parents about the hazard of household and drugs laws
 PAEDIATRIC PRESCRIBING
PRINCIPLES OF PAEDIATRIC PRESCRIBING
1. Painful intramuscular injections should be avoided in children as far as possible.
2. In children particularly neonates the risk of toxicity is increased by inefficient renal
filtration, relative enzyme deficiencies and inadequate detoxifying system causing delayed
excretion. So dose frequency is usually less (i.e. more spaced out in neonates according to
both gestational age and post-natal age.)
3. Paediatric doses should not be calculated as a portion of the adult dose e.g. ½ of the adult
dose for children less than 5 years old and ⅓ for children less than 1 year old etc.
4. Many children doses are calculated according to body weight in kilogram ( /kg) but that
again may result in much higher doses in overweight children.
5. Body-surface area (BSA) (M2) is more accurate and may be calculated from height and
weight by means of a normogram. (See figure 1)

Commonly used drugs

A. Anti-tuberculous drugs
Cautions &
Name Indication Route & dose Side effect
contraindication
Streptomycin - Tuberculosis - Deep IM - Not to be given - Dose related
sulphate in combination 15 (12-18) together with ototoxicity and
mg/kg od potentially ototoxic nephrotoxicity
diuretics (eg. especially in children
Frusemide). with renal failure.
- May impair
neuromuscular
transmission and
should not be given
to children with
myasthenia gravis.
Rifampicin - Tuberculosis PO 10 (8-12) Contraindication - On intermittent
in combination mg/kg. - Jaundice. therapy, influenza
- Prophylaxis of like symptoms
meningo-coccal 10 mg/ kg bd Caution - Alteration of liver
infection and Meningococc - Hepatic and renal function, jaundice,
Haemophilus al - 2 days impairment. - Flushing, urticaria,
influenzae type H. influezae rashes
b infection 4 days - Leucopenia,
eosinophila
- Urine, saliva and
other body secretions
colored
Isoniazid - Tuberculosis - PO 5 – 10 Caution - Nausea, vomiting,
in combination mg/kg (Max - Epilepsy - Peripheral neuritis
300 mg) - Malnutrition with high dose,
 - HIV (risk of - Hypersensitivity
peripheral neuritis) reaction e.g.
- Hepatic and renal erythema multiforme,
impairment. blood dyscrasia
- SLE like syndrome
Contraindication
Drug induced liver
diseases.
Pyrazinamide - Tuberculosis - PO 25 (20– Caution - Hepatotoxicity
in combination 30) mg/kg - Hepatic disorder - Nausea, vomiting
(for 2 months - Dysuria
initial phase Contraindication - Arthralgia
only ) - Severe hepatic - Sideroblastic
impairment anemia
- Rash and
occasionally
photosensitivity
Ethambutol - Tuberculosis - PO 25 (15 – Caution - Optic neuritis, poor
in combination 25) mg/kg - Test the visual vision, blindness,
acuity before - Peripheral neuritis
treatment and - Rash, pruritus,
warned patients to urticaria (rarely)
report visual - Thrombocytopenia
changes.
For young children NB – these side
– routine effects are very rare if
ophthalmological use in recommended
monitoring is dose, so now use
recommended. instead of inj.
Streptomycin
- In renal (to check with
impairment, reduce guideline)
the dose.

Contraindication
- Optic neuritis ,
poor vision

B. Anti–malaria dugs

Cautions &
Name Indication Route & dose Side effects
contraindication
Quinine - Treatment of - Quinine - Cardiac disease - Cinchonism
dihydrochloride falciparum should be given (so monitor ECG (tinnitus, headache
malaria by IV infusion, during parentral hot and flushed
 if the child is treatment.) skin)
seriously ill - Monitor for blood - Visual disturbance
- Loading dose glucose & - Confusion
20 mg/kg of electrolytes - Blood disorder
Quinine salt concentration including
over 4 hours during parentral thrombocytopenia &
than after 8 treatment. hemoglobinuria
hours - G6PD deficiency - Acute renal failure
- Maintenance - Renal impairment - Hypoglycemia
dose of 10 - Cardiovascular
mg/kg infused Contraindication effect are very toxic
over 4 hours - Haemoglobinuria in over dosage
for every 8 - Myasthenia
hours until gravis
child can - Optic neuritis
swallow tablet
to complete 7
day course

