Hyponatremic Dehydration (Na <130 mEq/L)

Here you calculate sodium deficit explicitly:Na⁺ deficit (mEq)=(135−Serum Na)×0.6×weight (kg)\textbf{Na⁺ deficit (mEq)} = (135 – \text{Serum Na}) \times 0.6 \times \text{weight (kg)}Na⁺ deficit (mEq)=(135−Serum Na)×0.6×weight (kg)

👉 135 mEq/L is taken as desired Na

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Example

10 kg child, Na = 125 mEq/L(135−125)×0.6×10=10×6=60 mEq(135 – 125) \times 0.6 \times 10 = 10 \times 6 = \textbf{60 mEq}(135−125)×0.6×10=10×6=60 mEq

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Important

• Correct slowly over 24–48 hrs
• Max rise: ≤8–10 mEq/L/day
• Give via DNS / NS + added Na as needed

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Isonatremic Dehydration (Na 130–150)

No sodium deficit calculation needed

Instead calculate:

• Fluid deficit = % dehydration × weight × 10

Example:

• 10% dehydration in 10 kg child →
  = 10 × 10 × 10 = 1000 mL deficit

Give:

• Deficit + maintenance + ongoing loss
• Usually NS / RL initially

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Hypernatremic Dehydration (Na >150)

👉 Do NOT calculate sodium deficit
Instead calculate free water deficit:Water deficit (L)=0.6×wt×(Na145−1)\textbf{Water deficit (L)} = 0.6 \times \text{wt} \times \left(\frac{\text{Na}}{145} – 1\right)Water deficit (L)=0.6×wt×(145Na​−1)

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Example

10 kg child, Na = 1600.6×10×(160/145−1)≈6×0.103=0.62 L0.6 \times 10 \times (160/145 – 1) \approx 6 \times 0.103 = \textbf{0.62 L}0.6×10×(160/145−1)≈6×0.103=0.62 L

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Key Pediatric Pearls (Exam Gold)

• Hyponatremia → calculate Na deficit
• Hypernatremia → calculate water deficit
• Isonatremia → calculate fluid deficit only

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Correction Rules

• Hyponatremia: ↑ Na ≤8 mEq/day
• Hypernatremia: ↓ Na ≤10–12 mEq/day
• Rapid correction → ODS (hypo) / cerebral edema (hyper)

First principle:
👉 Most overweight infants are exogenous (overfeeding).
👉 Investigations are needed only if there are red flags for endocrine, genetic, or metabolic causes.

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1️⃣ Step 1: Confirm Overweight / Obesity

Anthropometry

• Weight-for-length (WHO growth charts)
• BMI (if >2 years; not for infants)
• Head circumference
• Mid-upper arm circumference (optional)

Definitions (WHO)

• > +2 SD weight-for-length → Overweight
• > +3 SD → Obese

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2️⃣ When to Investigate?

Send investigations if:

• Rapid weight gain
• Short length/height (↓ linear growth)
• Dysmorphic features
• Developmental delay
• Hypotonia
• Organomegaly
• Hyperphagia
• Family history of endocrine/genetic disorders
• Signs of hypothyroidism, Cushing, etc.

If thriving, normal length, normal development → usually no labs required.

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3️⃣ Baseline Investigations (If Indicated)

Investigation	Why Send It
CBC	Baseline health
Fasting blood glucose	Insulin resistance (rare in infancy but possible in severe obesity)
Serum insulin (if strong suspicion)	Hyperinsulinemia
Lipid profile	If severe obesity or family history
LFT (ALT, AST)	NAFLD screening (rare but possible in severe cases)
Thyroid profile (TSH, Free T4)	Rule out hypothyroidism
Serum cortisol (8 AM)	If Cushing features
IGF-1	If growth failure

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4️⃣ Endocrine Causes to Rule Out

A. Hypothyroidism

• TSH
• Free T4

Clues:

• Constipation
• Large tongue
• Hypotonia
• Poor linear growth

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B. Cushing Syndrome (Very Rare in Infants)

• 8 AM cortisol
• Low-dose dexamethasone suppression test (if needed)

Clues:

• Moon face
• Hypertension
• Growth failure
• Thin skin

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C. Hyperinsulinism

• Fasting insulin
• Blood glucose

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5️⃣ Genetic / Syndromic Evaluation

If:

• Hypotonia
• Developmental delay
• Dysmorphism
• Hyperphagia

Consider:

• Karyotype
• Microarray
• Referral to genetics

Examples:

• Prader-Willi syndrome
• Beckwith-Wiedemann syndrome

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6️⃣ Metabolic Screening (If Suspicion)

If:

• Hepatomegaly
• Hypoglycemia
• Recurrent vomiting
• Developmental delay

Send:

• Serum ammonia
• Lactate
• Tandem mass spectrometry
• Urine organic acids

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7️⃣ If Severe Obesity (> +3 SD)

