Created by Turbolearn AI

Paediatrics Study Guide

Growth and Development
Growth is defined as a net increase in the size or mass of tissue. It is an essential feature that distinguishes a child
from an adult.

Laws of Growth
1. Continuous and orderly process:
Specific periods of acceleration, deceleration, and steady growth exist.
Rapid during intrauterine fetal life (especially the first few months), accelerated in postnatal life during the first two
years, then slows down and maintains a steady velocity.
Growth accelerates again at puberty.
Never haphazard, order is cephalocaudal and distal to proximal.
2. Unique pattern: Every individual's growth pattern is unique.
3. Different rates: Different tissues grow at different rates.

Somatic Growth
Body tissue is divided into two components: fat and lean body mass.
Fat: Deposited in subcutaneous adipose tissue, more in girls than boys.
Lean body mass: Includes muscle tissue, internal organs, and the skeleton. Correlates closely with stature.

Brain Growth
Fetal phase and the first two postnatal years are crucial.
Head reaches 90% of adult size by 2 years.
Head circumference reflects the growth and size of its contents, including the brain and ventricles.
Head circumference growth velocity is maximum up to 2 years of age, then slows down.

Lymphoid Growth
Most prominent during mid-childhood period (4-8 years).
Clinically seen as large tonsils and palpable lymph nodes.

Gonadal Growth
Dormant during childhood and becomes obvious during puberty.

Normal Height Milestones

At birth = 50 cm At 6 months = 65 cm At 1 year = 75 cm At 2 years = 90 cm At 4 years = 100 cm Af ter 4 years = In

Head Circumference

Page 1
 Created by Turbolearn AI

Also known as occipito-frontal circumference, it is a good parameter for a child's brain development.
During intrauterine life, head growth occurs before neck and arm growth before legs.
In postnatal life, growth of the head slows down, but limbs continue to grow rapidly.
Reaches 90% of the adult size by 2 years.
It’s best practice to plot head circumference on growth charts.
More than 2 standard deviations above the mean is called macrocephaly.
Below 3 standard deviations below the mean is known as microcephaly.
Age Head Circumference (cm)

Birth (term) 33-35

First 3 months Growth 2 cm/month
Next 3 months Growth 1 cm/month
Next 6 months Growth 0.5 cm/month
At 1 year 47
At 2 years 49
At 4 years 51

Assessment of Growth Parameters

Measured by:
Weight (bone and muscle mass)
Length or height (stature)
Head circumference (brain growth)
To be measured by a non-stretchable measuring tape.
The measuring tape is passed over the supra-orbital ridges in front and that part of the occiput which gives the maximum
diameter. Usually it is over the occipital protruberance but not always.
Recorded nearest to 0.1 cm.
Periodic plotting of child's growth parameters on a growth chart.

Growth Chart Basics

Recording growth measurements over time and plotting on a chart creates growth curves.
Contains growth standards representing norms.
Standards are obtained by cross-sectional or longitudinal studies in large populations.

Types of Growth Charts

According to References Standard:
WHO Growth Chart
CDC Growth Chart
IAP Growth Chart
According to growth parameters:
Weight for age
Height/length for age
Weight for height
BMI for age
Skin fold thickness for age
Head circumference
MAC for age

Growth charts are also available for different age groups and separately for boys and girls.

Utility of Growth Charts

Page 2
 Created by Turbolearn AI

Tool to diagnose deviations from normal.

Normal range between 3rd and 97th percentile curves (includes 94% of children, mean ± 2 standard deviations).
Refers to the position of an individual child on a given reference distribution.
Range of variation in observations is conventionally taken as values.
Periodic plotting of child's growth parameter on a growth chart is useful.
Growth velocity is the rate of growth over a fixed time interval.
One time measurement of growth parameter has no value rather than monitoring the trend of this parameter over time.
Plotting growth velocity in growth charts is a useful tool for early identification of growth disturbances, which may be the
first manifestation of an infectious disease.
Following the growth curves also helps in assessing utility of remedial measure. For example, upturning curve after
successful treatment and nutritional rehabilitation is reassuring.
Velocity of growth more accurately helps in predicting ultimate adult height.

WHO Growth Charts

Internationally accepted, from conception until the epiphyses close.
Published in 2006, based on the Multicentre Growth Reference Study (MGRS).
MGRS was a community-based, multi-country project conducted in Brazil, Ghana, India, Norway, Oman, and the United
States.
The pooled sample from these diverse locations consisting of children of both affluent and backward population makes it a
truly representative chart.
It also recapitulates the fact that child population across the world can attain similar growth patterns when their health
needs and basic care are met.
The WHO infant growth standards make breast feeding the normative model.

Bone Age Estimation

Important part of investigation for short stature.
Tells about skeletal maturity according to chronological age.
Depends on:
Number, size, and shape of epiphyseal centers.
Size, shape, and density of the ends of bones.
Classification Causes

Bone Age = Chronological age Normal, Familial short stature

Bone Age < Chronological age Hypothyroidism, Growth hormone deficiency, Malnutrition
Bone Age < Chronological age Constitutional delay of growth and puberty
Bone Age > Chronological age Thyrotoxicosis, Precocious puberty, Prolonged Steroid therapy

Location for Measurement

Hand and wrist (children between 1 and 13 years).
Elbow and hip (children between 12 and 14 years).
Carpal bones.
Metacarpal bones.
Patella.
Distal and proximal tees to both sexes.
Distal and middle phalanges in boys.
Distal and proximal phalanges in girls.

Methods
Greulich and Pyle - Atlas method.
Tanner Whitehouse - Rating method.

20 ossification centers are generally used for determining the bone age.

Page 3
 Created by Turbolearn AI

Disadvantages
Often Osteopenia provides erroneous reading.
It is macho assessment and needs to be interpreted in clinical context.

Growth Assessment of a One-Year-Old Child

This section covers the parameters and methods for assessing growth in a one-year-old child, including physical measurements
and developmental milestones.

Growth Parameters
The growth parameters to be measured include weight, length, and head circumference.

Weight
Recorded using a weighing scale (lever or electronic).
Ideally, the observed value should be plotted on an age- and sex-appropriate growth chart to determine the child's status
in reference to the percentile curve.
The normal range is between the 3rd to 97th percentile.
If a growth chart is unavailable, the expected weight can be calculated.
Any deficit or excess should be calculated from the expected weight and observed weight.
Approximate weight at 1 year of age is birth weight x 3.

Length
Measured by placing the baby on an infantometer or rigid measuring table.
Ideally, the observed value should be plotted on an age- and sex-appropriate growth chart.
The normal range is between the 3rd and 97th percentile.
Approximate length at 1 year of age is 75 cm (50 cm at birth + 25 cm in 1 year).

Head Circumference
Measured using a non-stretchable measuring tape around the head, just above the supraorbital ridge in front and the
maximum circumference of the head posteriorly.
Ideally, the observed value should be plotted on an age- and sex-appropriate growth chart.
Approximate head circumference at 1 year is 46-47 cm.
Average at birth is 33-35 cm and increases by 12 cm/1 year.

Chest Circumference
Measured using a non-stretchable measuring tape at the level of the nipples, ideally midway between inspiration and
expiration.
Chest circumference becomes equal to head circumference by 1 year of age (at birth, chest is 3 cm less than head).

Developmental Assessment

Stepwise Approach

Page 4
 Created by Turbolearn AI

1. History:

Detailed history to determine risk factors affecting development.

Differentiate between delay and regression.
Make a gross impression about the developmental age of the child.

2. Examination:

Detailed physical examination for physical growth.

Search for any dysmorphism or stigmata of intrauterine infection or hypothyroidism.
Screening for vision and hearing.
Detailed neurological examination and assessment of primitive reflexes (if required).
Detailed developmental assessment with appropriate tools (red ring, cube, spoon, cup, block, paper, pencil, etc.).

3. Evaluation:

Observation regarding baby's social responsiveness, alertness, concentration, interest, and movement.

Vision and hearing assessment to ensure intactness of response to sensory stimuli.

Vocal response: nature, frequency, and quality.

Fine motor assessment: interest, alertness, and rapidity of response by appropriate developmental tool.

Finally, perform annoying maneuvers that may hinder the child's cooperation:

Assessment of reflexes.
Head circumference measurement.
Ventral suspension.
Pull to sit.

After completion of the assessment, a conclusion is drawn whether the neurological and developmental status is age-
appropriate or not by calculating the Developmental Quotient (DQ) as follows:
Average age at attainment
DQ = × 100
Observed age at attainment

Considerations
In babies born preterm, corrected age rather than postnatal age is used to determine developmental status until 2 years of
age.
Retardation should not be diagnosed on a single examination; repeated examination is desirable.
A DQ < 70% is taken as delay and warrants detailed evaluation.
Remember the wide variation of normality.
Consider the opportunities provided to a child to achieve milestones.

Key Milestones by Age

Developmental milestones are divided into four segments:

1. Gross Motor
2. Fine Motor
3. Social and Personal
4. Language

Gross Motor Development

Gross motor development is the attainment of locomotion and complex motor tasks in an orderly sequence.

Page 5
 Created by Turbolearn AI

Age Milestones

3 months Neck holding

5 months Rolls over bed
6 months Sitting with own support
8 months Sitting without support
9 months Standing with support
12 months Creeping
Standing without support
Walking with fall
15 months Walking without support
18 months Running
2 years Walking up & down stairs
Riding tricycle
Going upstairs in alternate feet

Fine Motor Development

Fine motor development denotes the development of fine manipulation skills and coordination.

Age Milestones

4 months Bidextrous reach

6 months Unidextrous reach
Transfer objects
9 months Immature pincer grasp
12 months Mature pincer grasp
15 months Immature scribbling
Tower of 2 blocks
18 months Scribbling
Tower of 3 blocks
2 years Tower of 6 blocks
Vertical and circular stroke
3 years Tower of 9 blocks
Copies circle

Social and Personal Development

Social and personal development denotes cognitive development.

Age Milestones

2 months Social smile

3 months Recognizes mother
6 months Recognizes stranger, stranger anxiety
9 months Waves bye bye
12 months Plays simple ball game
18 months Copies parents in tasks
2 years Asks for food, drink, toilet
3 years Knows full name and gender

Language Development
Language development is the receptive and expressive abilities.

Page 6
 Created by Turbolearn AI

Age Milestones

3 months Cooing
4 months Laughs loud
6 months Monosyllable words
9 months Bisyllable words
12 months 1-2 words with meaning
18 months 8-10 words vocabulary
2 years 2-3 words simple sentences
3 years Asks questions and speaks full name

Nutritional Rickets and Vitamin D Metabolism

This section discusses vitamin D metabolism, its sources, and the pathological changes and clinical features of nutritional rickets.

Vitamin D Metabolism
Vitamin D is a generic term for secosteroids that play an important role in maintaining calcium and phosphorus
homeostasis.

It can be synthesized in epithelial cells of the skin.

Sources
1. Cutaneous Synthesis: Conversion of 7-dehydrocholesterol to vitamin D3 by ultraviolet B radiation (UVB) from the sun. This
is the most important source.
2. Dietary Source: Constitutes ≤10% of total vitamin D.
Vitamin D2 (Ergocalciferol): derived from plant sources.
Vitamin D3 (Cholecalciferol): derived from animal sources like fish liver oil, fatty fishes, and egg yolk.

Factors affecting cutaneous synthesis include skin pigmentation, timing of the day, clothing, and season. The RDA for vitamin D is
200 IU (5 μg) in infants and 400 IU (10 μg) in children.

Metabolism
1. In the Liver: The first step of hydroxylation occurs, converting vitamin D into 25-hydroxyvitamin D (25-D) or calcidiol by the
enzyme 25-hydroxylase. Measurement of 25-D is the standard method for determining a patient's vitamin D status.

2. In the Kidney: The final step of activation occurs, where 1α-hydroxylase converts 25-hydroxyvitamin D into 1,25-
dihydroxyvitamin D (1,25-D) or calcitriol, the active form of vitamin D.

1α-hydroxylase is upregulated by PTH and hypophosphatemia and inhibited by phosphate, 1,25-D (negative
feedback), and FGF-23.

Page 7
 Created by Turbolearn AI

The image above shows the metabolic pathway of Vitamin D. 7-dehydrocholesterol is converted to Vitamin D3 by UV light. It is
hydroxylated into 25-OH D3 in the liver, and again hydroxylated into 1,25-(OH)2 D3 in the kidneys. This is the active form of
Vitamin D and acts on the intestine, bones, and kidneys. The clinical and radiological features of the various types of vitamin D
deficiency rickets are almost the same.

Action
1,25-D (calcitriol) acts by binding to an intracellular receptor, affecting gene expression by interacting with vitamin D response
elements. Its actions in different target tissues include:

1. In the Intestine: Marked increase in calcium absorption and increase in phosphate absorption.
2. In the Kidney: Increase in calcium and phosphate reabsorption, inhibits its own synthesis by inhibiting 1α-hydroxylase, and
stimulates renal 24-hydroxylase activity, which converts 25-D to 24,25-D (inactive metabolite).
3. In the Bone: Increased mineralization.
4. In the Parathyroid: Suppresses PTH secretion directly and by increasing serum calcium concentration.

Pathological Changes in Bone in Nutritional Rickets

1. Loss of normal zone of provisional calcification adjacent to the metaphysis is usually the earliest change.
2. Increased distance between diaphysis and epiphysis due to hypertrophy of the growth plate cartilage.
3. Fraying: Edge of the metaphysis loses its sharp border.
4. Splaying: Widening of the distal end of the metaphysis.
5. Cupping: Edge of the metaphysis changes from a flat or convex surface to a more concave surface.
6. Coarse trabeculation of the diaphysis.
7. Generalized rarefaction of the bones.

Clinical Features of Rickets

1. General:
Failure to thrive
Listlessness
Muscle weakness (especially proximal)
Protruding abdomen
Fractures (due to osteopenia)
Seizures
Tetany
2. Head:
Craniotabes: Softening of the cranial bones, giving a "ping-pong ball" feeling.
Delayed closure of fontanelles.
Delayed dentition.
Frontal bossing.
3. Chest:
Rachitic rosary: Widening of the costochondral junctions.
Harrison groove: Horizontal depression along the lower anterior chest.
Repeated respiratory infections.
4. Extremities:
Enlargement of the wrists and ankles.
Anterior bowing of the tibia and femur.
Varus or valgus deformities.
Windswept deformity: Combination of valgus deformity of one leg with varus deformity of the other.
5. Back:
Kyphoscoliosis.

Radiological Features of Rickets

Page 8
 Created by Turbolearn AI

1. Metaphysis:
Changes are characteristically seen in rapidly growing bones.
Fraying at the ends of the metaphysis.
Splaying (widening) and cupping (concave edge) of the metaphysis.
Increased distance between the diaphysis and epiphysis due to hypertrophy of the growth plate cartilage.
2. Long Bones:
Osteopenia (reduced bone density).
Bowing of the legs due to weight bearing.
Windswept deformity.
3. Chest X-ray:
Widening of the costochondral junctions.
4. Skull:
Pronounced demineralization.
Indistinct sutural margins.
Delayed tooth eruption.
5. Spine:
May show kyphoscoliosis.

Investigations for Rickets

Investigations for rickets include:

Serum Calcium: Low or normal values.

Serum Phosphorus: Should always be low.
Alkaline Phosphatase: Raised.
PTH: Raised.
25-D: Low (<10 ng/mL indicates deficiency).
1,25-D: Levels may be low only in severe vitamin D deficiency.

Here is an image to represent the algorithm that would be used when approaching Refractory Rickets. The algorithm takes into
consideration serum phosphorus levels, blood pH, serum PTH, and calcium levels. Depending on the presentation of the patient,
the algorithm suggests diagnoses such as Fanconi Syndrome, Renal Tubular Acidosis (RTA), Vitamin D dependent rickets,
Hypophosphatemic Rickets, and Chronic Kidney Disease (CKD) or Chronic Renal Failure (CRF).

Management of Rickets
1. Vitamin D:
Stoss therapy: Single dose of 600,000 IU either orally or intramuscularly.
60,000 IU/day orally for 10 consecutive days.
After the initial dose, daily vitamin D supplementation (400 IU/day for infants and 600-800 IU/day for children > 1
year) should be continued.
2. Calcium:
Intravenous calcium is needed initially for children presenting with symptomatic hypocalcemia.
Oral calcium supplementation should be given to all patients of rickets @ 30-75mg/kg/day along with vitamin D.
3. Phosphorus: Oral phosphorus is supplemented along with calcium for vitamin D deficiency rickets.

Page 9
 Created by Turbolearn AI

Monitoring Response to Therapy

X-ray of wrist joints is repeated after 4 weeks to look for healing of bony changes (area of calcification at the metaphyseal end
that is denser than the diaphysis). If there is no sign of healing radiologically after 4 weeks, a second dose of vitamin D (600,000
IU) may be given. If no healing is observed even after the 2nd dose of vitamin D, the patient should be evaluated for refractory
rickets/resistant rickets.

Treatment for Nutritional Rickets

See Management of Rickets above.

Metabolic Interaction of Vitamin D, Calcium, and PTH

Maintaining calcium balance involves Vitamin D (Calcitriol), PTH (Parathormone), and Calcitonin, which regulate calcium and
phosphate metabolism.
2+ 2−
[Ca ] ⋅ [P O ] = Constant
4

Calcium Metabolism
Calcium balance is maintained by excreting the same amount absorbed from the gut through urine and stool.

Hormones Involved
1. Calcitriol: Increases P O level by helping in intestinal absorption and renal tubular reabsorption.
4

2. PTH: Decreases P O level by reducing tubular reabsorption in the kidneys.

4

Metabolic Action of PTH and Calcitriol

1. Calcitriol: Synthesized in the liver and kidney from cholecalciferol (vitamin D3). Helps in calcium metabolism by:

Aiding calcium absorption by synthesizing intracellular Ca binding proteins in the enterocytes.

2+

Assisting in the reabsorption of Ca from the distal nephron in the kidneys.

2+

Mobilizing calcium from the bones by increasing the number and activity of osteoclasts.

2. PTH: Secreted from the chief cells of the parathyroid glands and increases plasma calcium levels. It:

Increases calcium reabsorption in the DCT of the kidneys.

Increases calcium permeability of osteoclasts, osteoblasts, and osteocytes in the bones, leading to calcium
mobilization.

3. Calcitonin: Secreted by the perifollicular cells of the thyroid gland. It decreases serum Ca 2+
level.

Balanced Diet
A balanced diet is defined as a nutritionally adequate and appropriate intake of food items that provide all the nutrients in the
required amount and proper proportions. It should also be culturally and financially feasible to access and maintain.

Constituents of a Balanced Diet

A balanced diet consists of macronutrients and micronutrients:

Macronutrients

Page 10
 Created by Turbolearn AI

Carbohydrates: 55-60% of calories. Main energy source from cereals, grains, vegetables, fruits, sugar, etc.
Proteins: 10-15% of calories. Important for cell growth, repair, and maintenance. Sources include meat, egg, fish, pulses,
etc.
Fats: 25-30% of calories. Roles include thermal insulation, hormone production, and absorption of vitamins. Available in
oils and fats used for cooking (e.g., butter, ghee, etc.).

Micronutrients
Vitamins: Naturally occurring substances essential for health.
Fat-soluble vitamins: A, D, E, and K.
Water-soluble vitamins: B complex and C.
Minerals:
Iron
Calcium
Iodine
Copper

Additional Constituent
Water: Essential for life, maintaining hydration, and excreting harmful by-products of metabolism through urine and stool.

Vitamin A
Vitamin A refers to all-trans-retinol, the alcohol form of the vitamin.

Forms of Vitamin A
Forms of vitamin A are the oxidation products of retinol, such as:

All-trans-retinal: The aldehyde form.

All-trans-retinoic acid: Acid derivative.

Dietary Sources
Vitamin A cannot be generated de novo in the human body and must be obtained from dietary sources.

Preformed Vitamin A (Retinol): Found in animal sources.

Fish liver oils

Liver
Dairy products
Egg yolk

Provitamin A (Carotenoids): Found in plants.

α- and β-carotenes
β-cryptoxanthines
Carrots
Tomatoes
Oranges
Squash

Absorption of Vitamin A
Vitamin A and provitamin A are fat-soluble, and their absorption depends on the presence of adequate lipid and protein within
the meal.

Page 11
 Created by Turbolearn AI

1. Active transport with retinol-binding protein.

2. Dioxygenase (in the small intestine) converts provitamin A to vitamin A in the enterocyte.
3. Retinyl palmitate is formed.
4. Released into lymphatics via chylomicrons.
5. Transported to the liver.

Functions of Vitamin A
Vitamin A is required throughout the life cycle, beginning with embryogenesis.

1. Maintenance of Vision (Especially Night Vision): Mediated by the aldehyde form (retinal).

In the dark, low-intensity light induces photo-isomerization of 11-cis-retinal to all-trans retinal in the rhodopsin
prosthetic group.
This isomerization generates an electrical signal transmitted to the brain via the optic nerve.
Within the eye, 11-cis-retinal is bound to Rhodopsin (rod cells) and Iodopsin (cone cells).
All-trans-retinal dissociates from the opsin in a series of steps (bleaching), then is recycled and converted to 11-cis-
retinal for repeat of the cycle.

2. Maintenance of Epithelial Tissues: Pronounced in the intestinal mucosa and the respiratory mucosa. Vitamin A maintains
the normal mucus-secreting epithelium, acting as an effective barrier against pathogens and toxins.

3. Genetic Function: Retinoic acid helps in the differentiation of various tissues, particularly during reproduction and fetal life,
by regulating gene expression.

Retinoic acid binds to the Retinoid receptor RAR.

RAR combines with RXR (another retinoid receptor).
The resultant heterodimer binds to specific nuclear transcription factors.
Regulation of gene expression/differentiation occurs.

Vitamin D Deficiency (Rickets)

Rickets is a disease of growing bones caused by vitamin D deficiency.

Causes
1. Nutritional vitamin D deficiency.
2. Congenital vitamin D deficiency (due to maternal vitamin D deficiency).
3. Secondary vitamin D deficiency (e.g., malabsorption, CKD).
4. Vitamin D-dependent rickets (VDDR) — Type 1 and 2.

Pathogenesis
V itamin; D; def iciency ↓ Low; calcium; and; phosphate ↓ U nmineralized; matrix; at; the; growth; plate ↓ Rickets

Clinical Features
See lecture notes 0.3-0.5 for clinical features.

Radiological Features of Rickets

Active Rickets
See lecture note 0.6.

Healing Rickets

Page 12
 Created by Turbolearn AI

1. Earliest change is seen as an area of calcification (white line) at the metaphyseal end of the long bones that is denser than
the diaphysis of the same bone. This denotes de-novo calcium deposition due to the effect of vitamin D.
2. Fraying is gradually decreased.
3. The cupping becomes more prominent initially, which gradually wanes off over a longer time.

Biochemical Changes
See lecture note 0.6. (Investigations : Laboratory values/Biochemical Survey).

Treatment
See lecture note 0.6.

Complications
Hypothermia
Hypoglycemia
Sudden Infant Death Syndrome (SIDS)
Infections
Septicemia
Pneumonia
Diarrhea
Pyoderma
Scabies
TB
Measles
Bleeding (DIC)
Dyselectrolytemia
Dehydration, shock (including septic shock)

Role of Vitamin D
1. Role in Calcium and Phosphate Metabolism: See lecture note 0.7.

2. Role in Genetics:

Vitamin D receptor (VDR) acts as a heterodimer with Retinoid Receptor (RXR).

