Pediatric Anesthesia
Neonatal physiology, congenital syndromes, peds pharmacology, airway management, NRP, congenital cardiac. ← All topics
Q1. Pediatric airway anatomy
Compared to adults, the pediatric airway:
A. Has its narrowest point at the vocal cords, with the larynx positioned at C4–C5 similar to adults
B. Has its narrowest functional point at the cricoid ring, with the larynx more cephalad at C3–C4 and omega-shaped epiglottis
C. Has identical anatomic landmarks to adults, with the cricoid ring at the same cervical level and similar epiglottic shape
D. Has a thicker and more rigid epiglottis, with the larynx positioned more caudally at C5–C6 compared to adults
E. Has a wider trachea relative to body size, with the narrowest point at the vocal cords like in adults
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Answer: B. The pediatric airway differs significantly from the adult airway. The narrowest functional point is at the cricoid ring (subglottic region), though the anatomic narrowest point remains at the vocal cords. The larynx is positioned more cephalad at C3–C4 in children compared to C4–C5 in adults. The epiglottis is omega-shaped and floppy rather than flat. The vocal cords are angled with the anterior portion more caudad. Children also have a relatively large tongue and prominent occiput, necessitating a shoulder roll to achieve optimal sniffing position. A Miller (straight) blade is preferred in infants because it can directly lift the floppy epiglottis to visualize the vocal cords.
Q2. ETT size formula
For a 6-year-old, the appropriate uncuffed ETT size is approximately:
A. 4.0
B. 5.0
C. 5.5
D. 6.0
E. 6.5
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Answer: C. For uncuffed endotracheal tubes in pediatric patients, the appropriate size is calculated using the formula: age/4 + 4. For a 6-year-old child, this yields 6/4 + 4 = 1.5 + 4 = 5.5 mm internal diameter. For cuffed tubes, the formula is age/4 + 3.5 (or simply use a tube 0.5 mm smaller than the uncuffed size), which would be 5.0 mm for this patient. Modern microcuff endotracheal tubes are now considered acceptable from infancy onward. After placement, an audible air leak should be confirmed at less than 25 cm H₂O pressure to avoid excessive tracheal mucosal pressure and potential complications such as post-extubation stridor or subglottic stenosis.
Q3. Neonatal physiology — oxygen consumption
Neonatal oxygen consumption is approximately:
A. 2–3 mL/kg/min (similar to adult values)
B. 6–8 mL/kg/min (approximately double adult values)
C. 15 mL/kg/min (approximately quadruple adult values)
D. 0.5 mL/kg/min (approximately one-sixth adult values)
E. Cannot be measured reliably in neonates
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Answer: B. Neonatal oxygen consumption is approximately 6–8 mL/kg/min, which is roughly double the adult value of 3–4 mL/kg/min. This elevated metabolic rate, combined with a smaller functional residual capacity (FRC) of approximately 30 mL/kg (similar to adults on a per-kilogram basis but much smaller in absolute terms), leads to rapid oxygen desaturation during apnea. This makes adequate preoxygenation crucial before induction of anesthesia in neonates and infants. Additionally, closing capacity exceeds FRC in infants, predisposing them to early atelectasis and ventilation-perfusion mismatch under general anesthesia.
Q4. Fetal hemoglobin
HbF differs from HbA in that:
A. Right-shifted oxyhemoglobin dissociation curve with P50 approximately 35 mmHg
B. Left-shifted oxyhemoglobin dissociation curve with P50 approximately 19 mmHg
C. Higher affinity for 2,3-DPG resulting in P50 approximately 32 mmHg
D. Higher methemoglobin tendency with baseline MetHb levels above 3 percent
E. Identical oxygen-binding characteristics with P50 approximately 27 mmHg
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Answer: B. HbF contains γ-chains instead of β-chains and has low affinity for 2,3-DPG, resulting in a leftward shift of the oxyhemoglobin dissociation curve. This leftward shift reflects high oxygen affinity (P50 ~19 mmHg in fetus versus ~27 mmHg in adults) and facilitates efficient placental oxygen uptake and transfer from maternal to fetal circulation. By 6 months of age, HbF is replaced by HbA and the P50 normalizes to adult values. The hemoglobin nadir occurs at 8–12 weeks of life (~10–11 g/dL in term infants) and is a physiologic phenomenon.
