Paediatrics Notes

By Dr.G.Patil

GMC Nagpur
 Microcephaly
: Head circumference <3rd centile or < 3 SD below the mean for age and sex

OR

Defining microcephaly as >3 SD below the mean is more likely to be associated with genetic and non-
genetic disorders affecting brain than if defined as >2 SD below the mean, since the latter may include
intellectually normal healthy children with head circumference at the lower end of the population
distribution.

Primary causes Secondary causes

Phenylketonuria, Diabetes

of neueony
Reduced gene cation Seckel syndrome, Zika virus infection,
dueing development
Infections in infancy : Meningitis, Encephalitis

due to
iniuey trauma
,

Investigations

Evaluation for microcephaly should be initiated if a single head circumference measurement is more than
2-3 SD below the mean or when serial measurements reveal progressive decrease in head size.

Careful history and physical examination are necessary, including development assessment and
measurement of head size of parents.

Need for neuroimaging is determined by the age at onset, severity of microcephaly, head circumference in
parents, history of antenatal insult(s) and associated clinical features.

Pica
problem in children less than 5 years of age

month

mon non-edible substances like dust, clay, sand, and ice (pagophagia)
Etiology

⑨ on

⑨ maternal deprivation, parent neglect, abuse

⑤

Clinical associations:

Management- +
x

iron supplementation and

Thumb Sucking
Thumb sucking is normal behavior in infants and toddlers.

It peaks between the ages of 18-21 months and most children spontaneously drop the habit by 4 yr of age.

Its persistence in older children is socially unacceptable and can lead to dental malignancies.

Parents should be reassured and asked to ignore the habit if the child is younger than 4 yr of age.

If it persists beyond the age of 4-5 yr, the parents should motivate the child to stop thumb sucking and
encourage him when he restrains himself from sucking the thumb.

Application of noxious agents over the thumb is useful as an adjunctive second-line treatment .

Adolescence- SMR,Health Problems

Def :-

Stages of adolescence

Early adolescence (10 13 years) -

sexual characteristics

Mid adolescence (14 16 years) - Development of a separate identity from parents, experimentation,
new relationships with peer groups, and opposite sex.

Late adolescence (17 19 years) - Fully developed physical characteristics similar to adults. They have a
distinct identity, well-formed opinions and ideas.

Important Health problems during adolescence

Illness - 1) Problems related to growth and development like precocious or

delayed puberty and short stature

 2)Endemic infectious diseases like TB, malaria etc

Consequences of risk taking behavior - 1)Unintended injuries Automobile and sports related accidents

2)Intended injuries Violence, homicide, suicide

3)Sexually transmitted diseases HIV/AIDS, Herpes, UTI

4)Substance abuse Tobacco, alcohol, drug abuse

Nutritional problems - 1)Undernutrition 2)Micronutrient deficiencies like iron deficiency anemia,

iodine deficiency 3) Obesity 4) Eating disorders

Reproductive health problems - 1)Unprotected sexual intercourse 2)Teenage pregnancies

3)High maternal mortality 4) High perinatal mortality, high LBW rate 5)Abortion related problems 6)
Menstrual problems 7)Reproductive tract infections

Mental health and related problems - 1. Behavior disorders 2. Stress, anxiety 3.Depression and suicide

4. Substance use 5. Violent behavior 6. Eating disorders Bulimia and anorexia nervosa

Tanner staging/Sexual maturity rating (SMR)

Girls:

Stage Breast Pubic hair

1 No breast tissue Same as abdominal hair

2 Breast bud, enlargement Minimally pigmented, mainly over labia

Of areola

3 Further enlargement of Darker and coarser hair on mons pubis

breast bud and areola

4 Secondary mound formed Adult type, less distribution

by papilla and areola

5 Adult contour with projection Adult feminine distribution with spread to medial surface of thigh

of papilla alone

First visible sign of puberty is the Thelarche. It occurs between 8 and 12 years

Menses begins 2 2.5 years after thelarche (during SMR 3 4)

Growth spurt occurs in Tanner stage 3

Boys:
Stage Genital changes Testicular volume Pubic hair

1 Prepubertal <4 mL Same as abdominal hair

2 Early penile growth, scrotal 4 10 mL Fine pubic hair at the base of penis

enlargement, pink scrotum

3 Increase in penile length, 10 15 mL Increase in number of hair, darkening

scrotal growth

4 Increase in penile length and 15 20 mL Spread around thigh, less than adult distribution

width, pigmented scrotum

5 Adult size >20 mL Adult male distribution

First visible sign of puberty is testicular enlargement

It begins around 9 10 years

Testicular volume is assessed using an orchidometer

Growth spurt occurs in SMR 4 or when the testis volumes reach approximately 10 15 ml

Psychological Problems during Adolscence

1. Depression :-

from a loved one. These resolve in due course of time,occasionally after weeks or months.

-
guilt

in relationship to the dead. A psychiatric treatment is in order.

- ization of feelings of despair,

hopelessness and helplessness by the adolescent.

- -
running away

from home, multiple accidents, unexplained headache, abdominal pain, etc.

A psychiatric treatment is mandatory.

2. Sucide :-
 - Suicide is one of the important causes of deaths among adolescents.

- Its causes include serious conflicts and pressures, successive failures in examination, marriage
against will,

chronic illnesses causing fear of fatality, impotence, diminished competence, poor self-image,

vulnerability to loss of a loved one and easy and increased access to medication that could facilitate
suicide.

- Any suicidal attempt is an indication for a psychiatric evaluation and management.

- A short-term hospitalization is of distinct value in providing a secure environment to the subject and
helps the individual in the constructive resolution of his conflict

3. Substance Abuse :-

CNS stimulants (dexedrine, methedrine) CNS depressants (opiates)

Hallucinogens (LSD, phenylcyclidine, mushrooms, datura)

Volatile substances (gasoline sniffing, airplane glue, nitrites),

Marijuana (hashish), cocaine, alcohol, smoking, anabolic steroids

- The most important preventive measure is channelization of the energy of the adolescents and
creating awareness in them about the adverse effect of substance abuse

Metabolic Acidosis in Children

1. Loss of bicarbonate.
2. Elevated H+ ions or decreased excretion of acids.

elevated PaCO2.
Causes of metabolic acidosis:
Normal anion gap
1) Diarrhea 2)Renal tubular acidosis 3) Acetazolamide therapy 4)Urinary tract diversion
(uretero- sigmoidostomy, rectourethral fistula)

1)Diabetic ketoacidosis, starvation ketoacidosis

2)Lactic acidosis, shock, severe anemia, liver failure.
3)Poisoning: Salicylate, Paraldehyde, Methanol,Ethylene glycol
4)Uremia, Inborn errors of metabolism
5) Medications: Metformin, propofol.
Clinical features
Mild metabolic acidosis presents with nausea, vomiting, headache, and abdominal pain

vasodilatation leading to increased ICP, altered mentation and coma.

Anorexia, lethargy, poor weight gain and listlessness. Chronic acidemia
 also results in osteopenia and muscle wasting as a result of release of calcium carbonate and
glutamate respectively as buffers for H+
Management
Underlying cause should be identified and treated first.
Shock should be treated with aggressive fluid therapy and adequate oxygenation.
Vasoactive agents (dopamine, dobutamine) should be added only after volume replacement as
they can worsen acidosis.
Routine IV sodium bicarbonate for metabolic acidosis is not recommended

SAM c/f, complications , management

⇐
)

2) Visible wasting

:
3) Bilateral pitting type of edema
4) MUAC <11.5 cm between 6 to 60 months old

Clinical Features of PEM

Hair: Flag sign, hypochromotrichia, easily pluckable hair

:
Skin: Xerosis, follicular hyperkeratosis, flaky paint dermatosis, crazy pavement dermatosis,
purpura, Petechiae
Mucosa: Glossitis, stomatitis, cheilosis
• General: Irritability, apathy, tremors
• Face: Diffuse depigmentation, moon face, bitot spots, conjunctival xerosis, keratomalacia, angular

stomatitis, cheilosis
a Tongue: Atrophic papillae
• CVS: Microcardia, cardiomegaly

* CNS: Mental confusion, psychomotor change, sensory loss, loss of position sense, motor

weakness, loss of ankle and knee jerks and calf tenderness

a GIT: Hepatomegaly

Kwarshiorkor (edematous malnutrition)

Severe condition in protein energy malnutrition spectrum due to protein deficiency
The essential clinical tetrad to diagnose Kwarshiorkar
1) Growth retardation
2)Muscle wasting with retention of subcutaneous fat
3) Edema due to hypoalbuminemia
4)Mental changes
A typical child is listless, short, edematous along with hepatomegaly, anemia and skin lesions
Face: Moon face
- Skin: o Flaky paint dermatosis
o Dry inelastic mosaic appearance
- Hair changes: o Flag sign present
o Thin, dry, brittle, sparse, easily pluckable
 - Mental changes: o Lethargic, listless and apathic
o Takes little interest in the environment and does not play with his toy

&Clinical staging: Kwarshiorkar

Stage 1: Pedal edema
Stage 2: Pedal and facial edema

:
Stage 3: Pedal, facial, chest and paraspinal edema
Stage 4: Generalized edema with ascites

Marasmus
Marasmas in Greek means wasting.

- Age: highest incidence seen in infancy

- General features: o Gross wasting of muscle, poor muscle tone
o Loss of subcutaneous fat
o Bony prominences are seen
- Skin: o Wrinkled, dry and loose, inelastic
o Folds prominent over glutei and inner thigh
- Psychological: o Appears alert but irritable
o Voracious appetite
- Growth: o Marked deficit in weight and to a lesser extent in height
- GIT: Distended abdomen
Clinical staging: Marasmus
• Stage 1: Loose skin folds in axilla and groin
A Stage 2: Loose skin folds in buttocks and thighs
8 Stage 3: Wasting of chest and abdomen
A Stage 4: Wasting of buccal pad of fat

Assessment of the Severely Malnourished Child

History - The child with severe malnutrition has a complex backdrop with dietary, infective, social and
economic factors underlying the malnutrition.
A history of events leading to the child's admission should be obtained. Socioeconomic history
and family circumstances should be explored to understand the underlying and basic causes.
Particular attention should be given to:
(i) the usual diet (before the current illness) including breastfeeding;
(ii) presence of diarrhea (duration, watery /bloody);
(iii) information on vomiting, loss of appetite, cough;
(iv) contact with tuberculosis. Malnutrition may be the presentation of HIV infection

Examination - Anthropometry provides the main assessment of the severity of malnutrition.

Physical features of malnutrition as described above should be looked for.
Clinical features of prognostic significance include:
i. Signs of dehydration
ii. Shock (cold hands, slow capillary refill, weak andrapid pulse)
iii. Severe palmar pallor
 iv. Eye signs of vitamin A deficiency
v. Localizing signs of infections
vi. Skin infection or pneumonia, signs of HIV infection,fever (temperature 37.5°C or 99.5°F)
vii. Hypothermia (rectal temperature <35.5°C or <95.9°F), mouth ulcers, skin changes of
kwashiorkor

Treatment :-

The treatment involves 10 steps in 2 phases of treatment;

rehabilitation phase which might take several weeks to months

Look the flow chart on page no 45 of Arun Babu

Condition Treatment
1.Hypoglycemia (<54 mg/dL) Asymptomatic: 50 mL of 10% dextrose PO/NG
Symptomatic: 5 mL/kg of 10% dextrose IV
2.Hypothermia(<35.5°C) Warm clothes, KMC, warmer care, frequent feeds,
antibiotics
Severe hypothermia (<32°C) Oxygen,IV fluids(prewarmed), warmer care, antibiotics, temperature
monitoring

3.Dehydration Some dehydration: ORS 5 mL/kg every 30 min for 2 h, then 5 10 mL/kg/hr
for 5 10 h
Severe dehydration/ shock: RL with 5% D or 1/2 DNS@ 15 mL/kg over 1 h, repeat
after 1 h consider septic shock if no improvement. ORS once stable
4.Electrolyte imbalance Potassium and magnesium supplements for 2 weeks
5.Infection Ampicilin/gentamicin Cloxacillin for suspected staphylococcal infection
Cefotaxime (meningitis) Third generation cephalosporins (septic shock)
Ciprofloxacin (dysentery)
6.Micronutrient deficiency Vitamin A, D supplements, Vitamin B (twice RDA)
Folic acid (5 mg on D1 then 1 mg/day),
zinc (2 mg/kg/day) and copper (0.3 mg/kg/day)
Iron in rehabilitation phase
7.Start cautious feeding F75 diet-(75kcal+ 0.9g protein/100 mL)( rich in carbohydrate, low in protein/
fat)
8.Catch up growth F100 diet (100 kcal + 2.9 g protein/100 mL) (rich in protein/fat)
9.Sensory stimulation Emotional support
10.Discharge and follow up Sensitize caretaker, immunization complete, feeding and follow-
up advise

Complications Remarks
Superadded Both overt and hidden: Septicemia,pneumonia, diarrhea, pyoderma,
scabies,UTI, tuberculosis infections.
 Dehydration and Usually complicating accompanying
Dyslectrolytemia diarrhea, often with lactose intolerance.
Hypothermia An unattended rectal temperature of < 35 degree Celsius may prove
fatal, causing sudden infant death syndrome (SIDS)
Hypoglycemia It contributes to poor response to nutritional therapy and carries a poor prognosis.
CCF It is usually precipitated by excessive intake of sodium and fluid or severe anemia.
Since cardiac size is invariably small in PEM, even a normal sized heart in X-ray
should arouse suspicion of CCF.
Anemia Moderate to severe anemia may result from malnutrition as such or such factors as
superadded infection(s), contributing to development of CCF.
Bleeding DIC may complicate the clinical picture.
Suddent infant Sudden death 4-7 days after admission.
death syndrome( SIDS) Usually, the cause remains unclear

Complications of PEM:
S Sugar deficiency i.e hypoglycemia
H Hypothermia
I Infection and septic shock
EL Electrolyte imbalance
DE Dehydration
D Deficiencies of iron, vitamins and other micronutrients

Complementary feeding I
and development. Recently, the focus has been shifted to first 1000 days of nutrition that includes 270
days of intrauterine period and first 2 years of life (730 days).

by upto 6%.

UNICEF/WHO recommends the following strategies for optimal growth of infant and young child feeding

-
practices:

t 6 months

Principles of complementary feeding:

n
~
- ensity should be greater than breast milk.

a -containing foods like meat, iron-supplemented cereals should be preferred

-
absorption. &
yel size oven,
24 months
-
⑥
given

Age (months) Energy needed per day in addition Texture Frequency

To breast milk

6 8 200 kcal Thick porridge and mashed foods 2 3 meals per day

9 11 300 kcal Finely chopped and mashed foods 3 4 meals per day

12 23 550 kcal Family foods, chopped or mashed if necessary 3 4 meals per day

Nutrition Rehabilitation Center (NRC)

It aims at offering nutritional rehabilitation for mild to moderate PEM as a compromize between
domiciliary and hospital managements.

It offers a meeting point between classical treatment and prevention,embracing the positive points of
both hospital and home management.

Two types of NRCs are: Day care center and residential center.

Day care NRC - It consists of a room for children, a kitchen, an examination room and a teaching space.

At least one good meal is provided to children.Around 20 to 40 malnourished children

along with their mothers who are expected to involve themselves in various activities are taken care of.

The center remains open from 8 AM to 6 PM daily

Residential NRC -
with responsibilities that include daily work schedule of the mothers, purchase of food, issuing the correct
amount of food as decided by the nutritionist, and keeping stock and maintenance of cleanliness of the
center

. The supervisory staff is part time and includes a doctor, a medical assistant/nurse, a home
economist/nutritionist, and an agriculture teacher/extension worker

The criteria for admission to the NRC are:

 Children who do not catch up in growth after serious illness (measles, whooping cough,diarrhea)

receive at the under-5-clinic

Vitamin A deficiency WHO Classification , Management

Causes of deficiency:

Vitamin A is not synthesized in the body

Deficiency can be secondary to malnutrition, defective absorption, defective metabolism or increased

requirement

Inadequate breastfeeding is prime cause in first 6 months of life.

Requirement is increased in preterms and in infections like measles.

Zinc deficiency also increases the risk of vitamin A deficiency

WHO classification

Primary signs Secondary signs

X1A Conjunctival xerosis XN Night blindness

X1B Bitot spots XF Fundal changes

X2 Corneal xerosis XS Corneal scarring

X3A Corneal ulceration(<1/3 of cornea)

X3B Corneal ulceration(>1/3 of cornea

Clinical features:

tic early clinical feature is

Xerophthalmia.

Xerosis of the conjunctiva is generally the first clinical sign.

Bitot spots are the most characteristic feature. They appear as triangular area on the temporal aspects
of junction of cornea and sclera.

Corneal xerosis sets in leading to blindness.

Treatment:

Three doses of Vitamin A are given;

first dose immediately on diagnosis ,second dose 24 h later and third dose 1 4 weeks later.