Interacts with specific DNA sequences known as the vitamin D Response Elements (VDRE).
Causes activation or repression of gene transcriptions.
Suggested roles include:
Preventing cancers
Modulating immunity
Affecting the endocrine system (Renin-Angiotensin-Aldosterone Axis, Insulin release)

Scurvy
Deficiency of vitamin C leads to the clinical features of scurvy, the earliest recognized nutritional deficiency disease.

Pathogenesis
One of the many actions of vitamin C is the synthesis of collagen, which forms the basic supporting structure of multiple
connective tissues, including bones. In patients with scurvy, osteoid deposition by the osteoblasts remains defective, which leads
to the typical radiological changes.

Radiological Changes in Scurvy

Page 13
 Created by Turbolearn AI

Radiological changes are particularly common at the distal ends of the long bones, like knees and ankles.

1. Shafts of the long bones (diaphysis) have a characteristic ground-glass appearance due to trabecular atrophy.
2. Cortex is thin and dense, giving rise to the appearance of pencil outlining of diaphysis (Pencil-thin cortex).
3. White line of Frenkel: The most typical radiological finding, found at the metaphysis. It represents calcified cartilage at the
zone of calcification and appears as an irregular but thickened white line.
4. Trummerfeld zone: A more specific but late radiological feature of scurvy. This zone of rarefaction under the white line of
Frenkel appears as a linear break in the bone that is proximal and parallel to the white line.
5. Pelkan spur: Lateral prolongation of the white line with an underlying triangular area of rarefaction.
6. Epiphysis: Epiphyseal centers of ossification also have a ground-glass appearance and are surrounded by sclerotic rings,
known as Wimberger's Sign.
7. Occasionally, there may be subperiosteal hemorrhage, which is often missed in plain radiography. MRI can demonstrate
acute, as well as healing subperiosteal hemorrhages.

Vitamin A Deficiency and Xerophthalmia

Vitamin A or Retinal is an essential micronutrient needed for vision, epithelial integrity, and various other functions.

Xerophthalmia
Most characteristic and specific signs of vitamin A deficiency are the eye lesions known as Xerophthalmia, or dry eye.

Clinical Manifestations
1. Xerophthalmia: Eye lesions due to vitamin A deficiency develop insidiously and rarely occur before 2 years of age.

Delayed adaptation to the dark is the earliest symptom, progressing to complete night blindness in more advanced
stages of deficiency.
Photophobia is also a common symptom.
As vitamin A deficiency progresses, the epithelial tissues of the eye become severely altered, giving rise to the
classical signs of xerophthalmia or dry eye.
Conjunctiva is the first to be involved in the form of keratinization, xerosis, and plaque development (Bitot's Spot) in a
triangular fashion, lateral to the cornea.
Cornea also keratinizes, becomes opaque, and forms dry, scaly layers of cells (corneal xerosis).
In later stages, infection occurs, lymphocytes infiltrate, and irreversible damage occurs in the form of ulceration and
degeneration (keratomalacia).
Ultimately, there is corneal scarring, leading to obstruction of vision.
Finally, the pigment epithelium of the retina also degenerates, resulting in blindness.

2. Skin Changes: Epithelial changes in the skin are manifested as scattered, hyperkeratotic papules, commonly seen in the
arms, legs, shoulders, and buttocks.

3. Others:

Increased susceptibility to infections (e.g., respiratory infection, urinary tract infection, diarrhea).
Poor growth velocity.
Mental retardation.

WHO Classification of Xerophthalmia

Page 14
 Created by Turbolearn AI

Primary Signs:
XN: Night Blindness
X1A: Conjunctival xerosis
X1B: Bitot's spots
X2: Corneal xerosis
X3A: Corneal ulceration (< ⅓ of cornea)
X3B: Corneal ulceration (> ⅓ of cornea)
XF: Fundal changes
XS: Corneal scarring
Secondary Signs:
Radiological changes of scurvy - see O. 18.

Protein-Energy Malnutrition (PEM)

Assessment of Nutritional Status

Assessment of nutritional status in PEM is done according to the following parameters:

1. Weight for height (W/H) or weight for length.

2. Height (or length) for Age (H/A).
3. Weight for Age (W/A).
4. Presence of edema.

The WHO recommends the use of Z-scores or Standard Deviation Score (SDS) for evaluating anthropometric data to accurately
classify malnutrition.
Observed;value−M edian;ref erence;value
SDS; (or; Z − score) =
SD;of ;the;ref erence;population

Use of Z-score
Calculation of the Z-score gives a numerical value that indicates how far away from the 50th percentile for age (Median) the
child's measurement falls.

e.g., Z-score < -2 means the value is below (Median — 2SD)

Classification of Acute & Chronic Malnutrition

W/H H/A Interpretation

1. Normal Normal Normal (No PEM)

2. Decreased Normal Acute Malnutrition
3. Decreased Decreased Chronic Malnutrition
4. Decreased Decreased Acute-on-chronic malnutrition

WHO Classification of PEM

Features Moderate Severe

1. Edema No Yes
2. WH (Wasting) 70-79% (Z-score -2 to -3) <70% (Z-score <-3)
3. H/A (Stunting) 85-89% (Z-score -2 to -3) <85% (Z-score <-3)
Z-score W/H HA

1. > -2 (Normal) Normal Normal

2. < -2 (Decreased) Wasted Stunted

Page 15
 Created by Turbolearn AI

Severe Acute Malnutrition (SAM)

Definition: See lecture note 0.9 (Definition of SAM)
Management: See lecture note 0.9 (Steps of management and Inpatient management)
Complications: See lecture note 0.9
WHO Criteria for SAM: See lecture note 0.9 (Definition of SAM)

Complications of PEM
See lecture note 0.9 (complications)

Vitamin A Prophylaxis

Rationale
1. Vitamin A deficiency is the leading cause of blindness in children in developing countries.
2. There is also increased susceptibility to infections, like measles, diarrhea, ARI, etc., in children with vitamin A deficiency.
3. Early signs and symptoms of vitamin A deficiency, like delayed dark adaptation, night blindness, and Bitot's Spots, are often
not detectable by children or their caregivers.

Prophylaxis
1. Routine Prophylaxis:

Under the National Vitamin A Prophylaxis Programme, sponsored by the Ministry of Health and Family Welfare, all
children between 6 months to 5 years are given oral vitamin A supplementation along with routine immunization. The
first two doses are combined with routine vaccines to ensure maximum coverage.

Schedule:

1st dose: 9 months (along with measles/MMR vaccination).

2nd dose: 16-18 months (along with DPT booster).
3rd dose: 24 months.
4th dose: 30 months.
5th dose: 36 months.
6th dose: 42 months.
7th dose: 48 months.
8th dose: 54 months.
9th dose: 60 months (along with 2nd booster of DPT).

Dose:

< 6 months: 50,000 IU (Not applicable for routine prophylaxis)

6-12 months: 1,00,000 IU
> 1 year: 2,00,000 IU
Oral dose: Same as above.
IM dose: Half of the oral dose.

2. Prophylaxis in Special Situations: Children with measles and severe malnutrition should also receive vitamin A
prophylaxis (single dose) orally or intramuscularly.

Age-Independent Criteria of Malnutrition

Since it is often difficult to find the true age of the child in underprivileged and ignorant socioeconomic strata, the following age-
independent indices of nutritional status are devised to interpret anthropometric measurements:

Page 16
 Created by Turbolearn AI

1. Mid-Upper Arm Circumference (MUAC): Also known as Mid-Arm Circumference (MAC), it is the most widely used
measurement as it requires minimum equipment.

MAC has been found to be relatively stable between the ages of 1-5 years, at a value of 16-17 cm.
MAC is measured first, and then height. If the height is more than the expected height for the measured MAC, the
child is considered malnourished.
Grading:
MAC < 13.5 cm: Malnutrition
MAC < 12.5 cm: Severe malnutrition
MAC < 11.5 cm: Severe Acute malnutrition

2. Shakir Tape Method: This special tape has colored zones (red, yellow, and green) based on the measurement of MAC.

Red zone corresponds to < 12.5 cm (wasted)

Yellow zone: 12.5-13.5 cm (borderline)
Green zone: > 13.5 cm (normal)

3. Bangle Test: A bangle with an internal diameter of 4 cm is passed above the elbow. If it can be passed easily, the child is
having malnutrition.

4. OUAC Stick Method:

5. Skinfold Thickness: Measured over the Triceps by a standard caliper (e.g., Herpenden's caliper).

> 10mm: Normal

6-10 mm: Mild to moderate malnutrition
< 6 mm: Severe malnutrition

6. Mid-Arm Muscle Circumference:

Calculated by the formula: (M AC − π × triceps, skinf old, thickness)

It is partially age-independent and is calculated as: M AC

H eight;ratio

< 0.29 indicates severe malnutrition.

7. Weight for Height: W H (

8. Various Ratios:

a) Jellife's Ratio: CC

HC

b) Quetlet Index: Wt

[H t;(cm)]
2
× 100

c) Kanawati Index: Potential of malnutrition.

d) BMI (Body Mass Index):

W t;(kg)
2
[H t;(m)]

e) Rao's Index:
W t;(kg)

2
[H t;(cm)]

f) Dugdale Index:
W t;(kg)
1.5
[H t;(m)]

Kwashiorkor
Kwashiorkor is the type of PEM where there is predominantly protein deficiency rather than calorie deficiency. The
term Kwashiorkor originated from the local language of Ghana, meaning "the disease of the first child (after the arrival
of the second)."

Marasmus and Kwashiorkor are the 2 ends of the PEM spectrum with a lot of difference in clinical presentation.

Clinical Manifestations

Page 17
 Created by Turbolearn AI

Clinical features of a child with Kwashiorkor can be divided into essential features and non-essential features, which also helps in
the confirmation of diagnosis.

A) Essential Features:
1. Growth retardation, as evidenced by low weight and low height according to age.
2. Muscle wasting with the retention of some amount of subcutaneous fat.
3. Psychomotor changes, as evidenced by mental apathy in the form of listlessness and lack of interest in the surroundings.
4. Hypoalbuminemic (serum albumin < 2.5gm/dl) pitting edema, at least over the pretibial region (not of cardiac, renal, or
hepatic origin).

B) Non-Essential Features:
1. Hair Changes: Depigmented, sparse hair with the easy pluckability of light and dark-colored hairs are seen (Flag sign).
2. Skin Changes:
1. Flaky paint dermatosis.
2. Crazy pavement dermatosis.
3. GI System: Diarrhea, vomiting, anorexia.
4. Micronutrient Deficiency:
1. Anemia due to iron deficiency.
2. Deficient potassium & magnesium.
3. Vitamin A deficiency.
5. Hepatomegaly: Soft, rounded margin.
6. Superadded Infections: TB, Measles, Bronchopneumonia, Diarrhea, Pyoderma, Giardia, etc.

Grading of Kwashiorkor
Grading of kwashiorkor is based on the site & extent of edema.

1. Grade I → Pedal edema.

2. Grade II → I + Puffiness of face (Facial edema).
3. Grade III → II + Edema of the chest wall and back.
4. Grade IV → III + Ascites.

Difference Between Marasmus and Kwashiorkor

Features Marasmus Kwashiorkor

1. Appearance Old man appearance with generalised wasting Pully appearance with dependent edema.
2. Age Group Infants 1-5 years
3. Prevalence Common Rare
4. Etiology Predominantly calorie deficiency Predominantly protein deficiency
5. Weight < 50% of expected 60-80% of expected
6. Growth retardation ⊕ ⊕
7. Edema Nil ⊕
8. Subcutaneous fat Almost absent Some

Nutritional Recovery Syndrome

Nutritional Recovery Syndrome, also known as Gomez Syndrome, refers to a sequence of events observed in children being
treated with high quantities of proteins during rehabilitation from gross malnutrition.

Nutritional Rehabilitation Center (NRC)

Concept

Page 18
 Created by Turbolearn AI

The concept of Nutritional Rehabilitation Centres (NRC) originally came from Southern America.

Aim
The aim of NRC is to offer nutritional rehabilitation for mild to moderate PEM under the supervision of trained personnel,
bridging the gap between home management and hospital management.

Structure
An NRC consists of:

A room for children

A kitchen
An examination room
A teaching space/counseling room

Types
There are two types of NRCs:

1. Day Care NRC: Operates daily without overnight stay, typically from 8 AM to 6 PM.

2. Residential NRC: A larger, more organized center, usually attached to a health center, pediatric department of a teaching
hospital, or an under-5 clinic.

Caters to 20-40 malnourished children along with their mothers.

Mothers actively participate in activities like marketing and cooking.
At least one good meal is provided to the children.

Activities
Nutrition and health education
Daily work schedule of the mothers
Purchase of food
Keeping stock
Issuing the exact amount of food as decided by doctors/nutritionists
Maintenance of cleanliness

Staff
A "housemother" as the full-time head
Supervisory part-time staff
Doctor
Nurse/Medical assistant
Nutritionist
Home economist

Etiopathogenesis
Exact pathogenesis is still not known.
Initially described with Kwashiorkor, but seen in both Marasmus and Kwashiorkor in India.

Adaptive Mechanism in PEM

Page 19
 Created by Turbolearn AI

Function of the pituitary gland and its target glands are depressed.
Body activity, metabolic rate, and growth velocity are reduced during lower dietary intake.

Nutritional Rehabilitation Effects

Greater utilization of hormones stimulates the pituitary gland to produce trophic hormones (e.g., ACTH, TSH, FSH, LH).
Increases activity of target glands (e.g., adrenal gland, thyroid, gonads), producing hormones excessively (including
estrogen) and causing symptoms.

Clinical Features
Gynecomastia
Parotid swelling
Eosinophilia
Splenomegaly (sometimes)

Treatment
Wait and watch while continuing nutritional rehabilitation.

Prevention
Initiate treatment with a low protein diet, gradually increasing to the target level, may help prevent this entity and ensure a
smooth recovery.

Signs
Increasing hepatomegaly
Abdominal distension
Ascites
Prominent thoraco-abdominal venous network
Hypertrichosis (increased body hair)

Management of Severe Dehydration in PEM

Clinical Signs of Severe Dehydration

History of watery diarrhea or vomiting (i.e., fluid loss)
Increased thirst
Dry eyes and oral mucosa (absence of tears)
Sunken eyes (may be present in children with PEM without dehydration)
Slower skin pinch
Decreased urine output
Tachycardia
Tachypnea
Hypotension
Lethargic/unconscious

Important Considerations
Dehydration tends to be over diagnosed and its severity overestimated in severely malnourished children (particularly
marasmus).
In Kwashiorkor, edema often underestimates the severity of hypovolemia/dehydration.

Page 20
 Created by Turbolearn AI

Treatment Protocol
1. Initial Fluid Bolus:

Ringer's Lactate (RL) with 5% Dextrose or ½ Normal Saline at 15 ml/kg over 1 hour (IV or intraosseous).

2. Assessment After 1 Hour:

No Improvement or Worsening:

Consider septic shock. Start inotropes like dopamine or dobutamine.

Improvement:

PR slows
Faster capillary refill
Increase in BP
Increased urine output
Consider severe dehydration with shock.

3. Repeat Fluid Bolus:

Repeat fluid bolus of 15 ml/kg over 1 hour.

Assess

4. If Clinically Better, But Not Accepting Orally:

Give Oral Rehydration Solution (ORS) by Nasogastric (NG) tube at 5-10 ml/hour.
If accepting orally, start ORS 5-10 ml/kg/hour.

Rehydration Solution
Children with PEM are deficient in potassium, so extra potassium should be supplemented.
IAP recommends low-osmolality ORS (N a = 75 mmol/L, K = 20 mmol/L, Glucose = 75 mmol/L) with additional 20
+ +

mmol/L of potassium as Syrup Potassium Chloride (15 ml of potchlor syrup = 20 mmol of K ). +

Dose: 5 ml/kg every 30 minutes for the first 2 hours, then 5-10 ml/kg/hour for the next 4-10 hours.

Cautions
IV route of rehydration is not recommended, unlike in normal children (plan C for severe dehydration), due to the risk of
overhydration and heart failure.
NG tube is used if the child is unable to accept orally.

Monitoring
Monitor:

Pulse Rate (PR)

Respiratory Rate (RR)
Urine output
Oral mucosa, etc.

Half hourly initially then hourly.

Stop rehydration therapy if there are any signs of overhydration (e.g., ↑ in RR by > 5/min, ↑ in PR by > 15/min, pitting edema, etc.).

Feeding Pattern
Feeds are started at 2-hour intervals initially, then the volume of an individual feed is increased while decreasing the frequency.

Page 21
 Created by Turbolearn AI

Dietary Management of Severe PEM

Phases of Dietary Management

1. Initiation of feeding with starter diet (1st week)
2. Catch-up growth with catch-up diet (2nd week onwards)

Indications for Admission in NRC

Children at risk
Children who fail to gain weight over 3 months
Children who do not catch up in growth after serious illness (e.g., measles, diarrhea, etc.)
Failure of breastfeeding
Mothers and children who find it difficult to cope with their problems at home despite health teaching
Twins & triplets

Severe Dehydration Without Shock

1. Formula: F-75 starter diet (calorie content = 75 kcal per 100 ml)
2. Initiate feeding: As soon as possible. If the child is not able to take orally or takes <80% of the target amount, nasogastric
feeds are started.
3. Total amount of feed: 130 ml/kg/day; reduced to 100 ml/kg/day if there is generalized edema.
4. Recommended total energy: 100 kcal/kg/day.
5. Recommended protein intake: 1-1.5 gm/kg/day.
6. Breastfeeding to be continued ad-libitum.

Types of Diet
Milk-based diet
Milk + cereal based diet (low lactose diet) used in children with persistent diarrhea
Lactose-free diet (rarely needed; used only in those children having persistent diarrhea even on low-lactose diet)

Severe Dehydration With Shock

1. Formula: F-100 catch-up diet (calorie content = 100 kcal per 100ml).
2. Feeding Schedule:
Day Frequency Vol/kg/feed Total volume

D₁ - D₃ 2 hourly 11 ml 130 ml/kg/day

D₄ - D₅ 3 hourly 18 ml 130 ml/kg/day
D₆ - D₇ 4 hourly 22 ml 130 ml/kg/day
3. Transition to F-100: Diet is gradually transitioned from F-75 diet to F-100 diet with increase in energy & protein content.
4. Total volume of feed: 150-200 ml/kg/day.
5. Total energy: 150-200 kcal/kg/day.
6. Total protein: 4-6 gm/kg/day.
7. Types: Same as F-75 diet.
8. Complementary feeds are introduced once target nutrition is achieved with adequate weight gain.

Diet/Feeding of 6-12 Months Old Infants

Complementary Feeding
After 6 months of age, breast milk alone is not enough to make an infant grow well.

Page 22
 Created by Turbolearn AI

Complementary Feeding: Feeds that complement breast milk and ensures that the child continues to have energy,
protein, and other nutrients to grow normally.

Favorable Response
1. Resumption of alertness & appetite.
2. Initiation of weight gain @ 5-10 gm/kg/day.
3. Disappearance of edema (by 7-10 days).
4. Breastfeed as often as the child wants.

Factors Considered While Planning Diet

1. Energy density: Give small but energy dense foods at frequent intervals. Energy density can be increased by adding fats
(e.g., a teaspoon of oil or ghee) in every feed.
2. Amount of feed: Complementary foods should be started with small amounts (1-2 teaspoons) and quantity gradually
increased as the child gets older.
3. Consistency of feed: At 6 months, pureed/mashed semisolid foods are offered to infants. By 8 months, most infants can
also eat finger foods. By 12 months, most children can eat from the family pot.
4. Frequency of feeding: Breastfed healthy infants need 2-3 complementary feeds/day at 6-8 months and 3-4 feeds/day at 9-
12 months of age. Additionally, 1-2 snack meals can be given after 8 months.
5. Hygiene: Good hygiene and proper food handling should be practised to prevent infection.
6. Helping the child: Feeding the infant should be an active, engaging, and interactive affair.

Recommendations
1. Household budget teaching.
2. Complementary feed: Give at least 1 kalori serving at a time of mashed roti/bread/biscuit mixed in sweetened, undiluted
milk or mashed roti/rice/bread in thick dal with added ghee/oil or Khichri with added ghee/oil.
3. Add cooked vegetables in these servings or use dalia, halwa, kheer prepared in milk or mashed boiled potatoes.
4. Offer banana (after 9 months), mango, papaya, etc. as snacks in between the servings.
5. Keep the child in lap and feed with own hands.
6. Wash the hands of self and the child with soap and water every time before feeding.
7. Serve freshly cooked foods, cover food properly, avoid use of feeding bottles.

Unfavorable Responses
1. Nutritional Recovery Syndrome (Gomez Syndrome).
2. Pseudotumour cerebri.
3. Encephalitis-like syndrome.

Q's
Anorexia, nausea, vomiting
Lethargy, confusion or agitation
Headache
Seizures
Coma
Irregular respiration, cheyne stokes breathing

HYPONATREMIA
Hyponatremia (Serum Na < 135 mEq/L); Normal serum N a value is 135-145 mEq/L.
+

Causes

Page 23
 Created by Turbolearn AI

Hyponatremia may develop either due to net loss of sodium or due to net gain of water.

Pathophysiology
↓ Serum Na ↓ Serum (ECF) becomes hypotonic relative to ICF ↓ Water moves f rom ECF to ICF ↓ Cellular edema

Most problematic in the brain (as it is confined in skull)

Cerebral Edema
↓ Cerebral Blood Flow

Brainstem herniation (in acute severe hyponatremia)

Classification

Loss of Sodium (Hyponatremia) Gain of Water (Hyponatremia)

1. Hypovolemic hyponatremia 2. Hypervolemic hyponatremia

(a) Extrarenal losses (a) Nephrotic syndrome
(i) GI loss (Diarrhoea) (b) Cirrhosis of liver
(ii) Sweat (Cystic Fibrosis) (c) Congestive Cardiac failure
(iii) Third space loss (Peritonitis, Ileus) (d) Renal failure (Acute, chronic)
(b) Renal losses 3. Euvolemic hyponatremia
(i) Diuretics (a) Drugs (Desmopressin)
(ii) Hypoaldosteronism (Congenital Adrenal Hyperplasia, Adrenal
(b) SIADH (Syndrome of Inappropriate ADH secretion)
Insufficiency)
(iii) Salt-losing Nephropathy (Tubulo Interstitial Nephritis) (c) Hypothyroidism
(d) Water Intoxication (Primary polydypsia, Runner's
(iv) Bartter's syndrome
hyponatremia)

Factitious Hyponatremia
When serum osmolality is elevated due to increased amounts of osmotically active particles (Glucose, urea, mannitol), water is
drawn from ICF to ECF. Thus, a falsely low N a value is found.
+

Pseudo Hyponatremia
When the serum solids are increased (as in Hyperlipidemia or Hyperproteinemia) and sodium is measured in total serum (i.e.,
water + solids), a falsely low N a value is found.
+

Clinical Features
Symptoms are mostly related to CNS, like:

Other symptoms, like muscle cramps and weakness, may accompany.

Most problematic in the brain (as it is confined in the skull)
Cerebral Edema
↓ Cerebral Blood Flow

Brainstem herniation (in acute severe hyponatremia)

When hyponatremia develops slowly, cells have time to adapt, so patients may be relatively asymptomatic even
during very low levels of N a . +

Diagnosis

Page 24
 Created by Turbolearn AI

1. Exclusion of Pseudo hyponatremia and Factitious hyponatremia.

2. Assessment of volume status.
3. Clinical evaluation for a possible etiology.
4. Measurement of urinary N a .+

Management
1. Acute Cases:
(a) Hypovolemic: Rapid correction with 3% N aCl needed if N a < 120 mEq/L or patient is symptomatic. Otherwise,
+

correct slowly over 48 hours.