Q5. Neonatal blood volume
Term neonate blood volume is approximately:
A. 50 mL/kg
B. 80 mL/kg
C. 100 mL/kg
D. 120 mL/kg
E. 200 mL/kg
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Answer: B. Term neonates have a blood volume of approximately 80–90 mL/kg. This is higher than older children and adults but lower than premature infants. Blood volume varies by age: premature neonates have approximately 90–105 mL/kg, infants aged 3–12 months have approximately 75 mL/kg, children have approximately 70 mL/kg, and adults have approximately 65–70 mL/kg for males and 60 mL/kg for females. Maximum allowable blood loss (MABL) can be calculated using the formula: blood volume × (initial hematocrit − target hematocrit) / initial hematocrit. Blood loss should be replaced with blood products at a 1:1 ratio or with crystalloid at a 3:1 ratio depending on the clinical situation and type of blood product used.
Q6. Pediatric maintenance fluid
For a 25 kg child, the Holliday-Segar maintenance fluid rate is:
A. 25 mL/hr
B. 65 mL/hr
C. 100 mL/hr
D. 150 mL/hr
E. 250 mL/hr
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Answer: B. The Holliday-Segar method uses the 4-2-1 rule to calculate maintenance fluid rates: 4 mL/kg/hr for the first 10 kg of body weight, plus 2 mL/kg/hr for the next 10 kg (11-20 kg), plus 1 mL/kg/hr for each kilogram above 20 kg. For a 25 kg child, the calculation is (4 × 10) + (2 × 10) + (1 × 5) = 40 + 20 + 5 = 65 mL/hr. Recent studies have shown that isotonic fluids are preferred over hypotonic fluids for maintenance therapy in hospitalized children due to the increased risk of hyponatremia with hypotonic solutions.
Q7. Neonatal resuscitation HR
Per NRP, chest compressions in newborn are initiated when:
A. Heart rate remains below 100 beats per minute despite tactile stimulation and repositioning
B. Heart rate remains below 60 beats per minute after 30 seconds of adequate positive pressure ventilation
C. Heart rate remains below 80 beats per minute despite 60 seconds of supplemental oxygen administration
D. Apnea persists after initial tactile stimulation and warming measures have been performed appropriately
E. Immediate absence of respiratory effort is noted within the first 30 seconds after delivery
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Answer: B. Per Neonatal Resuscitation Program (NRP) guidelines, chest compressions are initiated when the heart rate remains below 60 beats per minute after 30 seconds of adequate positive pressure ventilation with supplemental oxygen. Compressions are delivered at a 3:1 ratio (90 compressions to 30 breaths per minute). If the heart rate remains below 60 despite compressions and ventilation, epinephrine 10–30 mcg/kg IV is given every 3–5 minutes. Volume bolus of 10 mL/kg is indicated if shock or blood loss is suspected. Initial FiO₂ should be 21% for term infants or 21–30% for preterm infants, titrated to the SpO₂ target curve. Heart rate below 100 (choice A) prompts positive pressure ventilation, not compressions. Heart rate below 80 (choice C) is not a specific threshold in NRP guidelines. Apnea alone (choice D) is managed with stimulation and PPV, not immediate compressions.
Q8. Postoperative apnea risk
Postop apnea monitoring is recommended for premature infants up to a postconceptual age of:
A. 40 weeks postconceptual age
B. 60 weeks postconceptual age (46 weeks for term infants)
C. 6 months chronological age regardless of prematurity
D. 1 year chronological age for all infants
E. 36 weeks postconceptual age (monitoring not needed beyond)
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Answer: B. Premature infants less than 60 weeks postconceptual age require 12 to 24 hours of postoperative apnea monitoring. Some institutional policies recommend monitoring term infants up to 46 weeks postconceptual age, though this varies by institution. Caffeine 10 mg/kg IV is a preventive option. Spinal anesthesia without sedation reduces but does not eliminate apnea risk. Anemia with hematocrit less than 30% is an independent risk factor for postoperative apnea.
