• EEG pattern: Periodic high-amplitude slow-wave complexes / burst-suppression pattern (Radermecker complexes) recurring every 4–10 seconds.

• Stage I: Insidious mental deterioration, behavioral/personality changes, decline in school performance.
• Stage II: Myoclonic jerks, choreoathetosis, seizures, motor and language deficits.
• Stage III: Severe dementia, rigidity, decorticate/decerebrate posturing, loss of vision/speech, vegetative state.
• Stage IV: Mutism, coma, loss of autonomic control, death.

• Characteristic EEG (periodic complexes)
• CSF and serum measles antibody titers (elevated anti-measles IgG with reduced serum-to-CSF ratio, oligoclonal bands)
• MRI brain (periventricular white matter hyperintensities)

• Treatment: Inosiplex (isoprinosine), intraventricular/intrathecal interferon-alpha, ribavirin, amantadine.
• Prevention: Measles vaccination (MR/MMR vaccine at 9 and 15 months).

• EEG pattern: Hypsarrhythmia (chaotic, high-voltage, disorganized background with multifocal sharp waves, spikes, and polyspikes).

• Symptomatic (Identifiable etiology): Tuberous sclerosis, hypoxic-ischemic encephalopathy (HIE), perinatal stroke, CNS infections, cortical dysplasia, inborn errors of metabolism.
• Cryptogenic / Genetic: Unknown etiology with normal development prior to onset.

• Adrenocorticotropic hormone (ACTH) (75 U/m²/day or 150 U/m²/day)
• Vigabatrin (first-line especially for tuberous sclerosis)
• Oral corticosteroids (prednisolone)
• Ketogenic diet, valproate, topiramate, or surgery if focal lesion.

• Diagnosis: Herpes Simplex Encephalitis (HSE).

• Unilateral facial clonic twitching / sensorimotor seizures
• Oropharyngeal symptoms: hypersalivation (drooling), guttural sounds, speech arrest / inability to speak.

• Treatment: Often observation only without antiepileptic therapy; if frequent/daytime seizures, Carbamazepine, Levetiracetam, or Oxcarbazepine.
• Prognosis: Excellent; spontaneously remits in almost all children by 14–16 years of age with normal neurocognition.

• EEG pattern: Slow generalized spike-and-wave discharges (<2.5 Hz) with disorganized, slow background and paroxysmal fast activity during sleep.

• Medical: Broad-spectrum AEDs (Valproate, Clobazam, Lamotrigine, Topiramate, Rufinamide, Cannabidiol), Ketogenic diet, IVIG.
• Surgical: Corpus callosotomy (effective for atonic drop attacks), Vagus Nerve Stimulation (VNS).

• EEG features: Continuous rhythmic spikes, sharp waves, or spike-wave discharges without overt convulsive motor movements, showing electrical improvement upon IV antiepileptic administration.

• CXR: Massive cardiomegaly (globular heart) in a floppy infant.
• ECG: Extremely tall QRS voltages (giant biventricular hypertrophy) requiring half-standard calibration, short PR interval, and deep T-wave inversions.

• Hemodynamically unstable (pulseless/hypotensive): Immediate synchronized cardioversion (0.5–1 J/kg, up to 2 J/kg) or defibrillation if pulseless.
• Hemodynamically stable: IV Amiodarone (5 mg/kg over 20–60 min), IV Lidocaine (1 mg/kg bolus), or IV Procainamide.

• Prolonged QT interval (congenital Long QT syndromes: Jervell-Lange-Nielsen, Romano-Ward)
• Electrolyte disturbances: Hypokalemia, Hypomagnesemia, Hypocalcemia
• Drugs: Macrolides, fluoroquinolones, ondansetron, antiarrhythmics (Class Ia, III), psychotropics.

• IV Magnesium sulphate (25–50 mg/kg IV over 10–15 min).
• If unstable: Immediate defibrillation/cardioversion.
• Overdrive pacing / Isoproterenol infusion.

• Wide QRS complex (>0.12 s in older children / >0.09 s in infants).
• "M" shaped rsR' / rSR' pattern in right precordial leads (V1, V2, V3R).
• Wide slurred S wave in lateral leads (I, aVL, V5, V6).