Na
+
correction needed = 0.6 × Body wt. × (135 − serum Na) mEq
(b) Hypervolemic/Euvolemic: Fluid restriction.
2. Chronic Cases: Corrected gradually by not more than 12 mEq/L/day. Rapid correction may cause central pontine
myelinolysis.

WATER BALANCE

Fluid Compartments
Total Body Water (TBW) [60%]
Extracellular fluid (ECF) [20%]
Plasma [5%] (Intravascular fluid)
Interstitial fluid [15%]
Intracellular fluid (ICF) [40%]

Total Body Water (TBW) as a percentage of body weight varies with age.

Fetus has a very high TBW, which gradually decreases to approximately 75% of birth weight for a term infant. Premature
infants have higher TBW than their term counterparts. TBW further decreases during the 1st year of life to approximately
60% of body weight.
Post puberty:
TBW in males remains at 60%.
TBW in females decreases to about 50% due to increased fat content (Fat has lower water content than muscle).

Balance Between Different Compartments

1. Balance between ECF and ICF:

ECF and ICF are usually in an 'Osmotic Equilibrium' because the cell membrane is permeable to water.

2. Balance between Intravascular and Interstitial fluid:

(a) \uparrow \text{ Hydrostatic force at intravascular space} ) OR

(b) \downarrow \text{ Oncotic force at intravascular space} )

Water moves from intravascular to interstitial space.

(a) \downarrow \text{ Hydrostatic force at interstitium} ) OR

(b) \uparrow \text{ Oncotic force at interstitium} )

The opposite is also true.

Depends on hydrostatic forces and oncotic forces of both the compartments. This interplay is critical for tissue
perfusion.

Regulation of TBW
Regulation of TBW is done by regulation of plasma osmolality.

Page 25
 Created by Turbolearn AI

( \uparrow \text{Serum Na} \rightarrow \uparrow \text{Serum osmolality} )

( \uparrow \text{ Serum osmolality} \downarrow \ \text{ Stimulation through hypothalamic osmoreceptors} \downarrow \
\text{Thirst } \ \text{Water intake} )

( \uparrow \text{ Serum osmolality} \downarrow \ \text{ Stimulation through hypothalamic osmoreceptors} \downarrow \
\text{Secretion of ADH} \downarrow \ \text{ADH binds to V2 receptors in the collecting duct cells of kidney} \downarrow \
\text{Insertion of Aquaporin-2 channels Into the renal collecting ducts} \downarrow \ \text{Water reabsorption} )

Interplay between different compartments

1. Volume depletion:
(\downarrow \text{ ECF volume} \downarrow )
(\uparrow \text{ ECF osmolality} (OSM_{ecf} > OSM_{icf}) \downarrow )
Water moves from ICF to ECF
2. Fluid retention:
(\downarrow \text{ ECF osmolality} \downarrow )
Water moves from ECF to ICF

HYPERNATREMIA
Hypernatremia is defined as serum N a > 145 mEq/L, but sometimes N a > 150 mEq/L is considered diagnostic of
+ +

hypernatremia.

Pathophysiology
( \uparrow \text{ Serum Na} \rightarrow \uparrow \text{ Serum osmolality} )

( \downarrow \ \text{Fluid shifts from ICF to ECF} \downarrow \ \text{Cell shrinkage} \downarrow )

Causes
Most commonly due to decreased free water losses.

1. Water deficit > Na deficit:

GI loss (diarrhea, lactulose)
Cutaneous loss (Burns)
Renal loss (Osmotic diuretic, Diabetes Mellitus)
2. Water deficit:
Diabetes Insipidus (Central, Nephrogenic)
Increased Insensible loss (warmer, phototherapy)
Decreased Intake
3. Na excess:
Iatrogenic (N S , N aH CO )3

Sea-water drowning
Hyperaldosteronism

Clinical Features
Thirst
Irritability, tremulousness
Excessive cry
Seizures, Focal deficits, coma

HYPOKALEMIA
Hypokalemia is defined as serum potassium < 3.5 mEq/L. Normal serum K +
level is 3.5 - 5 mEq/L.

Page 26
 Created by Turbolearn AI

Causes
1. Decreased intake:
Anorexia Nervosa
2. Increased loss:

(a) Extrarenal loss: Diarrhoea, vomiting.

(b) Renal loss:

Renal Tubular acidosis (Type I, II)

Diuretics
Bartter’s syndrome
Congenital Adrenal Hyperplasia
Cushing's syndrome
Primary Hyperaldosteronism
Renovascular Hypertension.
3. Transcellular shift: (Shift of K from ECF to ICF)
+

Alkalemia
Insulin
Catecholamines
Refeeding Syndrome

Clinical Features
C/Fs are limited to GI tract, musculoskeletal and cardiovascular systems

1. Musculoskeletal:

Muscle weakness
Hypotonia

2. GI:

Abdominal distension
Paralytic ileus.

3. CVS:

Bradycardia
Arrhythmias
ECG changes (low voltage QRS, ST depression, Flat T wave, appearance of U wave).

Diagnosis
1. Exclusion of spurious lab value by checking a second value.
2. History of drug intake.
3. Renal function (BUN, Creatinine)
4. Acid-base status (ABG)
5. Measurement of Renin and Aldosterone.

( \text{Serum K' < 3.5 mEq/L} \ \text{Exclude } \downarrow \text{ed intake, risk factors for transcettular shift} \ \text{Measure BP} )

( \text{BP normal } \ \text{Urine K'} \downarrow \ \text{ < 20 mEq Extrarenal losses} )

( \text{BP } \downarrow \ \text{Urine K'} \uparrow \ \text{ > 20 mEq/L Renal losses} \ \text{Renin, Aldosterone} )

Low Renin
Hyperaldosteronism
High Renin
Renovascular

Page 27
 Created by Turbolearn AI

Treatment
Fluid deficit to be corrected slowly over 48 hours or longer.

K
+
supplementation (KCl) → Oral/IV.
Correction is usually done slowly, and daily K should not exceed 4 mEq/Kg/day.
+

Rapid correction is needed in cases with → arrhythmias, bradycardia, shallow respiration etc.
Fluid deficit: ((0.6 \times \text{Body weight} \times [\text{Expected } Na^+ - \text{Lt. Na}^+]))
Usual fluid used for correction is 0.2 DNS.
In cases of central DI, Vasopressin is used. In nephrogenic DI, DOC is thiazide diuretics (DOC = Drug of Choice)

HYPERKALEMIA
Hyperkalemia is defined as serum potassium > 5 mEq/L.

Causes
1. Increased Intake:
Oral
Blood Transfusion.
2. Decreased excretion: (via kidney)
Renal Failure (AKI, CKD)
Addison's disease
Decreased Mineralocorticoid activity (CAH, Pseudohypoaldosteronism)
RTA, type IV.
Hyporeninemic Hypoaldosteronism (Decreased renin due to kidney damage in obstructive uropathy, sickle cell
disease).
Drugs (ACE Inhibitors, Aldosterone antagonists).
3. Transcellular shifts: (Shift from ICF to ECF).
Acidemia
Accidental
β-blockers

Crush injury, burn, rhabdomyolysis, hemolysis.

4. Spurious Lab. Value: Tissue ischemia during blood drawing.

Clinical Features
Mild degrees of hyperkalemia are generally well-tolerated with very few symptoms. But, when K +
value crosses 6-6.5 mEq/L,
there are risks of life-threatening cardiac arrhythmias.

ECG changes: Tall, peaked T waves (early change) that may progress to ST depression, prolonged P R interval, and
widening of QRS complex.
Ventricular ectopics, VT, VF.

Diagnosis
1. Exclusion of spurious lab. value by checking a second value.
2. History of drug intake, blood transfusion, injuries/burns.
3. Renal function (BUN, Creatinine)
4. Acid-base status (ABG)
5. Measurement of Renin and Aldosterone.

Measures to Tackle Hyperkalemia

Page 28
 Created by Turbolearn AI

1. To avoid all intake of potassium through dietary

2. Drugs to be avoided:
ACE inhibitors (Enalapril, Captopril etc.)
ARB (Losartan, Olmesartan etc.)
K
+
sparing diuretics (Spironolactone, Amiloride)
NSAIDS
Succinylcholine (during intubation).

Treatment
1. Calcium Gluconate (10%):
Used for immediate cardioprotective action when K > 6 mEq/L
+

Dose: 0.5-1 ml/kg over 5-10 mins, diluted in equal volume of 5% Dextrose.
MOA: Membrane stabilization.
2. N aH CO :
3

Cardioprotective action.
Dose: 1 mEq/kg.
MOA: Shifts K intracellularly.
+

3. Glucose + Insulin:
Slower onset of action (30 mins)
Dose: (0.5-1 gm/kg Glucose + 0.1 unit/kg Insulin) as infusion.
MOA: K shift into cells.
+

4. Nebulized β agonist: (Salbutamol)

2

Alternative to (glucose + insulin)

Dose: 5-10 mg.
MOA: K shift into the cells.
+

5. K exchange resins (Kayexalate):

+

Used for chronic hyperkalemia, as it excretes K from the body slowly.

+

Dose: 1 gm/kg PO or PR.

MOA: Exchanges N a for K across the colonic mucosa.
+ +

THERMOGENESIS/THERMOREGULATION
Thermogenesis: Production of heat in the body.

Thermoregulation: Involves maintenance of body temperature by means of thermogenesis in response to cold.

Heat regulating center at hypothalamus.

Mechanisms of Thermogenesis
1. Shivering (muscular)
2. Non-shivering (metabolic)

Shivering Thermogenesis
Shivering occurs by muscular activity in response to cold ambience. But in newborn infants, shivering is not a significant source of
heat production, and it appears only when the environmental temperature falls below 25°C.

Non-shivering Thermogenesis (NST)

It is the most important source of heat production in newborn and it occurs as a result of metabolism of the brown fat. Fetal
brown fat is laid down mostly during the third trimester of pregnancy. LBW babies are deficient in brown fat.

Page 29
 Created by Turbolearn AI

Brown Fat:
Characterized by: (In comparison to white fat)
Rounded nucleus and granular cytoplasm.
Large number of mitochondria.
Abundant fat vacuoles.
Increased vascularity.
The quantity of brown fat is directly related to the birth weight of the baby.
In a term baby, it accounts for 4% of body weight.
Extra O and glucose are needed for these metabolic efforts.
2

Location:
Nape of the neck
Interscapular region
Axillae
Groin
Around kidneys and adrenals

Mechanism of NST

Skin becomes cold Afferent Nerve Elferent Nerve Reaches Brown fat

( \text{BROWN FAT} \rightarrow \text{Local release of Noradrenaline (NA)} )

( \text{TG } \rightarrow \text{Glycerol + Fatty acids} )

Distributed to different parts of the body through circulation Heat generation.

Management of Hypothermia
1. Rapid rewarming
Started immediately using a radiant warmer or incubator.
Done up to 34°C.
2. Slow rewarming
As baby's temperature reaches 34°C, rewarming should be done slowly till 36.5°C.
3. Take all measures to reduce heat loss.
4. IVF (IV fluid) - Started as per maintenance requirement.
5. Hypoglycemia
CBG to be checked.
Treat any hypoglycemia with bolus of 10% Dextrose @ 2ml/kg.
6. Moist O provided with head box.
2

7. Give injection Vitamin K 1mg IM/IV if not already received recently.

8. If the baby doesn't improve with all these measures or there is recurrent/persistent hypothermia, think of causes like sepsis
and start IV antibiotics.

Grades of Hypothermia
Normal body temperature in newborn is 36.5 - 37.5°C. Body temperatures of < 36.5°C is abnormal and < 36°C is known as
hypothermia.

Hypothermia in a newborn baby is defined as core temperature of < 36°C.

Normal temperature → 36.5 - 37.5°C

Cold stress → 36-36.4°C

Hypothermia may persist because of any of the following: Inadequate Clothing

Hypothermia in Newborns
Hypothermia in a newborn is defined as a body temperature below 36°C. Normal temperature for a newborn is between 36.5°C
and 37.6°C. Newborns are more prone to hypothermia than hyperthermia.

Page 30
 Created by Turbolearn AI

Grading of Hypothermia
∘ ∘ ∘ ∘ ∘
Cold stress (Mild hypothermia) : 36 C − 36.4 C Moderate hypothermia : 32 C − 35.9 C Severe hypothermia :< 32 C

Etiology of Hypothermia
Situations and mechanisms contributing to excessive heat loss:

1. Situations Contributing to Excessive Heat Loss

Cold environment (winter, labor room, operation theatre)
During transport
Contact with cold linen
Bathing
Increased air flow with low humidity
2. Mechanisms Contributing to Heat Loss
Conduction
Convection
Radiation
Evaporation

Other factors:

Poor Ability to Conserve Heat: Common in preterm and LBW babies.

Poor Metabolic Heat Production (NST):
Deficiency of Brown Fat (preterm, SFD babies)
CNS damage (Asphyxia, intracranial hemorrhage)
Hypoxia
Hypoglycemia

Risk Factors for Hypothermia

Warm Delivery Room
Warm Resuscitation
Immediate Drying
Skin-to-skin contact
Breast feeding
Postponement of bathing and weighing
Appropriate clothing
Rooming-in
Warm transportation
Professional alertness and training

Clinical Features of Hypothermia

Baby is uncomfortable and restless.
Refusal to feed.
Peripheries are cold to touch.

Diagnosis of Cold Stress

Clinical Assessment: Touch the baby's abdomen and soles with the dorsum of your hand. If the abdomen is warm but the
soles are cold, cold stress is diagnosed.
Temperature Measurement:
Rectal temperature is ideal (30°C - 40°C).
Axillary temperature is commonly used (36°C - 36.4°C for cold stress, < 36°C for hypothermia).

Page 31
 Created by Turbolearn AI

Prevention of Hypothermia: Warm Chain

The warm chain consists of ten interlinked steps to reduce hypothermia in newborns. Risk of hypothermia is inversely
proportional to Birth Weight and Gestational Age. Preterm and Low Birth Weight (LBW) babies particularly need an additional
heat source.

1. Warm delivery room

2. Warm resuscitation
3. Immediate drying
4. Skin-to-skin contact
5. Breast feeding
6. Postponement of bathing and weighing
7. Appropriate clothing
8. Rooming-in
9. Warm transportation
10. Professional alertness and training

Monitoring Temperature
Temperature should be monitored in all babies diagnosed with hypothermia (including cold stress).

Initial Steps
1. Remove all wet/cold clothes from the baby.
2. Cover the baby with warm clothes/towel.
3. Cover peripheries with cap, socks, and mittens to decrease heat loss.
4. Warm the environment, including bed and room.
5. Ensure skin-to-skin contact with mother (Kangaroo Mother Care - KMC).
6. Immediately breast-feed the baby.

Additional Heat
1. Provide extra heat by radiant warmer, incubator, or room heater.
2. Take measures to reduce heat loss.
3. Warm environment and linen.

Management of Hypothermia
Cold Stress: Managed at home or by keeping the baby with the mother. Monitor temperature:
1. Every 1/2 hour until it reaches 36.5°C.
2. Hourly for the next 4 hours.
3. 2 hourly for 12 hours thereafter.
Moderate Hypothermia: Provide an additional source of heat.
Severe Hypothermia: Managed in a hospital setting.

Complications of Hypothermia
1. Hypoxia and hypoglycemia due to consumption of O2 and Glucose during metabolic heat production.
2. Metabolic acidosis due to anaerobic metabolism.
3. Rt to Lt. shunting of blood, which aggravates hypoxia.
4. Rise in serum K+ and NPN levels due to tissue catabolism (NPN = Non-protein Nitrogen).
5. Liver damage may cause coagulopathy.

Kangaroo Mother Care (KMC)

Page 32
 Created by Turbolearn AI

Kangaroo Mother Care (KMC) is a method of care for preterm or LBW infants involving skin-to-skin contact with the
mother or other caregiver to ensure optimum growth and development.

Prerequisites for KMC

All stable LBW babies are eligible.
Sick and very small babies (< 1200 gm) needing special care should be cared for under a radiant warmer, and KMC started
once they are hemodynamically stable.
Appropriate health facility: Allow parents in the neonatal unit, with separate space for KMC.
Appropriate support staffs and professionals: Trained, full-time health care workers.
Good quality monitoring and follow-up facility.
Mother's criteria: Willing, free from serious illness, and maintains good personal hygiene.
Supportive family members.
Social and community support.

Types of KMC
Continuous
Intermittent

Procedure for KMC

1. Counselling: Counsel parents and family about the benefits, procedure, and monitoring of KMC.
2. Mother’s Clothing: Mother can wear any front-open dress as per local culture.
3. Baby’s Clothing: Baby is dressed with cap, socks, mittens, nappy, and front-open steam shirt.
4. Positioning:
Baby is placed between mother’s breasts in an upright position.
Head is turned to one side and kept in a slightly extended position to keep the airway open.
Hips and arms are flexed and abducted to maintain a "frog-like" position.
Bottom of the body to be supported with a sling or binder.
Back of the baby to be covered by a woolen shawl.
5. Monitoring: Vitals (color, respiration, temperature).

Benefits of KMC
Improves bonding between mother and baby.
Promotes breast feeding with better yield of milk.
Stabilizes vital signs with effective thermal control.
Reduces risk of apnea.
Reduces risk of infections.
Babies cry less, sleep better, and show satisfactory neurobehavioral development.
Better weight gain occurs with early discharge from the hospital setup.

Limitations of Continuous KMC

1. Poor cultural acceptability in our society.
2. Lack of garment design for easy ambulation of mothers practicing KMC.
3. It is uncomfortable for the mother to remain constantly stuck with the baby throughout day and night during the hot
summer months.

Discontinuation and Weaning

KMC is continued until the baby achieves a weight of 2500 gms. Weaning occurs when the baby shows discomfort or there is
visible sweating.

Page 33
 Created by Turbolearn AI

Neonatal Sepsis
Neonatal sepsis is a clinical syndrome characterized by signs and symptoms of infection with or without
accompanying bacteremia in the first month of life.

Identification of the pathogenic organism by culture of blood or any other body fluids is confirmatory for sepsis.

Risk Factors
LBW
Preterm
SGA

Clinical Features of Neonatal Sepsis

Alteration in behavior and established feeding pattern.
Baby may become lethargic, inactive, and refuses to suck.
Hypothermia (including cold stress) - common in preterm babies.
Fever (very rare) - may manifest in term babies.
Prolonged jaundice
Hepatosplenomegaly
Apnea with cyanosis
Failure to gain weight may be the only feature.

Generalized Features
Cold extremities
Pale, grayish skin color with mottling
Increased CRT
Stretched out and shiny skin
Unpinchable skin
Progresses centripetally starting from face and legs, chest is involved last causing respiratory compromise.

Localized Features
Shock
Sclerema
Necrotizing enterocolitis
Disseminated Intravascular Coagulation

Complications
Excessive bleeding from venipuncture sites
Pulmonary hemorrhage
CNS bleeding

Sepsis Screen
All neonates suspected to have sepsis should have a sepsis screen to corroborate the diagnosis before blood culture report is
available.

Two positive markers out of the following 5 is suggestive of sepsis:

Page 34
 Created by Turbolearn AI

1. Total Leukocyte Count (TLC) - < 5,000/mm³

2. Absolute Neutrophil Count (ANC) - Low count as per Manroe's charts (or term intents and Mouzinho's chart for VLBW
babies. (On an average ANC < 1800/mm3. is considered abnormal).
3. Immature neutrophil (Band cell) : Total neutrophil ratio - (I : T ratio) > 0.2 or > 20%.
4. Micro—ESR —-) >15 mm in tst hour.
5. C-reactive protein (CRP) ‘ > 1 mgldl (varies among ditierent laboratories for different methods of estimation).

Interpretation
Considered positive when 2 or more parameters are positive.
If the initial screen is negative, but clinical suspicion of sepsis is high, it should be repeated after 12 hours.
Two consecutively negative sepsis screens exclude the diagnosis with reasonable certainty.
Sensitivity and specificity are approximately 93% and 88% respectively.
Negative predictive value is more than positive predictive value.

Specific/Localized Investigations
1. For pneumonia — Chest X-ray detects any pneumonic consolidation and also excludes other DD (like - RDS).
2. For Meningitis — Lumbar Puncture (LP) and neuro imaging should be done in all cases of Late Onset Sepsis (LOS).
Neuro imaging: USG of Brain is MC investigation done in LOS; MRI brain indicated in proved Clo meningitis later to
detect any brain damage. *Lumbar Puncture Results:
CSF cytology with cell count > 30 cells/mm³ *Cell type > 60% polymorphs
Glucose - < 50% of Blood glucose
Protein - > 150 mg/dl (Term) or > 180 mg/dl (preterm)
3. For UTI/Pyelonephritis
Urine culture and WE
USG — KUB region.
4. Arthritis/osteomyelitis - X-ray of concerned joint or bone is done.

Lab Diagnosis
Blood culture - Gold standard for confirmation of sepsis. Should always be sent before starting antibiotic therapy.
Conventional methods of culture usually take 7-10 days.
BACTEC and BACT/ALERT give faster results (Within 12-24 hours).

Acute Phase Reactants

CRP - Most commonly used marker and included in sepsis screen.
Micro-ESR - Can be done bedside and is also included in sepsis screen.
Procalcitonin - More reliable marker of sepsis compared to CRP.
Cytokines - e.g. IL-6.

Supportive Investigations (To detect complication/organ damage)

1. LFT - for jaundice
2. RFT - urea/creatinine
3. Glucose (both hypo and hyperglycemia can occur)
4. PT, aPTT- for DIC
5. Blood counts

General Investigations
Hb
Platelet count
Dohle bodies and Toxic granules in neutrophils.

Page 35
 Created by Turbolearn AI

Management of Neonatal Sepsis

1. Antimicrobial therapy: Mainstay of management. *Indication:
For early onset sepsis - (EOS)
≥ 3 risk factors for EOS (Risk factors include LBW, preterm. Meconium stained liquor. Prolonged rupture of
membranes, Prolonged labor, Birth asphyxia etc.)
≥ 2 risk factors + Positive septic screen.
Foul smelling liquor.
Strong clinical suspicion.
For LOS -
Positive sepsis screen
Strong clinical suspicion
Commonly used antibiotics are
Ampicillin + Gentamicin (1st line)
Cefotaxime + Amikacin (2nd line)
Piperacillin — Tazobactam/Meropenem/Ciprofloxacin + Amikacin (3rd line)

*Choice — Depends on local sensitivity pattern for each hospital setting, presence of meningitis and etiological agent. * For
septic arthritis/osteomyelitis - X-ray of concerned joint or bone * For Meningitis — Antibiotics with good CSF penetration used in
meningitis (eg. 3rd generation cephalosporins, cefuroxime, Meropenem) * For suspected Staphylococcal (MRSA) infection —>
Vancomycin * For suspected Pseudomonas infection —> Piperacillin — Tazobactam.

Change — Antibiotics are usually changed, if -

No response seen after 48 hrs, or
After receipt of sensitivity report (according to report).
Duration-
Presumed/clinical sepsis (screen and culture negative) -+ 5-7 days.
Screen + ve, but culture — ve -+ 7-10 days
Culture + ve (No meningitis) —i 14 days
Meningitis -+ 21 days
Ventriculitis/Arthritis ., 4-6 wks.
2. Supportive therapy:
Maintenance of temperature (nursed in warmer).
Moist O2 (for respiratory distress or desaturation).
Intravenous Fluid with maintenance of normoglycemia
Volume expansion and Inotropes for shock.
Anticonvulsants (for convulsion)
Respiratory Support (with CPAP or ventilator), if needed.
Blood products - Transfusion of Packed cells. FFP and Platelets. as and when required.
3. Newer therapies/Immunotherapy: Used in refractory cases.
Exchange Transfusion
Intravenous immunoglobulin
G-CSF/GM-CSF

Early recognition, prompt administration of effective and appropriate antibiotic & supportive therapy improve intact survival rate
of neonates with sepsis.