Q9. Pyloric stenosis
A 5-week-old male infant presents with projectile non-bilious vomiting, dehydration, and palpable epigastric mass. The classic electrolyte derangement is:
A. Hypochloremic, hypokalemic metabolic alkalosis with paradoxical aciduria
B. Hyperchloremic, hyperkalemic metabolic acidosis with compensatory respiratory alkalosis
C. Hypochloremic, hyponatremic metabolic acidosis with elevated anion gap
D. Hypernatremic, hypokalemic metabolic alkalosis with appropriate renal compensation
E. Normochloremic, hyperkalemic metabolic acidosis with paradoxical alkaluria
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Answer: A. Pyloric stenosis is a medical emergency requiring resuscitation before pyloromyotomy. The infant loses gastric hydrochloric acid through persistent vomiting, leading to metabolic alkalosis with hypochloremia. Volume depletion triggers secondary hyperaldosteronism, which causes renal potassium wasting and hypokalemia. As the kidneys attempt to retain sodium in the setting of volume depletion and aldosterone excess, they excrete hydrogen ions in exchange, leading to paradoxical aciduria despite systemic alkalosis. Correct identification and treatment of these fluid and electrolyte abnormalities must precede surgical intervention.
Q10. Tracheoesophageal fistula
The most common type of TEF is:
A. Type A — pure esophageal atresia without fistula
B. Type C — esophageal atresia with distal TEF
C. Type E — H-type isolated TEF without atresia
D. Type D — esophageal atresia with proximal and distal TEFs
E. Type B — esophageal atresia with proximal TEF
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Answer: B. Type C accounts for approximately 85% of all tracheoesophageal fistula cases, making it the most common type. It consists of esophageal atresia with a distal TEF. Workup includes VACTERL screening (vertebral, anal, cardiac with echocardiography, tracheoesophageal, renal, and limb anomalies). The primary anesthetic priority is to avoid gastric distention via the fistula. The endotracheal tube should be placed below the fistula, often with the surgeon performing rigid bronchoscopy to guide placement. Surgical repair is typically performed via right-sided thoracotomy unless a right aortic arch is present, in which case a left-sided approach is used.
Q11. Congenital diaphragmatic hernia ventilation
Anesthetic management of congenital diaphragmatic hernia includes:
A. Aggressive ventilation with high peak inspiratory pressures to recruit hypoplastic lung tissue and maximize oxygenation
B. Gentle ventilation with low tidal volumes, permissive hypercapnia up to 65 mmHg, and preductal SpO₂ 90–95%
C. High FiO₂ at 100% throughout the case to prevent hypoxemia and avoid pulmonary hypertensive crises
D. Aggressive volume resuscitation with crystalloid boluses to maintain cardiac output and systemic blood pressure targets
E. Mask ventilation as first-line airway management to avoid trauma from direct laryngoscopy and intubation attempts
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Answer: B. Congenital diaphragmatic hernia is characterized by pulmonary hypoplasia and pulmonary hypertension. The key principle is gentle ventilation to avoid volutrauma, which triggers inflammatory mediator release and worsens pulmonary hypertension. Permissive hypercapnia (PaCO₂ up to 65 mmHg) is accepted to avoid high airway pressures. Target preductal SpO₂ of 90–95% is appropriate. Additional management includes avoiding pulmonary hypertension triggers (acidosis, hypothermia, hypercarbia beyond permissive range, hypoxia), maintaining normothermia, and using inhaled nitric oxide for refractory pulmonary hypertension. Mask ventilation should be avoided because it causes gastric distention, which further compromises lung expansion and hemodynamics.
Q12. Tetralogy of Fallot — "tet spell"
A toddler with uncorrected TOF develops cyanosis, hyperventilation, lethargy during induction. Initial management:
A. 100% FiO₂, knee-chest position, IV fluids, phenylephrine to increase SVR, morphine for sedation, β-blocker if spasm persists
B. 100% FiO₂, Trendelenburg position, IV diuretics, ephedrine to increase cardiac output, midazolam for sedation, calcium channel blocker
C. 50% FiO₂, supine position, fluid restriction, nitroglycerin to decrease preload, ketamine for sedation, α-blocker for afterload reduction
D. 100% FiO₂, reverse Trendelenburg, IV fluids, dobutamine to augment contractility, fentanyl for sedation, nitroprusside for vasodilation
E. Room air, left lateral decubitus position, IV fluids, dopamine to increase renal perfusion, propofol for sedation, hydralazine for vasodilation
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Answer: A. A tet spell results from right ventricular outflow tract spasm, which increases the right-to-left shunt across the VSD and worsens cyanosis. Management aims to increase systemic vascular resistance (SVR) to reduce the shunt and decrease pulmonary vascular resistance (PVR). Knee-chest position and phenylephrine increase SVR, pushing more blood through the pulmonary outflow tract. 100% oxygen reduces PVR, and avoiding acidosis, hypercarbia, and sympathetic stimulation is critical. IV fluids increase right ventricular preload and filling. Morphine reduces sympathetic tone and calms the child. If infundibular spasm persists, a β-blocker such as esmolol or propranolol can relax the outflow tract. β-agonists, hyperventilation (causes hypocarbia and agitation), vasodilators (decrease SVR), and diuretics (decrease preload) all worsen the physiology of a tet spell.