< 6 months 50,000 IU 6 12 months 1 lac IU >12 months 2 lac IU

Severe PEM: repeat monthly doses of vitamin A till PEM resolves

Prevention and Control:

Prevention is achieved by:

itamin A supplementation to preschool children and during pregnancy

To healthy children:

ly) every 6 months up to the

age of 5 years

During pregnancy and neonates:

Breastfed neonates do not require additional supplementation

Rickets (Vit.D Deficiency)

Clinical Features:

1. Age: unusual below 3 months. Classically 6 months 2 years

2. Early signs: a. Restlessness, irritability, sweating over head

b. Craniotabes feeling of crackling over parietal bones

c. Rachitic rosary

3. General features: a. Flabby appearance

b. Muscle weakness and ligament laxity

4. Head: a. Anterior fontanelle remain open beyond 18 month

b. Bossing of head (hot cross bun appearance)

5. Che

b. Rachitic rosary
 c. Pigeon chest

d. Fiddle-shaped chest

6. Spine: kyphosis, scoliosis

7. Long bones bow leg, knock knees

8. Pelvis coxa vara

9. Abdomen a. Pot belly

b. Visceroptosis

10. Teeth: carries, delayed dentition

Swelling at wrist and ankle Laryngismus stridulus, tetany or convulsions due to hypocalcaemia

Radiological Features:

- Sites: growing bones of body around wrist and knee

- Changes: o Fraying of metaphysis

o Apparent in width of growth plate

o Splaying of metaphysis

o Cupping of metaphysis

o Decrease in the bone density

- Ribs:Rachitic rosary seen as headed enlargement of anterior metaphysis

- Pelvis: Coxa vara

- Spine: Kyphosis, scoliosis

Treatment of rickets:

1. Medical: STOSS regimen

Give 6 lac IU vit D3 oral/im

Healing line in X ray after 3 4 weeks

Yes no

Give 400 IU daily till full recovery Repeat the dose

 Yes------------------------------------- Responded

No

Vit D resistant rickets

Investigate further for cause

2. Surgical: a. Correction of deformities

b. Should be done after correction of rickets

Vitamin D dosage

Age group Daily regimen (8 12 weeks) Weekly Regimen 8 12 weeks) Stoss therapy Maintenance dose

<1 month 1,000 IU 50,000 IU Not recommended 400 1,000 IU

1 12 month 1,000 5,000 IU 50,000 IU 1 6 lakhs over 5 days 400 1,000 IU

1 18 years 5,000 IU 50,000 IU 3 6 lakhs units 1 5 days oral 600 1,000 IU

Vitamin B12 deficiency

-deoxyadenosyl cobalamine.

Deficiency:

: 1. Strict vegetarian/vegan diet

2.Breastfed infants of deficient mothers

3.Malabsorption

4.Drugs like PPI and H2 antihistaminics

Absorption:

Clinical manifestations:
1. Neurological features like irritability, hypotonia and developmental delay

2. Sensory deficits like parasthesias, peripheral neuritis.

3. Megaloblastic anemia and Knuckle hyper pigmentation.

4. Subacute combined degeneration of cord

Treatment and Prevention:

IV/IM 250 1000 mcg Vitamin B12, repeated daily for 1 week, followed by weekly
doses for 1 month.

pto 6
months or more

Vitamin C deficiency (Scurvy)

1.Hydroxylation of proline and lysine

2. Wound healing

3. Role in cholesterol metabolism, neurotransmitter metabolism and synthesis of carnitine

4. Important role in iron absorption

5.Antioxidant role

Dietary sources: Green leafy vegetables, Capsicum Green chillies, Amla, Guava, and Lemon

Deficiency:

Causes: 1. Children receiving heat treated milk or unfortified formula feeds

2.Children not receiving fruits or fruit juices

Clinical features:

a) Early: Irritability

Loss of appetite

Low grade fever

Pseudoparalysis due to knee and ankle swelling

b) Late: Scorbotic rosaries (wedge shaped) at costochondral junctions with sternal depression

Gum changes like blue purplish discoloration with swelling

Anemia due to impaired iron absorption

 Hemorrhagic manifestations like gum bleeding, petechiae, purpura, and ecchymoses at pressure
points, poor wound healing

Treatment:

1. 100 200 mg/day orally or parenterally for 3 months

2. Milk fortification with Vitamin C

Neonatal resuscitation Protocol,equipments,steps

Preparing for resuscitation

unexpected. Therefore, it is important to anticipate the need for resuscitation in every delivery and

ensure basic readiness to manage asphyxia.

ted delivery

Equipment required for Resuscitation

For Ventilation Ambu Bag,Face Mask (Appropriate sizes)

Laryngoscope Straight blade (Miller type)

Endotracheal tubes (Sizes 2.5 to 4)

Oxygen tubing with flow meter

Oxygen delivery devices Nasal mask,

Nasal prongs, Head box

Suction equipment Suction apparatus ,Suction catheter

Bulb suction ,Meconium aspirator

Medications Umbilical venous catheterization set

Infant feeding tubes ,IV catheters

Epinephrine, Naloxone ,Normal Saline

O negative blood, FFP

Miscellaneous Radiant warmer

Dry linen ,Stethoscope

Gloves ,Umbilical cord clamps

 Initial steps include drying, providing warmth, positioning the infant, clearing the airway secretions
followed by evaluation

Evaluation is based primarily on the following two signs:

1. Respiration key to effective neonatal resuscitation.

2. Heart rate the most sensitive indicator of response to resuscitation.

1. Positioning of the neonate

2. Suction of mouth followed by nose

: Initiate breathing if no spontaneous respirations

1. Tactile stimulation, such as flicking soles of foot, rubbing the back, etc.

2. Positive pressure ventilation (PPV) with a bag and mask or via endotracheal tube

: Maintain the circulation with

1. Chest compression and medications, if needed.

2. Chest compressions continued for 60 seconds before rechecking heart rate

Evaluating Color is not recommended as a useful indicator of oxygenation or effectiveness of

resuscitation. In the recent guidelines, spO2 is used instead of color evaluation.

AMBU bag can be used without oxygen /air source but ressed gas
source

PPV should be attempted immediately if tactile fails. Prolonged tactile stimulation should be avoided due

1.Primary apnea- revived with tactile stimulation

2. Secondary apnea is not revived by tactile stimulation but requires PPV. Absent respiratory efforts at
birth to be considered as secondary apnea and resuscitated.

Room air resuscitation is done for gestational age >35 weeks

Supplemental oxygen is used for resuscitating <35 weeks preterm babies

Free flow oxygen is started in a spontaneously breathing baby if target saturation is not attained.

Routine vigorous suction is not required. Secretions when excessive can be wiped with cloth

There is no role for tracheal suctioning in cases of meconium stained liquor.

Babies born out of meconium stained amniotic fluid are said to be vigorous or non-vigorous at birth
based on heart rate, respiratory efforts and tone.

Even nonvigorous babies need not be routinely intubated for tracheal suctioning at birth

Suction pressure should not exceed 100 mmHg

Ratio of chest compressions to ventilation 3:1(120 events/1 min)

Delayed cord clamping: Umbilical Cord clamping should be delayed for atleast 30 60 seconds for infants
 not requiring resuscitation

Immediately after birth, preterm neonates <32 weeksold should be completely covered in a plastic wrap

Adrenaline in Neonatal Resuscitation

1. Used in 1:10000 dilution 2. IV dose: 0.01 0.03 mg/kg (0.1 0.3 ml/kg) 3. ET dose: 0.05 0.1 mg/kg (0.5
1 ml/kg)

Administration of naloxone is not recommended.

APGAR Score:
It is a quantitative method for assessing the infantile respiratory, circulatory and neurological status

APGAR stands for A-Appearance (Skin colour), P-Pulse (Heart Rate), G Grimacing (Reflex), A Activity
(Tone) and R-Respiration (Chest movement)

APGAR Score System 0 1 2

Appearance Blue Body pink, extremities blue Pink completely

Pulse/min Absent <100 >100

Grimace (reflex stimulation) No response Grimace Cry, cough or sneezes.

Activity (muscle tone) Flaccid Some activity Actively moving limbs

Respiration None Slow irregular Good crying

Score: >8 normal

4-8 moderately asphyxiated

<4 severe distress

When to do: 1 min, 5 min, and 10 min

1. At first cry

2. After regular respiration established

3. Delayed

Importance: 1. Monitoring score to determine the efficacy of resuscitation

2. Gives overall view of condition of new born

3. Prognostic value if score <4 at min - indicates very bad prognosis

4. If low, it indicates one of following.

a. Birth asphyxia

b. Congenital malformations

c. Intrauterine infection/septicemia
Drawbacks: 1. Subjective scoring except HR

2. Ignores time of first cry

3. 1 minute score is not useful in deciding the intervention necessary for resuscitation

as action must be initiated before that

4. Cannot be used in

a. Preterm baby

c. Severely sedated baby

5. It does not give any idea of duration and severity of asphyxia.

NEONATAL HYPOTHERMIA
Etiology

The newborn, a preterm infant in particular, is highly susceptible to exposure to low environmental

temperature. This can happen in situations such as:

1. Winter months,

2. Sudden change in weather conditions,

3. Resuscitation procedure, and

4. Cold snap.

Normal axillary temperature in neonate -36.5 37.5°C.

Low reading thermometer should be preferably used in newborn which can record temperature as low as
30°C

1. Cold stress: 36 36.4°C

2. Moderate hypothermia: 32 35.9°C

3. Severe hypothermia: <32°C

- cold skin, acrocyanosis, sclerema, lethargy, refusal to feeds

- Examination reveals bradycardia, tachypnea and respiratory distress.

- Cold stress is diagnosed when feet are cold but trunk is warm.

Complications - Hypoglycemia, Hypoxia and metabolic acidosis

Disseminated intravascular coagulation Bleeding tendencies including pulmonary hemorrhage

Treatment

Mild-Moderate Hypothermia (32-36o C)

ming by skin-to-skin contact on a warm bed room in a warm room; may use radiant
warmer, convection-warmed incubator

Severe Hypothermia (body temp < 32oC)

mostatically-
controlled heated mattress)

ving 10 to 20 ml of 25% glucose intravenously,

the likely cause of hemorrhages,

Warm Chain
The 'warm chain' is a set of ten steps aimed at decreasing heat loss, promoting heat gain and ensuring that
baby is not exposed to the circumstances that can result in hypothermia.

1. Warm delivery room

2. Warm resuscitation

3. Immediate drying

4. Skin-to skin contact

5. Breastfeeding

6. Postponement of bathing (beyond 24 hours after birth)

7. Appropriate clothing and bedding

8. Nursing of baby and mother together

9. Warm transportation ( Weakest link )

10. Training and awareness of healthcare providers.

Normal Newborn Baby Routine Care

Care of the newborn should start much earlier than the time of birth. Newborn period is not a beginning
but a continuation of what has gone before.
Following important five stages are recognized for improving neonata cycle

First Stage: Care of the Girl Child

Particularly in developing countries like India measures to improve newborn care should start from

care of the girl child who is the future mother.

Her nutrition, immunization and education play a very crucial role in the well-being and outcome of her
future progeny

Second Stage: Care of the Adolescent Girls

Improving her nutritional status including anemia prevention, adequate immunizations including rubella

vaccine wherever possible, life cycle education,improving personal and reproductive hygiene,prevention of
early marriages (Before 18 years of age),

early motherhood (Before 21 years of age), improving general educational status are crucial for better

neonatal outcome in future.

Third Stage: Care during Pregnancy

Essential minimum antenatal care includes following measures aimed at improving neonatal outcome.

(a) Early registration of pregnancy

(b) At least three antenatal check ups

(c) Universal prophylaxis against nutritional anemia and tetanus.

Minimum of 2 injections of tetanus toxoids to be given at one monthly interval as early as possible
during pregnancy.

The second dose should have been given at least one month before the expected date of delivery.

(d) Iron folic acid tablets through pregnancy and lactation period.

(e) Identification of high-risk pregnancy and early referrals.

(f) Promotion of institutional deliveries, which are well equipped and have trained persons.

Fourth Stage: Immediate Care at the Time of Delivery

ivery by properly trained birth attendants including doctors, nurses or other category
of health workers in a well equipped institution.

stematic resuscitation whenever indicated

five cleans during every delivery

I. Clean surface
II. Clean hands

III. Clean cord tie

IV. Clean cord cut

V. Clean cord

prevent hypothermia

Fifth Stage: Routine Care of Newborn and Subsequent Fellow up

ral to special care / intensive care centers

Appropriate Immunizations

al assessment and follow-up, if required.

Neonatal jaundice c/f, D/D , Management

Hyperbilirubinemia is common and relatively benign problem in neonates during first week of life.

Defined as an increased level of bilirubin in the circulation.

Physiological jaundice

Due to functional immaturity of the neonates to handle the increased production of bilirubin due to
increased enterohepatic circulation, increased fetal erythrocyte breakdown, decreased hepatic excretion
and immature hepatic conjugation
Physiologic jaundice Pathologic jaundice

Appears on second to third day of life(term) Appear in first 24 h of life

Disappears by fifth day of life(term) Variable

peaks at second to third day of life Variable

Peak bilirubin<13mg/dL (term), <15 mg/dL(preterm) Unlimited

Rate of bilirubin rise <5mg/dL/day Usually>5mg/dL/day

Causes of indirect (unconjugated) hyperbilirubinemia

Physiological jaundice
 Breastfeeding jaundice, breast milk jaundice

Increased production

1. Blood group incompatibility (Rh, ABO, minor blood group)

2.RBC membrane defects (hereditary spherocytosis, elliptocytosis)

3. RBC enzyme defects (G6PD deficiency, pyruvate kinase deficiency)

Disorders of bilirubin uptake -

Disorders of conjugation - Crigler Najjar Types I and II, hypothyroidism, pyloric stenosis

Enhanced enterohepatic circulation - Small or large bowel obstruction or ileus

Idiopathic

Others - Prematurity, sepsis, polycythemia, infant of diabetic mother, extravascular blood

(cephalohematoma, bruising)

An Evidences-based Diagnostic Approach

History

The following points should be particularly noted:

family history with special reference to maternal infections during pregnancy, drugs given
during pregnancy or labor, previous sibling(s) affected by jaundice or anemia, diabetes, previous blood
transfusions

the parents and ancestors; h/o consanguinity for hemoglobinopathies

ice decreasing or increasing in intensity

ther healthy, having no feeding difficulty, no fever, no rash?

Type of feeding: whether breastfed?

Clinical Examination

tivity and general condition of the infant

techiae, etc.?

finding?
 tion and grading of severity of jaundice

Used for clinical assessment of jaundice

Zones Icterus upto TSB

1 Face 4 6 mg%

2 Upper trunk 6 8 mg%

3 Lower trunk and thigh 8 12 mg%

4 Arms and legs 12 14 mg%

5 Palms and soles > 15 mg%

Investigations

The initial investigations are as follows

Total and direct bilirubin

Mother and baby blood group

Hemoglobin or packed cell volume (PCV)

Peripheral blood smear (for RBC shape and evidence of hemolysis)

Reticulocyte count

G6PD assay

In case of sick infant with jaundice or prolonged jaundice (> 3 weeks), the following investigation are
needed

Complete blood count

Urine examination and culture

Evaluate for infection as indicated

Urine for reducing substances

Thyroid profile (T4, TSH)

Evaluate for cholestasis (if direct bilirubin is elevated)

Treatment

Management depends on gestation, weight, wellbeing and age of the infant. Phototherapy and exchange
transfusion are treatment of choice

Phototherapy remains as the mainstay in treatment of neonatal jaundice. It consists of compact

florescent lamps in wave length range of 460 to 490 nm.

Phototherapy acts by following

1.Configurational isomerization

2.Structural isomerization

3.Photo oxidation

Side effects of phototherapy

Insensible water loss ,Diarrhea , Bronze baby syndrome (when used in conjugated jaundice)

Double volume exchange transfusion (DVET) should be done if values exceed the age specific cut off.
Indications for DVET at birth

1. Cord bilirubin is 5mg/dL or more

2. Cord Hb is 10 g/dL or less

Medical management Not used routinely

- Oral Phenobarbitone Induces enzymes required for bilirubin conjugation

- Heavy metals Inhibits hemoxygenase enzyme and reduced hemoglobin break down.

Neonatal Sepsis - Management

It is the systemic bacterial infection of the new born which incorporates septicemia, pneumonia and
meningitis.

Etiology: - E.coli, Staphylococcus aureus, Klebsiella pneumonia

Two types of onset: Early v Late:

Early Late

Time <72 hours >72 hours

Complicated pregnancy + +/-

Source Genital tract of mother Post-natal environment

Clinical Features: Fulminant, multisystem Slowly progressive or localized

Symptomatology of neonatal sepsis:

General:- Lethargy CNS:- Not arousable, comatose

 - Refusal to suck - Poor cry - Seizures - High pitched cry

- Poor weight gain/excessive weight loss - Excessive crying/irritability - Neck retraction

Bulging fontanelle

Temperature problem:- Hypothermia - Fever

Respiratory System:- Cyanosis - Tachypnea Hypotension: - Poor profusion - Shock

- Chest retractions - Grunt Others:- Sclerema - Excessive jaundice

Apnea/gasping - Bleeding - Renal Failure-

GIT:- Abdominal distension

- Diarrhea Vomiting

Investigation:

- Blood counts Cultures - Gram stain

- X-Ray chest - Acute phase reactants

Management:

1. Antibiotics

2. Supportive therapy: a. Maintenance of nutrition49

b. Correction of electrolyte balance

c. Correct hypoglycemia

d. O2 ventilation in respiratory distress

Prevention of infections:

- Exclusive breastfeeding, no pre-lacteals

- Keeping the cord dry

- Hand washing by care givers before and after handling the baby.

- Hygiene of baby (sponging, clean clothing)

- Avoiding unnecessary iv fluids, injections, needle prick etc.

Expanded New Ballard Scores (ENBS)

- Has an accuracy of 1 week.
- New Ballard score physical and neurological criteria
Physical criteria Neurological criteria
Skin Posture
Lanugo Square window sign
Breast bud Scarf sign
Ear cartilage Heel-to-ear
Genitalia. Popliteal angle
Exclusive Breast Feeding Advantages,techniques,problems,C/I
Exclusive demand breast feeding is recommended during first 6 months of age

Exclusive breastfeeding: Giving a breastfeeding baby no other food or drink, including water, with the
exception of prescribed drugs.

BFHI, a global program organized by UNICEF was introduced in 1992 to promote exclusive breast feeding,
adopted in India in 1993

Mothers should consume additional 400 500 kcal and 25 g of protein during lactation

Breastfeeding should be initiated within half an hour after vaginal delivery and within 4 h after caesarean
delivery
Composition of Breast Milk Energy 67 Kcal/dl. Protein 0.9-1.3 gm/dl.

Fat 3.8-4.5gm/dl .Carbohydrate 6.8 gm/dl.