Late Onset Sepsis (LOS)

Neonatal sepsis with onset of symptoms occurring after 72 hours of life.

Page 36
 Created by Turbolearn AI

Source of infection is either nosocomial (hospital-acquired) or community-acquired.

Organisms:
Hospital-acquired:
Gram negative (about 2/3rd cases) - Like Klebsiella, E.Coli, Pseudomonas, Acenatobacter etc.
Gram positive (about 1/3rd cases) — Like Staphylococcus aureous, coagulase negative Staphylococcus etc.
Community-acquired:
Poor hygiene
Poor cord care
Bottle feeding
Pre lacteal feeds.

*Risk Factors * Hospital-acquired * LBW, Prematurity. * NICU admission * Mechanical Ventilation * Invasive procedures (e.g.
Exchange Transfusion) * Administration of IV fluid. *Community-acquired * Poor hygiene * Poor cord care

Hypoglycemia in Neonate
Hypoglycemia is defined as a blood glucose value of < 40 mg/dL (plasma glucose <45 mg/dL).

Clinical Features
Symptoms are mostly subtle and non-specific. The majority of hypoglycemic babies may remain asymptomatic. Babies may
present with:

Irritability of the CNS, like jitteriness, tremors, convulsions

Depression of CNS, like apathy, stupor, coma
Non-specific signs, like refusal to feed, apnea, cyanosis, hypothermia
Tachycardia and sweating (features of increased sympathetic activity)

Etiology
1. Hyperinsulinism:
Infant of Diabetic mother, LGA infants
Erythroblastosis fetalis.
Beckwith — Wiedemann syndrome.
Insulin producing tumors (Nesidioblastoma)
Genetic (mutation in ABCC8 gene)
2. Decreased store/intake:
Prematurity
IUGR/SGA
3. Increased utilization:
Birth asphyxia
Sepsis
4. Decreased production/Miscellaneous:
Defects in carbohydrate metabolism (Glycogen Storage Disease)
Defects in amino acid metabolism (organic acidemias).
Defects in fat metabolism (Fatty acid oxidation detect).
Adrenal insufficiency, Glucagon deficiency, Congenital Hypopituitarism

Risk Factors

Page 37
 Created by Turbolearn AI

LBW (< 2kg)

Preterm (< 35 wks)
SGA
LGA
IDM
Rh incompatibility
Any sick neonate on TPN or Total Parenteral Nutrition.
Polycythemia
Hypothermia

Diagnosis
Bedside reagent strips (Glucose oxidase): not reliable, useful for screening.
Laboratory diagnosis: all hypoglycemias diagnosed at bedside are to be confirmed by lab value.

Screening/Prevention
Screening is recommended in:

LBW (< 2kg)

Preterm (< 35 wks)
SGA
LGA
IDM
Rh incompatibility
Any sick neonate on TPN or Total Parenteral Nutrition. *Schedule of screening: 2, 6, 12, 24, 48 and 72 hrs. after birth. Sick
neonates on IVFITPN are usually screened 6-8 hrly.

Management

Blood Glucose (BG) Management

Symptomatic with/without Bolus of 2-ml/kg of 10% Dextrose Glucose infusion/IVF with GIR of 8 mg/kg/min Monitor every
Seizures BG < 20 mg/dl 30 mins. till BG >40. then 4 hrly
Bolus of 5-ml/kg of 10% Dextrose Glucose infusion/IVF with GIR of 6-8 mg/kg/min (Monitor
Asymptomatic BG < 40 mg/dl
every 30 mins. I till BG >40. then 4 hrly)
Trial of oral feeds & CBG after Continue feeding/Monitor BG If BG < 40 on subsequent recordings Uptitrate TGIR by 2mg/kg/min,
30 Minutes if BG < 40, Continue feeding/Monitor BG If BG < 40 on subsequent recordings upto 12mg/kg/min

Other Conditions

Hemorrhagic Disease of Newborn (HDN)

Hemorrhagic manifestations in a newborn baby due to deficiency of Vitamin K.

Transient Tachypnea of the Newborn (TTN)

Disruption or delay in clearance of lung fluids causes transient pulmonary edema that characterizes TTN (Wet lung
syndrome).

Diagnosis needs exclusion of other potentially severe etiologies of respiratory distress appearing in 1st 6 hours.

Early onset HDN : Risk factor is maternal intake of warfarin, anticonvulsants (Phenytoin, Phenobarbitone), Rifampicin etc.

Hemorrhagic Disease of Newborn (HDN)

Page 38
 Created by Turbolearn AI

Definition
Classical hemorrhagic disorder of the newborn

Etiology
Newborns are physiologically deficient in Vitamin K due to:

Minimal transplacental passage

Limited hepatic storage
Low content in breast milk
Malabsorption
Maternal drug intake

This deficiency leads to defective carboxylation of glutamic acid residues in Vitamin K dependent clotting factors (II, VII, IX, X),
impairing their activation and causing bleeding manifestations.

Types of HDN
1. Early HDN:

Presentation: Life-threatening hemorrhagic manifestations in-utero or within 24 hours of life (concealed hemorrhages
inside cranium, thorax, or abdomen).
Management: Predisposed infants receive Vitamin K1 (2 mg) at birth, preferably via LUCS (Lower Uterine Cesarean
Section).

2. Classical HDN:

Occurs due to physiological Vitamin K deficiency.

Most common type of HDN.
Aggravated by exclusive breastfeeding.
Presentation: Commonly during the 2nd or 3rd day of life (up to 1-7 days), presenting with umbilical stump bleeding,
nasal bleeding, or GI bleeding. Usually not life-threatening.
Treatment: Vitamin K1 (1 to 2 mg) intravenously or intramuscularly causes dramatic response.

3. Late HDN:

Presentation: Presents after the 1st week of life (2-16 weeks) with life-threatening bleeding manifestations
(intracranial bleed), but bleeding may occur from any site (skin, GIT, etc.). Mortality risk is around 20%.
Risk factors:
Chronic diarrhea
Malabsorption
Cholestasis
Prolonged administration of broad-spectrum antibiotics
Management: Predisposed infants should receive Vitamin K1 (1 mg) intramuscularly monthly until the underlying
disorder is controlled.

Diagnosis
1. Sepsis Screen: To rule out Early Onset Sepsis (EOS).
2. Coagulation Profile:
Bleeding Time - Normal
Clotting Time - Prolonged
Prothrombin Time - Prolonged
aPTT - Prolonged (may be normal initially, as Factor VII has the lowest half-life).
3. PIVKA (Protein Induced in Vitamin K Absence): Elevated.

Page 39
 Created by Turbolearn AI

Treatment
1. Vitamin K: K1 (plant source) and K2 (animal source) are safe in newborns, but K3 (synthetic) is potentially toxic.
2. Predisposed infants should receive Vitamin K1 (2 mg) at birth.
3. Life-threatening hemorrhage: Fresh Frozen Plasma (FFP) transfusion along with Vitamin K injection.
4. Whole Blood/Packed Red Blood Cells (PRBC) Transfusion: For large amounts of bleeding (> 20% blood loss).

Prophylaxis
All newborns born in hospital settings should be given 0.5-1 mg of Vitamin K intramuscularly at birth or within 24 hours of
life (0.5 mg for newborns < 1000 gms).

Transient Tachypnea of Newborn (TTN)

Definition
A benign, self-limiting condition affecting term or late preterm infants, characterized by tachypnea.

Risk Factors
1. Birth by cesarean section
2. Precipitated labor
3. Maternal diabetes

Pathophysiology
1. In utero, fetal lungs are fluid-filled (secretory mode) for normal lung growth.
2. At birth, lungs switch to an absorptive mode for normal breathing and gas exchange.
3. During normal labor and vaginal delivery:
Surge in Glucocorticoids and catecholamines
Fluid squeezes out from lungs
Absorption of fluids through capillaries and lymphatics

Clinical Features
1. Affected term or late preterm infants usually present within 1-6 hours of life.
2. Tachypnea (RR of 60-120/min) is the consistent sign.
3. May or may not be associated with signs of mild to moderate respiratory distress (retractions, grunting, nasal flaring).
4. Occasionally, mild cyanosis may occur, which responds to supplemental O2 at FiO2 < 0.4.
5. Increased anteroposterior diameter of chest due to hyperinflation (may also have pushed down liver and spleen).
6. Air entry is usually good.
7. Signs usually resolve by 12-24 hours in mild cases and within 72 hours in severe cases.

Investigations
CXR: Prominent perihilar streaking (Sunburst Pattern) due to engorgement of periarterial lymphatics is seen in TTN.

Treatment

Page 40
 Created by Turbolearn AI

Only supportive treatment is needed, as the disease is self-limiting.

Moist O2 inhalation by head box usually suffices.
More severe cases may need CPAP (Continuous Positive Airway Pressure) to improve lung recruitment.
NG or Nasogastric tube feeding may be required initially.
IV antibiotics may be started in dubious cases and stopped after 48-72 hours once symptoms resolve and sepsis screen is
negative.

Physiological Reflexes in Lactogenesis

Definition
Lactogenesis or milk production depends on 2 physiological reflexes, mediated by 2 separate hormones: Prolactin and
Oxytocin

Anatomy of the Breast

Before discussing prolactin and oxytocin reflexes, the anatomy of the breast tissue, including glands and ducts, should be known
well.

Milk-secreting cells - Prolactin

Myoepithelial cells - Oxytocin

Prolactin Reflex (Milk-Secretion Reflex)

Afferent pathway:
Baby sucks at breast
Sensory impulse travels to anterior pituitary
Prolactin hormone produced
Efferent pathway:
Prolactin passes through blood
Promotes milk secretion from milk-secreting cells
Enhancing factors:
Sucking (early and frequent sucking acts as good stimulus)
Expression of milk
Complete emptying of breast
Night feeds (as prolactin reflex is more active at night)
Hindering factors:
Worry
Stress
Pain
Doubt/low confidence

Oxytocin Reflex (Milk-Ejection Reflex)

Page 41
 Created by Turbolearn AI

Afferent pathway:
Baby sucks at breast
Sensory impulse travels to posterior pituitary
Oxytocin production
Efferent pathway:
Oxytocin released in blood
Contraction of myoepithelial cells around glands
Ejection of milk from the glands into the lactiferous sinuses through tubules.
Enhancing factors:
Loving thought of the baby by mother
Sound of baby
Sight of baby
Relaxed, comfortable and confident mother
Hindering factors:
Incorrect positioning during feeding
Painful breast
Prelacteal feeds or top feeding

Baby Friendly Hospital Initiative (BFHI)

Definition
A global program organized by UNICEF launched in 1992 and adopted by India in 1993.

After the introduction of BFHI, exclusive demand feeding is accepted as the only mode for early infant feeding, and exclusive
breastfeeding is recommended for the first 6 months of life.

Certification
A hospital is certified as a "Baby Friendly Hospital" if the facility promotes breastfeeding, maintaining all the 10 steps.

Certification is done by the national and state BFHI task forces if all the criteria are properly met.

Contact points where mothers can be counselled:

1. During antenatal visits
2. Delivery room/operation theatre
3. Primary immunization sessions

The Ten Steps in BFHI

1. Have a written breastfeeding policy that is routinely communicated to all health staff.
2. Train all health care staff in skills necessary to implement this policy.
3. Inform all pregnant women about the benefits and management of breastfeeding.
4. Help mothers initiate breastfeeding within an hour of birth.
5. Show mothers how to breastfeed and how to maintain lactation even if they are separated from their infants.
6. Give newborn infants no food or drink other than breast milk unless medically indicated.
7. Practice rooming-in and allow mothers and infants to remain together 24 hours a day.
8. Encourage breastfeeding on demand.
9. Give no artificial teats or pacifiers to breastfeeding infants.
10. Foster the establishment of breastfeeding support groups and refer mothers to them on discharge from the hospital or
clinic.

Types of Breast Milk with Advantages

Breast Milk Types According to the Stages of Lactation

Page 42
 Created by Turbolearn AI

1. Colostrum:

The golden-yellow milk secreted during the first 3 days after delivery. It transitions to mature milk over the next 2
weeks.
Often termed as “Liquid Gold”.
Characters:
Yellow and thick.
Secreted in small quantities.
Advantage:
Rich in antibodies and WBCs.
Loaded with secretory IgAs, which confers mucosal immunity (acts like a vaccine shot for the baby).
Higher protein content.
Never discard colostrum, as it is the ideal first meal for the baby.

2. Transitional Milk:

Secreted during the following 2 weeks.

The immunoglobulin and protein content decreases while the fat and sugar content increases.

3. Mature Milk:

Follows transitional milk.

Thinner and watery but contains all the nutrients essential for optimal growth of the baby.

Breast Milk Types According to the Phase of Feeding

1. Foremilk:

Secreted at the start of a feed from a particular breast.

Character: Watery, rich in protein, sugar, vitamins, and minerals.
Advantage: High water and sugar content alleviates baby's thirst and hunger quickly and calms the baby.

2. Hindmilk:

Released towards the end of a feed.

Character: Rich in fat content.
Advantage:
Provides more energy, as fat is the main source of energy (9kcal/gm, whereas protein and carbohydrate gives
4kcal/gm energy).

Helps in adequate postnatal weight gain.

Prevents frequent watery stools with perianal excoriation (seen in babies fed with foremilk only).
For optimum growth, the baby needs both foremilk and hindmilk. One breast should be completely emptied before
putting the baby on the opposite breast.

3. DRIP MILK:

Milk that drips from the opposite breast during breast-feeding

It is mainly foremilk with relatively low energy and fat content.

Breast Milk Types According to Baby's Gestational Age (GA)

Page 43
 Created by Turbolearn AI

1. Term Milk:

Milk of a mother who delivers a term baby after 37 completed weeks.

2. Preterm Milk:

The milk of a mother who delivers prematurely contains all the nutrients in adequate quantity needed by her preterm
infant.
Character (Compared with term milk):
Higher calories
Higher fat, protein and sodium
Lower lactose, calcium and phosphorus
Advantage: Meets the need for extra protein, fat and calorie in preterm babies for adequate catch up growth. Negates
the need for extraneous sources of protein and calorie (Preterm formula, HMF etc.).

Composition of Colostrum
Small in quantity, but enormous in quality.
Thicker than mature breast milk.
Color is yellow or golden yellow.
Higher protein content compared to mature milk.
Lower carbohydrate and fat content.
Sodium - higher
Potassium - lower
Rich in antibodies (IgG, IgA), cytokines, and WBCs.

Advantages of Colostrum
1. The ideal "first meal" for the baby due to its high protein content.
2. Often called "white blood" because it provides large amounts of living cells (lymphocytes and macrophages) which will
defend against infections.
3. Considered as baby's ‘first vaccine shot", as it is loaded with large amounts of Secretory IgAs (sIgA), which confers mucosal
immunity to the GI mucosa.
4. Colostrum has a laxative effect, which:
Helps in bowel movement and early passage of meconium in the baby.
Helps in clearing bilirubin → less enterohepatic circulation → prevents neonatal jaundice exaggeration.
5. Important role in protecting the GI tract:
Newborn's intestines are very permeable.
Colostrum seals the 'holes' by painting the GI tract with a barrier, which prevents most foreign proteins from
penetrating the gut and possibly sensitizing the baby to an allergy.
6. Proving to have neuroprotecting effects, which may prevent Alzheimer’s disease in the future (under research).

Advantages of Breastfeeding

Advantages to the Baby

Page 44
 Created by Turbolearn AI

1. Physical:
Breast milk is supplied at an optimum fluidity and warmth.
Protein is mostly whey protein (80%) rich in α-lactalbumin (precursor of serotonin) and lactoferrin (helps in iron
absorption). Rest is casein (20%).
Allergens like α-casein and lactoglobulin are absent.
Ca:P is more than 2, which helps in calcium absorption.
Solute load is low due to less protein and certain minerals.
2. Physiological:
Breast milk is the sweetest milk with high lactose content.
Protein is easily digestible.
Lipids are rich in essential fatty acids, polyunsaturated fatty acids (PUFA), and phospholipids.
Supplies various enzymes like amylase, lipase, oxidase, etc.
Contains several growth factors.
3. Biochemical:
Supplies passive immunity with WBCs, lysozymes, complements, and various antibodies.
sIgA provides mucosal protection to the GI tract and respiratory tract.
4. Microbiological:
Lactoferrin is bacteriostatic and inhibits E. coli.
PABA (Para amino benzoic acid) protects against malaria.
5. Immunological.
6. Psychological:
Promotes mother-infant bonding.
Helps in brain development and improves IQ.

Advantages to the Mother

1. Helps decrease Postpartum Hemorrhage (PPH).
2. Helps in involution of the uterus via oxytocin.
3. Burns off extra fat accumulated during pregnancy.
4. Decreases incidence of breast and ovarian cancer.
5. Helps in contraception through lactational amenorrhea.
6. Convenient for the mother (no need to carry or sterilize utensils).

Advantages to Family and Society

1. Breastfeeding is economical, saving the cost of packaged milk.
2. Prevents various infections, reducing healthcare expenses.

Causes of Failure of Breastfeeding

True Lactational Failure

Overall incidence of true lactational failure is very low, but it occurs more commonly due to the psychosocial causes.

Causes are:

1. Hypopituitarism/GH Deficiency: Impaired secretion of Prolactin and Growth Hormone (GH) from anterior pituitary.
2. Sheehan's Syndrome: Postpartum hypopituitarism due to ischemic necrosis from hypovolemia during and after childbirth.
3. Smoking/Nicotine Intake: Nicotine delays the suckling-induced release of prolactin.
4. Breast Hypoplasia: Inadequate glandular tissue of the breasts.
5. Obesity: Can result in lactational failure due to the inhibition of prolactin secretion.
6. Drugs: Drugs that stimulate D2 receptors suppress prolactin release by the dopaminergic pathway.
D2 receptor agonist: Bromocriptine, Pergolide.
Indirect D2 receptor activator: Amphetamines

Psychosocial Causes

Page 45
 Created by Turbolearn AI

These causes are more frequent and preventable with adequate maternal counselling:

1. Sickness of Mother: Minor illnesses (fever, cough, coryza, diarrhea) make the mother wary of transmitting the infection to
her baby.
2. Stress: Unnecessary stress about breastfeeding adequacy impairs milk secretion and ejection reflexes.

Other causes:

1. Nipple Confusion: Occurs when the baby is given water, artificial milk, or expressed breast milk through a bottle, leading to
preference for the bottle's wide opening.
2. Supplementation with Formula Feeds: The baby gets satisfied with formula milk and loses interest in breastfeeding.
3. Inverted Nipple: If not solved quickly, the mother gets frustrated and gives up breastfeeding.
4. Sore Nipple, Breast Engorgement, Breast Abscess: Result from improper positioning and attachment, causing pain during
breastfeeding and leading to failure.

Breaking the Myth About Colostrum

Many think colostrum is inadequate in quantity during the first few days of life and indulge in giving top feeding and
prelacteal feeds. It needs to be emphasized that the newborn needs very little fluid during early days, and colostrum is
sufficient to meet that need.
Many discard this yellow fluid from the mother's breast, showing concerns about hygiene. However, colostrum is rather
preventive against all infectious agents that may attack the baby in the neonatal period.

Mongolian Spot

Definition
Also known as Congenital Dermal Melanocytosis, is a benign, flat congenital birthmark seen at birth in over 80% of
Asian children.

Character
1. Flat patches of varying size and shape.
2. May be more than 1 in number.
3. Color: Bluish; may be bluish-gray or blackish-blue.
4. The color gradually fades as the child grows.
5. It normally disappears by 2-3 years and almost always by puberty.

Pathogenesis
Melanocytes (melanin-containing cells) are usually located in the epidermis. During their migration from the neural crest to the
epidermis during embryonic development, entrapment of melanocytes in the lower half to two-thirds of the dermis results in the
development of Mongolian Spots.

Site
Most common location is the lumbosacral area (lower back), but these are also seen at the buttocks, back (upper back), and
flanks. Rare locations include the shoulder, face, and extremities.

Differential Diagnosis
They may be mistaken for bruises and may raise concerns about child abuse.

Treatment
No treatment is required, as it is a benign condition with no malignant potential.

Page 46
 Created by Turbolearn AI

Congenital Diaphragmatic Hernia (CDH)

Definition
Congenital Diaphragmatic Hernia (CDH) is associated with congenital defects in the diaphragm and herniation of
abdominal contents into the thorax.

Incidence
1 in 2000-5000 live births.

Pathology
Defect in the diaphragm (most commonly left-sided foramen of Bochdalek).
Herniation of abdominal contents (stomach and intestine) into the thorax.
Hypoplasia of the ipsilateral lung.
Mediastinal shift to the opposite side.

Site
Left-sided hernias are more common than right-sided, and the posterior part (Foramen of Bochdalek) is usually involved.

Clinical Features
1. Babies with CDH usually present at birth with respiratory difficulty or gasping respiration or inadequate spontaneous
respiration.
2. Milder cases may present later, but rarely after the first week of life.
3. There is diminished air entry to the affected lung.
4. Occasionally, peristaltic sounds may be heard at the ipsilateral chest.
5. The heart is displaced to the opposite side, with shifting of the apex beat.
6. The abdomen usually appears scaphoid or flat.

Diagnosis
1. Prenatal diagnosis: Antenatal USG after 16 weeks of gestation can pick up CDH in the fetus. Polyhydramnios is present in
about 70% of cases.

2. Postnatal diagnosis: In all babies with difficult resuscitation should undergo urgent skiagram of the chest.

CXR shows:
Mediastinal shift
Finding of bowel loops in the hemithorax

Treatment
1. During resuscitation: Urgent endotracheal intubation should be done (assisted ventilation).
2. Bag and Mask Ventilation is contraindicated, as it causes gaseous distension of the bowel and respiratory difficulty worsens
with more compression of the lung.
3. Nasogastric Aspiration is done frequently to decompress the distended bowel of air and fluids.
4. Enteral feeding is contraindicated, and the baby is put on IV fluid and total parenteral nutrition if facilities are there.
5. Surgical Repair: Should be done as early as possible after correction of pH and blood gases.
Prenatal: Antenatally diagnosed CDH can be repaired in-utero by fetal surgery at around 26-28 weeks of gestation.
Postnatal: Surgical repair to correct the diaphragmatic defect.

Page 47
 Created by Turbolearn AI

Prognosis
Prognosis and outcome depend entirely on the degree of pulmonary hypoplasia.

Respiratory Distress in Newborn ‍

Definition
Respiratory distress in the neonate is defined as the presence of tachypnea (RR > 60/min) along with chest retractions
and/or grunting. Other less common signs of respiratory distress include nasal flaring, cyanosis, etc.