- PO 10mg/kg
every 8 hours
for 7 days
Artemisinin - Potent - IV, IM, Oral - Caution with - Generally well
and it’s antimalarials and rectal drugs that prolong tolerated at
derivatives - Basic of ACT preparations QT interval therapeutic doses,
(Artemisinin e.g. Quinine and - Nephrotoxicity
based Halofantrine and cardiotoxicity
combination in high doses in
therapy) animal studies
Artemether - Treatment of - PO - Electrolyte - Prolong QT
with acute imbalance interval
Lumefantrine uncomplicated - Abdominal pain
falciparum - Headache
malaria - Arthralgia

Clindamycin - Treatment of - PO 7 mg/kg - Discontinue - Diarrhea,

falciparum (maximum 450 immediately if abdominal
malaria mg) every 8 diarrhea or colitis discomfort
together with / hours for 7 develops. - Antibiotic
or followed by days associated colitis,
Quininine Contraindication - Jaundice
- Diarrhea states - Steven- Johnson
Other uses syndrome
- Staphylococal
 bone and joint
infection and
peritonitis
- Endocarditis
prophylaxis
Chloroquine - Prophylaxis Caution - GI disturbance
of malaria in - G6PD deficiency - Headache
areas of the - Ophthalmic - Hypotension
world where examination with - Convulsions
the risk of long-term therapy - Rashes, pruritus
chloroquine - Renal impairment
resistant
falciparum
malaria is still
low
Mefloquine Caution - Nausea, Vomiting,
- Cardiac Diarrhea
conduction - Abdominal pain
disorder, epilepsy - Dizziness
- Not - Loss of balance
recommended in - Headache
infants under 3 - Sleep disorders
months
- Hepatic
impairment

Contraindication
- Hypersensitivity
to quinine
Doxycycline - Treatment of Caution
falciparum - Patients receiving
mlaria together potentially
with or
hepatotoxic drugs
followed by
Quinine Hepatic and renal
(Doxycycline impairment
has a longer
duration of
action than
tetracycline and
need only be
given once
daily)

Other uses
- Leptospirosis
in penicillin
hypersensitivity
Tetracycline - Chlamydia Contraindication - Nausea, Vomiting,
infection - Deposition of Diarrhea
- Rickettsia tetracycline in - Dysphagia
(including Q growing bone and - Oesohageal
fever) teeth causing irritation
- Brucella staining,
infection occasionally dental Rarely
Spirochete hypolasia. - Hepatotoxicity
Mycoplasma - They should not - Blood disorder
be given to - Hypersensitivity
children under 12 reaction
years

C. Drugs used in Anaphylaxis reaction

Cautions &
Name Indication Route & dose Side effect
contraindication
Adrenaline - Acute - By continuous - Hyperthyroidism - Anxiety
hypotension IV infusion, IM - Diabetes Mellitus - Tremor
or SC - Heart disease - Tachycardia
Emergency 1 in 1000 - Hypertension - Arrhythmia
treatment of (1mg/ml) - Arrhythmia - Headache
acute <6 month - Cerebrovascular - Cold extremities
anaphylaxis 50μg ( 0.05ml) disease - Nausea
6 month to 6 yrs - Vomiting
120 μg (0.012 - Sweating
ml ) - Weakness
6-12 yrs - Dizziness
250 μg (0.25 - Hyperglycemia
ml)