Advantages of breastfeeding

To the Baby :- - Complete nutrition

- Species specific, baby specific, and time specific

-Bonding between mother and newborn

-Covers against infection

-Counters the risk of allergic disease, e.g. asthma, eczema

-Caries in teeth decreases

-Risk of CADs, cancer, obesity, type 2 diabetes, and hypertension decreased in later life

-More IQ promotes growth and mental development

-Cot death/SIDS risk decreased

-No risk of adulteration, dilution, contamination, and infection of breast milk

Anti-infective properties of breast milk

1.Boosts host defenses of newborn considered as 1st vaccine

2.Immunoglobulins IgA, IgM

3.Cellular elements macrophages, polymorphs

4.Bioactive factors lactoferrin

5.Probiotics Bifidobacterium and lactobacilli

6.Antimicrobials PABA protective against malaria, BSSL.

To Mother:- - Convenient

-Cheaper

-Risk of breast and ovarian cancer and risk of osteoporosis in later life reduced

- Assists in expulsion of the placenta and minimizes the risk of postpartum bleeding

-Helps in involution of uterus

- re spacing of baby.

- Contours of body come back to normal.

- Calming effect.
Technique of Breastfeeding

: Comfortable position for mother and her baby either sitting

neck should be supported in a straight line with his body and shoul should
.

: It means attachment of nipple along with

attachment at breast is a key to successful breastfeeding to suckle effectively a baby should be well latched
on the breast and should be able to take nipple and enough areola into the mouth for effective sucking.

: It means baby can be put on left shoulder the head has to hand
and then with the right arm support the buttocks and gen right hand. Is a
must after feeding the baby to avoid regurgitation.

Ten Steps of Successful Breastfeeding

stfeeding policy that is routinely communicated to all health care staff.

re staff in skills necessary to implement this policy.

nt women about the benefits and management of breast-feeding.

rs how to breastfeed and how to maintain lactation even if they should be separated from
their infants.

rn no food or drink other than breast milk,unless medically indicated.

-in: Allow mothers and infants to remain together 24 hours a day.

teats or pacifiers (also called dummies or soothers) to BF infants.

shment of breastfeeding support groups and refer mothers to them on discharge from
the hospital or clinic.

Problems in Breastfeeding

1.Primigravida mother problems: Inadequacy of feeds during initial 3 4 days, anxiety,worry, and lack of
confidence.

Treatment Antenatal and postnatal counseling of the mother.

2.Mechanical difficulties: Cleft lip, cleft palate, macroglossia, thrush, and incoordinated sucking and
swallowing by premature babies.

Treatment Treat the cause.

3.Retracted nipples and engorgement of breasts:

Treatment Syringe method (Nirmala Kesari method) a syringe is cut in the front and applied to the
actile nipple is pulled out and breastfeeding is established. However, new
guidelines suggest that syringing should be avoided as far as possible for retracted nipples.

If the baby is attached properly, inverted/retracted nipples soon become normal.

4.Sore/cracked nipples:

Pulling the baby forcefully from the breast without detaching.

Wrong position/attachment (latching) at the breast instead of major part

of areola. Ideally, should be checked and managed antenatally.

Treatment:

Avoid frequent washing of nipples with soap and water.

Emollient cream/hindmilk applied over the nipples in between the feeds.

5.Regurgitation of feeds

Treatment: Burping.

Right lateral position with head end slightly raised. Complementary feeds with bottle should be avoided.

CONTRAINDICATIONS TO BREASTFEEDING

- PKU

- Galactosemia

- Mother on anticancer drugs

- HIV Positive mother ( Should Continue*)

Low Birth Baby :- Def, Causes , Complications

-Def:- Low birth weight (LBW; birth weight less than 2500 g) babies have higher morbidity and mortality.
LBW results from either preterm birth (before 37 completed weeks of gestation) or due to intrauterine
growth restriction (IUGR) or both.

Some causes (risk factors) of preterm birth and IUGR

-Spontaneous , Racial, familial, and genetic

-Low socioeconomic status ,Low maternal weight

-Chronic and acute systemic maternal disease

-Antepartum hemorrhage ,Maternal genital tract infection

-Multiple pregnancy ,Congenital malformations ,Maternal smoking

-Induced labor: Maternal diabetes, PIH, and severe Rh isoimmunization.

 -Placental insufficiency

Complications

1.Preterm babies

-Hypothermia , Perinatal asphyxia

-Respiratory (hyaline membrane disease, pulmonary hemorrhage, pneumothorax, bronchopulmonary

dysplasia, pneumonia)

-Bacterial sepsis ,Apnea of prematurity

-Metabolic (hypoglycemia, hypocalcemia)

-Hematologic (anemia, hyperbilirubinemia)

-Feeding problems and poor weight gain

2.Babies with IUGR

-Perinatal asphyxia ,Meconium aspiration

-Hypothermia ,Hypoglycemia

-Feed intolerance ,Polycythemia ,Poor weight gain

Respiratory Distress Syndrome :- causes,c/f,management

Def :-Respiratory distress (RD) in newborn is the presence of one or more of the following features

1. Respiratory rate greater than or equal to 60/min

2. Chest retractions

3. Grunt.

Risk factors

Multiple gestation

Perinatal asphyxia Prematurity Cesarean section

ASSESSMENT OF RESPIRATORY DISTRESS:-

Downes score for respiratory distress in full terms.

Score 0 1 2
-
Respiratory rate/min <60 60 80 >80
④
Cyanosis (SpO2 < 80%) None in room air No with 40% oxygen Requiring >40% oxygen

a
Retractions None Mild Moderate to severe

Grunting None Audible with stethoscope Audible without stethoscope

-
-
Air entry Good Decreased Barely audible

Downes score >7 suggests impending respiratory failure.

CAUSES OF RESPIRATORY DISTRESS:-

1.Respiratory:- - Meconium aspiration syndrome ,Hyaline membrane disease

- Intrauterine pneumonia ,Postnatal aspiration

-Postnatal pneumonia ,Massive pulmonary hemorrhage

-Pneumothorax ,Transient tachypnea of newborn (TTNB)

- Bronchopulmonary dysplasia ,Pleural effusion

2.Congenital malformations:- -Choanal atresia ,Pierre Robin syndrome

-Laryngotracheomalacia ,Tracheoesophageal fistula

-Diaphragmatic hernia ,Pulmonary agenesis

3.Cardiovascular :- - Persistent pulmonary hypertension ,Congenital heart disease

-Arrhythmia ,Congestive heart failure

4.Central nervous system:- - Birth asphyxia or trauma ,Meningitis

- Diaphragmatic paralysis ,Maternal sedation/narcotic withdrawal

Clinical features:-

Usually presents within the first 6 h of delivery

Most commonly seen in premature infants as rapid and shallow respirations

Tachypnea

Retractions with grunting and cyanosis

Decreased air entry

Downe and silverman scoring are done to objectively quant

D/D Of Respiratory Distress:-

Conditions Clinical course Radiological features

Respiratory distress Onset at or soon after birth Low volume lungs, Fine reticulo granular
syndrome (RDS or HMD) Progresses in first 48 hours pattern ,Ground-glass appearance ,

Surfactant therapy modifies course of disease White-out lungs

Transient tachypnea of newborn Onset at birth or delayed Hyperinflated lungs ,Perihilar streaking
 Maximum severity at birth and improves gradually Mild pleural effusion ,

Mild cardiomegaly

Early-onset sepsis/pneumonia At birth or delayed Oxygen/CPAP required

Homogenous/heterogeneous

opacities bilaterally

Diagnosis

Chest x ray can confirm the diagnosis and is the investigation of choice.

X ray

1. Low volume lungs

2. Air bronchogram

3. Reticulogranular pattern

4. White out lung in severe cases

Shake test done using amniotic fluid or gastric aspirate Stable foam layer at air-liquid interface when
mixed with ethanol suggests adequate surfactant.

Management

Early supportive care of premature infants

Treatment of acidosis, hypoxia, hypotension and hypothermia, may lessen the severity of RDS.

Prevent or treat hypothermia Infant should be placed in incubator or radiant warmer and core
temperature should be maintained between 36.5 and 37 °C

Respiratory distress Requires Early Continuous positive airway pressure (CPAP) or ventilation

Provide warm humidified oxygen in order to maintain oxygen saturation of 89 -93%. Oxygen is given via
hood, prongs, CPAP or ventilator.

Mechanical ventilation and surfactant are indicated in infants with evidence of RDS

1. Severe hypoxemia

2. Poor ventilation

3. Xray evidence of RDS

4. Respiratory failure

5.Severe respiratory acidosis

Early CPAP Most important (reduces the need for ventilation)

Surfactant administration
a) Prophylactic- within min of delivery

b) Early rescue within 2 h of birth

c) Late rescue after 2 h of birth

Hyaline Membrane Diseases : C/F , Management

-One of the most common causes of respiratory distress at the time of birth is RDS or HMD.

- Def :-It is defined as an acute lung disease due to surfactant deficiency which leads to atelectasis and
subsequent failure of gas exchange.

- It is seen almost exclusively in preterms.

Risk Factors :-

1. Factors causing reduced lung development at birth and hence reduced surfactant preterm, infant of
diabetic mother, and diaphragmatic hernia.

2. Factors decreasing surfactant production birth asphyxia, LSCS without labor.

Clinical Features:-

1. Tachypnea

2. Expiratory grunting in a preterm/birth asphyxia

3. Inspiratory retraction

4. FiO2 requirement is more than 40%, surfactant modifies the typical course.

Time of presentation at birth or within 6 hours worsens over 24 hours.

Investigations:-

1.X-ray of chest , Low volume lungs

Fine reticulogranular pattern ground-glass appearance

Air bronchogram ,White-out lungs.

2.Blood gases hypoxia and hypercarbia

3.Others septic screen, blood chemistry, 2D echo for PDA, and cranial ultrasound as needed

Prevention :-

1. Prevent preterm delivery

2. Prevent birth asphyxia

3. ction dexamethasone to women in preterm

labor (24 34 weeks) at all levels of health facilities in public as well as in private

Dexamethasone 4 doses in 12 hours interval, last dose 48 hours before delivery.

 Betamethasone phosphate or acetate 12 mg IM 2 doses in 24 hours at 12 hours interval can also be used.

Treatment:-

1.Routine care:

Hemodynamic stabilization

Fluid management

Sepsis management

Temperature regulation

Caffeine: As CPAP becomes more effective if spontaneous breathing is effective, caffeine has a role in
reducing need for mechanical ventilation.

2.Oxygen delivery:

Give FiO2 as required, not more. Warm, humidified, and blended oxygen.

Target SpO2 is 88 92% for infants <30 weeks of gestation or <1,250 g.

Target SpO2 is 90 95% for >30 weeks of gestation.

3.Surfactant replacement therapy:-

- Timing :- In >28 weeks, as soon as HMD is diagnosed, preferably within 24 hours.

Role of prophylactic surfactant in >28 weeks is uncertain.

In <28 weeks, prophylactic surfactant is to be given if <25 weeks gestation,

PPV > 1 minute or no antenatal steroids

-Route: Intratracheal.

4. Continuous Positive Airway Pressure (CPAP)

-Bubble CPAP or NIPPV can be used

-Start at pressure of 4 7 cm H2O and FiO2 as required and flow at 5 10 L/min.

-Discontinue CPAP when FiO2 < 30% and no distress.

-CPAP care is considered to be associated with less incidence of adverse neurodevelopmental outcome in
preterms as compared to mechanical ventilation

5.Mechanical ventilation:

-If despite 8 cm H2O CPAP and 60% FiO2 , SpO2 remains <90%, pCO2 > 50 mm Hg and pO2 < 50 mm Hg,
ventilator care is required

-Initial settings: PiP 20 25 mm Hg, PEEP 4 6 mm Hg, rate 25 30/min, and Ti 0.3 seconds.

-Continuous flow, time-cycled pressure limited ventilators are useful.

-Goal is to limit tidal volume without promoting atelectasis and wean as soon as possible.

Hypoglycemia
: Blood glucose less than 40 mg/dL in general, regardless of the gestational age

Cornblath operative threshold based on risk factors

1. During first 24 h 45 mg/dL. Levels of 30 to 35 mg/dL may be acceptable once, but raised to if the level
persists after feeding or recurs in first 24 h.

2. After 24 h 45 to 50 mg/dL.

3. Infant with abnormal signs or symptoms 45 mg/dL.

4. Asymptomatic infants with risk factors 36 mg/dL.

5. For any baby <20 to 25 mg/dL requires immediate therapy

Clinical Features

Poor correlation between blood glucose levels and occurrence of symptoms

Approximately 50% cases present with symptoms.

Common symptoms include irritability, poor feeding, jitteriness, lethargy, tachycardia, tremors and
sweating

Severe cases can lead to apnea, cyanosis and seizures

Investigations

Insulin plus c-peptide

Additional testing

1. Growth hormone assay 2. Thyroid hormone assay

3. ACTH assay 4. Glucagon assay

Treatment

In Asymptomatic neonates

a. Determine Babies at Risk of Hypoglycemia

b. Early and frequent enteral feeding if tolerating feeds

c. Additional IV glucose maintenance if persistent hypoglycemia

Treatment in symptomatic neonates

a. Immediate therapy: Bolus dose of 10% Dextrose, 2 ml/kg (IV)

b. Maintenance therapy: Glucose infusion rate (GIR) of 4 10 mg/kg/minute

 Target: Titrate glucose infusion to achieve stable blood sugar values of > 40 mg/dL

Close monitoring of glucose levels (Every 15 30 min in acute phase followed by every 4-6 h)

IV glucose is gradually tapered and switched to oral feeding under glucose monitoring

In refractory hypoglycemia, not responding to IV glucose therapy, steroids are indicated. Prednisone, 1-2
mg/kg/day or hydrocortisone, 5 mg/kg, every 12 h is used

Steroids reduces peripheral glucose utilization and increases gluconeogenesis.

Second line drugs

1.Glucagon 2.Diazoxide

BCG Vaccine :-
Vaccine - Live-attenuated vaccine

0.1 0.4 million bacilli

Danish 1331 strain, freeze-dried multidose powder form in brown vials

Schedule - At birth, single dose or first contact earliest before 5 years

Dose/route - 0.1 mL intradermal left upper arm at deltoid insertion (5 mm wheal indicates

injection successful). Dose remains same for all ages

Diluent - Lyophilized NS only, never with diluted water

Side effects - Axillary lymphadenitis (BCGosis)

Regress on their own, no treatment nee antituberculous

Therapy , If abscess, I&D or aspiration

Contraindications - Cellular immunodeficiency, not with measles/MMR, hypogammagobulinemia

and SCID (severe combined immunodeficiency disease)

Typical reactionat BCG site - Instructions to mother:

3weeks

8 mm by 5 6 we scar

after 6 12 weeks
Measles Vaccine /MMR Vaccine :-
Contents - Measles: Edmonston-Zagreb virus 1,000 TCID50

Mumps: L-Zagreb strain 5,000 TCID50

Rubella: Wistar 1,000 TCID50

Trade names - Tresivac

Schedule 2019 IAP schedule:

MMR at 9 months, 15 months, and 4 6 years or 2 doses at 12 months and 4 6 years

Additional dose of MR vaccine during MR campaign irrespective of the vaccination status

NIS: MR vaccine 2 doses: 9 months and 16 24 months , Rubella to adolescents

Dose/route, volume - 0.5 mL SC in thigh

Side effects- Mild measles like illness after 7 days, rarely parotid swelling

Complications - anaphylaxis, TSS due to Staphylococcus contamination

C/I- immunocompromised, pregnant women, symptomatic HIV with CD4 < 15%

Avoid for 1 month if child on steroids >14 days prednisolone 2 mg/kg or equivalent

Injectable Polio Vaccine (IPV) / Inactivated Polio Vaccine

Vaccine- Killed vaccine

eIPV enhanced potency of IPV better vaccine stability now

Class/contents- 40, 20, and 32 kDa antigen units of type 1, 2, and 3 viruses, salk strain

UIP schedule: As of 2019, two fractional doses of IPV intradermally at 6 and14 weeks along with 5 doses

of bOPV at 0, 6, 10, 14 weeks and 16 18 months

Dose/route,volume - 0.5 mL IM/SC in thigh

S/E - Major S/E none, very safe

C/I - allergic reaction to previous dose

Hep B Vaccine
Content Killed subunit vaccine 20 mg/mL of antigen by recombinant DNA technique

Schedule At birth within 24 hours, 6, 14 weeks or 6, 10, and 14 weeks as pentavalent or 0, 1, and 6 months

Dose and route 0.5 mL IM in thigh >18 years 1 mL

Side effects Major S/E none

C/I serious hypersensitivity

Special remarks 1st dose within 24 hours is important to protect baby from hepatitis B infection from
 mother during delivery

DPT Vaccine
Contents:

- Diphtheria toxoid 25 Lf

- Tetanus toxoid 5 Lf

- B. pertussis 20000 million killed bacteria 4 IU

- Al. phosphate 1.5 mg

- Thiomersal BP 0.01 %

Age: 6 weeks, 10 weeks, and 14 weeks

Booster: 1 18 months , 2 4 ½ - 5 years

Route: Deep im

Site: Anterolateral aspect of thigh

Dose: 0.5 ml
Adverse Effects :-

from which the child invariably recovers in an hour or two

Typhoid Vaccine:
im: - Type: Vi polysaccharide vaccine

- Age : after 2 years

- Dose: 0.5 ml im single dose. Booster every 3 years

Oral: - Type: Live attenuated vaccine. S.typhi Ty2la strain

- Age: after 6 years

- Dose: on 1, 3,5 days 1 capsule

Differences between IPV and OPV:

IPV OPV
History Developed by Salk Developed by Sabin

Type Killed formalized vaccine Live attenuated vaccine

Contents Type 1 40D Attenuated strain conc

Type 2 8D Type 1 106 TCI D50

Type 3 32D Type 2 105 TCI D50

Type 3 105.5TCI D50

Schedule 3 dose at 6-8 week interval Zero dose at birth, 6, 10, 14 weeks

Route Im Oral

MOA (immunity) Induce circulating antibody Prevent paralysis as well as intestinal infection

Prevents paralysis but does not prevent infection

No intestinal immunity .