Respiratory Causes
1. Respiratory Distress Syndrome (RDS):
Also known as Hyaline Membrane Disease (HMD), it is a disease of the preterms due to immaturity of the lungs.
There is a deficiency of surfactant, which leads to alveolar collapse during expiration.
2. Meconium Aspiration Syndrome (MAS):
In-utero passage of meconium causes Meconium Stained Amniotic Fluid (MSAF), aspiration of which during delivery
may cause respiratory distress in term babies.
3. Pneumonia:
The common presentation of early onset sepsis can involve both term and preterm babies.
4. Transient Tachypnea of Newborn (TTN):
A benign condition affecting mostly term and late preterm babies born by cesarean section. Delayed absorption of
lung fluids is thought to be responsible for tachypnea and respiratory distress.
5. Others (Less Common):
Persistent pulmonary hypertension (PPHN)
Pneumothorax
Chronic Lung disease or Bronchopulmonary Dysplasia (BPD)
Tracheo-esophageal fistula
Congenital Diaphragmatic Hernia
Congenital Lobar Emphysema

Cardiologial Causes
1. Left-to-right shunts: Like VSD, PDA, etc., cause respiratory distress due to pulmonary edema associated with congestive
heart failure.
2. Cyanotic heart diseases: Like transposition of great vessels (TGV), Hypoplastic Left Heart Syndrome (HLHS), etc.
3. Heart failure: May also occur with cardiomyopathies and cardiac rhythm disorders.

Neurological Causes
1. Birth Asphyxia
2. Intracranial hemorrhage
3. Cerebral edema

Metabolic Causes
1. Hypothermia
2. Hypoglycemia
3. Metabolic acidosis (shock, late metabolic acidosis).

Chest Wall Abnormalities

Page 48
 Created by Turbolearn AI

1. Asphyxiating Thoracic Dystrophy (hampers lung expansion).

2. Werdnig-Hoffman disease (Spinal Muscular Atrophy type 1): Weakness of respiratory muscles causes RD in this condition.

Respiratory Distress Syndrome (RDS)/Hyaline Membrane Disease

(HMD) 🫁

Definition
Respiratory Distress Syndrome (RDS), formerly known as Hyaline Membrane Disease (HMD), is primarily caused by
inadequate pulmonary surfactant in preterm babies. However, surfactant may be deficient in term babies also due to
various risk factors.

Clinical Features
Preterm babies or within the first 6 hours of life present with signs of respiratory distress immediately after birth.
1. Tachypnea (RR>60/min)
2. Chest retractions (Intercostal, subcostal)
3. Grunting (expiratory)
4. Cyanosis

Pathogenesis
Pulmonary surfactant is composed of phospholipid (Lecithin and Phosphatidyl Glycerol) and proteins. It decreases surface
tension inside the alveoli to maintain stability.

RDS/H M D ⟹ ↓ Surf actant ⟹ ↑ Surf ace T ension inside alveoli ⟹ Alveoli tends to collapse at end − expiration ⟹ ↓

Risk Factors
1. Factors that affect lung development (and subsequent surfactant production):
Prematurity (Most important etiologic factor)
Gestational diabetes in the mother
Genetic factors
2. Factors that impair surfactant production:
Perinatal Asphyxia
Congenital surfactant deficiency (Mutation of genes producing surfactant proteins B and C).

Complications
1. Pulmonary hypertension.
2. Pneumothorax (of the opposite healthy lung).

Prevention
Administration of antenatal steroids (Betamethasone or Dexamethasone) to mothers in preterm labor (GA 24-34 weeks)
accelerates lung maturity and surfactant production within 24 hours.

Additional Information
The clinical assessment of gestational age at birth by physical and neurological examination of the baby is more reliable
compared to the methods of assessment of the baby in-utero.
Assessment should be done at 24-48 hours of life.
Physical criteria help to divide babies between term (≥ 37 completed weeks) and preterm (< 37 weeks).

Page 49
 Created by Turbolearn AI

Gestational Age Assessment

Physical Criteria
Gestational age can be assessed in newborns based on several physical criteria:

Skin: Preterm babies have smoother, more transparent skin with visible veins, while term babies have rare veins and may
show superficial peeling or cracking.
Lanugo hair: Abundant in preterm babies, less so in term babies.
Ear cartilage: Deficient in preterm babies, causing poor recoil; well-formed in term babies.
Genitalia:
Male: Testes are at or above the external spermatic ring and scrotum is less rugosed in preterm babies; testes are
well-descended in term babies.
Female: Labia majora are widely separated, exposing labia minora in preterm babies; labia majora completely covers
labia minora in term babies.
Sole creases: Preterm babies have a single deep crease over the anterior 1/3 of the sole or no deep creases at all, while
term babies have deep sole creases covering the entire sole.
Breast nodule: < 5 mm in preterm, > 5 mm in term babies.

Neurological Criteria
Neurological parameters are more reliable for precise gestational age estimation:

Muscle tone: Progressively increases in utero as maturity progresses.

Posture or attitude: Term babies have a more flexed attitude, while preterms show a frog-like posture with extended
limbs.
Arm Recoil: More instantaneous recoil in term babies.
Traction response: Term infants can maintain their head in line with the trunk when lifted by the hands, whereas
preterms show head lag.
Scarf sign: Elbow crosses midline in preterm babies.
Popliteal angle: Angle is more in preterms.
Heel-to-ear test: Heel goes more close to ear in preterm.
Reflexes:
Pupillary reflex (light reflex): Present after 30 weeks.
Rooting and coordinated sucking: Appears at 34 weeks.
Moro reflex: Appears at 28-30 weeks, but complete adduction occurs after 38 weeks.
Joint mobility: Limited flexion at ankle and wrist (square window) in preterm babies due to relative stiffness of joints.

Scoring Systems
Modified Ballard Score is widely used, including 6 physical and 6 neurological criteria.

Meconium Aspiration Syndrome (MAS) 🫁

Pathophysiology
Meconium Aspiration Syndrome (MAS) is a significant cause of respiratory distress in term newborns.

Meconium Stained Amniotic Fluid (MSAF) occurs due to in-utero passage of meconium physiologically in post-term
babies or pathologically due to fetal distress (hypoxia).

Clinical Features
Respiratory distress appears within 24 hours of life (usually within 6 hours) in term, post-term, and IUGR babies.
Without treatment, it progresses rapidly to respiratory failure.

Page 50
 Created by Turbolearn AI

Other clinical signs include:

Signs of respiratory distress (tachypnea, retractions, grunting, cyanosis).

Increased anterior-posterior diameter of the chest.
Variable percussion note.
Bilateral wet sounds on auscultation.
Yellowish stain in umbilical cord, nails, and generalized skin surface (Meconium stain).

Diagnosis is confirmed by chest X-ray showing:

Bilateral hyperaeration due to obstructive emphysema.

Coarse nodular opacities due to areas of atelectasis and consolidation.
Groundglass opacity with air bronchogram.
White out lungs (severe RDS).

Etiology
History of MSAF.
Onset of respiratory distress within 24 hours.
Other clinical features suggestive of MAS.
CXR findings.
Exclusion of other causes like sepsis.

Delivery Room Management

Here is a decision-making guide on the delivery room management of MSAF

For a non-vigorous baby:

1. Endotracheal intubation.
2. Direct laryngoscopy.
3. Intratracheal suctioning of meconium.
4. Proceed for resuscitation.

For a vigorous baby:

1. Routine care.

Treatment
In the absence of any definitive therapy, supportive treatment is administered:

Page 51
 Created by Turbolearn AI

1. IV Fluid: As per maintenance fluid requirement.

2. Moist O2: Through head box.
3. Monitoring of O2 saturation: By Pulse oximetry.
4. Assessment of severity of respiratory distress: By Downe’s score.
5. Respiratory Support.
6. Surfactant Replacement.
Exogenous surfactant replacement is the treatment of choice in moderate and severe RDS along with respiratory
support.
Babies with moderate RDS are given surfactant by INSURE approach (tubation, SURfactant replacement and
Extubation to CPAP).

Complications
Air leaks (like pneumothorax)
Persistent Pulmonary Hypertension of the Newborn (PPHN)
Bronchopulmonary Dysplasia (BPD)

Apnea in Newborn ‍

Definition
Apnea in newborns is defined as cessation of respiration for > 20 seconds or shorter duration in presence of cyanosis
or bradycardia.

Classification
Central apnea: Absent inspiratory efforts (40%).
Obstructive apnea: Inspiratory efforts persist with airway obstruction (10%).
Mixed apnea: Airway obstruction precedes or follows central apnea (50%).

Etiology
1. Apnea of Prematurity: Common in babies with GA < 34 weeks.
2. Pulmonary causes: RDS, Pneumonia, Pulmonary hemorrhage etc.
3. Neurological causes: Perinatal asphyxia, intracranial hemorrhage, seizures, Maternal medications, meningitis etc.
4. Metabolic causes: Hypoglycemia, hypocalcemia etc.
5. Septicemia
6. Congenital malformations: Choanal atresia, Tracheoesophageal fistula (TEF) etc.

Investigations
All infants who attend an episode of apnea should undergo the following investigations:

Sepsis screen (CBC, CRP, ESR)

Electrolytes (Na, K, Ca)
Glucose
CXR
Cranial USG
ABG

Management

Page 52
 Created by Turbolearn AI

1. Thermoneutral environment to prevent hypothermia.

2. Maintenance of normoglycemia with appropriate IV Fluids.
3. Moist O2 inhalation (through head-box).
4. Respiratory support: CPAP or Mechanical ventilation, according to severity of respiratory distress (assessed by Downe's
score).
5. Use of exogenous surfactant may be beneficial, as meconium causes surfactant deficiency. But, the routine use is still
controversial.

Monitoring
All premature babies < 34 weeks gestation should be monitored at least during the 1st week of life.

Drugs
Drugs used to treat apnea of prematurity are caffeine citrate and aminophylline (Methylxanthines).
NB.: Dose of caffeine citrate is 20 mg/kg (loading dose), followed by 5-7mg/kg/day once daily (maintenance dose).
Nasal CPAP: Very useful in case at obstructive and mixed apneas, as it helps to keep the upper airway open.
Mechanical ventilation: Used for apneas not responding to above modalities of treatment.
Treatment of the underlying cause: In do secondary causes.

Prophylaxis
All newborns < 1.25 kg or < 30 weeks' GA should be given prophylactic caffeine until they attain 37 weeks' maturity and
are apnea-free for 7 days.

Anterior Fontanelle (AF)

Definition
Anterior Fontanelle (AF) is the largest of the fontanelles and is placed at the junction of the sagittal suture, coronal
suture, and frontal (metopic) suture.

Shape
AF is diamond-shaped with its corners extended into the respective sutures.

Obliteration
AF is an unossified, membranous area between the skull bones (Frontal and Parietal bone).
It is the last fontanelle to be obliterated, completely closing at around 1 ½ to 2 years of age.

Measurement
Clinical examination of newborn includes measurement of AF and its palpation.

Diagram of measurement landmarks on an infant head for calculating AF area

Measurement is done as: AF is measured as (AC + BD) / 2 cm (AC = Distance between A and C, BD = Distance between B and
D).

Clinical Significance (Advantages)

Page 53
 Created by Turbolearn AI

1. Allows skull deformation during birth to ease passage through the birth canal.
2. Allows brain expansion after birth to help in brain growth.
3. Any rise in intracranial pressure can be temporarily alleviated in infants due to the presence of AF, which protects against
ICP-induced brain injuries.
4. AF gives a window to see the brain parenchyma and ventricles by means of an ultrasound probe. Thus, more costly and
deleterious investigations like CT and MRI are not needed routinely to newborn and infants.

Clinical Signs
Bulged fontanelle: Indicates raised Intracranial pressure, which is seen in:
Meningitis
Intracranial hemorrhage
Benign Intracranial Hypertension (Pseudotumor Cerebri).
Sunken fontanelle: Indicates dehydration
Very large AF may be seen In:
Hypothyroidism (Congenital)
Trisomy Syndromes
Intrauterine Growth Restriction (IUGR)
Rickets
Osteogenesis imperfecta.
Very small or almost closed AF may be seen In:
Craniosynostosis.

Loose Stools in Newborn

Physiological Causes
Exclusively breastfed infants tend to pass softer and more frequent stools due to higher lactose content and lower casein.
Transitional stools: During the third and fourth day of life, neonates often pass semi-loose, greenish-yellow stools due to
the change in breast milk contents (colostrum to transitional milk). This settles spontaneously within 24-48 hours.
Gastrocolic reflex: Many babies pass loose stools while being fed or soon after feeding due to an exaggerated gastrocolic
reflex. It may persist for 1-2 weeks.
Newborn infants are physiologically very prone to develop loose stools. So, in most of the intents presenting with loose
stools, no intervention is needed and counseling and reassurance suffices.

Pathological Causes
Change in baby's established bowel pattern towards increased frequency and looseness should be taken seriously. Other
markers for pathological causes include:

Improper feeding technique: Babies fed only on foremilk get only lactose and water in higher concentration in the expense
of protein and fat of hind milk. They may present with loose stools, perianal excoriation and inadequate weight gain. Proper
feeding history points towards this possibility and correction of feeding technique corrects the problem.
Infection: Infective diarrhea is more common in babies fed by bottle. There may be poor feeding, oliguria and blood/mucus in
stools as presentation. They should be treated as sepsis with parenteral antibiotics.
Other rare causes:
Developmental defects of brain
Congenital thyrotoxicosis.
Salt-losing variety of CAH.
Malabsorption Syndromes (e.g., disaccharidase and enterokinase deficiency).
Maternal drugs (e.g., ampicillin, tetracycline, laxatives).
Perianal excoriation
Blood and mucus in stool.

Care of Umbilical Stump 🫱‍🫲

The umbilical cord stump is an important site of entry for infections (including tetanus).

Page 54
 Created by Turbolearn AI

Procedure
1. After delivery umbilical cord should be clamped and cut at about 2-3 cm from abdominal wall.
2. Sterile blades should be used for cutting the cord.
3. Cut end of the cord should be ligated with sterile ligatures, like:
Disposable clamps. or
Rubber band.
Thread (It is not preferred. as it loosens once the cord shrinks after a few hours of birth, resulting in bleeding from the
umbilical stump.
4. Cord should be repeatedly inspected every 15-30 minutes for the first few hours after birth
5. Nothing previous should be applied over cord and it should be kept dry to prevent infections.

If there is bleeding from stump check the tightness of the clamp.

If there is any discharge or oozing, local antiseptics can be used (like betadine, spirit etc).

Parenteral antibiotics are indicated for umbilical sepsis (criteria for diagnosis -+ redness and induration of > 2 cm around
umbilicus).

Management of Neonatal Seizures

Seizure is defined as a paroxysmal alteration in neurologic function, e.g., motor, behavioral or function. Commonest
type of neonatal seizure is subtle seizures (about 50% of all seizures).

1. Secure airway, breathing, circulation and temperature

2. Start O2 (if seizures continue)
3. Secure IV access and send routine investigations
4. Measure CBG

Here is a flowchart of the management of neonatal seizures:

Etiologies
Common causes of neonatal seizure are:

1. Perinatal asphyxia (MC)

2. Metabolic causes:
Hypoglycemia
Hypocalcemia
Hypomagnesemia
3. Meningitis: as part of late-onset sepsis.
4. Intracranial hemorrhage
5. Developmental defects of brain

Investigations

Page 55
 Created by Turbolearn AI

1. General/Routine Investigations:
Blood sugar
Electrolytes (calcium, sodium etc.)
CSF examination (for seizures appearing after 72 hrs of life)
Cranial ultrasound
2. 2nd line Investigations:
Neurolmaging (CT, MRI)
EEG
Screening for congenital infections (TORCH)
Metabolic screen (for Inborn Errors of Metabolism)

Neonatal Hyperbilirubinemia: Causes

Jaundice or Hyperbilirubinemia is the commonest abnormal physical finding during the first week of life. Commonest cause of
neonatal hyperbilirubinemia is Physiological Jaundice, which affects about 60% of the term and 80% of the preterm babies.

Physiological Jaundice
Jaundice due to physiological immaturity of the newborn is known as physiological jaundice. It occurs in about 60% of
the term babies and nearly 80% of the preterm babies.

Characteristic Term Preterm

Appearance 36-72 hrs Earlier, but never before 24 hrs (24-48 hrs)
Maximum intensity Day 4 Day 5-Day 6
Disappearance 7-10 days of life 10-14 days of life

Causes of Physiological Jaundice

1. Overproduction of bilirubin, due to:
Polycythemia
Reduced lifespan of fetal RBCs (around 90 days) compared to adult RBCs (120 days).
2. Reduced uptake of bilirubin by the liver due to deficiency of ligandin or Y-acceptor protein in the hepatocytee.
3. Reduced conjugation of bilirubin due to relative deficiency of the conjugating enzyme and substrate (UDP glucuronic acid).
4. Reduced excretion of conjugated bilirubin due to immaturity of liver.
5. Conjugated bilirubin entering the gut cannot be converted to stercobilin due to relative lack of bacteria in the gut.
6. Increased enterohepatic circulation, due to overactivity of B-glucuronidase enzyme. deconjugates the bilirubin.
7. These handicaps are more pronounced in preterm babies, resulting in increased severity and duration of physiological
jaundice in them.
8. As bilirubin is a potent antioxidant, physiological jaundice may actually protect the baby against oxygen free radical induced
damages in the earlier days of life.

Management
1. It doesn't need any therapy, but the baby should be closely monitored for increasing severity of jaundice (> 15 mg/dl) and
its persistence beyond normal period (> 14 days)
2. Mother should be instructed to give frequent feeds.
3. Mother to be reassured about benign nature of the condition.

Conditions that cause Exaggerated Physiological Jaundice

1. Lack of colonization of the gut is delayed in breastfed infants, resulting in greater deconjugation of bilirubin and enhanced
enterohepatic circulation.
2. Hepatic conjugation of bilirubin is compromised due to the presence of 3-a, 20-ßpregnanediol in breast milk of 1-2% of
women.
3. High concentrations of unsaturated fatty acids in human milk may also inhibit conjugation and uptake of bilirubin.
4. Breast milk jaundice.
5. Hypothyroidism.

Page 56
 Created by Turbolearn AI

Pathological Jaundice
When jaundice in the newborn crosses the physiological limit or does not conform to the timetable deserted for
physiological jaundice, it is designated as 'Pathological Jaundice' and demands investigations for the cause and
therapeutic interventions (like phototherapy or exchange transfusion).

Criteria
There is no clean demarcation between physiological and pathological jaundice. But, the following characters raise the suspicion
of pathological jaundice:

1. Appearance of jaundice within 1st 24 hours.

2. Total Serum Bilirubin (TSB) level above the expected normal range according to age, e.g.:
TSB >5 mg/dl on Day 1.
TSB >10 mg/dl on Day 2.
TSB >15 mg/dl on Day 3.
3. Rise of serum bilirubin >0.5 mg/dl/hour.
4. Conjugated hyperbilirubinemia, evidenced by:
Dark urine staining of the nappy.
Conjugated Bilirubin >2 mg/dl or 15% of TSB.
5. Persistence of clinical jaundice beyond 3 weeks of life (Persistent jaundice/Prolonged jaundice).

Causes of Pathological Jaundice

Unconjugated Hyperbilirubinemia

1. Hemolysis:
Hemolytic disease of newborn (Rh-incompatibility, ABO incompatibility, Minor blood group incompatibilities).
RBC enzyme defects (e.g., G6PD deficiency).
RBC membrane defect (e.g., Hereditary Spherocytosis).
Homozygous a-thalassemia.
Acquired hemolysis by drugs (e.g., Vitamin K, Sulfonamides etc.)
Extravasated blood
Polycythemia
2. Defects In conjugation (Hereditary):
Crigler-Najjar syndrome.
Gilbert syndrome
Hypothyroidism.

Conjugated Hyperbilirubinemia

1. Infections:
Sepsis
Intrauterine infections (TORCH)
2. Obstructive:
Biliary atresia
Choledochal cyst.
3. Defects in hepatic excretion (Hereditary):
Dubin Johnson syndrome
Rotor syndrome
4. Metabolic diseases
Galactosemia
Hereditary Fructose intolerance
Tyrosinemia
a1-antitrypsin deficiency etc.
5. Total Parenteral Nutrition

Page 57
 Created by Turbolearn AI

Investigations
1. Serum Bilirubin:
Total.
Direct.
Indirect.
2. Blood group of
Mother
Baby (if mother is 'O' or Rh negative).
3. Direct Coombs Test—Positive in immune hemolysis.
4. Hematocrit—Reduced in hemolysis
5. Reticulocyte count—Increased in Hemolysis
6. G6PD level
7. Others
Sepsis screen
Liver function test
Thyroid function (FT3, FT4, TSH)
TORCH screening
USG abdomen (in conjugated hyperbilirubinemia)

Management
1. Phototherapy - Mainstay of therapy during initial 7-10 days of life.
2. Exchange transfusion — In more severe cases.
3. Specific therapy — According to the cause, like:
Antibiotic for sepsis
Thyroxine in hypothyroidism

Persistent Unconjugated Hyperbilirubinemia

When clinically evident hyperbilirubinemia persists beyond 3 weeks of life, it is known as persistent jaundice.
Persistent hyperbilirubinemia may be both unconjugated and conjugated, and there are separate lists of causes for
both types.

Diagnosis of breast milk jaundice should be considered in newborns with prolongation of jaundice, when:

1. There is unconjugated hyperbilirubinemia, and

2. Other common causes of prolonged unconjugated jaundice are excluded by investigation (e.g., Blood group incompatibility,
G6PD deficiency, extravasated blood, hypothyroidism etc.)
3. Cessation of breastfeeding for about 48-72 hours results in prompt fall of serum bilirubin (by 2-6 mg/dl), and breastfeeding
can be reestablished without any risk of recurrence

Characteristics of Breast Milk Jaundice

1. Jaundice is maximum in intensity between 10-14 days, but may persist up to 6-8 weeks.
2. Total serum bilirubin level is usually in the range of 10-15 mg/dl or occasionally higher, but never severe enough to need
exchange transfusion.
3. Factors responsible for this hyperbilirubinemia in breastfed babies are as follows:
Lack of colonization of the gut is delayed in breastfed infants, resulting in greater deconjugation of bilirubin and
enhanced enterohepatic circulation.
Hepatic conjugation of bilirubin is compromised due to the presence of 3-a, 20-ßpregnanediol in breast milk of 1-2%
of women.
High concentrations of unsaturated fatty acids in the human milk may also inhibit conjugation and uptake of bilirubin.
4. Breast milk jaundice is different from Breastfeeding jaundice, which is seen in the early neonatal period due to inadequate
breast milk production and inadequate feeding and resultant dehydration.

But, in view of the transient and benign nature of the disease, breastfeeding should not be stopped either for diagnosis or for
treatment of breast milk jaundice.

Page 58
 Created by Turbolearn AI

Kernicterus
Kernicterus or Bilirubin encephalopathy is the most dreaded complication of unconjugated hyperbilirubinemia in the
newborn during the first week of life, when the blood brain barrier remains immature.

Clinical features
1. First year of life:
Hypotonia
Active Deep Tendon Reflex (DTR)
2. Beyond 1 year:
Movement disorders (tremor, choreoathetoid movements)
Upward gaze palsy
Sensorineural hearing loss
Brownish staining of teeth
Various degrees of intellectual retardation.

Investigations
1. LFT:
To confirm elevated hyperbilirubinemia
Liver enzymes (SGOT, SGPT) usually normal
2. WBC: Increased
3. RBC count: Reduced
4. Peripheral blood smear: Anisocytosis, Poikilocytosis nucleated RBCs, Target cells.
5. Blood group of mother & baby.
6. G6PD level in cases of hemolysis

Delayed Fall of Umbilical Cord 🫴

The cord normally falls off after 5 to 10 days.

Etiopathogenesis
Causes of delayed fall of the umbilical cord include:

1. Immunodeficiency
Leukocyte Adhesion Defect
Neonatal Alloimmune neutropenia
2. Excessive use of antiseptics to cleanse the cord.
3. Parenteral antibiotic therapy for sepsis.
4. Premature birth
5. Urachal anomalies
6. Histiocytosis X.