• Wide QRS complex (>0.12 s).
• "M" shaped broad notched R wave in lateral leads (V5, V6, lead I, aVL).
• "W" shaped QS / rS pattern in lead V1.

• Vagal maneuver: Ice bag / ice-cold water bag applied to forehead and mid-face for 10–15 seconds (without occluding airway). Max 2 attempts.

• Adenosine: Initial dose 0.1 mg/kg (0.4 mg for 4 kg baby; max first dose 6 mg for adult/70 kg), followed by 0.2 mg/kg if needed.
• Precautions: Rapid IV push via a large proximal vein (antecubital/central) followed immediately by rapid normal saline flush (5–10 mL); continuous ECG monitoring.

• A: Atrial Fibrillation (irregularly irregular baseline, absent P waves)
• B: Ventricular Fibrillation (chaotic, disorganized waveforms)
• C: Ventricular Tachycardia (wide regular monomorphic complexes)
• D: Atrial Flutter (regular "sawtooth" flutter waves / F waves)

• Multifocal / multiform PVCs
• Runs of consecutive PVCs (couplets, triplets, non-sustained VT)
• PVCs that increase with exercise / exertion
• Presence of underlying structural heart disease or LV dysfunction
• "R-on-T" phenomenon

• Deep, wide Q waves in lateral leads (I, aVL, V5, V6)
• ST segment elevation / depression and T wave inversion in anterolateral leads
• Signs of anterolateral myocardial ischemia / infarction and left ventricular hypertrophy

• Diagnosis: Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA / Bland-White-Garland syndrome).
• Differential Diagnosis: Dilated cardiomyopathy (DCM), acute viral myocarditis, severe infantile colic / intussusception (due to episodic irritability/crying during angina).

• Deep and wide Q waves in leads I, aVL, V5, V6
• ST-segment elevation or depression in leads I, aVL, V5, V6
• Inverted T waves in anterolateral leads (I, aVL, V5-V6)
• Diminished R wave progression or left ventricular hypertrophy / strain pattern

• Medical: Anti-failure therapy (diuretics, ACE inhibitors, inotropic support) and afterload reduction.
• Surgical (Definitive): Direct coronary reimplantation into the aorta (preferred) or Takeuchi procedure (intrapulmonary baffle) / ligation of ALCAPA.

• A: Normal acid-base status.
• B: High Anion Gap Metabolic Acidosis (HAGMA) with expected respiratory compensation (Winter's formula: 1.5×14 + 8 = 29 ± 2). Delta ratio ~0.8–1.0 represents pure high AG metabolic acidosis.
• C: Mixed High Anion Gap Metabolic Acidosis + Metabolic Alkalosis (Delta ratio 3.5 > 2.0 indicates concurrent metabolic alkalosis elevating HCO₃⁻).
• D: Mixed High Anion Gap Metabolic Acidosis + Normal Anion Gap Metabolic Acidosis (Delta ratio 0.55 < 0.8 indicates additional non-AG metabolic acidosis).

• Measured AG = Na - (Cl + HCO₃) = 131 - (104 + 19) = 8 mEq/L
• Expected Normal AG = 12 - 2.5 × (4.0 - Albumin) = 12 - 2.5 × (4.0 - 2.0) = 7 mEq/L.
• Measured AG (8) equals the expected corrected AG, so this is a Normal Anion Gap (Hyperchloremic) Metabolic Acidosis (NAGMA).

• ΔAG = 8 - 8 = 0
• ΔHCO₃⁻ = 24 - 19 = 5
• Delta ratio = 0 (Confirms pure NAGMA).

• $\text{UAG}=({\text{Urine Na}}^{+}+{\text{Urine K}}^{+})-{\text{Urine Cl}}^{-}=(146+27.6)-146=+27.6\text{ mEq/L}$ (Positive UAG indicates impaired urinary ammonium excretion).

• Immediately administer supplemental oxygen (increase FiO₂ via face mask / high-flow nasal cannula) to achieve PaO₂ > 80 mm Hg / SpO₂ 94–98%.
• Investigate underlying pulmonary etiology (e.g., CXR for pneumonia, atelectasis, pneumothorax, pulmonary edema).