Use Not useful in controlling epidemic Can be effectively used

Cost Very costly, difficult to manufacture Cheap, easy to manufacture

Contraindication None - Acute infections

- Febrile illness

- Diarrhea and dysentery

- Malignancy - Corticosteroid therapy

Rabies Vaccine
Postexposure prophylaxis

Dose 1 mL IM injection anterolateral aspect of thigh/deltoid region (never in gluteal region) 0.5 mL for
PVRV

Schedule IAP 2019 recommendation Now shortened regimens are recommended

Postexposure prophylaxis:

4 doses of either

1 site IM of vaccine on days 0, 3, and 7 and between 14 days and 28 days

2 sites IM on day 0 and then 1 site on days 7, 21

Human RIG (rabies immunoglobulin) 20 U/kg (human) or ERIG 40 U/kg (equine) for all category III bites
Pre-exposure rophylaxis

Indications: Children exposed to pets at home or veterinary healthcare personnel

Schedule: 1 site IM on days 0 and 7

For reexposure after completed pre-/postexposure prophylaxis, only 2 doses on days 0 and 3

RIG is not required during reexposure treatment

Fever With Rash Causes, Measles c/f,Complications , Prevention

Causes :- 1. On the basis of day of appearance 2.On the basis of etiology

1.On the basis of day of appearance Varicella (D1) , Scarlet Fever(D2) , Small Pox(D3) ,Measles(D4)

Typhus(D5) , Dengue (D6) , Typhoid (D7)

2. On the basis of etiology

a. Viral Infections Measles , Rubella , Roseola ,CMV , EBV ,Parvovirus

b. Bacterial Infections Scarlet Fever , Lyme Diseases

c. Rheumat. Diseases ARF,PAN,Kawasaki ,HSP

Measles

Clinical features

Begins with secondary viremia

High fever, dry cough, coryza, conjunctivitis

Seen 2 days after the onset of fever

a.Tiny white raised spots on the reddish buccal mucosa opposite the second molars

b.Pathognomonic of measles

Typical morbilliform rash (Fig. 10.3) Seen 4 days after onset of fever

a. Starts behind the ears, then spreads to face, trunk, extremities, palms and soles

b. Confluent rash that desquamates in a week

c. Fades in about 7 days leaving brawny desquamation

Fever peaks with the rash and falls 2 3 days later

Measles complications:

1. Respiratory tract: otitis media, laryngitis, pneumonia

2. Encephalitis and subacute sclerosing panencephalitis (SSPE)

3. Digestive system Persistent diarrhea, appendicitis, hepatitis

4. Malnutrition vitamin A deficiency

5. Other acute glomerulonephritis, DIC

For Prevention Refer MMR Vaccine

Malaria Lab Inv. , Complications , Treatment

Diagnosis

Peripheral Smear- both thick and thin smear Gold standard for diagnosis

1. Thick smear is used to identify malarial parasites

2.Thin smear is used for species identification

Rapid Diagnostic Test

1.Parasite lactate dehydrogenase

2.Histidine rich protein 2 (HRP-2)

Quantitative Buffy Coat Technique Molecular Probes PCR Assay

Serology

1. Indirect Fluorescent antibody test (IFAT)

2. Indirect Hemagglutination antibody (IHA) test

3. Enzyme-linked immunosorbent assay (ELISA)

Complications:

- Algid malaria - Acidosis - Anemia - Black water fever

- Cerebral malaria - DIC - Pulmonary edema - Renal failure (acute) - Hypoglycemia

Treatment

Supportive treatment

Fluid Resuscitation

Hypoglycemia correction Antipyretics Blood Transfusion Diazepam/Midazolam For Seizures

- Chloroquine sensitive malaria:

o Chloroquine 10 mg base/kg stat followed by 5 mg base/kg at 6, 24, 48 hours. Repeat the dose if child
vomits within 30 min

Chloroquine resistant:

Quinine 10 mg salt/day orally TID x 7 days95

Or

Pyrimethamine 1.25 mg/kg + sulfadoxine 25 mg/kg as a single dose orally

 Or

Mefloquine 15 mg base/kg orally stat followed by 10 mg/kg 12 hours later

Complicated malaria:

o Quinine 20 mg salt/day (loading dose) diluted in 10ml/kg 5% dextrose iv over 4 hours;

followed 8 hrs later with 10 mg salt/kg (maintenance dose) over 4 hours 8 hourly,

until child can swallow oral quinine 10 mg/kg TID to complete 7 days of treatment.

Or

o Artemether 3.2 mg/kg im (loading dose) followed by 1.6 mg/kg im daily for 6 days.

Chemoprophylaxis:

- Chloroquine sensitive: Chloroquine 5 mg/kg daily

- Chloroquine resistant: Doxycycline 2 mg/kg daily

- Begins 1 week before entering the area (doxycycline is started 1-2 days before departure) and continued
for 4 weeks after leaving transmission area.

Enteric Fever Pathology,c/f,Complications ,Management

Incubation period: 14 days (3 60 days)

Clinical Features:

- First week of illness: o Step ladder pattern of fever not seen which is characteristically seen in adults

o Sudden onset fever with headache and vomiting

o Fever is continuous with little diurnal variations o Constipation o Coated tongue at center.

o Typhoid rash (nose spots) occurs on 6th day of illness.

Second and third week: o Abdomen distended and gives a tympanic note on gentle percussion

o Spleen palpable o Rales over bases of lungs

- In severe toxemia, child may have typhoid state in which child has muttering delirium and may pick at
bed clothes.

Complications:

- Oral: parotitis - Chest: pneumonia and pulmonary infarct

- Heart myocarditis - Liver and GB Fatty liver, hepatitis, cholecystitis, pancreatitis

- GIT Diarrhea, constipation - Neurological meningitis, encephalitis

- Musculoskeletal chronic osteomyelitis - Other Alopecia, uveitis

Diagnosis:

Clinical signs pathognomic of typhoid:

- In endemic area, typhoid should be a diagnostic possibility in all fevers > 7 days duration, especially those
without localizing signs - Bradycardia

Lab diagnosis:

- Hematology:

o Moderate neutropenia leading to relative lymphocytosis

o Thrombocytopenia

- Blood culture:

o Blood 1st week

o Stool and urine after 2 weeks

- Serology Widal test

o Diagnostic titer of > 1 in 80 after 7 10 days of illness

o 4 fold rise in titer is diagnostic

Treatment:

- Specific:

o Amoxicillin 100 mg/kg/day in 4 divided doses 10-14 days

o Ceftriaxone 50-100 mg/kg/day iv for 5-7 days

o Corticosteroid in children with altered mental state or shock

- Supportive treatment:

o Good nursing care o Nutritious diet

o Fluid and electrolyte o Antipyretics:

Prevention of HIV Parent to child transmission (PTCT)

1. Education

2. Take precautions while using blood/blood products

3.Screening blood/blood products

4. Use sterile injection equipment

5.No sharing of needles by drug users

6.Antenatal mother

7. Voluntary counseling and testing to test AN HIV status

8.Management of high risk factors

9. HAART when indicated for the mother

- Tenofovir (TDF) 300 mg + Lamivudine (3TC) 300 mg + Efavirenz (EFV) 600 mg to mother and

Single daily dose of Syrup Nevirapine (2mg/kg) for 6 weeks to newborn

Acute Diarrhoea causes , c/f,Complications , Management

Etiology Of Diarrhoea

A. Enteric Infections

Bacteria: E. coli, Shigella, Salmonella, Staphylococcus, Cholera vibrio, Yersinia enterocolitica,

Campylobacter jejuni, Clostridium difficile, Aeromonas hydrophilia. Vibrio parahemolyticus, Plesiomonas
shigelloides.

Viruses: Rotavirus, Norwalk and allied viruses, enterovirus. Influenza virus, measles virus.

Parasites: Ent. histolytica, Giardia lamblia, Cryptosporidium,H. nana, malaria

Fungi: Candida albicans.

Parental: URI, otitis media, tonsillitis, pneumonia, urinary tract infection.

B. Dietic/Nutritional: Overfeeding, starvation, food allergy, food poisoning.

C. Drugs: Antibiotics

D. Nonspecific

Clinical picture of differnt grades of dehydration

Mild - (3 to 5% weight loss) - Irritability or drowsiness; pallor; somewhat sunken eyes.

Moderate (6 to 10%weight loss) - Sick-looking child; pallor;weight loss) depressed fontanel; sunken
eyes;dry mucous membrane; dry and inelastic skin.

Severe (>10% weight loss) - Signs of superimposed shock,like coma, limpness, pallor, cold and clammy
skin, thin rapid or almost impalpable peripheral pulses; metabolic acidosis; oliguria or anu

C/F - vomiting,pyrexia,URTI, seizures,toxemia

Management

Objective: Prevention of dehydration It is carried at home and consists of

< 6 months 50 ml (1/4th glass)

7 months 2 yr 50-100 ml (1/4 ½ glass)

2 yrs 5 yr 100 200 ml (1/2 1 glass)

Later As much as the child accepts

caretaker to bring back the child after 2 days (even earlier in the presence of such danger
signals (fever, repeated vomiting, dehydration)

Plan B for Some Dehydration

Objective: Correction of dehydration and preventionof malnutrition

dration is carried out by administering ORS, 75 ml (50-100 ml)/kg over a period of 4

hours.

If adequately rehydrated, deal as in Plan A

If poor response to ORS, treat as in Plan C

Plan C for Severe Dehydration

Objective:

ml/kg over next 2 ½ hour.

-2 hour

If no improvement, give IV fluid more rapidly

If improvement, complement with ORS as soon the infant starts accepting it.

After 6 hours in infants and 3 hours in older children, opt for the suitable plan A, B or C depending on the
assessed hydration status

Complications/Sequelae

thromboembolism, seizures.

site of cut down.

 mental retardation in later life.

Assessment of Dehydration WHO

Signs No dehydration Some dehydration Severe dehydration

Look at Well alert Restless, irritable Lethargic or unconscious, floppy

Gen. condition

Eyes Normal Sunken Very sunken and dry

Tears Present Absent Absent

Mouth and Moist Dry Very dry

tongue

Thirst Drinks normally, not thirsty Thirsty, drinks eagerly Drinks poorly or not able

to drink

Feel skin

Pinch Goes backquickly Goes back slowly Goes back very slowly

Decide No dehydration 2/more signs Some dehydration 2/more signs Severe dehydration

Treat Plan A Plan B Plan C

Hirschsprung disease (congenital aganglionic megacolon)

Developmental disorder of enteric nervous system.

Failure of migration of neural crest cells down the gut during embryogenesis.

Characterized by absence of ganglionic cells in submucosal and myentric plexuses of distal intestine

Most common cause of lower intestinal obstruction in neonates

Clinical features

Usually diagnosed in neonatal period. Common features include failure to pass meconium in first 48
hours of life, abdominal distension, bilious or nonbilious vomiting, gastric aspirates and feeding intolerance

Older children present with long standing constipation with the onset since birth. Examination often
reveals distended, tympanitic abdomen with palpable fecal masses.

Can be associated with

Trisomy 21 Anorectal abnormalities MEN syndrome

Investigations

Plain X ray abdomen

1. Bowel distension with multiple air fluid levels

2.Absence of rectal gas

3. In enterocolitis Bowel wall thickening, mucosal irregularity with fluid levels.

Barium enema narrow aganglionic segment(Transition zone) with proximally distended bowel

Treatment

Surgery is only treatment of choice. Three-stage Surgery is done

Stage 1: Initially temporary colostomy is preformed to relieve obstruction before definitive surgery.
Biopsies are done to confirm the site of transition zone

Stage 2: Pull through procedure done to anastomose ganglionic colon and anus

Stage 3: Closure of colostomy

Acute viral hepatitis

Virus can affect the liver directly or a part of systemic involvement

Etiology

Hepatitis virus A, B, C, E

1. Hepatitis A virus is most common cause

2. HAV and HEV transmitted by feco oral route

3. HCV transmitted by parenteral or vertical

Herpes simplex virus

Clinical features

Prodromal symptoms are low grade fever, malaise, anorexia

Jaundice
 Examination shows icterus Mild ascites

Over next few weeks appetite improves and child gets better

Anicetric presentation of hepatitis A can occur

Complications

Pancreatitis

Serum sic Hem Chronic liver disease

Investigations

Normal albumin

Milk leukopenia with relative lymphocytosis

Ultrasound shows enlarged liver with increased echogenicity

Viral serologies

Management

Viral hepatitis is self-limiting which requires no active intervention if there is no complications

Maintain hydration with adequate oral intake

No specific dietary modification is recommended

Monitor the child for appearance of complications

Replacement of fat soluble vitamins A, D, E & K

Reduce stool transit time with syrup Lactulose

GI sterilization with non-absorbable oral antibiotics

Ursodeoxycholic acid (UDCA) 20 mg/kg/day for cholestasis

No antiviral drugs are required for acute HAV, HBV and HEV infection

Tenofovir and entecavir can be used in selective cases of acute HBV infection

Acute Liver Failure Management

Pediatric Acute Liver Failure Study Group (PALFSG) definition:

1.No history of known chronic liver disease

2.Evidence of acute liver injury (increased SGPT, serum bilirubin, PT)

3.Coagulopathy unresponsive to vitamin K

4.Prothrombin time (PT) >15 seconds or INR >1.5 with encephalopathy

PT >20 seconds or INR >2 without encephalopathy.

5.Coagulopathy is the only dependable symptom.

Signs of Liver Cell Failure:

a. Jaundice b. Diminished body hair c. Spider naevi d. Palmar erythema

h. Ascites i. Gynaecomastia j. Testicular atrophy Adults only k. Menstrual irregularities

Management

1. Immediate intensive care

Get two IV lines

Volume resuscitation followed by 10% D to maintain RBS 100 300 mg%

Hemodynamic monitoring

Strict input/output chart

Hepatic coma feeds nitrogen content 4% of total calories

Elective mechanical ventilation if grade III/IV encephalopathy

2.Basic workup

Liver function test - Serum bilirubin, sGPT a sharp rise may be seen , Low albumin Prolonged PT, USG
abdomen

Blood biochemistry: Electrolytes, blood urea, serum creatinine,sugar, calcium

Evidence of infection: Culture, viral markers, CBC, X-rays

Hyperammonemia a useful prognosticator, though not infallible diagnostic test

3.Management of hepatic encephalopathy

Bowel washes With acidic fluid (1 tsp vinegar in 0.5 liter water 6 hourly)

Lactulose oral/nasogastric 0.5 mL/kg/dose four times(adjusted till 3 4 loose stools/day

Enteral feeds No restrictions in grade I and II encephalopathy, vegetable protein preferred

Protein restricted to <0.5 g/kg in grade III

Phenytoin sodium if seizures

Avoid sedatives.

4.Management of coagulopathy
Gastrointestinal bleed ,Cold saline washes 4 6 hourly ,Antacids Ranitidine

5.Management of cerebral edema

Head end elevation ,Mannitol

No role of steroids ,Elective ventilation if needed.

6.Treatment of infections

At the earliest possible suspicion of infection

With broad-spectrum coverage ceftriaxone ± metrogyl

Take aseptic care

7.Definitive treatment liver transplant, especially if prognosis is poor

Indications :- PT >60 seconds ,Decreased transaminases ,Encephalopathy grade III.

Lactose Intolerance:
Definition: Lactose intolerance is the development of clinical symptoms resulting from lactase

deficiency following ingestion of lactose in water in a standard dose.

Cause: - Primary Autosomal recessive condition

- Secondary Acute gastroenteritis PEM Worm infestation

Malabsorption syndrome Animal milk allergy

Consequences: - Osmotic diarrhea - Metabolic acidosis

- Bacterial proliferation - Caloric loss

Clinical Features:

- Diarrhea Watery, frothy, greenish yellow, sour smelling stool

- Perianal excoriation - Failure to thrive

- Abdominal distension - Borborygmi, flatulence

Investigations:

- Stool pH <5.5 Reducing substance >0.5%

- Lactose tolerance test - Interstitial enzyme activity by biops

Treatment: - Primary Eliminate lactose from diet

- Secondary Treatment of primary cause.

Lactose free diet if persistent diarrhea, weight loss, reducing substance >1%

Idiopathic thrombocytopenic purpura (ITP) c/f , Management

 Immune thrombocytopenia due to autoantibody mediated consumption of platelets

Presents between 1 and 7 years of age

Two types based on duration of thrombocytopenia

Acute lasting less than 6 months

Chronic more than 6 months

Clinical features

Antecedent history of febrile illness but usually afebrile at presentation

Signs and symptoms depends on platelet count

Presents with sudden appearance of bruises and mucosal bleeding

Epistaxis, oral oozing, prolonged bleeding with superficial trauma

Petechiae and ecchymoses

Healthy child without any hepatosplenomegaly, lymphadenopathy and bony tenderness

Investigations

Complete blood count show low platelet count and other hematological parameters are normal

Circulating platelets are larger in size

Bone marrow examination shows increased megakaryocytes

Management

Routine Platelet transfusion should be avoided

Children with active bleeding should be given intravenous immunoglobulin 1 g/kg/day for 1 2 days or 50
75mg/kg of anti D-immunoglobulinin Rh positive children

Prednisolone 1 4 mg/kg/day for 2 4 weeks then tapered

3 weeks for 4 6 courses

Refractory cases immunosuppressive drugs like vincristine, cyclosporine, azathioprine, rituximab

Hemophilia
Most common hereditary clotting defects

Hemophilia B is caused by factor IX deficiency

Manifestations of hemophilia depends on level of clotting factors in blood.