Treatment
1. If there is any discharge or oozing, local antiseptics can be used (like betadine, spirit etc).
2. Parenteral antibiotics are indicated for umbilical sepsis (criteria for diagnosis -+ redness and induration of > 2 cm around
umbilicus).

Neonatal Jaundice

Biliary Atresia
Biliary atresia is a condition that can lead to chronic jaundice in newborns.

Page 59
 Created by Turbolearn AI

Investigations for Neonatal Jaundice

Prematurity
Hemolytic disease of newborn due to fetomaternal blood group incompatibility
Other hemolytic jaundice (e.g., G6PD deficiency)
Breast milk jaundice
Hypertrophic pyloric stenosis and other conditions associated with intestinal stasis
Crigler-Najjar syndrome
Gilbert syndrome
Concealed hemorrhages
Malaria

Treatment for Neonatal Jaundice

1. According to the cause.
2. Reassurance, if no cause is found, as breast milk jaundice (in exclusively breastfed babies) is a benign condition and
resolves spontaneously within 6-8 weeks.

Kernicterus
Kernicterus is a type of brain damage that can result from high levels of bilirubin in a baby's blood.

Diagnosis: Kernicterus is a clinical diagnosis.

Suggestive clinical features in a newborn with severe unconjugated hyperbilirubinemia.

Diagnostic Tests
1. Thyroid function: FT4, TSH
2. USG abdomen: For pyloric stenosis or other causes of intestinal obstruction
3. UDP-Glucuronyl transferase activity: For Crigler-Najjar and Gilbert syndrome
4. Breast milk jaundice is the diagnosis of exclusion.

Pathogenesis of Kernicterus
1. Bilirubin in plasma exists as an albumin-bound complex, which cannot penetrate the cell wall.
1gm Albumin binds to 8.5mg of Bilirubin $

2. When the bilirubin-binding capacity of albumin is exhausted (e.g., low albumin, high bilirubin), free bilirubin diffuses into
the interstitial compartment and binds to tissue proteins in the interstitium.
3. Further rise of bilirubin causes bilirubin to cross the blood-brain barrier.
4. Bilirubin gains access into the neurons located at basal ganglia, hippocampus, auditory nuclei, etc.

Clinical Features of Neonatal Unconjugated Hyperbilirubinemia

Jaundice, clinically evident up to leg or sole.
Colorless urine.
Yellow or normal colored stool.
Pallor in cases of hemolysis
Typical phenotype in Down syndrome.
Clinical features of hypothyroidism (e.g., Lethargy, hypotonia, dry skin, constipation, large tongue) in cretinism.

Acute Form of Kernicterus

Page 60
 Created by Turbolearn AI

Phase I:
Poor suck
Hypotonia
Seizures
Phase II:
Hypertonia of extensor muscles
Opisthotonus
Retrocollis
Fever
Phase III: Generalised hypertonia

Phototherapy
Phototherapy is a treatment for neonatal hyperbilirubinemia that involves exposing the baby's skin to a special blue
light, which helps to break down bilirubin into a form that can be excreted in the stool and urine.

Phototherapy has been accepted widely as a relatively safe and effective therapy for neonatal hyperbilirubinemia.

Mechanism of Phototherapy
Converts unconjugated bilirubin into water-soluble isomers, which are excreted in stool and urine.
Bilirubin absorbs light maximally at a wavelength of 425-475 nm; emissions at this range lower serum bilirubin by 3
mechanisms:
1. Photo-oxidation (slow and ineffective)
2. Photo-isomerization: Z-isomers to E-isomers, which are not stable and revert back to Z-isomers.
3. Lumirubin isomerization (Most effective method, where lumirubin is produced and it is excreted without the need for
hepatic conjugation).

Indications for Phototherapy

Grossly, Total Serum Bilirubin (TSB) > 15mg/dl is considered an indication for phototherapy.
Timely phototherapy and exchange transfusion can prevent the menace and neurological sequelae in the early stages of
the disease.

Phototherapy Thresholds Based on Birth Weight

Birth Weight Cut-off for Phototherapy (mg/dl)

< 1kg 5-7

1 − 1.25kg 7-9
1.25 − 1.5kg 9-11
1.5 − 2kg 11-13
2 − 2.5kg 13-15
> 2.5kg 15-17

Risk Categories for Term and Near-Term Infants (>35 Weeks)

Lower risk: Well infants ≥ 38 weeks
Medium risk: Well infants of 35-37 weeks and infants ≥ 38 weeks with risk factors like blood group incompatibility, G6PD
deficiency, asphyxia, sepsis, etc.
Higher risk: Infants of 35-37 weeks with risk factors

Complications of Phototherapy

Page 61
 Created by Turbolearn AI

1. Passage of loose green stools.

2. Hyperthermia and dehydration due to increased insensible water loss.
3. Flea-bite rashes on trunk or extremities.
4. Risk of opening of Ductus Arteriosus
5. Hypocalcemia (due to secretion of melatonin)
6. May cause hemolysis and increased platelet turnover.
7. Disturbance in the circadian rhythm of the sex hormones.
8. Decreased mother-child interaction.
9. Bronze Baby Syndrome (in conjugated hyperbilirubinemia).

Intensification of Phototherapy
Reducing distance to 15-20 cm.
Providing double surface phototherapy by placing the baby on Biliblanket or LED mattress
Using white slings or curtains around the baby which reflect light on the baby.
Using Special blue CFL tubes.

Practical Aspects of Phototherapy

The baby's clothes are removed, except diaper (in male infants) and eye shield.
The light is kept at a distance of 45 cm from the skin surface of the baby.
Baby's position should be changed often to expose the maximal area of skin to light.
Breast feeding should be continued.

Rh-Isoimmunization
Rh-isoimmunization occurs when a Rh-negative mother carries a Rh-positive fetus.

Rh-incompatibility is the most fatal of the blood group incompatibilities causing hyperbilirubinemia in the newborns.
This is the type of Hemolytic Disease of the Newborn (HDN) which is entirely preventable by appropriate measures in Rh-
negative mother.

Pathogenesis
1. Once placental circulation is well established after 3 months of pregnancy, fetal RBCs may seep into maternal circulation.
2. Rh antigen of fetal RBCs invoke antibody response by the maternal immune system.
Though enough Ab is not produced in first pregnancy, each subsequent pregnancy with Rh+ve fetus leads to rising
Ab response and more severe disease.
3. The anti-D antibodies are IgG in type and crosses placenta to reach fetal circulation
4. They destroy D+ve (Rh +ve) fetal RBCs [Hemolysis].

Prevention and Treatment

Prevention is always better than cure, because once neuronal damage becomes irreversible, no treatment is available to
stop the progression of the disease spectrum.
Anti-D immunoglobulin given to Rh-ve mother within 72 hours of delivery.

Sequelae
1. Choreo-athetoid cerebral palsy.
2. Intellectual impairment.
3. Sensorineural deafness.

Small for Gestational Age (SGA) Babies

SGA (Small for Gestational Age) babies are newborn infants that are smaller in size than normal for their gestational
age.

Page 62
 Created by Turbolearn AI

Babies with birth weights below the 10th percentile for the corresponding gestational age.
Intrauterine growth retardation (e.g., placental insufficiency, maternal malnutrition, chronic hypoxia, etc.)

Complications of SGA/IUGR Babies

1. Phototherapy: Almost all babies need phototherapy.
2. Exchange transfusion:
Early exchange transfusion on Day 1 of life is indicated if:
Cord Hb < 10gm/dl
Cord Bilirubin ≥ 5mg/dl
3. IVIg: Can be used.
4. Hypoglycemia: (HBC breakdown product glutathione inactivates circulating insulin → Hyperplasia of islet cells of pancreas
→ Hyperinsulinemia → Hypoglycemia).
5. Lukopenia and Thrombocytopenia: (due to increased erythropoiesis in bone marrow).
6. Polycythemia:
Fetal hypoxia ↓ ↑ Erythropoietin ↓ ↑ RBC mass (polycythemia)

7. Congenital malformations: including intrauterine infections are common in IUGR babies.

8. Pulmonary hemorrhage: due to unknown cause.
9. Hyperbilirubinemia
10. Thermoregulation: Unsatisfactory thermoregulation may occur due to scanty brown fat.
11. Vulnerability to infections.
12. Long-term complications:
Poor catch-up growth in future (due to decreased number of cells in the body)
Increased risk of development of metabolic syndrome X, diabetes mellitus, hypertension and coronary artery disease
in adult life.

Preterm Babies
Preterm infants are neonates born at less than 37 completed weeks of gestation

Complications of Preterm Babies

Page 63
 Created by Turbolearn AI

1. CNS:
Lethargy, reactivity.
Poor sucking and swallowing in babies born before 34 weeks of gestation.
Apnea of prematurity (due to immaturity of the respiratory centre).
Intraventricular hemorrhage.
Periventricular leukomalacia.
Retinopathy of prematurity.
2. Respiratory:
Hyaline Membrane Disease (due to deficiency of surfactants in immature lungs).
Bronchopulmonary dysplasia.
3. CVS: Delayed closure of ductus arteriosus
4. GI System:
Feeding difficulties (due to poor reflexes)
Feed intolerance, regurgitation.
Abdominal distension (due to decreased peristaltic movements: may progress to Necrotizing Enterocolitis).
5. Liver:
Exaggeration of physiological jaundice (due to immature conjugation system)
Development of Kernicterus at lower bilirubin levels (due to low serum albumin & poor blood-brain barrier).
6. Renal:
Low GFR (Glomerular Filtration Rate).
Poor capacity to concentrate urine.
Azotemia.
7. Thermoregulation:
Increased propensity to develop hypothermia occurs in preterm babies due to:
Excessive heat loss due to larger surface area.
Poor generation of heat due to paucity of brown fat.
8. Infections: Preterm infants are more prone to infections (sepsis) due to:
Low IgG level.
Insufficient cellular immunity.
9. Metabolic:
Hypoglycemia
Hypocalcemia (Predispose to seizure)
Metabolic acidosis
10. Deficiency of micronutrients:
Iron deficiency anemia (due to low iron store)
Vitamin E deficiency.
Osteopenia of prematurity.

Feeding of Low Birth Weight (LBW) Newborns

Babies with a birth weight of < 2.5kg are classified as low birth weight (LBW) babies.
These include both preterm babies (i.e., those born at less than 37 completed weeks of gestation) and term small for
gestational age (SGA) babies.
Nutritional management influences immediate survival as well as subsequent growth and development of LBW infants

Difficulties in Feeding LBW Infants

1. May have inadequate sucking skills and require other methods of feeding other than breastfeeding.
2. They are often sick in the early days precluding enteral loading.
3. They have higher fluid requirements in the first week.
4. They often have low body stores of various nutrients.
5. Owing to gut immaturity, feed intolerance is common.

Initial Feeding Method Based on Gestational Age

Page 64
 Created by Turbolearn AI

Gestational
Maturation of feeding skills Initial feeding method
age

< 28 weeks • No sucking • No propulsive gut motility IV fluid

• Sucking bursts develop • No coordination between sucking, swallowing Orogastric (or Nasogastric tube
28-31 weeks
and breathing feeding)
32-34 weeks • Sucking and coordination with breathing mature slightly Feeding by cup and spoon/ paladai
> 34 weeks • Complete maturation of sucking and coordination with breathing Breastfeeding

Feeding Approaches
1. Sick infants:
Often started on IV fluids.
Enteral feeds, however, should be started as soon as they are hemodynamically stable, with choice of feeding method
based on the infants' gestational age and clinical condition.
2. Healthy infants:
Initial feeding method in healthy LBW infants depends on maturation of feeding skills according to gestational age

Non-Nutritive Sucking (NNS)

Non-Nutritive Sucking is when stable LBW infants are put on their mother's breast for immature sucking.

All stable LBW infants, irrespective of their initial feeding method, should be put on their mother's breast.
The immature sucking (NNS) helps in:
Rapid maturation of their feeding skills.
Improves milk secretion in their mothers.

Choice of Milk
All LBW infants should receive only breast milk, irrespective of their feeding method, in the form of:
Mother’s own milk (best): Expressed Breast Milk (EBM).
Donor human milk (from milk bank, if available)
In case, the mother is sick (and milk bank is not there) or there is any contraindication to breast feeding, options are:
Formula feeds:
Preterm formula — in VLBW infants (< 1.5kg).
Term formula - in infants weighing > 1.5kg.
Animal milk: e.g., cow's milk (last option).

Amount of Feeding
1. Infants, who are breastfed are given demand feeding every 2-3 hours, sometimes more frequently.
2. Infants, who are not breastfed (i.e. cup and spoon feeding, tube feeding): total amount of feed required per day is calculated
and given in divided volumes 2-3 hourly.
> 1.5kg: 60ml/kg/day on day 1, then increasing by 15ml/kg/day daily into 150ml/kg/day on day 7.

< 1.5kg: 80ml/kg/day on day 1, then gradually increasing by 10-15ml/kg/day daily to reach 160-170 ml/kg/day at the

end of first week.

Nutritional Supplements
1. Vitamin D to all LBW Infants.
2. Iron to only VLBW Infants.
3. Calcium
4. Folic acid
5. Phosphorus

Hypoxic-Ischemic Encephalopathy (HIE) due to Birth Asphyxia

Page 65
 Created by Turbolearn AI

Birth Asphyxia or perinatal Asphyxia is the leading cause of neonatal mortality and morbidity that can lead to
hypoxic-ischemic injury to various organ systems.

Neonatal encephalopathy following severe birth asphyxia is referred to as Hypoxic Ischemic Encephalopathy (HIE).
About 25-30% of infants are likely to develop HIE following perinatal asphyxia.

Pathogenesis
Hypoxia → Relative ischemia (Existing blood flow not able to maintain adequate O supply) 2

Protective mechanisms like Diving Reflex ensues, which redistributes available blood flow from lesser to more vital organs.
As a result, blood flow to the brain, heart, and adrenals is preserved at the expense of blood flow to the kidneys,
lungs, GI tract, liver, skin, skeletal muscles, etc.
When asphyxial damage is severe and prolonged → Compensatory mechanisms overwhelmed → Hypoxic and ischemic
damage to the brain. (Neuronal necrosis) Cerebral edema (both cytotoxic and vasogenic)

Neuropathology

In term newborns:
1. Selective neuronal necrosis (cortical).
2. Status marmoratus of basal ganglia and thalamus.
3. Parasagittal cerebral Injury.

In preterms:
1. Selective neuronal necrosis (sub-cortical).
2. Periventricular Leukomalacia.
3. Periventricular and Intraventricular hemorrhage.

Clinical Features
1. Seizures: Mostly within 6-12 hours and invariably by 36-48 hours of birth.
2. Features of CNS irritability: like jitteriness, excessive crying etc. primarily occurs.

Management

Page 66
 Created by Turbolearn AI

1. Resuscitation:
Resuscitation-preparedness, as there is a high risk for the need for resuscitation.
Gentle resuscitation using appropriate-sized small bags (to deliver small tidal volume).
2. Temperature control:
Maintenance of warm chain starting from warm resuscitation and use of radiant warmer whenever necessary.
Frequent monitoring of temperature and education of parents about the importance of checking the temperature.
Kangaroo Mother Care.
3. Feeding:
Choosing appropriate method of feeding according to gestational age:

34 weeks: Breast feeding.

31-34 weeks: Cup & spoon feeding.

28-31 weeks: Tube feeding (Nasogastric / orogastric)
< 28 weeks: IV fluid.
Looking for feed intolerance.
Supplementation with micronutrients.
4. Infection:
Strict adherence to asepsis, hand hygiene.
Minimal handling.
Low threshold for suspicion of sepsis and start antibiotics (IV) at minimum suspicion.
5. Metabolic derangements:
Hypoglycemia: Frequent monitoring of blood glucose, particularly in SGA babies & VLBW babies in the first 48 hours.
Hypocalcemia: Prophylactic calcium gluconate (10%) @ 4 ml/kg/day in VLBW Infants.
6. Hyperbilirubinemia:
Early use of phototherapy and exchange transfusion at comparatively lower bilirubin levels than their term
counterparts.
Phototherapy can be used up to 10-14 days in preterm infants, as their skin is more slender and transparent.
7. Hematological problems:
Polycythemia: Extra fluid is given and partial exchange is done, if needed, in plethoric babies.
Anemia: Iron supplementation @ 2-3 mg/kg/day starting from 6-8 weeks of life to prevent anemia of prematurity.
8. Respiratory problems:
Early use of CPAP and surfactant for prevention and treatment of RDS.
Prophylactic caffeine therapy with caffeine citrate for prevention of apnea of prematurity in all infants with Hypoxic
ischemic encephalopathy who received O , ventilation etc. < 32 weeks and in selected babies with GA > 32 weeks.
2

9. Retinopathy of prematurity screening: In all babies with birth weight <1.5 kg and gestational age
10. Hearing screening: If there is prolonged stay in NICU (Neonatal Intensive Care Unit).
11. Screening for intraventricular haemorrhage: by USG of the brain.
12. Follow-up: at high-risk clinic.

Organ Involvement in Perinatal Asphyxia

Perinatal asphyxia (PA) can affect every system of the body due to hypoxia and Ischemia.
Non-vital organs are affected first due to the diving reflex, which redistributes blood flow to support the vital organs of the
body.

Page 67
 Created by Turbolearn AI

1. Brain: PA involves the brain in about 33% of cases. Brain lesion is also known as Hypoxic-Ischemic Encephalopathy (HIE),
which may have following manifestations:
Danger signs:
Seizures, coma, apnea, hypotonia.
Intracranial hemorrhage.
Cerebral edema.
Long-term neurological sequelae.
2. Kidney: Kidney is the most common organ to be involved in perinatal asphyxia and the incidence of renal involvement is
about 50% in the form of:
Acute tubular necrosis.
Renal vein thrombosis.
Renal failure etc.
3. Heart: Cardiac involvement occurs in 25% of cases, in the form of:
Myocardial damage causing dysrhythmia.
Tachycardia
Congestive cardiac failure.
4. Lungs: Pulmonary complications include:
Meconium aspiration.
Surfactant impairment causing RDS.
Persistent pulmonary hypertension.
Pneumothorax.
5. GI Tract:
Necrotizing enterocolitis (NEC)
Hepatic dysfunction.
Paralytic ileus.
6. Hematological:
Thrombocytopenia.
Disseminated intravascular coagulation.
7. Endocrine:
SIADH (Syndrome of inappropriate ADH secretion).
Transient hypoparathyroidism, leading to hypocalcemia.
Adrenal hemorrhage.
8. Metabolic:
Hypoglycemia.
Hyponatremia, hyperkalemia.
Acidosis.

Staging of HIE
1. Haley:
2. Levene grading (clinical method, can be used at bedside): Uses 4 features, namely — a) Consciousness, b) Tone, c) Seizures
and d) Sucking / Breathing.
3. Sarnat and Sarnat staging (more elaborate).

Danger Signs of Newborn

The following danger signs are always important as early features of severe diseases:

Page 68
 Created by Turbolearn AI

1. Bleeding: From any site, like - hematemesis, melena, hematochezia, hematuria, umbilical bleeding etc.
2. Jaundice: Appearance of jaundice within 24 hours or deep jaundice.
3. Meconium: Not passed within 24 hours.
4. Urine: Not passed within 48 hours.
5. Repeated vomiting or diarrhea.
6. Poor feeding/ refusal to suck.
7. Undue lethargy or excessive crying.
8. Excessive frothing or drooling of saliva.
9. Respiratory difficulty:
Hurried breathing (RR > 60/min).
Chest indrawing.
Nasal flaring.
10. Cyanosis: Peripheral or central.
11. Apneic attacks.
12. Choking during feeding.
13. Seizures.
14. Temperature Instability:
Hypothermia - Term < 35.5\degreeC .
Hyperthermia - Temp > 38\degreeC .
15. Skin Infections:
Macules.
Pustules.
Oral thrush.
Umbilical sepsis (Redness and induration around umbilicus)

Management of Danger Signs

1. Management of seizures.
2. Maintenance of temperature, glucose, and perfusion.
3. Maintenance of fluid and electrolytes.
4. Newer modalities, like therapeutic hypothermia.

Breast Milk vs. Cow's Milk

There are several biochemical, nutritional and physiological differences between breast milk and cow's milk.

Nutritional Comparison (per 100 ml)

Page 69
 Created by Turbolearn AI

Nutrients Breast milk (Human milk) Cow's milk

1. Protein content 1.1gm 3.5gm

2. Protein quality:
a. Whey : Casein 60 : 40 20 : 80

Mainly lactalbumin & lactoferrin

b. Whey protein Mainly lactoglobulin (allergen)
(bacteriostatic)
(easily digestible)
c. Casein: β-casein is more. α-casein is predominant
3. Lactose 7gm 4.5gm

(High lactose content helps in calcium & iron

absorption)
4. Fat content 3.5gm 4gm

5. Fat quality
a. Essential fatty acid 13 2

b. PUFA: Saturated fatty acid 1.2 : 1 1 : 2

6. Calcium 36mg 140mg

7. Phosphorus 15mg 90mg

< 2(may produce

8. Ca: P > 2
hypocalcemia)
9. Sodium 0.7mEq 2.2mEq

10. Potassium 1.4mEq 3.5mEq

11. Vitamin K 15μg 60μg

12. Osmolality 290mosm/L 350mosm/L

13. Calories 67Kcal 67Kcal

14. Energy: Protein 70 : 1 25 : 1

15. Solute load (Protein, Na, K, Ca, P etc.) Low High (may ↑ dehydration)

Inter-Hospital Transport
From peripheral health facilities to the tertiary care centre having NICU
When a high-risk pregnancy is identified, it is best to transfer the mother to a higher center, because the uterus is an ideal
transport incubator.

Steps for inter-hospital transport

1. Ensure a genuine indication for referral.
2. Explain the condition and reason for transportation to the parents / family members.
3. Stabilize temperature, airway, breathing, circulation and blood glucose before transport.
4. A precise note should be written providing birth details, need for referral, treatment given etc.
5. The mother should be encouraged to accompany the baby.
6. A health worker (doctor, nurse, etc.) should accompany the baby.
7. The referral facility should be informed in advance.
8. Take the baby to the nearest NICU by the shortest route, using the fastest possible and affordable mode of transport.
9. All the essential equipments, instruments, and emergency drugs should be checked before transport.
10. The referring hospital should be informed about safe arrival at the referral center.

Intra-Hospital Transport
Like NICU to operation theatre, imaging department etc.

Indications for NICU Admission

Page 70
 Created by Turbolearn AI

1. Preterm infant < 32 weeks GA or birth weight < 1.5kg.

2. Respiratory distress requiring CPAP or ventilation.
3. Severe HIE.
4. Severe sepsis.
5. Intractable seizure.
6. 3 | Eng lee.
7. Severe Jaundice.
8. Others (e.g., congenital anomalies, surgical conditions etc.)

Determining Initial Feeding Method

The first step is assessment of gestational age.
Then an appropriate initial feeding method is determined.

Vigilance in the Maternity Ward

All healthcare staff including nurses, doctors, attendants etc. should always be vigilant in the maternity ward to diagnose
neonatal abnormalities at the earliest.
Even mother and family members are also educated about the possible danger signs, which should be brought to the notice
of the pediatricians immediately.
Because, if the early symptoms go unnoticed, the health of a newborn may deteriorate rapidly, even resulting in death
sometimes.## Neonatal Transport

Principles of Neonatal Transport

Transport equipment is crucial.

Write out your care plan for feeding a premature, very low birth weight newborn.

Usual indications for transport within the hospital can be accomplished by a transport incubator.