• Stepwise reduce FiO₂ from 0.80 to 0.35–0.40 to target a safe PaO₂ of ~80–100 mm Hg and prevent oxygen toxicity.
• Slightly reduce minute ventilation to normalize pH and PaCO₂.

• Increase minute ventilation by increasing the Respiratory Rate (RR).
• Formula: ${\text{RR}}_{\text{new}}\times {\text{PaCO}}_{2\text{ new}}={\text{RR}}_{\text{current}}\times {\text{PaCO}}_{2\text{ current}}$
• ${\text{RR}}_{\text{new}}\times 40=12\times 60=720⟹{\text{RR}}_{\text{new}}=\frac{720}{40}=18\text{ breaths/min}$.
• Increase ventilator Respiratory Rate from 12 to 18 breaths/min (and slightly titrate down FiO₂ to 30–35%).

Alveolar-arterial oxygen gradient ($P_{(A-a)}{O}_2$) Calculation:

• Alveolar $PA{O}_2$:
  $PA{O}_2=Fi{O}_2\times (P_{\text{atm}}-P_{H_{2}O})-\frac{PaC{O}_2}{RQ}$
  $PA{O}_2=1.0\times (760-47)-\frac{50}{0.8}=713-62.5=650.5\text{ mm Hg}$
• $P_{(A-a)}{O}_2$ Gradient:
  $P_{(A-a)}{O}_2=PA{O}_2-Pa{O}_2=650.5-50=600.5\text{ mm Hg}$

Indications for ECMO:

• Oxygenation Index (OI) > 40 on 100% oxygen for > 2–4 hours, or OI > 25 for > 12–24 hours.
• $P_{(A-a)}{O}_2>600\text{--}620\text{ mm Hg}$ for > 8–12 hours (>80% predicted mortality without ECMO).
• Intractable severe hypoxemia / acidosis unresponsive to maximal medical therapy (inhaled nitric oxide, HFOV, surfactant, inotropic support).
• Acute reversible respiratory/cardiac failure in gestational age ≥ 34 weeks and birth weight ≥ 2.0 kg without major intracranial hemorrhage (Grade III/IV) or lethal chromosomal anomalies.

• Severe uncompensated / partially compensated Metabolic Acidosis with marked acidemia (pH 6.64, HCO₃⁻ 5 mEq/L, compensatory hyperventilation with PaCO₂ 25.8 mm Hg).
• Hyperoxia (PaO₂ 396.4 mm Hg).

• Inborn errors of metabolism (organic acidemias, maple syrup urine disease, methylmalonic acidemia)
• Lactic acidosis (sepsis, mitochondrial disorders, severe tissue hypoxia)
• Diabetic ketoacidosis (DKA)
• Renal failure / Uremia
• Toxic ingestions (salicylates, methanol, ethylene glycol)

• Hypoalbuminemia (most common)
• Severe hypercalcemia, hypermagnesemia
• Lithium toxicity
• Multiple myeloma (monoclonal IgG paraproteinemia)
• Severe bromide / iodide ingestion

• Formula: $PA{O}_2=Fi{O}_2\times (760-47)-\frac{PaC{O}_2}{0.8}=(0.50\times 713)-\frac{25}{0.8}=356.5-31.25=325.25\text{ mm Hg}$
• $AaD{O}_2=PA{O}_2-Pa{O}_2=325.25-160=165.25\text{ mm Hg}$.

• a. Diagnosis: Fully compensated Chronic Respiratory Acidosis (pH normal 7.38, elevated PaCO₂ 65 mm Hg with compensatory renal retention of HCO₃⁻ 34 mEq/L) with severe hypoxemia / V-Q mismatch (PaO₂ 48 mm Hg on 60% oxygen).
• b. Expected PaO₂ on room air: 80–100 mm Hg.

• Formula: $Ca{O}_2=(\text{Hb}\times 1.34\times \frac{{\text{SpO}}_2}{100})+(0.0031\times {\text{PaO}}_2)$
• $Ca{O}_2=(8.2\times 1.34\times 0.99)+(0.0031\times 120)=10.88+0.37=11.25\text{ mL }{O}_2/\text{dL}$ of blood.