Clinical features

Severity Clotting factor (% activity) Bleeding episodes

Mild 5 40 Severe bleeding with major trauma or surgery

Moderate 1 5 Mild spontaneous bleeding, severe bleeding with trauma, surgery

Severe <1 Spontaneous bleeding predominantly in joints and muscles

Treatment

Appropriate factor replacement

Judicious physiotherapy to prevent chronic joint disease

Counselling for injury prevention

Monitoring development of factor VIII and IX inhibitors

Desmopressin, synthetic analogue of vasopressin can induce factor VIII levels and is tried in mild cases

Acute bleeds should be treated early (within 2 h if possible)

Cryoprecipitate and fresh frozen plasma are used to control bleeding

Iron Deficiency Anemia c/f,Management

Iron deficiency anemia is the most common micronutrient deficiency.
Clinical Features:

Symptoms:

- Failure to thrive - Appear off color and easily fatigued

- Suffer from frequent infection - Pica

- Mental performance is reduced - Attention span decreased - Anorexia

Signs:

- Pallor - Tongue papillae are atrophied Koilonychia

- Thin brittle and flat nails - In case of CCF, cardiac enlargement, systolic murmur, JVP raised

Lab Diagnosis:

1. RBC Changes:

a. Hb, PCV, MCH, MCV, MCHC All decreased

b. PS 1. Microcytic, hypochromic red cells

2. Anisocytosis
 3. Poikilocytosis

4. Reticulocyte count decreased

2. Marrow changes: a. Persian blue staining decreased iron stores

3. Iron studies: a. Serum iron low <30 µg/dl

b. TIBC increased >350µg/dl

c. Transferrin saturation less than 15%

d. Serum ferritin less <10 ng/ml

Goals of treatment

1. Iron therapy including replenishing stores oral/parenteral

2. Treatment of underlying cause

3. Prevent recurrence by Diet counseling ,Iron supplements ,Fortification

Oral therapy

Ferrous sulfate is most effective and started at 3 6 mg/kg/ day in 3 divided doses for 4 6 months

Reticulocyte count increase in 72 96 h after initiating treatment

Absorption is best if taken on an empty stomach

Side-effects of oral iron therapy include nausea, vomiting, diarrhea, constipation, abdominal cramps

Hemoglobin rise following oral iron therapy is around 0.1 g/dL/day

Response to iron therapy:

- Child becomes less irritable in 24 hours and appetite improves

- Initial marrow response is observed within 48 hours

- Rise in reticulocyte count occurs by 2nd or 3rd day

- Elevation of Hb level

-Indications for parenteral therapy:- -Intolerance to oral iron Malabsorption Ongoing blood loss

- Commercially available preparations:- Iron dextran Iron sucrose

Iron ferric gluconate Ferric carboxymaltose injection

- intravenous iron sucrose is safe and effective

-Formula to calculate the dose of Iron (mg) = Weight in kg × Hb deficit (g/dL) × 4

-Rarely needed

Red cell transfusion are given in

emergency situation like severe anemia with cardiac failure or

with ongoing blood loss

when Hb levels are below 3 4 g/dL

Prevention

Exclusive breastfeeding for 6 months

Timely introduction of complementary feeding at 6 months

Iron supplementation for preterm/ LBW infants from 2 months

Intake of green leafy vegetables and sprouting green grams

Periodic deworming in endemic areas

Iron supplements for susceptible infants and children and at puberty, especially in girls

National Nutritional Anemia Control Program recommends 20 mg of iron and 100 µg of folic acid daily for
100 days every year

Thalassemia Major :- etiology,c/f, Management , Chelation Therapy

The hemoglobin consists of two pairs of amino acid -

Adult hemoglobin (HbA) consists of two pairs of

Fetal Hb is constitut
HbA2 is constitute

Deficiency or abnormalities in any of the Hb chains leads to thalassemia syndromes or abnormal

hemoglobinopathies

C/F:- 1.transfusion-dependent anemia 2. Splenomegaly 3.bone deformities

4.growth retardation and hemolytic facies in untreated or inadequately treated individuals.

5. Severe pallor 6. Symptoms of anemia irritability, intolerance to exercise, heart murmur

Investigations

1. Complete blood count Hemoglobin ranges from 2 8 gm/dL

MCV and MCH are low Reticulocyte count is elevated

Leukocytosis with shift to left Platelet count is normal

2.Peripheral smear: - Microcytic hypochromic cells

 - Anisocytosis tear drop cells, target cells - Poikilocytosis

- Marked basophilic stippling and various polychromasia - Fragmented RBC

3.Iron studies shows Increased Serum iron

Total iron binding capacity is normal Serum ferritin is increased

4.Osmotic fragility test reduced fragility

5.Xray skull shows hair on end appearance due to widening of diploic space

Treatment of Thalassemia Major

Principles 1.Packed red cell transfusions 2.Management of complications

3.Causative treatment 4.Future treatment

1.Transfusion Therapy Packed RBCs are the corner stone of treatment.

Aims :- a. To improve anemia

b.Suppress ineffective erythropoiesis

c.To prevent serious growth, neurological, and skeletal complications of thalassemia

d.To prevent hepatosplenomegaly hemolytic facies

When to start? Hb <7 g/dL ;

What is the Ideal Blood Transfusion? :- Volume 15 cc/kg ; Packed RBCs Fresh (4 5 days old)

Leukodepleted (bedside filters) or saline washed

ABO- and Rh-compatible ; Screened for HBV, HCV, CMV, TPI (syphilis)

Daycare Transfusion Centers New concept

Advantages

No hospitalization and transfusion on outdoor basis ; Children become familiar with the staff

Much cheaper ; Decreased chance of hospital-acquired infection

2.Management of Complications :-

Management of endocrine and cardiac complications

a.Curative treatment BMT/SCT

b.Hypersplenism role of splenectomy

Management of other complications

a.Gall stones/anemia/hypoxia/leg ulcers

b. Pharmacological methods to increase gamma chain synthesis

Iron Chelation Therapy :- Iron overload in thalassemia major is because of:

Excess GI absorption of iron

Lack of excretory mechanism for excess iron in the body ; Chronic red cell transfusions

Investigations Serum ferritin, liver biopsy/MRI, and ECG

Cardiac T2 MRI to assess cardiac iron overload

Indications Usually started at around 2 years or when 10 transfusions have been given.

Cumulative transfusion load of 120 mL/kg or greater

Indicated when serum ferritin is above 1,000 mg/L

Liver iron >3.2 mg/g of dry weight.

Aims of chelation: To keep serum ferritin <1,000.

Effect:- Promotes growth Decreases iron overload complications

Improves gonadal function Improves endocrinal complications.

Chelators Used

Desferrioxamine (DFO) SC/IM Deferiprone (DFP) oral Deferasirox (DFX) oral

40 mg/kg/day IV/SC infusion 75 mg/kg/day orally TDS with meals 30 mg/kg/day orally OD dispersible

over 8 hours for 6 nights/week Tablets dissolve in glass of water or

Vitamin C 100 mg daily helps DFO treatment orange juice Safe up to 80 mL/kg,

long t1/2 (18hours) once a day dose

3.Future treatment Gene replacement therapy, intrauterine BMT

4. Prevention of disease by antenatal diagnosis and genetic counseling

Sickle cell anemia:- enumerate crisis, c/f,Management

Autosomal recessive inheritance

Disease results from the substitution of valine for glutamic acid at position 6 of the beta globlin gene

Homozygous state for HbS gene manifest as sickle cell disease

Heterozygous state for HbS gene have sickle cell trait

Four types of crisis in sickle cell anemia:

1. Painful crisis/Vaso occlusive Crisis

2. Hyperhemolytic crisis
3. Aplastic crisis

4. Splenic sequestration crisis

Clinical features

1.Painful/Vaso-occlusive crisis :- Occurs due to obstruction to microvascular circulation by sickled red cells

Painful abdominal crisis occurs due to localized areas of bowel dysfunction

Severe abdominal pain and signs of peritoneal irritation

2. Hyperhemolytic Crisis :- Rare ,Due to rapid fall in Hb level

3.Aplastic crisis:- The causative organism is Parvovirus B19

The child presents with acute anemia, without eticulocytosis

Condition is always self-limiting with duration of 7 10 days

4.Sequestration crisis:- Sudden trapping of large amount of blood in spleen or less commonly in liver

Splenic dysfunction occurs due to obstruction of sinusoidal blood flow

5.Other clinical features:- Priapism, Megaloblastic crisis, Epistaxis, Retinal infarcts

Renal involvement Hyposthenuria, nephrotic syndrome

Gall stones, Delayed somatic and sexual growth

Investigations :- Anemia and thrombocytopenia Leukocytosis; Shift to left indicates infection

Peripheral Presence of Howell jolly bodies indicates asplenism

Sickling te Hemoglobin electrophoresis

Radiograph of chest and bones are taken during crisis period

Management

Hydration and analgesics are mainstay of treatment

Oxygen supplementation if hypoxia is present

Blood transfusion is useful in patients with aplastic crisis and acute sequestration crisis

Exchange blood transfusion is indicated in case of cerebrovascular accidents and acute chest syndrome

Pneumonia- etiology,c/f,Management
Pneumonia inflammation of lung parenchyma due to microorganisms.

Pneumonitis inflammation of lung parenchyma due to noninfectious cause.

Etiology:-
Age Bacteria Virus

Neonate GBS, Klebsiella ,Escherichia coli ,Listeria CMV

1 3 months S. pneumonia ,H. influenza CMV,RSV,Influenza

4 months 5 years S. pneumonia,HiB,Staphylococcus,TB, Adenovirus,Influenza virus,Measles

>5 years S. pneumonia,Mycoplasma,Staphylococcus, TBInfluenza,Varicella

Most common S. pneumoniae and H. influenza

Clinical features

Symptoms:- Triad of fever, cough, rapid and difficult breathing

Other features include lethargy, poor feeding, vomiting, irritability, and cyanosis

Localized chest, abdominal, or neck pain can be present

Signs:- Sick looking, toxic child Tachypnea, Nasal flaring, Chest indrawing, or Chest retractions

Oxy End inspiratory coarse crackles over the affected area

Classical signs of consolidation are

a.Dullness on percussion

b.Decreased breath sounds

c. Bronchial breathing over the affected area

Complications:-

Diagnosis:- Complete hemogram Acute phase reactants like CRP and ESR

Staphylococcal pneumonia Pneumatoceles

2.Streptococcal pneumonia Interstitial pneumonia

3.Atypical pneumonia Hazy or fluffy exudates from hilar regions

4.Pneumonia due to Gram negative organisms Unilateral/bilateral consolidation

5.Viral pneumonia perihilar and peribronchial infiltrates

6.Bronchopneumonia

7. Lobar pneumonia

Sputum culture (Only in suspected tuberculosis) or blood culture

 Serology serology, urinary antigens, rapid antigen detection test (RADT) and cold agglutinins for
mycoplasma

Nasopharyngeal swab for swine flu (H1N1)

Invasive procedures Bronchoscopy, BAL and lung aspiration, have high sensitivity and specificity

Treatment

Mainstay of management are antibiotics and supportive therapy

Supportive Treatment

Antipyretics ,Hydration ,Oxygen ,Antitussives have no/limited place in treatment.

Duration of antibiotics 10 days irrespective of the route of administration

Outpatient management

All nonsevere pneumonias more than 3 months of age First line oral antibiotics should be given for
minimum period of 5 days and second line for days

Age First line Second line

3 months to 5 years Amoxicillin Coamoxiclav/Cefuroxime/ Chloramphenicol

> 5 years Amoxicillin Macrolides/Coamoxiclav/ Cefuroxime

Indications of Hospitalization

Age <3 years , Severe acute malnutrition

Respiratory rate >70/min in infants and >50/minute in older children

Respiratory distress grunting, ICR or SCR , Dehydration

Comorbidities/complications/nonresponders within 48 72 hours.

Antibiotics :- <3 months Cefotaxime/Ceftriaxone ±Aminoglycosides

Bronchial Asthma :- c/f, Management

Def:- a chronic inflammatory disorder of the lower airway characterized by bouts of dyspnea
(predominantly esult of temporary narrowing of the bronchi by bronchospasm,
mucosal edema and thick secretions .

Clinical Features:-

1. Mild: Cough, tachypnea and wheeze without any chest indrawing and difficulty in speech and feeding.

Oxygen saturation >95%. PEFR > 80%.

2. Moderate: Cough, tachypnea and wheeze together with chest indrawing,

 difficulty in speech and feeding, pulsus paradoxus. PEFR and oxygen saturation are reduced.

Sensorium is normal.

3. Severe: Cyanosis, poor respiratory effort, silent chest, fatigue, altered sensorium.

Oxygen saturation and PEFR may be reduced (say <90% and 30%, respectively)

Investigations :-

1.Less than 3 years mostly, a clinical diagnosis.

Three episodes of wheeze in 1 year + Family history of asthma + Atopy personal family history

Cough >2 weeks without fever with good response to bronchodilators.

2.More than 5 years: IgE-increased possibility of persistent asthma, but good response to steroids

Peak Expiratory Flow Rate (PEF) 15% improvement after salbutamol inhalation

Spirometry decreased FEV1 ;Eosinophilia ;Skin testing for allergens to identify allergens

Management

1.Education: About noncommunicability, fear of allergens, etc.

Written action plan should be provided and detailed counseling about medications and inhalational
devices.

2.Environmental control:

Dust mites avoid carpets and wet mopping

Cockroach cover garbage, etc.

Fungus attend to damp walls

Avoid smoke and tobacco.

3.Pharmacotherapy: Inhalation therapy ideal and drugs three groups.

Quick relievers Preventers (controllers) Long-term (hours)/symptom relievers

Long-acting b2 agonists, e.g.
Short acting b2 agonists Steroids inhaled (ICS) and oral,
Salbutamol Salmeterol, Formoterol
Salbutamol, Terbutaline ,Adrenaline e.g. Budesonide Cycloserine ,
Bambuterol
LT receptor antagonists, e.g. montelukast

Stepwise treatment of asthma:-

Step 1: Intermittent :- Inhaled short-acting Beta-agonist as required for symptomatic relief. If needed >3

times/ week, move to step 2

Step 2: Mild persistent :- Inhaled short-acting Beta-agonist as required +

 inhaled budesonide, fluticasone or beclomethasone (100-200 µg) or

cromolyn sodium or sustained release theophylline or leukotriene modifiers

Step 3: Moderate persistent:- Inhaled short-acting Beta-agonist as required +

inhaled budesonide, fluticasone or beclomethasone (100-200 µg q 12 hr).

If needed, salmeterol (50 µg q 12-24 hr) and/ or sustained release theophylline

Step 4: Severe persistent:- Inhaled short-acting Beta-agonist as required +

inhaled budesonide, fluticasone or beclomethasone (200-400 µg q 12-24 hr) +

salmeterol or formoterol and/or sustained release theophylline +

oral low dose prednisolone on alternate days (if symptoms not relieved with above treatment)

Acute bronchiolitis
Bronchiolitis is inflammation and narrowing of bronchial tree, secondary to acute lower respiratory tract
infection. Infants are commonly affected, but can also affect children upto 2 years of age

Etiology: Viral: Respiratory syncytial virus ; Adenovirus, influenza virus ; Parainfluenza virus 1, 2, 3

Bacterial: Mycoplasma pneumonia

Clinical Features:

Symptoms: - Cough, dyspnea, fever

- Gradual development of respiratory distress - Rhinorrhea

- Characterized by paroxysmal wheezing cough - Difficulty in feeding.

Signs: - Tachypnea - Tachycardia

- Use of accessory muscles of respiration Chest retraction

- Respiratory distress is out of proportion to the extent of physical sign in lungs.

- Expiration prolonged, fine rale and rhonchi are auscultated.

Investigations:

- X Ray: Hyperinflation and infiltrates , Lung field and abnormality translucent , Diaphragm pushed down

- ABG - Serum electrolytes

Treatment:

- Nursing care: humid atmosphere preferably sitting position at 30o-40o angle with head and neck elevated

- Oxygen: keep O2 saturation above 95% - IV fluids - Antibiotics

- Ribavirin: shortens the course if given in the early stages delivered by an nebulizer 16 hours a day for 3-5
days.
Acute respiratory infection (ARI) control programme:-
Crux of the program is to diagnose and treat children with symptoms and signs of ARI at the community

level by training the field workers & early referral if needed.

WHO protocol comprises 3 steps:

Case finding & Assessment

Case Classification

Institution of appropriate therapy

Step 1: Case finding & Assessment

Cough & difficult breathing in children < 5 years age

Fever is not an efficient criteria

Step 2: Case Classification

Children are divided into 2 groups: - Infants < 2months & -Older children 2 59 months

Specific signs to be looked: In younger children, signs like feeding difficulty, lethargy, hypothermia,
convulsions.

In infants < 2 months

Pneumonia is diagnosed if RR 60/min with other clinical signs

All cases should be hospitalized

All cases should receive IV medications

Minimum duration of antibiotic therapy - 10 days

Combination of Ampicillin & Gentamicin is Preferred.

Child 2 months to 5 years

Severe pneumonia

No pneumonia (cold & cough)

Step 3: Institution of appropriate therapy - Antibiotics

Cotrimoxazole: 6-10 mg/kg per day

Chloramphenicol: 25 mg/kg every 6- Amoxicillin: 20-30 mg/kg/day in three divided doses

Prevention of ARI

Keep young Exclusive breast feeding up to 6 months

Better MCH Vitamin A prophylaxis

CCF :- c/f,Management
Def:- Clinical syndrome characterized by inability of the heart to pump enough blood to meet the
demands of the body, to maintain systemic or pulmonary venous return adequately or both.