Routine Care of Newborns

Routine care of newborns in the delivery room includes:

Vitamin K: Injection of Vitamin K (1 mg; 0.5 mg for birth weight < 1 kg) is given IM at the anterolateral thigh for all
newborns.
Identification Band: Each newborn must have an identification band containing the mother's name, hospital registration
number, gender, and birth weight.

The following three questions are asked:

1. Term gestation?
2. Breathing or crying?
3. Good muscle tone?

If all three answers are "Yes," proceed with routine care. If any answer is "No," proceed with initial steps.

Initial Steps of Resuscitation

Page 71
 Created by Turbolearn AI

One health provider (doctor or nurse) trained in neonatal resuscitation must be physically present during each delivery,
irrespective of risk status.
In high-risk deliveries, two people should be present solely to manage the baby.
The health provider designated for neonatal care should check the resuscitation equipment well before the delivery.
Delayed cord clamping: Usually delayed for 1-2 minutes to allow slow transfer of additional blood from placenta to the
infant.
Cord is clamped 2-3 cm away from the abdomen.
Cord stump should be clean, and nothing applied.

Maintaining the Airway

Secretions are removed from the airway by wiping the nose and mouth with a clean cloth or by suctioning with a suction
catheter.
Mouth is suctioned first before nose (as alphabetically 'M' comes before 'N') to prevent aspiration while gasping during
nasal suction.
Size of suction catheter: 12 to 14 Fr.
Suction pressure: 80-100 mm Hg.

Positioning
Body is placed on back or side with the neck slightly extended. This brings the posterior pharynx, larynx, and trachea in line
to facilitate breathing.
To help maintain this position, a rolled towel or blanket is placed under the shoulders, elevating them 3/4" to 1" off the
mattress; this is known as a "shoulder roll."

Prevention of Hypothermia
Temperature of the delivery room around 25°C.
Baby received in pre-warmed linen sheet.
Baby is immediately dried, including head and face, and then covered in a separate, dry sheet.
Baby is placed under a heat source, preferably a radiant warmer, without being covered to allow full visualization and
permit the radiant heat to reach the baby.

Standard Aseptic Measures

Gloves, mask, and gown should be worn by the health provider during resuscitation.
Observe "5 cleans" to prevent sepsis at birth:
1. Clean hand
2. Clean surface
3. Clean blade
4. Clean cord-tie
5. Clean cord-stump (nothing to be applied)

Stimulation
The act of steaming and drying itself provides adequate stimulation to initiate breathing. If the baby doesn't still respond,
additional tactile stimulation is provided in the form of:

Flicking the back gently, or

Flicking the soles.

Bag Mask Ventilation (BMV)

Positive Pressure Ventilation (PPV) is the single most effective step in babies who fail to breathe normally at birth.
PPV is usually given by using a self-inflating bag and a face mask, together known as Bag and Mask Ventilation (BMV).

Page 72
 Created by Turbolearn AI

Indications for BMV

BMV is indicated if:

HR < 100/min, or
Labored breathing or Gasping or apneic
Persistent cyanosis

Contraindications for BMV

1. In suspected or continued diaphragmatic hernia because the air pumped into little lungs also passes into the stomach,
partly as the opening is free. This air will distend the stomach, which is more often in the thoracic cavity, and will further
compromise lung inflation.
2. In non-vigorous babies born through meconium-stained liquor (MSL), because any meconium in the larynx and trachea will
be further pushed into the lungs. BMV is done only after tracheal suctioning, if indicated.

Corrective Steps for Ventilation (MRSOPA)

M: Mask re-applied
R: Reposition the head and neck
S: Suction the airway
O: Open the mouth slightly
P: Pressure increased slightly
A: Airway alternative (e.g., ET tube)

Modifications in Babies Born Through Meconium Stained Liquor (MSL)

Postpone drying and suctioning to prevent stimulation.
Removal of residual meconium from mouth and posterior pharynx by suctioning under direct vision using a laryngoscope.
Intubation and suctioning of trachea by applying suction directly to the Endotracheal tube (ET tube) and gradually
withdrawing the ET tube.

Newborn Resuscitation

This flowchart summarizes newborn care, starting with assessing if the newborn is breathing/crying, has a heart rate > 100, and
good muscle tone. A "yes" to all leads to routine care, while a "no" triggers further evaluation. The flow chart is detailed in the
image, showing initial stabilization, ventilation, and chest compression steps based on the newborn's heart rate and response to
care.

Chest Compression
Chest compression is always given simultaneously with PPV at a 3:1 ratio (chest compression: PPV) and a total of 120 events in
1 minute (i.e., 90 chest compressions and 30 breaths).

Page 73
 Created by Turbolearn AI

Medications
Epinephrine: 0.1-0.3 ml/kg IV of 1:10,000 solution.

Reflexes of a Newborn

Neonatal Reflexes
Neonatal reflexes are brainstem-mediated automatic responses that disappear after a certain age.

Commonly Used Reflexes

1. Grasp Reflexes:
Palmar grasp: Flexion of the fingers when the examiner's finger is placed on the palmar surface.
Plantar grasp: Flexion of the toes while pressing the anterior part of the sole by the examiner's finger.
Disappears by 2-4 months (palmar grasp) and 6 months (plantar grasp).
2. Rooting Reflex:
When the baby's cheek is touched softly near the angle of the mouth, the head turns towards that side with deviation
of the tongue and angle of the mouth to the same side.
Appears at 32 weeks and disappears by 4-6 months.
3. Sucking Reflex:
When a clean index finger of the examiner is introduced into the mouth, sucking movement ensues.
Appears at 28 weeks and disappears by 4-6 months.
4. Glabellar Tap:
Tapping the nasion is followed by closure of the eyes in infants above 30 weeks of gestation.
5. Asymmetric Tonic Neck Reflex (ATNR):
Rotation of the baby's head to one side causes extension of upper and lower limbs of that side and flexion of the
limbs at the opposite side.
Disappears by 5 months of age, and its persistence precludes turning of the baby from supine to prone position.
6. Moro Reflex:
The baby is held in a semi-upright position. The head is then allowed to drop suddenly by 15-30 degrees with the
head flexed on the examiner's arm and hand, and supported by the hand again.
1st phase (Rapid)
a) Abduction and extension of shoulders
b) Extension of elbows
c) Opening of hands, followed by
2nd phase (Slow)
d) Adduction and flexion at shoulders
e) Flexion at elbows
f) Closing of hands
Associated features
g) Opening of eyes
h) Lusty cry
Disappears by 3-6 months.

Abnormalities in Reflexes
1. Depressed in:
Asphyxia
Sepsis
Hypoglycemia
2. Exaggerated in:
Early meningitis
3. Asymmetric in:
Erb's palsy
Fracture of clavicle
Humerus, etc.

Page 74
 Created by Turbolearn AI

Jitteriness vs. Convulsion

Feature Jitteriness Convulsion

Movement Fast (4-6 jerks/second) Slow (1-3 jerks/second)

To-and-fro, equal speed &
Nature of Movement Fast and slow components occur alternately
amplitude
Provoked by Stimulation Yes No
Stopped by Restraint Yes No
Neurological Exam Usually normal Often abnormal
Associated Eye Movements/Autonomic Often associated with eye movements or autonomic changes
No
Changes (e.g., changes in heart rate)

Jaundice and Bilirubin Metabolism

Bilirubin Metabolism
1. History: Any risk factors for exaggeration of physiological jaundice, such as prematurity, LBW, perinatal asphyxia, etc.
2. History: Parenteral nutrition.
3. Urine and stool color:
Normal in unconjugated jaundice.
High-colored urine and white stool in conjugated jaundice (white stool is mainly found in obstructive causes).

Differential Diagnosis Approach

Clinical Features:
6-day-old neonate
Pallor in hemolysis
Plethoric in polycythemia
Features of intestinal obstruction, like abdominal distension, constipation, etc.
Bulging anterior fontanelle in meningitis/meningoencephalitis.
Gestational age of the baby is also important, as preterm infants are more prone to severe infection.

Causes of Jaundice
Massive extravasation of blood
Hemolysis
Infections
Metabolic causes

Types of Jaundice
1. 6-day-old neonate: All the causes listed, excluding:
Breast milk jaundice
Pyloric stenosis
Hypothyroidism
2. 7-day-old term neonate with unconjugated jaundice (TSB=15 mg/dl): All the causes of unconjugated pathological
jaundice, except the above three causes, which present later than physiological jaundice.
3. 3-day-old baby with sole staining (TSB > 15 mg/dl): All the causes of pathological jaundice, except:
The above three causes, which present later (>1-2 weeks)
Increased enterohepatic circulation
Sepsis
Metabolic diseases (usually presents later - causes of persistent jaundice)

Investigations

Page 75
 Created by Turbolearn AI

1. Serum Bilirubin:
Total
Direct fraction (CB)
Indirect fraction (UCB) (=Total — Direct)
If Direct Bilirubin is > 20% of total bilirubin, it is known as conjugated hyperbilirubinemia. Otherwise, the diagnosis
remains unconjugated hyperbilirubinemia.
2. Blood Group of Mother and Baby: If the mother is 'O' or Rh-ve.
3. Direct Coombs Test: Positive in immune hemolysis (e.g., ABO incompatibility & Rh-incompatibility).
4. Hematocrit: Decreased in hemolysis, infections (sepsis or intrauterine infections), massive extravasation of blood.
5. Reticulocyte Count: Increased in hemolysis.
6. Sepsis Screen: Positive in sepsis (confirmed by blood culture).
7. Liver Function Test: Deranged in cases of sepsis-induced hepatitis, metabolic diseases, or other causes of hepatitis.
8. TORCH Screening: For diagnosis of intrauterine infections.
9. Straight X-ray Abdomen: For intestinal obstruction.
10. USG Abdomen: For diagnosis of obstructive causes.
11. Metabolic Screen
12. G6PD Level: For diagnosis of G6PD deficiency.

Treatment
1. Double Surface Phototherapy: Usually the mainstay of therapy during the initial 7-10 days of life for unconjugated
hyperbilirubinemia. It lowers serum bilirubin level through photo-oxidation, photoisomerization, and structural isomerization
(most effective mechanism).
2. Exchange Transfusion: In more severe cases, when the initial bilirubin level is too high or phototherapy fails to decrease
jaundice adequately.

Selection of blood group for exchange transfusion is done according to the following rule:

Rh incompatibility: Rh-ve blood with ABO group of the baby.

ABO Incompatibility: ‘O’ group blood with Rh group of the baby.
In all other cases, the baby's blood group is used.

Anti-Infective Properties of Breast Milk

See GI system.

Neonatal Convulsion ‍
Neonatal convulsion or neonatal seizures are the most frequent and distinctive clinical manifestations of neurological
dysfunction in the newborn infant.

Possible Causes

Page 76
 Created by Turbolearn AI

1. Hypoxic Ischemic Encephalopathy (HIE): Secondary to perinatal asphyxia and the commonest cause of neonatal seizure.
Subtle seizures are the commonest type of seizures following HIE in neonates.
2. Metabolic causes:
Hypoglycemia
Hypocalcemia
3. Infections:
Meningitis/meningoencephalitis secondary to Intrauterine infections (e.g., TORCH, Syphilis, etc.)
4. Intracranial hemorrhage:
Subarachnoid hemorrhage (SAH)
Intraparenchymal hemorrhage (common in terms)
Subdural hemorrhage (SDH)
Intraventricular hemorrhage (IVH) – common in preterms
5. Developmental defects of brain
6. Miscellaneous:
Polycythemia
Accidental maternal local anesthetic injection into the scalp
Benign idiopathic neonatal convulsions, etc.

Investigations
1. Blood sugar: To detect hypoglycemia
2. Serum calcium: To detect hypocalcemia
3. Cranial ultrasound (GUS): An excellent tool for detection of IVH and intraparenchymal hemorrhage but is unable to detect
SAH and SDH.
4. Sepsis screen: As sepsis may precipitate hypoglycemia.
5. PCV: For diagnosing polycythemia
6. CT scan / MRI: To diagnose SAH, SDH, and sequelae of HIE and hypoglycemia.
7. EEG: Has both diagnostic and prognostic role in seizures.
8. Metabolic screening: Includes blood pH, ammonia, urine for reducing substance, serum and CSF lactate, etc.
9. Amino acid screening: If the metabolic screen is positive.

Approach

A) History
1. Complete description of members.
2. Leading questions to be asked to enquire about any seizure activity (e.g., subtle seizure) in the first 24 hours of life.
3. Antenatal History:
Maternal diabetes (leads to both hypoglycemia and hypocalcemia)
Maternal narcotic addiction (leads to withdrawal seizures in the newborn infant)
4. Natal history:
History of perinatal asphyxia (e.g., less fetal movements, prolonged labor, need for resuscitation, timing of cry after
birth, etc.)
History of instrumental delivery (may lead to hemorrhage).
5. Postnatal history: History of associated lethargy, drowsiness, vomiting after breastfeeding may be suggestive of IEM.
6. Family history: History of consanguinity in parents, family history of seizures, mental retardation, or early neonatal deaths
may suggest IEM.

B) Examination

Page 77
 Created by Turbolearn AI

1. General Examination:
Vital signs recorded in all infants with seizure.
Bulging anterior fontanelle seen in IVH, SAH, etc.
2. Systemic examination:
Hepatosplenomegaly or abnormal urine odor
3. CNS examination:
Consciousness, tone, and reflexes noted.
Any obvious malformation or dysmorphic feature.
Pallor seen in intracranial hemorrhage
Plethora seen in preterm babies (mainly) with polycythemia

Three-Day-Old Baby with Maternal Chickenpox

1. Whether the mother developed the rashes on the same day or she had any evidence of infection for the last 1-2 days. This
is because if the mother develops rashes up to 2 days after delivery, the initial viremia may have occurred before delivery,
resulting in transplacental infection of the baby (which is more severe and fatal).
2. Whatever may be the time of onset of rash, the mother was definitely devoid of immunity against Varicella. So, there is no
protecting Ab against Varicella Zoster Virus (VZV) in the newborn also.
3. The gestational age of the baby is also important, as preterm infants are more prone to severe infection.

Indications for Post-Exposure Prophylaxis (PEP)

If the mother had the onset of rash up to 2 days after delivery.
If the baby is preterm (i.e., GA < 37 completed weeks) as the mother possibly has no evidence of varicella immunity.
If GA < 28 weeks/weight < 1 kg, PEP is to be given irrespective of maternal immunity.

Options for PEP

Varicella Zoster Immunoglobulin (VZIG) - Most preferred, but it is presently unavailable in India, and the cost is also
prohibitive.
IVIG - Second option in the absence of VZIG; dose is 400 mg/kg single dose.
Isolation should be done, and breastfeeding is withheld.
Treatment - if the baby subsequently develops rashes or any other complications (like pneumonia, hepatitis, encephalitis,
etc.), IV Acyclovir should be started, irrespective of the PEP status.
The mother should be treated aggressively with oral acyclovir and other supportive measures.

Immunization

MMR Vaccine
Globally, most countries use the MMR vaccine instead of just the measles vaccine due to the complications associated with
mumps, such as:

Aseptic Meningitis
Encephalitis
Oophoritis
Deafness
Pancreatitis
Orchitis

Additionally, Rubella during the first trimester of pregnancy can lead to Congenital Rubella Syndrome (CRS).

Page 78
 Created by Turbolearn AI

Strains Used: Different formulations exist among manufacturers.

Mumps component: Jeryl Lynn strain
Rubella component: RA 27/3 strain
Measles Component: Edmonston Zagreb Strain
Efficacy: Seroconversion rate is over 95%.
Storage: 2-8° C, protected from light.
Usage: Reconstituted unused vaccine should be used within 4 hours.

IPV (Inactivated Polio Vaccine)

Developed by Jonas Salk in the 1950s, IPV is an effective vaccine against poliomyelitis.

Type: Formaldehyde-killed polio virus grown in monkey kidney cells or human diploid cells.
Potency: Current IPV vaccines contain 40, 8, and 320 antigen units of type 1, 2, and 3 respectively, known as 'enhanced
potency IPV (eIPV)'.
Availability: Available as a lyophilized (freeze-dried) product in a vacuum-sealed dark multidose vial.
Diluent: Sterile normal saline.
Storage: At 2-8° C.
Dose and Route: 0.5 ml, intramuscular or subcutaneous.

OPV (Oral Polio Vaccine)

Type: Live attenuated vaccine.
Mechanism:
Produces secretory IgA antibody.
Induces herd immunity, although lower than OPV.
Does not cause VAPP (Vaccine-associated paralytic poliomyelitis) with sequential administration of IPV with OPV.
Sequential Administration: Maintains high rates of mucosal immunity and prevents VAPP.

BCG Vaccine
BCG Vaccine is derived from the bovine tuberculosis strain and first developed in 1921.

Page 79
 Created by Turbolearn AI

Action: Primarily induces cell-mediated immunity.

Protection:
Protects against severe forms of tuberculosis (Miliary TB, TB meningitis).
Significant reduction of the risk of death from TB.
Site: Left upper arm, at the insertion of the deltoid to allow easy identification of the BCG scar.
Dose Route: 0.1 ml, intradermal.
Injection Results:
Intradermal injection
↓
Wheal of about 5 mm
↓
Small papule by 2-3 weeks
↓
Enlarges to 4-8 mm by 5-6 weeks
↓
Ulcerates and heals by scarring at 6-12 weeks
Contraindications:
Known allergy.
Cellular immunodeficiency.
Symptomatic HIV.
Osteomyelitis or scrofuloderma in immune-compromised patients.
Adverse Reactions:
Local ulceration or discharging sinus.
Axillary or cervical lymphadenopathy (more likely if given subcutaneously).
Disseminated infection.

Typhoid Vaccine
Typhoid fever is a significant public health problem in many developing countries, including India. Three types of typhoid vaccines
have been developed to combat this infection:

1. Vi Polysaccharide Vaccine:
Purified Vi antigen prevents phagocytosis of S. typhi and inhibits serum bactericidal action.
Types: Unconjugated and conjugated.
Unconjugated vaccine elicits anti-Vi antibodies in children > 2 years; revaccination every 3 years.
Conjugated vaccine immunogenicity and safety are insufficient to recommend its use.
2. Live Attenuated Vaccine:
Contains live attenuated bacteria of the Ty21a strain of S. typhi.
Vaccine is stable at 4-43° C for 3-4 months and can withstand temperature fluctuations.
Potency is monitored using the Vaccine Vial Monitor (VVM), a heat-sensitive patch displayed on the vial label.
Storage: Stable at 2-8° C for a year but potency drops rapidly with storage at -20° C.
Primary immunization: 3 doses on alternate days on an empty stomach.
Capsules must be swallowed intact, unsuitable for administration in children < 6 years.
3. Whole Cell Inactivated Typhoid Vaccine (TNT AB):
Contains heat-killed whole cell Salmonella typhi and S. Paratyphi A and B.
Protected efficacy: 50-70%.
Two doses, 4 weeks apart in children > 6 months old; revaccination every 2-3 years.
Adverse Reactions: Local pain, swelling, redness for injectable vaccine.
Contraindications:
Immunodeficiency state.
Immunosuppressive drugs.
Malignancy.
Advanced HIV.
Untreated tuberculosis.
Pregnancy.

Pulse Polio Immunization 🫶

Page 80
 Created by Turbolearn AI

Pulse Polio Immunization Programme was launched in India in 1995 as a result of WHO Global polio Eradication
initiative.

Objective: Achieving hundred percent coverage with OPV.

Method: Mass immunization campaigns known as Supplementary Immunization Activities (SIAs), including National
Immunization Days (NIDs) and Sub National Immunization Days (SNIDs).
Schedule: Conducted in two rounds one month apart, usually in December and January.
Target: All children < 5 years of age are given 2 doses of OPV.
Frequency: Three to five NIDs are usually required to eradicate polio.
Timing: Conducted during cooler months (December, January) to simplify logistics and improve the immunological response
to OPV.

NIP (National Immunization Programme)

Goal: Intensification of the PPI program is accomplished by extra immunization rounds, adding house-to-house ‘search &
vaccinate’ components in addition to mass immunization at a fixed date.

Objectives:

To increase immunization coverage.

To improve the quality of service.
To achieve self-sufficiency in vaccine production.
To train health personnel.
To supply cold chain equipment and establish a good surveillance network.
To ensure district-wise monitoring areas are covered.

Coverage: Universal coverage of all infants under 1 year and pregnant women with the recommended vaccine schedule.

EPI (Expanded Programme of Immunization): First organized global immunization initiative by WHO in 1974; India
adopted it in 1978.

Vaccines Included: BCG, DTwP, Oral Polio Vaccine (OPV), and Typhoid vaccine (chiefly in urban areas).

National Immunization Schedule

Age Vaccines

0 (Birth) BCG, OPV, HepB

6 weeks DTwP1, OPV1, HepB2, Hb1
10 weeks DTwP2, OPV2, HepB3, Hb2
14 weeks DTwP3, OPV3, HepB4, Hb3
9 months Measles, Vitamin A* (First dose)
15 months MMR (in selected states)
16-24 months DTwP, OFV (Booster 1 dose), Japanese Encephalitis (in selected endemic districts)
5 years DTwP (Booster 2 dose)
10 years TT
16 years TT

OPV (Sabin) vs. IPV (Salk)

Page 81
 Created by Turbolearn AI

OPV (Sabin) IPV (Salk)

Inactivated formaldehyde-killed
Vaccine Type Live attenuated vaccine.
vaccine.
Administration Administered orally. Intramuscular or subcutaneous.
Local mucosal gut immunity
production is much less than OPV, but
Immunity Produces local mucosal gut immunity through secretory IgA.
there is local production of secretory
IgA.
Heard immunity production, though
Herd Immunity Produces herd immunity in the unimmunized segment of the population. less than OPV, results from spillover
of antibody to gut.
Humoral Produces a strong humoral immunity
Humoral immunity production is less.
Immunity response.
Expertise of administrator is required
Administration is technically easy; expertise is not required. Dose - 2
Technical Ease as the vaccine is given I.M./S.C. Dose -
drops.
0.5 ml I.M./S.C.
Outbreak Control Ideal vaccine for outbreak control. Not ideal for outbreak control.
Heat Sensitivity Vaccine is very much heat sensitive. Not so much heat sensitive.
Live OPV is associated with serious side effects like Vaccine-associated
Paralytic Poliomyelitis (VAPP) and circulating vaccine-derived poliovirus
Side Effects Not associated with those side effects.
(CVOPV), especially with conventional trivalent OPV, though very
uncommon.
Cannot be given in severely immunocompromised patients like Can be given in immuno-
Contraindications
symptomatic HIV patients. compromised patients.

Catch-Up Immunization
If a child is unimmunized until 2 years of age, not all vaccination doses are mandatory.

Evaluation (1st contact):

BCG
OPV - 1 dose
DTwP / DTaP
Hepatitis B
After 1 month:
OPV - 1 dose
DTwP / DTaP
Hepatitis B
After 2 months:
MMR (Preferred) or Measles
Typhoid
After 6 months:
DWP/DTap
Hepatitis B

DTwP Vaccine
DTwP, popularly known as Triple antigen, is composed of Diphtheria and Tetanus toxoids as well as killed whole-cell
pertussis bacilli absorbed on insoluble aluminum salts as adjuvant.

Page 82
 Created by Turbolearn AI

Schedule (National Programme): DTwP at 6, 10, and 14 weeks (primary).

Boosters: 15-18 months and 5, 6, 10 years.
Catch Up: At 0, 1, and 6 months (if age is < 7 years).
Dose: 0.5 ml intramuscular.
Site: Anterolateral aspect of the mid-thigh.
Adverse Reactions: Local pain, swelling, redness, fever, anorexia, vomiting.
Frequency of systemic reactions reduces, and local reactions increase with increasing doses.