Q13. Patent ductus arteriosus closure pharmacology
To maintain ductal patency in a duct-dependent congenital heart lesion, give:
A. Indomethacin infusion to inhibit cyclooxygenase and promote ductal closure
B. Alprostadil (PGE1) infusion to relax smooth muscle and maintain ductal patency
C. Ibuprofen infusion to inhibit prostaglandin synthesis and promote ductal closure
D. Furosemide infusion to reduce fluid overload and improve pulmonary edema
E. Acetaminophen infusion to inhibit peroxidase activity and promote ductal closure
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Answer: B. PGE1 (alprostadil) opens and maintains ductal patency in duct-dependent congenital heart lesions including hypoplastic left heart syndrome, pulmonary atresia, aortic atresia, critical coarctation of the aorta, and transposition of the great arteries. It works by relaxing ductal smooth muscle through prostaglandin-mediated vasodilation. Important side effects include apnea (requiring airway equipment at bedside), hypotension, fever, and flushing. In contrast, to close a patent ductus arteriosus in premature infants, cyclooxygenase inhibitors are used: indomethacin, ibuprofen, or acetaminophen. These agents work by blocking prostaglandin synthesis, promoting ductal constriction and closure.
Q14. Pediatric drug dosing — pharmacology
Neonatal codeine metabolism is affected by:
A. CYP2D6, which has low activity at birth and variable genetic polymorphisms
B. UGT2B7, which conjugates codeine directly without requiring demethylation
C. CYP3A4, which shows reduced hepatic expression in the neonatal period
D. Plasma esterases, which hydrolyze codeine similarly to other ester opioids
E. Renal excretion alone, as codeine undergoes minimal hepatic biotransformation
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Answer: A. Codeine is converted to morphine via CYP2D6. This enzyme has low activity at birth but demonstrates significant genetic polymorphism. Ultrarapid metabolizers can produce dangerously high morphine levels, leading to respiratory depression and death. The FDA issued a black-box warning contraindicating codeine in children under 12 years and after tonsillectomy/adenoidectomy. Breastfeeding mothers who are ultrarapid metabolizers have caused infant deaths through breast milk transmission of excess morphine. Codeine should be avoided in pediatrics. UGT2B7 is relevant for morphine glucuronidation, not codeine metabolism. CYP3A4 does metabolize some codeine to norcodeine but is not the primary pathway. Codeine is not an ester and does not rely on plasma esterases. Codeine requires hepatic metabolism to exert analgesic effects.
Q15. Pediatric MAC
Compared to adults, pediatric MAC for sevoflurane is:
A. Highest in neonates, peaks at 1–6 months, then declines through childhood
B. Highest in adults, progressively lower in younger age groups
C. Identical at all ages, approximately 2% in all populations
D. Lowest in toddlers, higher in infants and school-age children
E. Independent of age, determined only by individual patient factors
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Answer: A. MAC for sevoflurane is highest in infants aged 1–6 months at approximately 3.2%, then declines progressively through childhood to reach adult values of approximately 2%. Premature infants have lower MAC than term neonates. The increased cardiac output and decreased functional residual capacity in pediatric patients lead to faster anesthetic equilibration and emergence compared to adults. Sevoflurane is the preferred agent for inhalation induction in children because it is non-pungent and has bronchodilator properties.