- By slow IV
injection, 1 in
10,000 solution
In neonate
10μg/kg
(0.1ml/kg)
1 month to 12
yrs
10μg/kg
(0.1ml/kg)
By inhalation of
nebulized
solution of
adrenalin 1 in
1000 ( 1mg/
kg )
1 month -12 yrs
Other uses 4000 μg/kg
- Croup (maximum
 5mg) Repeated
after 30 minutes
if necessary
Hydrocortisone - Acute - IM or IV Caution - GI effect-
hypersensitivity 1 month to 1 yr - Adrenal dyspepsia, peptic
reaction initially 25 mg/ suppression ulcer, abdominal
- Angioedema kg 3 times daily - Infection distension
- Severe acute adjusted after - Growth - Candidiasis
asthma response retardation - Proximal
- Congenital 1-6 yrs - Hypertension myopathy
adrenal initially 50 - Endocrine effects
hyperplasia mg/kg 3 times Contraindication including
- Acute daily - Systemic infection - Adrenal
adrenocortical 6-12 yrs (unless specific suppression
insufficiency initially antimicrobial - Cushing 's
(Addisonian 100mg/kg 3 therapy given) syndrome (with high
crisis) times daily dose )
- Adrenal - Hirsutism
hypoplasia - Weight gain
- Addison's - Negative nitrogen
disease balance
- Acute - Increase appetite
hypersensitivity - Increase suscepti-
reaction bility to and severity
of infection
- Psychological
dependence
- Depression
Chlophenara- - Symptomatic
mine maleate relief of allergy
- Injection can
also be used for
anaphylactic
reactions in
emergency

D. Penicillins and Cephalosporins

Cautions &
Name Indication Route & dose Side effect
contraindication
Benzyl - G (+) ve Newborn Contraindication - Anaphylatic
penicillin bacteria - 7days – 25 - Hypersensitivity reactions
(streptococci, mg/kg/dose 12 to penicillins or - Immediate and
pneumococci) hourly cephalosporins delayed
- G (-) ve diplo- - >7days - 25 hypersensitivity
cocci mg/kg/dose 8 Caution reactions
(meningococci, hourly (Double - Monitor renal and
gonococci), dose in hepatic function
- G (+) ve meningitis) especially if
bacilli prolonged therapy,
(clostridia, Child high doses or pre-
anthrax) – 25mg/kg/dose existing renal or
 - G (-) ve bacilli 6 hourly hepatic
(corynibacteriu - Severe insufficiency
m diphtheriae) infection
Spirochete including
(syphilis, meningitis -
leptospirosis) 50mg/kg 6
- Some hourly
anaerobic
organisms

- Pneumonia
- Meningitis
- Diphtheria
- Tetanus
- Gas gangrene
- Gonorrhoea
- Neonatal
sepsis (in
combination
with amino-
glycosides)

Ampicillin and - Otitis media Neonate Contraindication - GI upsets (nausea,

Amoxicillin - Tonsillitis Amoxicillin (or) - Hypersensitivity diarrhea)
- Respiratory Ampicillin to penicillins or - Uritcarial rash
tract infection - PO/IV/IM 50 cephalosporins - Erythematous
(pneumonia) mg/kg 12 maculopapular rash
- Urinary tract hourly ≤ 7days Caution
infection - PO/IV/IM 50 - Monitor renal and
- Listeriosis mg/kg 8 hourly hepatic function
- Helicobacter 7-21days especially if
pylori - PO/IV/IM 50 prolonged therapy,
eradication, - mg/kg 6 hourly high doses or pre-
Endocarditis >21days existing renal or
prophylaxis *Increase IV hepatic
- Anthrax and dose to 100 insufficiency
dental infection. mg/kg/ dose in
meningitis

Child
Amoxicillin
- 1/12 - 2 yr –
IV/IM 125 mg
tds oral
- 2-12 yr-
IV/IM 125-250
mg tds oral
- All ages -
IV/IM 30
mg/kg 8 hourly
(Double dose in
severe
 infection)

Ampicillin
- 1/12 - 2yr -
125 mg qid
- 2 - 12yr - 250
mg qid
- All ages - 25
mg/kg 6 hourly
(maximum
single dose 1 G)

100 mg/kg 6
hourly
(meningitis,
septicaemia -
maximum
single dose 3 G)