Dengue Fever

Clinical Features:
Classical Dengue Fever:
High-grade fever with abrupt onset, lasts for 3-7 days.
Severe headache
Retro-orbital pain
Myalgia
Arthralgia
Transient maculo-papular rash over the chest, back, and limbs.

For the above symptoms, classical Dengue fever has acquired the epithet of "Break-bone fever".

Undifferentiated Dengue Fever: Seen in the majority of children with Dengue infection.

Investigations:
Complete Blood Count:
Leukopenia is a feature in the early phase of illness
Platelet count may drop
Haematocrit may be raising (-> 20% or more rise is suggestive of hypovolaemia)
Other Tests:
Virus isolation in cell culture, viral RNA (expensive and time-consuming, not used practically).
Viral antigen detection by ELISA (easy and quick method of detection of Dengue antigen (NS1) during the early phase
of infection, within 5 days).
Detection of Dengue Antibody (after 5 days, dengue viruses disappear from blood, and antibodies appear).

Complications:
Raising haematocrit and a drop in platelet count indicate an impending complication of Dengue.
Chest X-ray, USG abdomen, Echocardiography to detect pleural effusion, ascites, myocardial dysfunction in complicated
Dengue infection.

Measles Complications

Page 83
 Created by Turbolearn AI

Respiratory:
Post-measles Bronchopneumonia
Croup
Tracheitis
Empyema
Bronchiolitis
Giant cell pneumonia
Flaring up of Tuberculosis
ENT: Otitis media (most common complication).
Eye: Keratitis.
GIT:
Frequent or persistent diarrhea (significant cause of dehydration and malnutrition).
Appendicitis
Hepatitis
CNS:
Acute encephalitis caused by direct invasion of the brain by the Measles virus or post-infectious immune-mediated
encephalitis (rare but serious).
SSPE (Subacute sclerosing Panencephalitis): May occur as a degenerative brain disease due to persistent infection by
the Measles virus after several years (7 years) after primary infection.
Others:
Widespread mucosal damage and significant immunosuppression.
Cancrum oris, stomatitis (names at different sites of the mouth and face).

Falciparum Malaria Complications

Severe Malaria: Potentially fatal condition caused by P. falciparum parasites.

Impaired consciousness, coma (GCS < 8).

Prostration (severe weakness).
Multiple convulsions (≥3 seizures in 24 hours).
Acidosis (PH < 7.25 and HCO3 < 15 mEq/L).
Hypoglycemia (Blood glucose < 40 mg/dL).
Severe Anaemia (Hemoglobin < 5 mg/dL).
Renal impairment (Serum creatinine > 3 mg/dL).
Jaundice (Bilirubin > 3 mg/dL).
Pulmonary oedema.
Significant bleeding.
Shock (Systolic pressure < 80 mm of Hg).
Hyperparasitemia (> 10% red cells parasitized).

Algid Malaria: Characterized by shock, hypovolemia, vasodilation, and postural hypotension.

Blackwater Fever: Sudden severe hemolysis, red smoky urine (hemoglobinuria), and renal failure.

Cerebral Malaria: Dreaded complication with high mortality and neurological sequelae.

Risk Factors:

Degree of parasitemia
Cyto-adherence and sequestration capacity of individual
Age (infants and children are more vulnerable)
Immune status
Geographic region

Treatment of Cerebral Malaria

Page 84
 Created by Turbolearn AI

Drugs:

Parenteral antimalarial drug Quinine or Artesunate or Artemether in full course.

See doses in the table that follows
Anti-malarial drug Loading dose Maintenance dose

Quinine dihydrochloride 20 mg salt/kg over 4 hours I.V 10 mg salt/kg over 4 hours repeated every 8 hours
Artisunate IV route 2.4 mg/kg 1.2 mg/kg repeated at 12 and 24 hours, then 1.2 mg/kg/day
Artemether IM route 3.2 mg/kg 1.6 mg/kg repeated 12-24 hours

Good Supportive management:

Patient should be ideally managed in PICU.

Assessment of airway, breathing, and circulation.
Detection of hypoglycemia (Blood glucose < 40 mg/dL) and treated by I.V. bolus of 10% or 25% Dextrose.
Diagnosis of dyselectrolytemia and treatment accordingly.
Convulsion should be promptly managed with the use of anticonvulsants.
CSF study to rule out meningitis.
Assessment of hydration status and proper fluid management (avoid overhydration).
For hyperpyrexia, repeated cold sponging and use of antipyretics (Paracetamol I.V. - 10 mg/kg).
Consideration of blood transfusion in the presence of severe anemia.
Correction of lactic acidosis with proper oxygenation, tissue perfusion, and judicious use of sodium bicarbonate.
A rapidly rising serum creatinine level is an indication of dialysis.
Raised intracranial pressure is to be managed by I.V. Mannitol or 3% NaCl.

Treatment of Chloroquine-Resistant Falciparum Malaria

Artesunate + Sulfadoxine - Pyrimethamine:
Artesunate tablet 4 mg/kg daily for 3 days.
Sulfadoxine (25 mg/kg body weight) + Pyrimethamine (1.25 mg/kg body weight) on the first day.
Primaquine: 0.75 mg/kg body weight on day 2.
Available as co-formulated tablet of Artemether (20 mg) + Lumefantrine (120 mg).

Dosage
Artemether + Lumefantrine:

5-14 kg (5 months - < 3 years): 20 mg/120 mg BD for 3 days

15-24 kg (> 3 years - 8 years): 40 mg/240 mg BD for 3 days
25-34 kg (> 9 years - 14 years): 60 mg/360 mg BD for 3 days

Primaquine: 0.75 mg/kg body weight on day 2

Resistance to chloroquine is a common occurrence in case of falciparum malaria. In such a situation, Artemisinin derivative-
based combination therapy is the treatment of choice.

Monitoring Glucose and the Heart

Quinine has a strong stimulant effect on pancreatic secretion leading to Iatrogenic hypoglycemia and also causes significant
cardiotoxicity. So, monitoring blood glucose and electrocardiogram is necessary if quinine is used as an antimalarial.

Cerebral Malaria Therapy

Therapy for cerebral malaria, caused by infection with P. falciparum, includes:

1. Antimalarial Therapy: Artenether-lumefantrine.

2. Supportive Management: Addressing complications in the CNS, respiratory, cardiovascular, and hematological systems.

Rabies Prophylaxis

Page 85
 Created by Turbolearn AI

Rabies is endemic in India, primarily affecting animals, and is often fatal if not properly managed. Prevention involves:

Wound Management
Washing: Use running tap water for at least 10 minutes to reduce viral load.
Disinfection: Apply povidone-iodine, spirit, or household antiseptics.
Soap/Detergent: Use for chemical treatment and to alter the pH of the wound.

Post-Exposure Prophylaxis
The type of prophylaxis depends on the wound category:

Category Type of Contact Recommended Post-Exposure Prophylaxis

I Touching or feeding animals, licks on intact skin None if the history is reliable
II Nibbling of uncovered skin, minor abrasion without bleeding Wound management + antirabies vaccine
Single or multiple transdermal bites, licks on broken skin, contamination of Wound management, rabies
III
mucous membrane with saliva, bite over face/head immunoglobulin, antirabies vaccine

Rabies Immunoglobulin (RIG)

RIG provides passive immunity by binding to the rabies virus, leading to neutralization.

Types:
Equine RIG: 40 IU/kg body weight
Human RIG: 20 IU/kg body weight
Administration: Infiltrate as much as possible into and around the wound, with the remainder given intramuscularly.

Antirabies Vaccine
Active immunization against rabies.
Intradermal (ID) dose: 1/4 of the intramuscular dose.
Dose: 1 ml for all vaccines except PVEV.
PVEV (IM): 0.5 ml
Types of vaccines:
Cell culture rabies vaccine (CCRV)
Human diploid cell vaccine (HDCV)
Purified chick embryo cell vaccine (PCEC)
Purified vero cell rabies vaccine (PVRV)
Purified duck embryo vaccine (PDEV)
Site: Anterolateral thigh/deltoid.
Schedules: Various schedules exist for intramuscular and intradermal routes. The Essen schedule is common, with five
single doses on days 0, 3, 7, 14, and 28.
Updated TRC-ID Schedule: 2-2-2-0-2: 0.1 ml per site, two ID sites (one on each deltoid area) on days 0, 3, 7, and 28.

Pre-Exposure Prophylaxis
For individuals at high risk of animal contact.
Dose & Schedule: IM on days 0, 7, 21 or 28; booster after 1 year and every 5 years thereafter.
Tetanus Toxoid & Tetanus Immunoglobulin given as required.

Severe Falciparum Malaria Complications

Severe falciparum malaria can affect various systems:

Page 86
 Created by Turbolearn AI

(a) CNS:
Prolonged, uncontrolled headache
Prolonged, recurrent convulsions (2 or more in 2-4 hours)
Unconsciousness
Subtle seizure-like activity (facial twitching, eye deviation)
Irregular breathing
Opisthotonus posturing
Hypotonia
Visual difficulty
(b) Hematological:
Severe Anemia
Jaundice
Passage of dark red smoky urine
Abnormal bleeding, petechiae
(c) Respiratory: Rapid, deep breathing.
(d) Circulatory:
Postural hypotension
Shock
(e) Renal:
Oliguria or anuria
Passage of red smoky urine
(f) G.I.:
Vomiting
Diarrhea
Dehydration
(g) Other: Hyperpyrexia (> 38.5°C)

Mumps Complications
Mumps is a generalized viral infection primarily affecting children and young adults, mainly impacting salivary glands but can
infect almost any organ.

Pancreatitis (5% of cases)

Possible cause of juvenile-onset diabetes, developing weeks after parotitis.
CNS Complications:
Aseptic Meningitis (40% of patients)
Encephalitis (can be serious with seizures and cortical blindness, but prognosis is usually good).
Aqueductal stenosis and hydrocephalus
Other CNS manifestations: Cerebellar ataxia, Transverse Myelitis, Guillain-Barré syndrome.
Orchitis (testis and epididymis infection)
Occurs 1-2 weeks after parotitis, mostly unilateral.
Testicular swelling, tenderness, nausea, vomiting
Testis enlargement (two to four times larger and very tender)
Atrophy may develop, but sterility is rare.
Oophoritis (ovary infection, especially in postpubertal females)
Usually no evidence of impaired fertility.
Deafness
Sensory neural deafness may develop.
Can be unilateral/bilateral, transient/permanent.
Other less common complications: Myocarditis, Arthritis, Optic neuritis, Mastitis, Thyroiditis, Endocardial fibroelastosis

Acute Suppurative Otitis Media (ASOM)

ASOM is an inflammation of the mucoperiosteal lining of the middle ear, lasting less than 2 weeks.

Clinical Features

Page 87
 Created by Turbolearn AI

Moderate to high-grade fever

Ear pain (older children), excessive crying (younger children)
Ear discharge
Sometimes lower motor neurone facial palsy
Hearing loss (older children)
Ear tenderness
Otoscopic examination: Tympanic membrane inflamed, bulging, loss of normal anatomy, fluid in the middle ear.

Treatment
Antibiotics are primary:
Initial choice: Amoxicillin / Amoxicillin + Clavulanic acid
Severe case: Injectable third-generation cephalosporin
Children < 2 years: Antibiotics
Children > 2 years with mild disease: Observe for 2-3 days before starting antibiotics
Severe disease at any age: Antibiotics at diagnosis
Duration: 10 days
Supportive treatment:
Adequate hydration
Oral paracetamol (pain and fever relief)
Tympanocentesis (occasionally to relieve severe pain)

Tubercular Meningitis (TBM)

Tubercular meningitis is the most frequent manifestation of CNS tuberculosis and is potentially curable with early diagnosis and
anti-tubercular chemotherapy.

Clinical Manifestations
Divided into three stages:

Stage I (Prodromal):
Non-specific symptoms: Low-grade fever, loss of appetite, disturbed sleep, vomiting, constipation, headache (older
children), irritability, restlessness, apathy, less playful.
Photophobia in older children
Stage II (Meningitis):
Alteration of sensorium, drowsiness, or delirium
Signs of meningeal irritation: Neck rigidity and Kernig sign
Convulsions (65% of cases)
Cranial nerve palsy (squint, vision disturbances, facial asymmetry, ptosis, dilated irregular pupils)
Paralysis: Hemiplegia, monoplegia, or quadriplegia
Features of raised intracranial tension (ICT): Headache, vomiting, visual disturbances, pulse/BP changes, bulging
fontanelle and separation of sutures (infants)
Stage III (Coma):
Deep coma
Well-marked meningeal signs, progressive neurological deficits
Dilated and fixed pupils
Cheyne-Stokes or Biot-type breathing
Neck retraction, opisthotonus, decorticate and decerebrate rigidity
Central origin hyperpyrexia

CSF Changes

Page 88
 Created by Turbolearn AI

Feature CSF Finding

Physical Appearance Clear, colorless, cobweb coagulation forms on standing (composed of TB bacilli and fibrin)
Pressure (mm H2O) Usually elevated
Leukocyte (mm3) 6 - 500 PMN early, but lymphocytes predominate (>60%)
Protein (mg/dl) 100 - 3,000 (may be higher with CSF flow block)
Glucose (mg/dl) <50 in most cases
Staining/Microscopy Acid-fast bacilli rarely seen on smear. Culture: Organism can be recovered if CSF volume is large (> 5 ml)
ADA level and PCR Mycobacterium tuberculosis can be detected by PCR. >10 U/L supports TB meningitis

Tuberculin Test (Mantoux Test)

Most common test for childhood TB diagnosis.
Dose: 5 TU of PPD-S or 2 TU of Tuberculin PPD RT-23.
Administration: 0.1 ml of PPD intradermally into the volar aspect of forearm using a 26G needle and Tuberculin syringe.
Reading: Measure the diameter of induration transversely to the long axis of the forearm after 48-72 hours.
Size of Induration Interpretation

< 10 mm Negative, no active disease

5-10 mm Borderline, consider positive in immunocompromised child and contact with sputum. Positive TB in adult.
> 10 mm Positive, suggests disease in presence of clinical features.

Miliary Tuberculosis
Miliary tuberculosis is another name of disseminated tuberculosis.

Risk Factors
Age < 3 years
Weak immune system (HIV)
Not vaccinated with BCG
Viral, bacterial infection (Measles, mumps, chicken pox, HIV, typhoid)
Live vaccination
Lymphoma, leukemia
Immunosuppressive drugs
Surgery
Wrong method of administration, improper dilution, storage
Inexperienced reader

Organs Affected
Lung
CNS
Liver
Bone marrow
Pericardium

Clinical Features

Page 89
 Created by Turbolearn AI

Symptoms are vague and nonspecific

Intermittent febrile episodes and gradual weight loss
Prolonged cough not responding to antibiotics
Respiratory distress
Headache/vomiting
Alteration of sensorium
Cranial nerve palsies
Hepatosplenomegaly
Jaundice
Anemia
Chest pain
Features of pericardial effusion
Other symptoms per organ involvement

Diagnosis
Chest X-ray to detect miliary focus in the lung
Tuberculin skin test often falsely negative
CSF study-cells protein sugar, PCR. cutture, ADA CBNAT if meningitis is sus'iiected
CBC with ESR - High ESFi with high lymphocyte count is suggestive.
Fluid collected from the affected organ like, pleural fluid, pericardial or joint fluid to
Imaging studies — CT scan, USG, MRI of the affected organs as required.

Treatment
Supportive treatment: Organ function support (lung, kidney, brain), blood transfusion, drainage of effusion.
Anti-TB drugs (6-9 months). Corticosteroids in meningitis

Chikungunya Fever
Chikungunya is a viral fever caused by an alphavirus and transmitted by the bite of infected Aedes aegypti mosquitoes.

Clinical Features
Acute onset
Fever rises abruptly to 103-104°F, accompanied by rigors and chills.
Associated with headache, fatigue, muscle ache, nausea, vomiting
A ‘saddle back’ fever may occur.
Rash:
Flushing of the face and trunk, followed by maculopapular rash
Trunk and limbs are commonly involved
May be itchy
May fade or desquamate
Arthralgia/Arthritis:
Polyarticular, migratory
Affects small joints of hands, wrists, ankles, feet
Intense pain in the acute stage
Pain worse in the morning, improves with mild exercise
Swelling may occur
May persist for weeks to months

Congenital Toxoplasmosis
Toxoplasmosis occurs when a mother gets a primary infection with Toxoplasma gondii during pregnancy, leading to
transplacental transmission.

Clinical Features

Page 90
 Created by Turbolearn AI

Mild to severe neonatal disease or with sequelae

Infants may be asymptomatic at birth and later present with mental retardation, deafness.
Classical Triad: Chorioretinitis, Hydrocephalus. Cerebral calcification

Other Clinical Features

Prematurity
IUGR
Jaundice
Hepatosplenomegaly
Myocarditis
Pneumonitis
Various rashes
Sensorineural hearing loss

Diagnosis
Prenatal Diagnosis:
Fetal ultrasound
PCR analysis of amniotic fluid
Post-natal Diagnosis:
Serological test Serum lgM and lgG
CT Scan — Hydrocephalus, cerem calci fi cation
Analysis Toxoplasma speci fi demonstrate

Treatment
Pyrimethamine + Sulfadiazine
Pyrimethamine: 2 mg/kg/day BD for 2 days, then 1 mg/kg/day for 2 or 6 months, then 1 mg/kg twice weekly P.O.
Sulfadiazine: 100 mg/kg/day BDPO
Leukovorin: 5-10 mg given twice weekly P.O.
Duration of treatment: 1 year

Acute Flaccid Paralysis (AFP) Surveillance Programme

Acute Flaccid Paralysis implies paralysis of acute onset (less than 4 weeks) and affected limb or limbs are flaccid i.e.
floppy or limp in a child < 15 year old or paralysis in a person of any age in whom polio is suspected.

AFP Rate
Sensitive surveillance detects a background AFP rate of 1/100,000 children.

AFP Action Plan

All health facilities must notify every AFP case immediately to the District Immunization Officer (DIO).
Stool sample must be collected from all AFP cases within 14 days of onset.
DIO must revisit every case of AFP 60 days after the onset of paralysis to confirm the presence or absence of residual
paralysis.

Stool Sample
Two stool specimens should be collected within 14 days of onset.
Maintain temperature below (to 8°C)

Page 91
 Created by Turbolearn AI

Polio Classification
Confirmed Polio case: Isolation of wild polio virus from any stool specimen.
'Non-Polio AFP' case: if the 69 day AF fOIIOW up examination shows no residual weakness, the case is classified as non-
polro y AFP.

Dengue Fever

Pathology
1. Intracellular dengue viral killing
2. Vasculoparhy causing damage to the vessels walls
3. Extravasation of plasma from Intravascular to extravascular space
4. Shock and Bleeding

Clinical Features
Warning signs of Dengue in children:
Intense anorexia
Nausea, vomiting
Pain abdomen
Hepatomegaly
Giddiness
Cold extremities
Oliguria
Restlessness, irritability
Progression to Dengue Haemorrhagic Fever (DHF) and/or Dengue Shock Syndrome (DSS).
After a febrile period of 2-7 days, signs of circulatory failure develop:
Postural hypotension
Cold periphery
Thready, rapid pulse
Tachycardia
Circumoral cyanosis
Peripheral pulses difficult to palpate
Puffy swollen face
Generalized oedema
Polyserositis
Low or unrecordable pulse
Narrow pulse pressure
Progressive p otic. to a is
Uncorrected shoclr
DIC
Other Features
Recurrent Vomiting .
Pleural effusion / ascites / gall bladder oedema on imaging.
Minor bleedng from different sites : haemoptysis, haematomyelis. haematuria, gum bleeding etc.
Pain abdomen or discomfort
Palpitation, breathiessness
Hepatic dysfunction or hepatomegaly (> 2 cm) with or without tenderness
Decrease urine output
High haematocrit (> 45%} or increase in 20%
Rapid fall of platelet count
Cold. clammy extremities
Narrow pulse pressure
Rapid pulse
Hypotension
General weakness I lethargy! restlessness

Page 92
 Created by Turbolearn AI

Investigation
1. Positive Toumiquet Test

Signs of plasma leakage

1. Ansaofhaematocritforageandaex 220%
2. A more than 20% drop In haematocrit following volume replacement treatment
3. Signs of plasma leakage (pleural effusion. ascites. hypoproteinemia]

DSS Treatment
Immediate rapid volume replacement
Fluid is bolus —- 20 ml/kg. up to 3 boluses
Look for Anaemia, acidosis, myocardial

Dengue Hemorrhagic Fever

Dengue Hemorrhagic Fever (DHF) is a severe form of dengue fever with high mortality if not detected and managed early.

Key Characteristics of DHF

Thrombocytopenia: Platelet count < 100,000
Bleeding manifestations:
Petechiae, ecchymosis, or purpura
Bleeding from mucosa, GI tract, or injection sites
Plasma leakage: Indicated by a rise in hematocrit > 20% for age and sex

Clinical Features
Positive tourniquet test
Prolonged bleeding from venipuncture sites
Fine purpuric rash all over the body
Mild GI bleeding (in < 10% cases)
Severe GI or other forms of bleeding
Low platelet count (< 100,000) in the presence of bleeding
Initial symptoms similar to dengue fever: high fever, intense headache, backache, myalgia, joint pain
Hemorrhagic tendencies as fever subsides

DHF Diagnosis Criteria

Clinical criteria for dengue fever + hemorrhagic manifestation + thrombocytopenia + hypotension

Treatment
Volume replacement is the mainstay of treatment
All patients with danger signs should be admitted to the hospital and need IV fluids, preferably crystalloids.

IV Fluid Therapy

Page 93
 Created by Turbolearn AI

1. Initial therapy: 10-20 ml/kg/hr for 1-2 hours

If improvement: Crystalloid therapy with successive reduction of rate and then discontinuation.
If no improvement: Proceed to step 2.

2. Successive IV therapy with crystalloids, reduced from 10 to 6 ml/kg, then 6 to 3 ml/kg.

If further improvement: Discontinue IV therapy over 24-48 hours.

If hematocrit falls: Colloid therapy 10 ml/kg.
If hematocrit rises: Blood transfusion 10 ml/kg.

Acute Encephalitic Syndrome (AES)

Symptoms
Followed by stiffness of neck, difficulty in swallowing, and rigidity of abdominal muscles
Rigidity of facial muscles: Leads to sardonic smile or risus sardonicus
Rigidity of back and abdominal muscles: Leads to opisthotonos posturing
Rigidity of laryngeal and respiratory muscles: Leads to airway obstruction and asphyxia
Spasms precipitated by stimuli like bright light, noise, touch
Constipation and urinary retention
Sympathetic nerve involvement: Hyperpyrexia, hypertension, excessive sweating, tachycardia

Potential Causes
Japanese Encephalitis virus
Herpes simplex 1
Dengue virus
Measles virus
Chikungunya virus
Epstein-Barr virus
Human Herpes virus 6
West Nile virus
Nipah virus

Generalized Tetanus

Characteristics
Descending pattern of involvement of generalized muscle.
Incubation period: Around 10 days

Types of Tetanus
Generalized Tetanus (most common)
Localized Tetanus
Cephalic Tetanus

Symptoms
Typically occur within 3-12 days of birth

This is a serious condition

Progressive difficulty in feeding (sucking and swallowing)

Stiffness and spasm of body and in extreme cases opisthotonos occurs

Page 94
 Created by Turbolearn AI

Condition is invariably fatal.

Diagnosis
Careful history taking is very important
History of fever, headache, vomiting, seizure, abnormal posturing

Page 95