Q16. Postintubation croup
A 3-year-old develops stridor after extubation following an 8 hr case. The most appropriate management is:
A. Reintubation immediately without prior medical management
B. Humidified oxygen, racemic epinephrine nebulizer, and IV dexamethasone 0.5 mg/kg
C. Steroid bolus only without additional respiratory support
D. Continue observation only without any medical intervention
E. Ipratropium nebulizer with humidified oxygen and observation
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Answer: B. Postintubation croup is best managed with humidified oxygen, racemic epinephrine nebulizer, and IV dexamethasone 0.5 mg/kg. Racemic epinephrine causes vasoconstriction of subglottic edema, providing rapid relief. Dexamethasone reduces inflammation and prevents recurrence. Close monitoring is essential because rebound stridor can occur approximately 2 hours after racemic epinephrine administration. Risk factors for postintubation croup include prolonged intubation, oversized endotracheal tube, traumatic intubation, and age 1-4 years. Immediate reintubation is reserved for severe respiratory distress or failure of medical management. Observation alone or single-agent therapy is insufficient for symptomatic postintubation croup.
Q17. Necrotizing enterocolitis
A premature infant with feeding intolerance, abdominal distention, bloody stools, and pneumatosis intestinalis on imaging is diagnosed with NEC. Most appropriate initial management:
A. Stop feedings, IV fluids, broad-spectrum antibiotics, NG decompression, surgical consult
B. Continue current feedings, add probiotics, IV fluids, monitor vital signs, serial exams
C. Immediate exploratory laparotomy, bowel resection, ostomy creation, postoperative broad-spectrum antibiotics
D. Oral antibiotics, continue trophic feeds, probiotics, serial abdominal exams, outpatient follow-up
E. NG decompression, probiotics alone, continue feedings at reduced volume, observe for improvement
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Answer: A. The initial management of NEC is medical: make the patient NPO, provide IV fluids for resuscitation and maintenance, initiate broad-spectrum antibiotics (typically ampicillin, gentamicin, and clindamycin or metronidazole), place an NG tube for gastric decompression, and obtain a surgical consult for monitoring. Surgery is indicated for perforation (pneumoperitoneum on imaging), bowel necrosis, abdominal mass with obstruction, or clinical deterioration despite maximal medical therapy. Continuing feedings would worsen bowel ischemia. Immediate laparotomy is not indicated unless there is evidence of perforation or necrosis. Oral antibiotics are inadequate for systemic infection and ileus. Probiotics have a role in prevention but not in acute treatment. Risk factors for NEC include prematurity, formula feeding, and intestinal dysbiosis.
Q18. Foreign body aspiration
A toddler with sudden cough, wheeze, decreased breath sounds on the right side is suspected of foreign body aspiration. The anesthetic plan is:
A. Awake intubation with topical anesthesia and minimal sedation to preserve airway reflexes
B. Inhalation induction with sevoflurane maintaining spontaneous ventilation followed by rigid bronchoscopy
C. Rapid sequence induction with propofol and rocuronium followed by endotracheal intubation
D. Mask sedation only with spontaneous ventilation without instrumentation of the airway
E. Volatile anesthetic induction with neuromuscular blockade and controlled positive pressure ventilation
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Answer: B. The key principle in foreign body aspiration is to maintain spontaneous ventilation until the foreign body is removed, as positive pressure ventilation can drive the object distally into smaller airways. Inhalation induction with sevoflurane allows gradual deepening of anesthesia while preserving spontaneous breathing. Once adequate depth is achieved, rigid bronchoscopy (typically performed by ENT) allows visualization and removal of the foreign body. Awake intubation is not appropriate in toddlers due to lack of cooperation. Rapid sequence induction with neuromuscular blockade eliminates spontaneous ventilation and requires positive pressure, risking distal migration of the foreign body. Mask sedation alone does not provide adequate conditions for bronchoscopy. Postoperative complications including laryngospasm and bronchospasm are common and should be anticipated.