Clinical Features:

A. Symptoms: a. Poor weight gain b. Difficulty in feeding c. Breathes too fast

d. Breathes better when held against the shoulder e. Persistent cough and wheezing

f. Irritating, excessive perspiration and restlessness g. Puffiness of face h. Pedal edema

B. Signs:

Left Both Side Right

Tachypnea Cardiac enlargement Hepatomegaly

Tachycardia Gallop rhythm (S3) Facial edema

Cough Peripheral cyanosis Jugular venous engorgement

Wheezing Small volume pulse Edema affect

Rales in chest Absence of weight gain

Diagnosis

History of poor feeding (suck rest suck cycle), fore head sweating in infants. Dyspnea on exertion, easy
fatigue, puffy eyelid, and swollen feet is seen in older children.

Findings on examination are,

Compensatory mechanism tachycardia, cardiomegaly, perspiration.

Pulmonary congestion tachypnea, dyspnea, orthopnea, PND, lung crept.

Systemic congestion hepatomegaly, puffy eyelid, distended neck vein

The chest radiography shows Cardiomegaly,

ECG used to find the cause Echo shows LV dysfunction

Treatment:

Management consists of four pronged attack for the correcting of inadequate output.

a. Reducing cardiac work

b. Augmenting myocardial activity

c. Improving cardiac performance by reducing heart size

d. Correcting underlying cause.

Aim of the treatment is to

Eliminate cause (Thyroid, Congenital Heart Disease, Hypertension, Fever, Infection)

Treat contributing factor(Anemia, Arrhythmias)

Control failure features

General measures:

Infant seat (head end elevation)

Oxygen supplementation

Providing adequate calories (160 kcal/kg/day)

Salt restriction (<0.5 gm/day)

Bed rest

a. Reducing cardiac work.

1. Restriction of activities nursing in propped up position

2. Sedative morphine 0.05mg/kg sc

3. Treatment of fever, anemia, obesity

4. Vasodilators

b. Augmenting myocardial activity

1. Digitalis

2. Dopamine, dobutamine

3. Amrinone and Milrinone

Digitalis: Total digitalizing 0.04 mg/kg

Maintenance 0.01 mg/kg/day

Dose given in fraction ½, ¼, ¼ at 0, 8, 16 hours

Parenteral dose is 7/10 of oral One day drug holiday in a week

c. Improving cardiac performance

1. Digitalis

2. Diuretics

3. Salt restriction
Stepwise management:

1. Frusemide 1mg/kg/dose + Amiloride/Triamterene

2. Add Digoxin

3. Add ACE inhibitor and stop K+sparing diuretics

4. Add Isosorbide nitrate

5. Intermittent dopamine + dobutamine (in separate iv) or dobutamine.

6. Myocardial biopsy & add immunosuppression with steroids in case of active myocarditis -Blocker in
cases without active myocarditis

7. Cardiac transplantation

TOF:- Components , Cyanotic Spell C/F , Management

It is the most common cyanotic congenital heart disease

TOF Components:

1. VSD

2. Pulmonic stenosis

3. Overriding dextroposed aorta

4. Right ventricular hypertrophy

Cyanotic spell :- Events like waking up in the morning or exertion (excessive crying/straining for
defecation) which decreases the systemic vascular resistance, initiates the spell.

Onset: 1 month 12 year usually.

Peak: 6 12 months

Natural History: Gradual decrease in frequency with increase in the age

Decrease in severity beyond 2-3 years

Typical Attack:

Usually occurs in the morning.

Any valsalva maneuver (crying, feeding, defecation)

Increase rate and depth of respiration with restlessness

Cyanosis
 Increasing cyanosis

Gasping respiration

Syncope (convulsion may occur)

Mechanism:

Valsalva maneuver

Increased O2 demand

19

Hyperpnoea

Cyanotic spell

Investigation:

ECG: Right ventricular hypertrophy and right axis deviation.

Chest X ray shows boot shaped heart; lung fields may be oligemic or normal (due to PS or right to left
shunt) or with right sided aortic arch.

ECHO confirms the diagnosis, coronary angiogram delineates the origin of the left anterior descending
coronary

Treatment :-

1. Knee chest position/ squatting position

2. Humidified O2

3. Morphine 0.1mg/kg sc for sedation

4. Correct acidosis. Obtain pH give sodium bicarbonate iv.

5. Propranolol 0.1 mg/kg iv during spell.

Long term 1 mg/kg 4-6 hourly orally.

6. Vasopressor methoxamine(vasoxyl) im/iv

7. Correct anemia

8. Consider operation. -Long term

a. Blalock Taussig shunt

c. Waterston shunt

PDA:
Clinical Features:

Symptoms: Small: Asymptomatic. Poor exercise tolerance

Large: Effort intolerance ; Palpitation ; Recurrent chest infection

Signs:

Cyanosis / clubbing of lower limbs if severe.

Pulse: Water hammer pulse

Precordium: Hyper dynamic apex Palpable D2 Right ventricular heave

Auscultation: S1 accentuated and D2 loud.

Gibsons/machinery/mill wheel murmur (continuous murmur)

Investigation:

Chest radiograph: May be normal in small PDA; Cardiomegaly and increased pulmonary vascular
markings in large PDA

- LVH ; RVH if pulmonary vascular obstructive disease develops

Biventricular hypertrophy in large PDAs

ECHO

Treatment:
 Asymptomatic sm and they should be followed for 6 months for
spontaneous closure.

Medical management:

Pharmacological closure with indomethacin/ibuprofen is attempted in preterm with symptomatic PDA,

unless contraindicated by renal failure or bleeding tendency in the infant.

Surgical closure:

Surgical ligation is done if medical management fails. Commonly used approach is by posterolateral
thoracotomy PDA either ligated/hemoclipped.

Acute Rheumatic Fever :- etiolopathogenesis,c/f,Jones Criteria , Management

Definition: ARF is delayed, nonsuppurative sequelae of upper respiratory tract infection caused by Group A
beta hemolytic Streptococci (GAS).

-It affects joints, skin, subcutaneous tissue, brain and heart. Except heart involvement, all others are
reversible, requiring only symptomatic therapy during the acute episodes.

Epidemiology:- - The incidence of rheumatic fever is closely related the incidence of group A

streptococcal pharyngitis.

- Rheumatic fever is more common in the age group of 5-15 years.

- Both the sexes are equally affected.

- predisposing factors :- poor socioeconomic status, overcrowding and

unhygienic living conditions.

-more common during fall, winter and early spring, coinciding with increased incidence of

streptococcal infections.

The etiology of rheumatic fever is unknown. A strong association with beta hemolytic streptococci of
group A is indicated by a number of observations:

i. History of preceding sore throat is available in less than 50% patients

ii. Epidemics of streptococcal infection are followed by higher incidence of rheumatic fever

iii. The seasonal variation of rheumatic fever and streptococcal infection are identical

iv. In patients with established RHD streptococcal infection is followed by recurrence of acute rheumatic
fever

v. Penicillin prophylaxis for streptococcal infection prevents recurrences of rheumatic fever in those
patients who have had it earlier

Etiopathogenesis:- Delayed, non-suppurative sequelae of Group A Beta hemolytic Streptococcal

pharyngitis.
 Molecular mimicry theory M proteins of GAS (M1, M5, M6, and M19) and myocardial

proteins like myosin.

- Mean latent period between the sore throat and clinical manifestations is 18 days.

Valvular involvement Mitral valve is more affected than aortic, tricuspid and pulmonary valves.

Aschoffs bodies in the atrial myocardium is pathognomonic of ARF.

Clinical features:-

History of streptococcal pharyngitis 1 to 4 weeks before the onset of symptoms is usually present.

Other features like pallor, easy fatigability, malaise, epistaxis, and abdomen pain may be seen.

Revised jones criteria 1993 (Updated 2015)

Major criteria Minor criteria

1. Pan carditis a) Clinical

2. Polyarthritis 1. Fever > 38.5°F

3. Chorea 2. Polyarthralgia (in the absence of arthritis as major criteria)

4. Subcutaneous nodule b) Laboratory

5. Erythema marginatum 3. Elevated acute phase reactants (ESR, CRP)

4. ECG: Prolonged PR interval > 0.16 s (in the absence of carditis as

major criteria)

Essential Criteria Supportive evidence of preceding streptococcal infection

1. Positive throat culture or rapid streptococcal antigen test (Streptozyme test)

2. Elevated or increasing streptococcal antibody titer

a. Anti streptolysin O (ASO titer: >333 unit for children and >250 for adults)

b. Antideoxyribonuclease B

1.Carditis (Pancarditis) :-

a. Pericarditis: Chest pain, Pericardial Rub, Pericardial effusion (never tamponade)

Myocarditis: a. Resting tachycardia (look for sleeping PR) or disproportionate tachycardia for fever

b. Soft S1, S3 gallop c. Cardiomegaly, CHF is more common in recurrence.

d. Myocardial contractility is not impaired and serum level of troponin not elevated

b. Endocarditis: a. Mitral systolic murmur Pan systolic murmur of MR

b. Mitral diastolic (Carey Coombs) murmur with no presystolic accentuation.

 c. Aortic diastolic murmur. 80% of carditis occurs within first 2 wks

2. Arthritis (Migratory polyarthritis):- Earliest, Least specific, Large joints (ankle, knee, wrist, elbow)

affected simultaneously/succession.

Swelling, pain, warmth, severe tenderness and limited motion of joint. No residual deformity.

):- Irregular, non-repetitive, quasi purposive involuntary movements

can last for18 months.

Usually proximal, but may affect fingers, hands, face.

4.Subcutaneous nodules:- Hard, painless, freely mobile, non-pruritic on Extensor aspect.

5. Erythema marginatum:- Red macules with serpengineous margins, are non-pruritic.

Diagnosis:

2 Major Criteria

Or

1 Major and 2 Minor criteria

Plus

Essential criteria

Investigations

To detect presence of inflammation/ rheumatic activity.

1.ESR Always elevated in Acute Rheumatic Fever

2. Abnormal ESR > 60 mm/1 h in Rheumatic Fever

3.CRP A value more than 6 mg/dL is diagnostic.

Throat culture positive only in 20% 30% (Positive throat culture is less reliable than
antibody test for GAS

- ECHO

To know severity of valvular involvement stenosis/regurgitation.

-ray (cardiomegaly suggest severe carditis)

) prolonged PR interval, ventricles and left atrial enlargement.

Treatment:

Principles of treatment:

a. Treatment of group A streptococcal infection.

b.Control of inflammation with anti-inflammatory drug.

c.Treatment of complications.

relief:

a.Analgesics for pain relief (Aspirin should be avoided till diagnosis is confirmed).

b.Indications for Hospitalization is needed for

Moderate to severe carditis

Severe arthritis

Chorea.

c.Rest is individualized according to symptoms

Specific measure:

Control of inflammation with Anti-inflammatory agents:

Total duration of antiinflammatory therapy 12weeks

Aspirin and steroids are primarily used to control inflammation. Naproxen and methylprednisolone can be
used alternatively

Prevention:

Primary Prevention:

1.10 day course of Penicillin. Penicillin-V (oral) children: 250 mg qid ; adult: 500 mg tid

2.30% have sub clinical pharyngitis, hence may not seek medical treatment.

3. 30% develop ARF without symptoms of streptococcal pharyngitis.

- Chronic antibiotic therapy in confirmed cases to prevent secondary steptococcal infection.

Infective Endocarditis : Management

Definition:- IE is defined as infection of endocardium lining the heart valves, mural endocardium and blood
vessels.

Diagnosis:

Underlying heart disease, tooth ache or dental procedure , tonsillectomy, prolonged low

grade fever , loss of weight and appetite , myalgia, arthralgia, and easy fatigability.
1. Heart murmurs new or changing intensity of murmur.

2. Fever 101 103°F. 3. Splenomegaly

4. Dermatological finding due to embolization/immune phenomenon.

5. Petechiae mucus membrane/skin, Splinter hemorrhage, Janeway lesion, Oslers nodes

6. Pulmonary emboli (in VSD, PDA), CNS emboli seizures/focal neurological deficit (in aortic/mitral valve

7. Caries tooth, clubbing of finger, appearance of new signs of CCF.

1. Positive blood culture is seen in more than 90% of cases and previous antibiotic use decreases the yield
to 40%.

2. Three separate blood samples for culture in 24 h;

If no growth in second day, 2 more cultures can be obtained.

a. No more than 5 cultures in 2 days are advisable (3 mL in infant, 5 mL in children).

b. CBC shows anemia,thrombocytopenia and raised ESR.

Treatment:

: The antibiotic therapy should be instituted immediately once a definitive diagnosis is

made and a total of 4 6 week of treatment is recommended.

Initial empirical antibiotic is antistaphylococcal semisynthetic penicillin + aminoglycoside and if MRSA is

suspected then vancomycin instead of penicillin is used.

Final antibiotic choice depends on blood culture antibiotic sensitivity test.

Indications are

1.Progressive CCF 2. Malfunction of prosthetic valve

3.Positive blood culture positive even after 2 weeks of antibiotics 4. Bacteriological relapse cases

Prevention & Prophylaxis

-The best method to prevent infective endocarditis is early appropriate surgical treatment of the
underlying heart disease.

. Proper hygiene and treatment of other foci of infections are also important.

Antibiotics before various medical procedures (dental manipulation, colostomy, etc.) may reduce the
incidence of infective endocarditis in susceptible patients

Appropriate dental care and oral hygiene.

Acute GN :- Etiopathogenesis,c/f,Complications,Management (PSGN is Same)

Def:-Acute glomerulonephritis (GN) is characterized by abrupt onset of hematuria, oliguria, edema and
hypertension.

Def :- PSGN is a postinfectious sequelae secondary to nephritis and pharyngitis caused by group A beta
haemolytic streptococcus.

-It occurs most often beyond the age of2 years. Males suffer more frequently.

-Postinfectious GN is the most common cause of GN in children out of which approximately 80% cases
have poststreptococcal etiology.

- IgA nephropathy is the most common cause of acute nephritis in less than 5 years

Etiopathogenesis:- Cause of Acute Glomerulonephritis (Acute GN)

1. Postinfectious:-

a.Bacteria: Gr -hemolytic Streptococci (M/C), Staphylococci, Pneumococci, Meningococci,

b.Viruses: Hepatitis B and C, Cytomegalovirus, Ebstein-Barr virus

c. Parasites: Plasmodium malariae, P. falciparum, Toxoplasma

d.Misc: Infective endocarditis, Infection of indwelling catheters.

2. Noninfectious:-

a.Primary renal diseases:-

IgA nephropathy Mesangial proliferative glomerulonephritis

Focal segmental glomerulosclerosis

Membranoproliferative glomerulonephritis

b.Systemic diseases:- Vasculi Microscopic polyangiitis , HSP

Connective tissue diseases: Lupus nephritis

c.Drugs:- Gold, Penicillamine

-In all probabilities, it results secondary to a preceding streptococcal (beta-hemolyticus type 12) infection

of throat or skin.

-A history of upper respiratory infection, infected scabies or impetigo, 7 to 14 days previously,

is positive in most of the patients.* In some it may complicate scarlet fever

1. Basic mechanism of pathogenesis in AGN is due to Molecular mimicry.

Antibodies against streptococcal antigens react with normal glomerular antigens leading on to immune
complex formation and subsequent complement activation.

2. Deposition of immune complexes formed either in the circulation or binding of antibodies to antigens
 trapped in the glomerulus leads to activation of complement pathway.

Depression in the serum complement(C3) provides a strong evidence of immune mediated renal injury.

3. Release of leukocyte, macrophages, cytokines further accentuates renal injury.

Clinical features:-

1.PSGN is commonly seen in children aged 5 12 years with male preponderance.

Affected children classically present with acute onset nephritic syndrome

- 1 2 weeks following streptococcal pharyngitis or 3 6 weeks after a streptococcal skin infection.

- Acute nephritic syndrome occurring within 3 4 days following respiratory or GI infection

suggests IgA nephropathy or Alport syndrome.

-Patients present with edema, hypertension and oliguria depending on the severity of renal involvement.

2.Edema starts as Facial puffiness and can progress to Pedal edema, ascites and anasarca in severe cases.

3. Gross hematuria, often described as

4. Patients with hypertension should be monitored for symptoms of encephalopathy such as blurred
vision, headaches, altered mental status and seizures.

5.Nonspecific symptoms like malaise, lethargy, abdominal/flank pain can occur.

Complications

Hypertension (60%) and Hypertensive emergency (10% cases)

Heart failure and Pulmonary edema

Dyselectrolemia: Hyperphosphatemia, Hypocalcemia

Differential Diagnosis

a. hemolytic uremic syndrome b. infective endocarditis c. acute pyelonephritis

d. acute glomerulonephritis occurring in vasculitis (anaphylactoid purpura, SLE, polyarteritis nodosa,

Wegener granulomatosis)

e. membranoproliferative glomerulonephritis d. hepatitis B

g. nephrotic syndrome accompanied by hematuria, IgA nephropathy and familial nephropathy(Alport

syndrome).

These conditions are easily excluded by their associated features.

Investigations :-

1.Laboratory findings

Urine analysis reveals dysmorphic RBC cells,

 RBC cast, polymorphonuclear leukocytes and proteinuria

Normochromic anemia (hemodilution), Low grade Hemolysis, Raised ESR

Increased blood urea and creatinine

Electrolyte abnormality Hyponatremia, Hyperkalemia, Metabolic acidosis

Low serum C3 level can be demonstrated in the acute phase but usually normalizes by 5 6 weeks.

Evidence of prior streptococcal infection required for confirming diagnosis

a. ASO titres (Sore throat) and Anti DNAase B titres (Skin infection) increased

b.Streptozyme test

c.Throat swab for Beta hemolytic streptococcus

2.Light microscopy

a. Enlarged and ischemic glomeruli

b. Endothelial and diffuse mesangial cell proliferation

c. Neutrophilic infiltration in early stages

d.Crescents and interstitial inflammation seen in severe cases

3.Electron microscopy and complement on sub-epithelial side of

glomerular basement membrane and in mesangium

4.Immunofluorescence - Granular deposits of IgG and complement along

deposit

5. X-ray chest prominent broncho-vascular marking indicating hypervolemia, rarely, cardiomegaly and
pulmonary edema

6. Indications for Renal biopsy :- a. Acute Renal failure b.Nephrotic syndrome

c. Renal function impaired severely beyond 10 14 days

d. Serum C3 remains low for more than 2 months e. Unresolving glomerulonephritis

Management :- Treatment is mainly symptomatic.