Consider screening for:

• Lipid profile
• LFT (NAFLD)
• Blood pressure monitoring
• HbA1c (if strong suspicion)

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8️⃣ What NOT to Routinely Send

❌ Insulin levels in every overweight baby
❌ Extensive metabolic panels without red flags
❌ Hormone panels without growth failure

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9️⃣ Practical Clinical Algorithm (Exam-Friendly)

Normal length + normal development + formula overfeeding → NO LABS

Overweight + short length → TSH + Free T4

Overweight + hypotonia + hyperphagia → genetic workup

Overweight + moon face + hypertension → cortisol evaluation

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🔟 For Your Clinical Practice in Nepal

In most cases in our setup:

• It is formula concentration error or early complementary feeding.
• Counseling on feeding practice is more important than investigations.

Perforated Acute Otitis Media (AOM with tympanic membrane perforation) is treated slightly differently from uncomplicated AOM because the perforation allows topical therapy to reach the middle ear.

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1. First-line Treatment

A. Topical Antibiotic Ear Drops (Most Important)

Use quinolone ear drops because they are safe in perforated TM.

• Ofloxacin ear drops
  • Dose: 5 drops in affected ear twice daily
  • Duration: 7–10 days

OR

• Ciprofloxacin ear drops
  • Dose: 4–5 drops twice daily
  • Duration: 7–10 days

Avoid aminoglycoside drops (e.g., Gentamicin, Neomycin) because they can be ototoxic if TM is perforated.

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2. Oral Antibiotics (if indicated)

Give systemic antibiotics if:

• Moderate/severe infection
• Fever
• Young child (<2 years)
• Bilateral disease
• Systemic symptoms

First line:

• Amoxicillin
  • 80–90 mg/kg/day divided BID
  • Duration 7–10 days

If severe infection or recent amoxicillin use:

• Amoxicillin‑clavulanate
  • 90 mg/kg/day (amoxicillin component)

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3. Analgesics

• Paracetamol 10–15 mg/kg every 6 hours
  OR
• Ibuprofen 10 mg/kg every 8 hours

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4. Local Care

• Keep ear dry (no water entry).
• Do not plug ear tightly.
• Gentle ear toilet/suction if discharge excessive.

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5. Follow-up

• Re-examine after 1–2 weeks.
• Most perforations heal spontaneously within 2–4 weeks.
• If persistent perforation >6 weeks → ENT referral.

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6. Red Flags (Refer ENT)

• Persistent otorrhea >2 weeks
• Suspected mastoiditis
• Hearing loss
• Recurrent perforations

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Example Pediatric Prescription

• Ofloxacin ear drops: 5 drops BD × 7 days
• Amoxicillin: 80–90 mg/kg/day divided BD × 7 days
• Paracetamol: 10–15 mg/kg every 6 hr PRN pain

• Nelson Textbook of Pediatrics
• First Aid for the USMLE Step 1
• Cloherty and Stark’s Manual of Neonatal Care

Introduction

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Cerebral palsy (CP) is the most common cause of permanent motor disability in childhood. It results from injury or abnormal development of the immature brain, leading to abnormalities of movement, posture, and coordination.

Despite the term palsy, cerebral palsy is not a progressive disease—the brain injury is static. However, symptoms may change as the child grows.

The worldwide prevalence is approximately 2–3 per 1000 live births, and the condition is more common in premature infants and low-birth-weight neonates.

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Overview of Cerebral Palsy

Definition

Cerebral palsy is defined as:

A group of permanent disorders of movement and posture causing activity limitation, attributed to non-progressive disturbances in the developing fetal or infant brain.

Key Characteristics

Feature	Description
Nature	Non-progressive brain injury
Onset	Early childhood
Primary problem	Motor dysfunction
Associated problems	Cognitive, sensory, and behavioral issues

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Pathophysiology

According to First Aid for the USMLE Step 1, cerebral palsy results from injury to motor control systems of the developing brain.

Brain Areas Involved

Brain Structure	Resulting Clinical Type
Motor cortex	Spastic CP
Basal ganglia	Dyskinetic CP
Cerebellum	Ataxic CP
Multiple regions	Mixed CP

Mechanisms of Brain Injury

Major mechanisms include:

• Hypoxic-ischemic injury
• White matter injury
• Intracranial hemorrhage
• Inflammation
• Toxic injury (bilirubin toxicity)

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Periventricular Leukomalacia (Common Mechanism in Preterm Infants)

Periventricular leukomalacia (PVL) is the most common neuropathologic lesion in premature infants who develop CP.

Pathogenesis

1. Immature cerebral circulation
2. Hypoxia or ischemia
3. White matter injury near ventricles
4. Damage to descending corticospinal tracts

Clinical Outcome

PVL is strongly associated with spastic diplegia.