Q19. Cardiac defect — coarctation BP measurement
A child with coarctation of the aorta has:
A. Upper extremity hypertension with weak and delayed lower extremity pulses
B. Systemic hypotension affecting all four extremities equally throughout the cardiac cycle
C. Equal blood pressures in all extremities with normal pulse timing
D. Lower extremity hypertension with weak and delayed upper extremity pulses
E. Variable pressures in all extremities associated with underlying cardiac arrhythmia
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Answer: A. Coarctation of the aorta is a stenosis typically located distal to the left subclavian artery. This anatomic narrowing creates a significant blood pressure gradient between the upper and lower extremities. The upper extremities demonstrate hypertension because they receive blood proximal to the obstruction, while the lower extremities have weak, delayed femoral pulses and lower blood pressures due to reduced flow distal to the coarctation. Repair is usually performed electively in childhood. Anesthetic considerations include monitoring blood pressure in the arms (not legs), anticipating cross-clamp hypertension during repair and rebound hypotension after clamp release, and preserving spinal cord perfusion by maintaining adequate collateral flow through the artery of Adamkiewicz.
Q20. Emergence delirium in children
The most evidence-based prophylaxis for emergence delirium after sevoflurane in a 5-year-old is:
A. Dexmedetomidine 0.15 mcg/kg IV before emergence
B. Diphenhydramine 0.5 mg/kg IV before emergence
C. Ondansetron 0.1 mg/kg IV before emergence
D. Naloxone 0.01 mg/kg IV before emergence
E. Atropine 0.02 mg/kg IV before emergence
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Answer: A. Dexmedetomidine 0.15 mcg/kg IV given before emergence has the strongest evidence for preventing emergence delirium in children. Sevoflurane causes emergence delirium more frequently than desflurane, which in turn causes it more than other volatile agents. Other evidence-based prophylactic options include clonidine, fentanyl, propofol bolus before emergence, and ketamine. Diphenhydramine (an antihistamine), ondansetron (an antiemetic), naloxone (an opioid antagonist), and atropine (an anticholinergic) lack evidence for emergence delirium prophylaxis. Always address contributing factors such as pain, hypoxia, and full bladder. Emergence delirium is typically self-limited, resolving within 10 to 30 minutes.
Q21. Crouzon syndrome
Anesthetic considerations in Crouzon syndrome include:
A. Mandibular hypoplasia with glossoptosis causing difficult mask ventilation and difficult intubation similar to Pierre Robin sequence
B. Craniosynostosis with maxillary hypoplasia causing upper airway obstruction and difficult mask ventilation but intubation usually manageable if cervical mobility preserved
C. Normal craniofacial anatomy with preserved airway patency allowing routine mask ventilation and direct laryngoscopy without anticipated difficulty
D. Isolated macroglossia without other craniofacial abnormalities causing mild airway obstruction but generally allowing successful mask ventilation and intubation
E. Atlantoaxial instability with cervical spine abnormalities mandating awake fiberoptic intubation and strict avoidance of neck manipulation during airway management
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Answer: B. Crouzon syndrome is characterized by craniosynostosis with midface hypoplasia. Key features include shallow orbits with proptosis, maxillary hypoplasia, and beaked nose appearance. The airway management challenge is primarily difficult mask ventilation due to the midface abnormalities and upper airway obstruction, but direct laryngoscopy and intubation are usually manageable if cervical spine mobility is preserved. This contrasts with Pierre Robin sequence (micrognathia, glossoptosis, cleft palate causing both difficult mask ventilation AND difficult intubation, where LMA is useful), Treacher Collins syndrome (mandibular hypoplasia with similar challenges to Pierre Robin), and Goldenhar syndrome (unilateral facial asymmetry where LMA is also useful). Crouzon syndrome does not typically involve mandibular hypoplasia, isolated macroglossia, or atlantoaxial instability.
Q22. Down syndrome (Trisomy 21)
Anesthetic considerations in Down syndrome include:
A. Atlantoaxial instability, congenital heart disease, subglottic stenosis, obstructive sleep apnea, hypothyroidism, and increased sensitivity to atropine
B. Cervical spine hypermobility, pulmonary hypertension, tracheal stenosis, central sleep apnea, hyperthyroidism, and increased sensitivity to succinylcholine
C. Occipitocervical fusion, acquired valvular disease, laryngeal stenosis, periodic breathing, hyperparathyroidism, and increased sensitivity to benzodiazepines
D. Basilar invagination, systemic hypertension, glottic webs, hypoventilation syndrome, adrenal insufficiency, and increased sensitivity to volatile anesthetics
E. Craniocervical instability, coronary artery disease, supraglottic stenosis, restrictive lung disease, diabetes mellitus, and increased sensitivity to opioids
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Answer: A. Down syndrome patients require multiple anesthetic considerations. Atlantoaxial instability occurs in approximately 15% of patients; avoid neck extension and screen with C-spine films per current guidelines or proceed cautiously. Congenital heart disease is present in approximately 50% of patients, with atrioventricular septal defects and ventricular septal defects being most common. Subglottic stenosis is common and necessitates use of a smaller endotracheal tube than predicted by age. Obstructive sleep apnea is frequent due to midface hypoplasia and macroglossia. Hypothyroidism is common and should be screened preoperatively. Patients demonstrate increased sensitivity to atropine, which should be used cautiously. The other options list conditions that are not characteristic associations with Down syndrome.