Patients with oliguria and hypertension should be hospitalized. Strict bed rest is not required in mild cases.

Diet: -Sodium and fluid restriction

- Protein and Potassium restriction till renal insufficiency normalizes

- Diet protein should be restricted until blood levels of urea reduces and urine output increases

Daily weight monitoring - Fluid intake is to be reduced if weight gain is evident.

Fluid restriction - Fluid intake should be restricted to insensible losses and 24 h urine output.
Hypervolemia can worsen hypertension and precipitate pulmonary edema secondary to left ventricular
failure

Diuretics -Not indicated in mild edema

-Furosemide (2 4 mg/kg) in presence of pulmonary edema

Hypertension -Fluid and salt restriction

- Antihypertensives include beta blockers, ACE inhibitors and nifedipine

- Malignant hypertension would require prompt treatment with IV nitroprusside or labetalol

Left ventricular failure -Hypertension should be controlled

- Intravenous furosemide to induce diuresis

- Urgent dialysis if no immediate diuresis after IV furosemide administration.

required in severe renal failure, prolonged oligoanuria, fluid overload and severe electrolyte
abnormalities.

: Penicillin course for 10 days to limit the spread of nephritogenic strains.

Nephrotic Syndrome :- Etiopathogenesis,c/f,Complications ,Management of 1st Attack

Definition: Clinical condition characterized by massive proteinuria, hypoalbuminemia, generalized edema
and associated hyperlipidemia.

Values:

a. Proteinuria: >40mg/m2/hour ; >1g/m2/day ; >50mg/kg/hour ; 3+/4+ by dipstick

b. Hypoalbuminemia Serum albumin <2.5g%

c. Hyperlipidemia Cholesterol >250mg%

Causes of Nephrotic syndrome:-

1.Idiopathic Nephrotic syndrome

disease (Most common)

glomerulosclerosis

nephropathy

2.Secondary causes

- Endocarditis ; Hepatitis B, C, HIV-1 ; Malaria ; Toxoplasmosis, Schistosomiasis

- Captopril ; Penicillamine ; NSAIDs

Allergic Disorders :- Vasculitis syndromes ; Food allergens ; Serum sickness

3.Genetic causes

-typecongenital nephrotic syndrome glomerulosclerosis

-Drash syndrome

Pathogenesis :-

- Increased permeability of glomerular capillary wall is basic abnormality in nephrotic syndrome.

-Podocytes are epithelial cells of the glomerular capillary loop.

-Foot processes of a podocyte are connected by slit diaphragm.

-Components of slit diaphragm inlcude -actinin 4.

- Foot process and slit diaphragm forms glomerular filtration barrier for proteins.

-Podocyte injury leading on to its effacement or genetic mutations of genes producing podocyte proteins

may cause nephrotic-range proteinuria

Clinical features

Age of onset ars with male predisposition (2:1 ratio)

Insidious onset with peri-orbital facial puffiness and pedal edema. Edema progresses to involve

extremities, trunk, Abdomen (Ascites), pleura (hydrothorax) and genitalia.

Anorexia, irritability, abdominal pain and diarrhea are common alongwith Classical Features.

Blood pressure is normal

Increase in cholesterol, triglycerides, LDL and VLDL.

Spontaneous bacterial peritonitis:-

a.Presents with fever, abdominal pain, and peritoneal signs.

b.Peritoneal leukocyte counts >250 cells/uL are highly suggestive of spontaneous bacterial peritonitis.

Investigation:

A. To confirm the diagnosis:

a. CBP: Anemia ; Leukocytosis

b. ESR: Elevated.

c. Urine: Proteinuria 4+ ; Hematuria +/- ; WBC to rule out UTI

d. Serum Albumin:< 2.5g%

e. Serum Cholesterol: > 250mg%

f. Serum BUN & Serum creatinine MCNS

B. To rule out infection:

a. Blood culture b. Mantoux test TB

c. X Ray chest Pneumonia, TB d. Urine culture

e. Peripheral smear malaria f. Australia Ag Hepatitis B g. VDRL Syphilis

C. Additional test:- Frequent relapses

Resistant to steroids

C3 level -

ASO titer -

Throat swab - + in GN

Complications

Edema Infections Pneumonia, Peritonitis, Cellulitis, Meningitis are common

Thrombosis of rena Hypovolemia and Acute renal failure

Steroid toxicity Cushingoid facies, Fluid retention, Hypokalemia, Hypertension, Gastritis, Infections, and
Osteoporosis

Treatment

Salt restriction

Diuretics to reduce edema day in 2 divided doses

Steroids are mainstay therapy in nephrotic syndrome.

Prednisolone is the drug of choice. Prednisolone is started at 60 mg/m2/day or 2 mg/kg/day for 4 6 weeks.

weeks), maintenance treatment

with alternate day low dose prednisolone is started (40 mg/m2 / day or 1.5 mg/kg/day).
Hematuria:- Define , Causes , Evaluation
Hematuria is defined as the presence of at least 5 red blood cells (RBCs)/microliter of urine

Presence of blood in urine can impart various hues to urine, deep red, brown and pink

Concentrated urine can sometime be mistaken as hematuria

Porphyria and beet ingestion and certain drugs like rifampicin can also lead to red/orange coloured urine

Uric acid crystals can lead to faint pink color of urine.

Causes of hematuria in children

1.Upper Urinary Tract Disease

Alport syndrome

- nephropathy Rapidly progressive GN

2.Multisystem disease:- -uremic syndrome

 granulomatosis

3.Vascular:- Renal vein thrombosis

Crystals in urine

4.Lower Urinary Tract Disease:- Trauma

Coagulopathy

Lab investigation

Fresh urine specimen is examined for

a.Red cells/casts and protein, Dysmorphic RBC

b.Urinary calcium creatinine ratio for hypercalciuria

Plain X-ray and ultrasound abdomen to rule out renal and urinary tract anomalies and calculi

Blood levels of urea and creatinine

Renal biopsy for light microscopy, immunofluorescence and electron microsocpy

a. Hematuria associated with heavy proteinuria b. History of Renal disease in the family

c. Evidence of Chronic kidney disease d.Persistent Hypertension e.Persistent microscopic hematuria

Vesico uretric reflux (VUR):-
Retrograde urinary flow from bladder into upper urinary tract during micturition.

Underlying pathology includes i junction due to shortening and

lack of obliquity of submucosal and intravesical segment.

VUR can lead to progressive renal damage and scarring in the presence of UTI
 - 1. Acute pyelonephritis 2. Reflux nephropathy

Etiology

a. Autosomal dominant condition.

b.Valve at the uretero-vesicle junction preventing retrograde flow of urine is defective.

High intravesical pressure seen in

a. Neurogenic bladder (Myelomeningocele/Spinal cord injury)

b. Bladder outlet obstruction (Posterior urethral valve)

c. Bladder dysfunction

Clinical features

Recurrent febrile urinary tract infection

Renal insufficiency

Grading of vesicouretric reflux

Grade I Reflux limited to ureter (no dilatation)

Grade II Reflux upto pelvis. calyces not dilated and fornices are normal

Grade III Reflux + Mild dilatation of Ureter ± blunting of fornices.

Grade IV Reflux + Moderate dilatation of Ureter and calcyes ±, blunting of fornices but presereved

papillary impressions

Grade V Reflux + Severe ureteral dilation and tortuosity and loss of fornices and papillary impression.

Diagnosis:-

Radio nuclide cystogram More sensitive and specific

Radio contras DMSA to detect renal scarring

Treatment

Asymptomatic bacteriuria does not require treatment.

In symptomatic UTI, the major aim is to prevent renal scarring and its complications.

Children less than 3 months and those with complicated UTI should be hospitalized and receive
parenteral antibiotics

Amount of oral fluids should be increased and child should be encouraged to frequently empty

bladder.
 Cephalosporins and aminoglycosides are safe and effective drugs for empirical therapy.

Oral drugs for empirical therapy include amoxicillin, cotrimoxazole and nitrofurantoin.

Drugs are modified based on organism growth in urine culture and sensitivity pattern

Differentiate Between AGN And Nephrotic Syndrome In Urine Analysis:

AGN NEPHROTIC SYNDROME

- Hematuria -

Gross >5 RBC/HPF +/-

RBC Cast: + -

- WBC, granular cast Cellular and granular cast

- Oliguria Rare

- Proteinuria 1+/2+ Massive proteinuria,

> 2 g/day

>40 mg/m2/day

>1 g/m2/day

>50 mg/kg/hour

3+/4+ dipstick

Diabetic Ketoacidosis :- Management

1. DKA is a life threatening emergency.

2. Principles of DKA management

Immediate restoration of fluid volume

Correction of acid-base status

Correction of Dyselectrolemia

Treatment of hyperglycemia

3. Initial lab evaluation should include

Blood sugar, blood and/or urine ketone

Serum Electrolytes - Sodium, potassium, chloride, bicarbonate, calcium and phosphorus

Electrocardiogram, ABG analysis Blood culture and urine microscopic examination.

Classification of severity in DKA

Blood glucose mg/dL Arterial pH Serum HCO3mEq/L

Mild DKA 200 - 250 7.24 7.3 15 18

Moderate DKA >250 7.0 7.2 10 15

Severe DKA >250 <7.0 <1

Treatment of mild DKA:-

(200-250 mg/dl glucose, mild dehydration, pH 7.2-7.3 and bicarbonate 10-15 mmol/L)

Oral rehydration with sugar free fluid

Insulin therapy: 1 - 2 units/kg of soluble insulin

(50% dose given intravenously and other 50% subcutaneously followed by 20% of the initial dose every 1
to 2 hours subcutaneously.

Treatment of Moderate and Severe DKA

orrection of Dyselectrolemia

a. Hypotension is treated with boluses of 10-20 ml/kg of 0.9 normal saline

b.For moderate to severe dehydration, replacement of 75-85 ml/kg fluid for 48 hours is indicated.

Normal Saline is the crystalloid fluid of choice for initial volume expansion. Half normal saline is started
after 6 hours of rehydration.

c. Potassium (40 mEq/L) should be added to the rehydration fluid after ruling out hyperkalemia.

a. Routine sodium bicarbonate infusion is contraindicated due to severe adverse effects like

Cerebral edema Hypokalemia

Left shifting of oxygen dissociation curve Metabolic Alkalosis

b. Sodium bicarbonate is only indicated in cases of refractory severe metabolic acidosis (pH< 6.9) not
responding to rehydration

c. Dose of Sodium bicarbonate in ml = 0.15 × base deficit × kg body weight. It is given as infusion over 2
hour period and stopped when pH reaches 7.0

a. Current preferred treatment of choice is Continuous low dose insulin infusion.

b.Regular insulin is given along with normal saline at the rate of 0.1units/Kg/hour.
 Insulin boluses should be avoided. Target of therapy is to slowly reduce blood sugar by 50-100 mg/dL
every hour

c. The endpoint for stopping insulin infusion is correction of acidosis and not just hyperglycemia.

5% dextrose is added to rehydration fluid when blood glucose dips below 250 300 mg/dL.

d. After correcting acidosis, subcutaneous insulin is started at a dose of (0.2 0.4 units/kg).

Insulin infusion is stopped after 30 minutes and oral feeding is resumed.

e. This regimen of insulin plus meal is carried out every 6 8 hours until the child can feed orally.

f. Two daily doses (before breakfast and dinner) of regular plus intermediate acting NPH insulin are started.

a.Vitals, hydration, sensorium, urine output should be continuously monitored during rehydration phase

b.Serial monitoring of Serum glucose, sodium, potassium, bicarbonate, phosphorus and urine ketones are
required.

Hypothyroidism in Children :- C/F , Management( Congenital Hypo.)

Hypothyroidism in children may be congenital or acquired

Hypothyroidism is also classified as primary (thyroid disease) or secondary (Pituitary or Hypothalamic

dysfunction)
Common causes of hypothyroidism

1.Primary hypothyroidism

-Hashimoto thyroiditis, Autoimmune

- polyglandular syndrome (APS)

Thyroid dysgenesis (aplasia

, hypoplasia, ectopic thyroid)
Iodine deficiency

- Amiodarone, phenytoin, methimazole,propylthiouracil

2. Secondary hypothyroidism

Hypothalamo pituitary disease

0
✓ A I - 4 • Radiation

A.Congenital hypothyroidism (CH)

Most commonest type of hypothyroidism seen in children.

-

Clinical features are present since birth or early infancy.

Etiology

Thyroid dysgenesis is the most common etiology accounting for 85% cases.
I
 Approximately 98% of cases occur sporadically while 2% are familial.
- -

Other causes include

a. Dyshormonogenesis - Inborn errors of thyroid hormone synthesis b. Deficiency of Iodine

c. Congenital anomalies of thyroid gland d. Disorders of thyroid metabolism

Clinical features

Early manifestations include hypotonia, hoarse cry, decreased activity, wide anterior fontanelle,

prolonged hyperbilirubinemia and decreased passage of stools or constipation.

Examination reveals coarse facial features , large protruding tongue, umbilical hernias and mottled, cold
and dry skin (Cutis marmoratus).

These children also have delayed dentition, poor feeding, short stature and poor growth

Untreated children have severe involvement with myxedema, severe mental retardation, developmental
delay, growth failure and goiter termed as cretinism. / L
Somu
TSH >
Total
Diagnosis

1. Demonstrating decreased total or free T4 and elevated TSH levels. Total TSH levels >20 mU/L is
diagnostic.

2. Assay should be done after 72 hours of life (3 -5 days) in order to prevent false positive diagnosis due to
postnatal physiological rise in TSH levels seen in first 48 hours.

3. Thyroid-binding globulin (TBG) deficiency manifests with reduced total T4 levels and normal TSH levels.

: Ultrasound examination to confirm normal location of thyroid gland and to rule out ectopic
thyroid in lingual or sublingual areas.

Differential diagnosis :- Mucopolysaccharidosis

Treatment

Management is aimed at early diagnosis and immediate exogenous replacement of thyroid hormone

All cases of confirmed hypothyroidism should promptly receive thyroid hormone supplementation
regardless of the etiology.

Drug of choice is synthetic oral levothyroxine (Eltroxin). It is started at a dose of 10-15 mcg/kg/day

Adequacy of therapy is indicated by increased activity, relief from constipation, improving appetite and
feeding.

@
B.Acquired hypothyroidism

Hypothyroidism acquired beyond infancy is most commonly due to autoimmune thyroid disease known
as Hashimoto thyroiditis (Chronic lymphocytic thyroiditis)
 Children present beyond 5 years of age.

Clinical manifestation

Short stature due to deceleration of growth may be the earliest presenting feature.

Other classical features include cold intolerance, constipation, lethargy and excessive sleepiness.

Myxedematous change of the skin, unexplained anemia, precocious or delayed puberty

Pseudotumour cerebri, muscle weakness, muscular hypertrophy, nerve entrapment and ataxia

Delayed dental and skeletal maturation.

Investigations:

Thyroid hormone assay: Serum Free T4, T3 and TSH Compare with age specific reference ranges

Assay of Anti-thyroglobulin and anti-peroxidase antibodies Autoimmune thyroiditis

Imaging: Ul Bone age assessment

Treatment

Principles are similar to treatment of congenital hypothyroidism

Hormonal replacement with synthetic oral levothyroxine is the treatment of choice.

Medical:

•Anti-thyroid drugs (propylthiouracil or carbimazole) or radioactive iodine

Saturated solution of•

Potassium iodide (1 drop per day) may be added

Symptomatic control with B•

blockers (propranolol),

In the thyro-toxic state severe, parenteral fluid therapy, corticosteroids and digitalization may be
=
indicated if heart failure occurs.

Surgery:-

•Complications of surgery - Hypoparathyroidism, vocal cord paralysis.

Acute bacterial meningitis/pyogenic meningitis:- Etiology,C/F,Management

.

More common in neonates and infants than older children because of immature immune system.

Patients on immunosuppressive drugs are more susceptible to meningitis especially by fungi, listeria and
mycoplasma.
Causes:

1. Neonates: E.coli, Streptococcus pneumonia, Salmonella, Pseudomonas aeruginosa,

Strep aureus, Streptococcus faecalis

2. 3 months 2-3 year: H.influenzea, S.pneumoniae, H.meningitidis

3. >3yrs: S.pneumoniae, H.meningitidis

Pathogenesis: Hematogenous spread

Head injury can lead to purulent meningitis

Extension from contiguous septic foci: Infected paranasal sinus, mastoiditis, osteomyelitis,

Skull base fracture

Clinical Features:

Onset is usually acute and febrile.

Symptoms -Lethargy and irritability - Headache

- Infants presents with Projectile vomiting, shrill cry and bulging fontanelle

- Seizures, altered sensorium progressing to coma -Photophobia - Myalgia, arthralgia

a. Tachycardia, cutaneous signs such as petechiae, macular rashes may be seen.

b.Papilledema, hypertension with bradycardia due to increased ICP

c. Generalised hypertonia and neck rigidity

d. Signs of Meningeal Irritiation

Neck stiffness

Kernig sign Limited extension of knee beyond 135 degrees

Brudzinski sign Hips and knees flex with passive neck flexion

e. Focal neurological deficits

Hemiparesis

Cranial neuropathies are seen usually involving nerves II, III, VI, VII, VIII.

Hemianopsia

Presentation in neonates & Young infants

Neck rigidity and kernig sign are not prominent

Common presenting symptoms are

- Irritability, Refusal to feed & Vomiting -Poor cry, lethargy & Drowsiness

- Fever or hypothermia -Vacant stare, posturing or clonic seizures

- Shock & circulatory collapse - Focal neurological deficits

Diagnosis:

CSF Analysis:

- Pressure: elevated (>180mm of H2O) - Appearance : turbid - Cell count: >1000/mm2

- elevated (polymorphonuclear) - Protein: >100 mg/dl elevated

- Sugar: <40 mg/dl below 50% of blood sugar

- Gram stain: positive - Culture: Positive

MRI

Treatment:

Based on choice of antibiotic and duration of therapy

Meningococcal or pneumococcal meningitis: Penicillin 400, 000 - 500,000 units/kg/day every 4th hourly.