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Etiology of Cerebral Palsy

Modern research shows most CP originates before birth, rather than during delivery.

Causes by Timing of Brain Injury

Timing	Causes
Prenatal	Brain malformations, infections, genetic disorders
Perinatal	Prematurity, birth asphyxia, intracranial hemorrhage
Postnatal	Infection, trauma, stroke

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Major Risk Factors

Based on Cloherty and Stark’s Manual of Neonatal Care.

Maternal Factors	Neonatal Factors
Maternal infection	Prematurity
Placental insufficiency	Low birth weight
Preeclampsia	Neonatal seizures
Multiple pregnancy	Intraventricular hemorrhage

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Classification of Cerebral Palsy

Types Based on Motor Pattern

Table: Major Types of Cerebral Palsy

Type	Brain Region	Key Features	Frequency
Spastic	Motor cortex	Stiff muscles, hyperreflexia	~70–80%
Dyskinetic	Basal ganglia	Involuntary movements	~6–10%
Ataxic	Cerebellum	Poor balance and coordination	~5–10%
Mixed	Multiple areas	Combination of symptoms	Variable

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Spastic Cerebral Palsy

Most common type.

Pathophysiology

Damage to corticospinal tracts leads to:

• Increased muscle tone
• Hyperreflexia
• Clonus

Distribution Patterns

Type	Body Areas Involved
Hemiplegia	One side of body
Diplegia	Legs > arms
Quadriplegia	All limbs
Monoplegia	Single limb

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Dyskinetic Cerebral Palsy

Associated with basal ganglia injury.

Clinical Features

• Dystonia
• Chorea
• Athetosis
• Involuntary twisting movements

Important Cause

Severe neonatal jaundice causing
Kernicterus.

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Ataxic Cerebral Palsy

Results from cerebellar damage.

Symptoms

Symptom	Description
Ataxia	Unsteady walking
Intention tremor	Tremor during movement
Poor coordination	Difficulty performing fine motor tasks
Wide-based gait	Instability while walking

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Clinical Features of Cerebral Palsy

Symptoms depend on severity and brain area affected.

Early Warning Signs

Age	Red Flag
3 months	Poor head control
6 months	Stiff or floppy muscles
9 months	Not sitting
12 months	Early hand preference

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Associated Conditions

Children with CP often have additional neurological problems.

Condition	Frequency
Epilepsy	30–50%
Intellectual disability	40–60%
Visual impairment	20–40%
Speech disorders	common
Hearing loss	10–15%

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Diagnosis

Diagnosis is mainly clinical, supported by imaging.

Diagnostic Evaluation

Evaluation	Purpose
Developmental history	Identify delays
Neurological exam	Tone, reflexes
MRI brain	Identify structural lesion
EEG	If seizures present
Genetic testing	If atypical features

Neuroimaging Findings

Common MRI findings include:

• Periventricular leukomalacia
• Cortical malformations
• Brain atrophy
• Old infarction

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Gross Motor Function Classification System (GMFCS)

This system classifies severity of CP.

Level	Functional Ability
Level I	Walks independently
Level II	Walks with limitations
Level III	Walks with assistive device
Level IV	Limited self mobility
Level V	Wheelchair dependent

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Management of Cerebral Palsy

There is no cure, but multidisciplinary management improves function.

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Multidisciplinary Treatment

Therapy	Role
Physiotherapy	Improve mobility
Occupational therapy	Daily living skills
Speech therapy	Communication
Special education	Cognitive development

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Pharmacological Treatment

Used mainly for spasticity management.

Drug	Mechanism
Baclofen	GABA agonist
Diazepam	Muscle relaxant
Tizanidine	Alpha-2 agonist
Botulinum toxin	Local spasticity control

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Surgical Management

Indicated in severe deformities.

Examples include:

• Tendon lengthening
• Hip reconstruction
• Selective dorsal rhizotomy
• Spinal surgery for scoliosis

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Prevention Strategies

Important preventive measures include:

Strategy	Benefit
Antenatal care	Prevent infections
Prevention of prematurity	Reduce PVL
Neonatal intensive care	Prevent brain injury
Early jaundice treatment	Prevent kernicterus

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Prognosis

Outcome depends on:

• Severity of brain injury
• Type of cerebral palsy
• Associated neurological deficits
• Access to rehabilitation

Many individuals with CP can live productive lives with appropriate therapy and support.

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Clinical Pearls (High-Yield)

• Spastic diplegia → periventricular leukomalacia
• Dyskinetic CP → basal ganglia injury
• Ataxic CP → cerebellar damage
• Kernicterus → dyskinetic cerebral palsy

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Conclusion

Cerebral palsy is a lifelong neurological disorder caused by early brain injury. Although the underlying brain damage is permanent, early diagnosis, multidisciplinary therapy, and supportive care can significantly improve functional outcomes and quality of life.

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