Q23. Pediatric defibrillation dose
Pediatric defibrillation initial dose:
A. 0.5 J/kg initial, 1 J/kg subsequent
B. 1 J/kg initial, 2 J/kg subsequent
C. 2 J/kg initial, 4 J/kg subsequent
D. 4 J/kg initial, 6 J/kg subsequent
E. 5 J/kg initial, 10 J/kg subsequent
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Answer: C. Per PALS guidelines, pediatric defibrillation dosing is 2 J/kg for the initial shock and 4 J/kg for subsequent shocks, with a maximum of 10 J/kg or the adult maximum dose. This differs from synchronized cardioversion, which uses lower energy: 0.5–1 J/kg initially and 2 J/kg for subsequent attempts. An automated external defibrillator (AED) may be used in children older than 1 year if pediatric pads are unavailable, though pediatric attenuator pads are preferred when available.
Q24. Sickle cell perioperative
A child with sickle cell disease undergoing tonsillectomy. Perioperative priorities:
A. Avoid hypoxia, hypothermia, dehydration, and acidosis; consider preoperative simple transfusion to hemoglobin 10 g/dL for moderate-risk surgery
B. Maintain hyperventilation to decrease PaCO2 below 25 mmHg; restrict fluid administration to prevent pulmonary edema and vaso-occlusive crisis
C. Apply tourniquet with pressures above systolic to minimize blood loss; maintain normothermia and avoid supplemental oxygen to prevent rebound sickling
D. Extend NPO status to 12 hours for solids and liquids; avoid preoperative transfusion to prevent hyperviscosity and increased sickling risk
E. Minimize all intravenous fluid administration to prevent hemodilution and decreased oxygen-carrying capacity; allow mild hypothermia for neuroprotection during surgery
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Answer: A. Perioperative management of sickle cell disease focuses on preventing the 6 H's of sickling: hypoxia, hyperthermia, hypothermia, hypotension, hypovolemia, and H⁺ (acidosis). The TAPS trial demonstrated that simple transfusion to hemoglobin 10 g/dL is noninferior to exchange transfusion for low-to-medium risk surgeries like tonsillectomy. Target hemoglobin S percentage should be 30–40% (lower than the 21–30% seen in healthy sickle cell patients at baseline). Hematology consultation is recommended for high-risk procedures. Hyperventilation causes respiratory alkalosis and vasoconstriction, which can precipitate sickling. Tourniquets create ischemia and acidosis, promoting sickling. Prolonged NPO times risk dehydration. Adequate IV hydration is essential to prevent hypovolemia and vaso-occlusive crises.
Q25. Pediatric pharmacology — total body water
Compared to adults, neonates have:
A. Lower total body water (~50%) and proportionally higher fat content than adults
B. Higher total body water (~75–80%) and larger volume of distribution for hydrophilic drugs
C. Identical body composition with equivalent distribution volumes for all drug classes
D. Higher fat content (~40%) and larger volume of distribution for lipophilic drugs
E. Lower protein binding capacity but unchanged total body water compared to adults
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Answer: B. Neonates have higher total body water (~75–80% vs ~60% in adults) and increased extracellular fluid, along with decreased fat, decreased muscle mass, and decreased albumin levels. This results in a larger volume of distribution for hydrophilic drugs such as succinylcholine, antibiotics, and digoxin, requiring larger weight-based loading doses. The decreased protein binding also means more free drug is available for highly protein-bound medications like phenytoin, barbiturates, and bupivacaine. Hepatic enzyme systems mature over the first 1–2 years of life. Renal function is approximately 30% of adult capacity at birth and matures by 1 year of age.