Cefotaxime 150-200 mg/kg/day every 8th hourly.

Ceftriaxone 100-150 mg/kg/day every 12th hourly.

H.influenzae meningitis: Ceftriaxone / Cefotaxime / Combination of Ampicillin (300mg/kg/day q6h) and

Chloramphenicol (100mg/kg/day)

Staph meningitis - Vancomycin is the treatment of choice if Penicillin or Methicillin resistance is

suspected.

Lumbar puncture should not be done in case of increased intracranial pressure and osmotic diuresis with
mannitol should be done.

Anticonvulsants for convulsion.

Fluid and Electrolyte imbalance and Hypotension should be corrected.

Tuberculous meningitis:- etiopathogenesis,c/f,Management

May occur at any age but more common between 6 and 24 months of age

Caused by M.tuberculosis an aerobic gram-positivebacteria

There is usually a focus of primary infection or military tuberculosis

Pathogenesis
 Infection reaches meninges by hematogenous route, rarely by lymphatics

Has predilecti

The bacilli is discharged into subarachnoid space intermittently leading on to

- Proliferation - Perivascular exudation

- Caseation - Gliosis - Giant cell formation

Miliary tuberculosis can also be associated with tubercles in choroid plexus.

Clinical features:

Clinical features of untreated case classically goes through 3 stages

A) Prodromal stage or Stage of invasion:

- Insidious onset with low grade fever - Irritability and restlessness

- Loss of appetite and disturbed sleep - Vomiting and headache

-Child may exhibit head banging and photophobia

B) Stage of meningitis:

-Neck rigidity and kerning sign positive. - Remittent or intermittent Fever

- Disturbed breathing -Child is drowsy or delirious -Sphincter control is usually lost.

-Convulsions and focal neurological deficit like monoplegia and hemiplegia may occur.

C) Stage of coma: Loss of consciousness, rise of temperature and altered respiratory pattern.

- Dilated pupils, nystagmus and squint -Ptosis and ophthalmoplegia

-Cheyne- - Bradycardia -If untreated, is lethal in 4 weeks

Diagnosis:-

alysis:-

- Pressure: Elevated - Appearance: Clear cobweb formation after sometime

- Cells: Elevated lymphocyte 10-500/mm3 - Protein: Elevated 80-400 mg%

- Sugar: Decreased 30-50 mg% (less than 2/3rd of blood sugar)

- AFB: Positive - Culture: Positive

Mantoux test may be positive. If negative does not rule out diagnosis

Chest X ray may provide supporting evidence of pulmonary TB.

Culture of gastric aspirate and urine.

 CT and MRI show basal exudates and inflammatory granulomas, hypodense lesions or infarcts and
hydrocephalus.

BACTEC & PCR

Treatment:

- should be prompt, adequate and prolonged for at least 12 months.

At least 4 anti-tubercular drugs should be used for initial 2 months comprising

-Isoniazid( 5mg/kg/day, max 300 mg )

- Rifampicin(10mg/kg orally,max 600 mg) ; - Ethambutol(15-20 mg/kg/day)

- Pyrazinamide (30mg/kg/day orally) ; -Streptomycin (30-40 mg/kg/day)

- parenteral dexamethasone 0.15mg/kg, every 6 hrIV, Change to oral prednisolone once brain
edema

Symptomatic therapy of raised intracranial pressure, seizures, dyselectrolytemia should be done.

The patient should be kept under observation for papilloedema, optic atrophy or increased head
circumference.

Seizures(Convulsions) :- Define,causes,febrile(typical&Atypical),Management
A seizure is a brief syndrome of manifestations resulting from abnormally increased neuronal
firing in the brain.

Causes of convulsions

1.Early neonatal period (0-7 days)

-Birth asphyxia, difficult obstructed labor

-Intraventricular, intracerebral hemorrhage

-Pyridoxine dependency, hypoglycemia, hypocalcemia

-Inborn errors of metabolism -Maternal withdrawal of medications

2. Neonatal period (7-30 days)

-Transient metabolic: Hypocalcemia, hypomagnesemia, hypoglycemia, dyselectrolytemia

-Developmental malformations

-Infections: Meningitis, septicemia, tetanus neonatorum, intrauterine infections

-Metabolic errors: Phenylketonuria, maple syrup urine disease, galactosemia, urea cycle disorders.

3. Beyond neonatal period

-Simple febrile convulsions ; Epilepsy syndromes

-Infections: Bacterial meningitis, intrauterine infections, tuberculous meningitis, aseptic meningitis,
encephalitis, cerebral malaria, Reye syndrome

-Metabolic causes: Dyselectrolytemia, hypocalcemia, hypomagnesemia, inborn errors of metabolism

-Space occupying lesions: Neoplasm, brain abscess, tuberculoma, cysticercosis

-Vascular: AV malformations, intra cranial thrombosis, hemorrhage.

Types of febrile seizures

-Age group 6 months to 6 years - Generalized seizure - Lasting < 15 minutes

-Not recurring within 24 hours -No post ictal neurological abnormality

- Age < 5 months or above 6 years - Focal or focal becoming generalized seizure

-Prolonged > 15 minutes -Multiple episodes within 24 hours

-Associated with postictal neurological abnormality.

Clinical features

Seizures are usually generalized tonic clonic type. In infants, uprolling of eyes and fixed gaze can be the
only feature or may be associated with tonic movements of limbs.

Approach to a Child with Convulsons

-A good description of the seizures including mode of onset, details of aura, type of seizure, automatism,
associated behavioral abnormalities and the postictal phase should be obtained.

-An accurate seizure description is more informative than detailed neurological examination or
investigations.

-Perinatal, developmental, and family history of seizures help in determining the cause.

- The child should be examined for evidence of raised intracranial tension, degenerative, metabolic or
congenital disorders.

Investigations

A) In cases of typical febrile seizures :- No neuroimaging or LP required

B) In cases of atypical febrile seizures - Lumbar puncture - EEG if risk or recurrence or future epilepsy

C) To identify the cause of fever

- Investigations based on clinical presentation and differential diagnosis for fever

- Hemogram, ESR - Blood, Urine culture -Serology

- Age < 6 month -Toxic and ill appearing child
a

-Any clinical suspicion of intracranial infection

- Age 6 - 12 month if Hib-2 and pneumococcal vaccination not done or if status unknown.

Management

1.Immediate management

⑩
In children with active seizures IV or rectal diazepam is the first choice (0.3mg/kg/dose).

If facilities for intubation are available, IV or nasalo

midazolam(0.1 -0.2 mg / kg) can be tried.

o o
Other options are IV lorazepam and Rectal clonazepam.

2. Long term management

Goal is to prevent recurrence

Management options depends on the risk of recurrence and epilepsy

*Continuous daily prophylaxis with antiepileptics or diazepam is not required in simple febrile seizures.

In cases of parental anxiety, Intermittent diazepam prophylaxis can be given during febrile episodes
(Dose - 0.3 mg / kg / dose every 8 12 hours if temperature > 38° C)

Antipyretic measures and Drug prophylaxis reduces but does not completely prevent the recurrence or
development of seizure disorder

Status epilepticus:- Management

Status epilepticus is defined as seizures that continue for more than 30 minutes or recurrent seizures for
more than 30 minutes without recovery of consciousness in between the attacks.

Investigations

All cases

-Blood biochemistry: Glucose and electrolytes, and other metabolic parameters

-Blood gases assessment

- - Blood counts -Cerebral spinal fluid examination

- Urine examination - Necessary cultures

:- - Electroencephalogram - Neuroimaging - Drug levels

Treatment Protocol

Emergency management focuses on securing the airway, maintaining oxygenation, ensuring perfusion by
obtaining intravenous access and protecting the patient from injury.
Specific therapy:

a. Glucose for hypoglycemia b. Pyridoxine 50 100mg if deficiency

c. IV calcium if hypocalcaemia d. Im Magnesium

Cerebral Palsy :- Define,Classification, c/f,Management
Cerebral palsy (CP) is a non-progressive neurological disorder of movement and posture.

It causes limitation of activity due to a static lesion affecting the developing brain

The neurological insult can happen during fetal life or during birth or after birth

Though CP is static disorder, the neurological features can change over a period of time. It usually
presents at 2-5 years of life.

Classification of cerebral palsy

1. Based on Motor deficit

Spastic CP (Pyramidal CP)

1.Quadriplegia (20%) -Most severe form of CP. It involves all the four extremities with generalized
spasticity with mental retardation and seizures

2. Diplegia (30%) - Spasticity and weakness predominantly involving the lower limbs with minimal or no
involvement of upper limbs

3. Hemiplegia (25%) - It involves either left or right side of the extremities. Upper limbs are more
commonly affected at early stage than lower limbs

4. Monoplegia 5. Triplegia

- - Choreoathetosis -Dystonia

- -Atonic diplegia - Congenital cerebellar ataxia

2. According to patients functional status

Class I No practical limitation of activity

Class II Slight to moderate limitation

Class III Moderate to gross limitation

Class IV Inability to carry out any useful activity

3.According to patient therapeutic requirement:

Class I no active treatment required

Class II require minimal bracing and treatment

Class III Require bracing and service of CP team

Class IV Long term hospitalization and management

Clinical Features:

1. Spastic: - Quadriplegia, hemiplegia - Hyperirritable, ophisthotonus

- Babinski positive beyond 2 years of age

- Pseudobulbar palsy swallowing difficulty with drooling of saliva and expression less face

2. Atonic: - Hypotonia, delayed talking - Cerebellar sign present

Associated features:

Eye: Strabismus, cataract, refractiveness ; Ear: Deafness partial/complete

Speech: Dysarthria, Aphasia, dyslalia ; Sensory defects: Astereognosis, spatial disorientation

Seizures: Generalized/focal tonic ; Intelligence: Borderline/moderately/severely mental retardation

GIT: Constipation, feeding difficulties ; Teeth: Malocclusion, caries

- thumb is persistently flexed across palm after 1st month of life.

Management: Depending on severity and type of neurological deficit and associated problem.

1. Symptomatic treatment:

- Anticonvulsant for seizures - Tranquilizers for behavioral disturbances

- Muscle relaxants Dantrolene sodium

- Balcofen to reduce spasticity - Diazepam athetosis and spasticity

2. Physiotherapy: - Massage/exercise - Encourage basic movements - Special therapy

3. Occupational therapy 4. Educational management: vision, speech and learning problems.

5. Orthopedic support: splints and surgeries 6. Social Support

CP Team: Pediatrician, orthopedic and general surgeon, physical and occupation therapist,

speech therapist, psychologist, medical, social worker.

Breath Holding Spell :- read in

dweolopmet chapter
.

- Breath holding spells are reflexive events typically initiated by a provocative event that causes anger,

frustration or pain causing the child to cry.

- The crying stops at full expiration and the child becomes apneic and cyanotic or pale.

In some cases the child may lose consciousness, become hypotonic and fall.

If the spell lasts for more than a few seconds, brief tonic-clonic seizure may occur.

- Breathholding spells always revert on their own within several seconds, with the child resuming normal
Ee lived their own
activity or falling asleep for some time. Ta =
own

do not the child

pick upevent
Be calm during .
sideway shift
 do not cnhi bit undue concern hoagie into child 's demand
if spell was provoked by anger
.

- Breath holding spells are rare before 6 months of age, peak at 2 yr and abate by 5 yr of age.

- Diagnosis is based on the setting and the typical sequence of crying, cyanosis or pallor with or without

brief loss of consciousness.

-The differential diagnoses include seizures, cardiac arrhythmias or brainstem malformation.

- The history of provoking event, stereotyped pattern of events and presence of color change preceding

the loss of consciousness help in distinguishing breath holding spells from seizures.

Guillian-barre syndrome
Post infectious polyneuritis

Two third patients have history of viral infection preceding the illness

Neurologic manifestations begins 2-4 weeks after viral infection.

Etiology: Viral: EBV, mumps, measles ; Post vaccination ; Bacteria: Campylobacter

Clinical features

Pain in the muscles is early symptom

Weakness starting in legs then spreading to upper extremities and trunk muscles (Ascending type of
palsy)

Weakness is more marked in proximal muscles

Tendon reflexes are diminished, plantar is normal with hypotonia

Cranial nerve involvement seen in three fourth cases

Sensory symptoms are subjective rather than objective

Autonomic nervous system involvement :- - Urinary retention -Hypertension - Postural hypotension

Respiratory insufficiency due to paralysis of intercostal muscles.

Investigations

CSF analysis shows al Protein are elevated > 45mg/dl

Treatment

Self-limiting with gradual recovery in 6 months 2 years

Intravenous immunoglobulin 300 400 mg/kg for 5 days

Plasmapheresis

Physiotherapy is mainstay to prevent handicaps.

 Acute Flaccid Paralysis :- etiology,,surveillance,Management
Case definition

Sudden onset of weakness and floppiness in any part of the body in a child < 15 years of age or paralysis
in a person of any age in which polio is suspected.

Principles of AFP surveillance

All AFP cases must be reported, not just suspected polio.

All
✓

Nil reporting to be considered as important as case reporting. →

-

AFP cases must be reported immediately.

-

Nil reports need to be sent weekly, after a thorough search.

-0
With improved surveillance more AFP cases will be reported (Polio & non polio)

→
Reporting of more cases is a sign of improved surveillance and not failed eradication

It is needed to assure successful eradication of polio in the shortest possible time.

Steps of AFP surveillance

•Establishment & maintenance of Reporting Network

•AFP case notification by reporting units

AFP case investigation

: Stool specimen collection & transportation

÷
Search for active cases in community

Outbreak response Immunization

Follow-up for 60 days

Adequate specimen:

- 2 specimens at least 24 hours apart

- Collected within 14 days of AFP

- Adequate amount 8-10g

- Reaching WHO lab in good condition

- Sent by reverse cold chain

Indicator for effectiveness of surveillance:

- Sensitivity non-polio AFP at least 1/100000 in children < 15 years

- Completion of survey:- 2 adequate specimen from at least 60% of all AFP cases
r

Down Syndrome (Trisomy 21):-

The extra 21st chromosome could be either maternal or paternal in origin

Advanced maternal ag syndrome.

Trisomy 21 (95% cases) Extra copy of chromosome 21. It occurs due to nondisjunction of maternal
chromosome in meiosis stage I

Clinical features

These children have very characteristic facies resembling Mongolian race.

Typical facial features :- brachycephaly with flat occiput , wide open anterior fontanelle , flat facies with

flat nasal bridge, protruding tongue, dysplastic,

low set ears, upward slant of eyes, and epicanthic folds

- short neck with abundant neck skin, hypoplastic middle phalanx of 5th finger

(clinodactyly), characteristic single transverse palmar crease (Simian crease),

incomplete second transverse crease (Sydney line)

Investigations

Karyotyping

- -Fluorescent in situ hybridization test - Quantitative fluorescence PCR

Radiology:- - Only 11 pairs of ribs - 2 3 ossification centers of manubrium

- Hypoplasia of base of skull, facial bones -Hypoplasia of middle phalanx of 5th finger.
Management

Multidisciplinary management by a team of pediatricians, geneticists, physiotherapists, occupational

therapists, and other specialties based on organ involvement

siotherapy, and speech therapy form the basis of therapy

Early stimulation is recommended for all cases and should be started as soon as possible

Screening for associated abnormalities should be done and treated.

Kerosene Poisoning:-
Kerosene poisoning is the most common accidental poisoning seen in children .

Storing kerosene in disposable water or cool drink plastic bottle is a risk factor.

Kerosene is not absorbed from gastrointestinal tract.

Hypoxia secondary to aspiration pneumonia causes neurological symptoms.

Clinical features:

Immediate symptoms include violent coughing, flushing of the face and vomiting following ingestion.

Examination invariably reveals the characteristic kerosene odour from mouth and vomitus.

Respiratory findings include cough, tachypnea, retractions, wheeze and crepitations.

Older children often complain of headache, abdominal pain abdominal distension, dry throat and
difficulty in swallowing. Fever is very common.

Neurological manifestations in the form of restlessness, convulsion and coma can occur in severe cases.

Management:

All suspected cases should be hospitalized. Preserving airway is of utmost importance in unconscious
patients. Patients should be put on left lateral position to avoid aspiration.

induced vomiting are contraindicated due to the risk of aspiration. Commonly used
household antidotes such as milk and oil should be avoided. ✗
a - -

Oxygen and respiratory support are mainstay therapy in symptomatic children. Oxygen saturation should
be continuously monitored during acute phase.

agonists nebulisation might offer symptomatic relief in patients with predominant wheezing.

Hospitalization
left lateral positions
No vomiting , Gastric emptying milk oil
relief
p!= symptomatic
.

saspieatus support
>

: 02 .
Assessment of Infant with Diarrhoea IMNCI :-
Fever in Child IMNCI:-
Primary Complex TB Etiopathogenesis,Management
-Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis.

Etiopathogenesis

- A child is infected by the bacilli from an open case of tuberculosis, usually an adult.

The most common site is the lung though lymph nodes, tonsils, skin, intestine.

- About 2 to 10 weeks (average 6 weeks) after this primary infection, many viable bacilli are transported to
the regional lymph glands. There is an exudative reaction locally.

- The original focus of infection develops an accumulation of polymorphs.

This is followed by epithelioid cell formation. Finally, there results a typical tubercle formation with its
surrounding layer of mononuclear leukocytes and occasional giant cells.

This is what has been described as the Ghon focus.

- It is about a centimeter in diameter and, together with lymphatic drainage of the area and regional lymph
glands, is termed the primary complex.

- Primary complex is liable to g reinfection, especially about the time of puberty.