Cefotaxime - Streptococci, Cefotaxime Contraindication

and ceftriaxone Staph. aureus, Neonate - Known or
Gram (-)ve - ≤ 7days, 50 suspected allergy to
bacteria, mg/kg/dose 12 cephalosporins /
particularly hourly penicillins
against - > 7days, 50
penicillin mg/kg/dose 6-8 Caution
resistant hourly Ceftriaxone
pneumococci Child - Pre-existing
and H. - 50 mg/kg 12 disease of biliary
influenzae. hourly (6 hourly tract, gall bladder,
in meningitis & liver or pancreas
Meningitis, other severe - Should probably
meningococcal sepsis) not be used in
septicaemia, premature infants
severe sepsis, Ceftriazone
epiglottitis, (slow infusion)
respiratory tract Neonate
and urinary - 20-50 mg/kg
tract infection, once daily
soft tissue (Avoid in
infection preterm,
acidotic or
hyper-
bilirubinaemic
neonate)
Child
- 20-50 mg/kg
once daily
(80 mg/kg once
daily in severe
infection &
meningitis)
E. Aminoglycosides

Cautions &
Name Indication Route & dose Side effect
contraindication
Gentamycin IM or slow IV Contraindication - Hypersensitivity
Newborn - Myasthenia gravis - Ototoxicity
<32 week - 5 (tinnitus, deafness,
mg/kg 36 H Caution vestibular damage)
>32 week - 5 - Pregnancy - - Nephrotoxicity -
mg/kg 24H auditory & usually reversible;
vestibular damage directly related to
Child in fetus (rise duration of therapy
2.5mg/kg 8H greatest with (whenever possible
streptomycin; very treatment should not
small with exceed 7 days)
gentamycin - avoid - Impairment of
unless essential) neuromuscular
Renal impairment, transmission -
infant and elderly should not be given
Avoid prolong use in myasthenia gravis
Condition with - Concurrent use
muscular weakness with diuretic is
(can be reversed by avoided if possible
IV calcium to prevent
gluconate) ototoxicity (if
unavoidable,
interval between
these two drugs
should be separated
by as long as
practicable.
-Two
aminoglycosides
must never be given
simultaneously.
- Serum
concentration should
be measured in all
patient if possible
thus preventing
toxicity and
ensuring efficacy.
- Antibiotic
associated colitis,
nausea, vomiting,
rash
F. Chloramphenicol
Cautions &
Name Indication Route & dose Side effect
contraindication
Chloramphenic - Bacterial Newborn Contraindication - Blood disorder
ol meningitis & - < 2 weeks - IV - Pregnancy, breast (reversible and
brain abscess 12.5 mg/kg 12 feeding irreversible
- Acute hourly - Porphyria (idiosyncratic),
epiglottis - - > 2 weeks - IV aplastic anaemia)
Pneumonia 12.5 mg/kg 6- Caution - Nocturnal
- Typhoid fever 12 hourly - Avoid repeated haemoglobinaemia
- salmonella courses and - CNS - Peripheral
septicaemia Child prolonged treatment neuritis, optic
- Ricketsial - 12.5 mg/kg 6 - Reduce doses in neuritic
infection (scrub hourly (double hepatic impairment - Erythema
typhus, Q fever) dose in - Renal impairment multiforme
meningitis and (avoid unless no - Nausea, vomiting,
severe alternatives) diarrhoea,
infection) - Blood count stomatitis,
required before and candidiasis,
during treatment superinfection
- Grey baby
syndrome
(abdominal
distension, pallid
cyanosis, circulatory
collapse) may
follow excessive
doses in neonate.
G. Co-trimoxazole
Cautions &
Name Indication Route & dose Side effect
contraindication
Co-trimoxazole - UTI - Oral – 20 Contraindications -
- RTI mg/kg - Pregnancy, infant syndrome
- Invasive sulfamethoxazo < 6weeks - Bone marrow
salmonalla, le & 4 mg/kg (especially with depression
shigella trimethoprim bd neonatal - Allergy
infection, - PCP jaundice/preterm), - - GI disturbance -
in AIDS & - - Liver disease antibiotic associated
malignancy - Blood disorder. colitis

Cautions
- Renal impairment
breast feeding
mother
- Check blood
count
Increased fluid
intake
- G6PD deficiency
- Asthma