Pediatric and Neonatal Anesthesia Flashcards

A 28-week preterm neonate (1.1 kg) requires emergency laparotomy for necrotizing enterocolitis. Intraoperatively, you notice persistent metabolic acidosis despite adequate ventilation. Which of the following is the MOST likely cause in this specific scenario?

Answer: Hypothermia-induced impaired lactate clearance

Premature neonates have extremely limited capacity for thermogenesis and virtually no brown adipose tissue reserves at 28 weeks. The open abdominal cavity during laparotomy, combined with wet surgical drapes, cold irrigation fluids, and a large surface-area-to-volume ratio leads to rapid hypothermia. Hypothermia impairs hepatic lactate clearance (the liver is the primary lactate consumer), reduces cardiac output, and shifts the oxyhemoglobin dissociation curve leftward — all compounding a persistent metabolic acidosis that will not respond to bicarbonate without addressing the temperature deficit. While the other options are plausible, hypothermia is the most immediate and correctable cause uniquely amplified in this gestational age and surgical context.

During awake fiberoptic intubation preparation for a 4-year-old with Pierre Robin sequence, the child becomes increasingly agitated and desaturates to 78% despite 15 L/min oxygen via facemask. The most appropriate immediate maneuver BEFORE any pharmacological intervention is:

Answer: Lateral decubitus positioning with jaw thrust

In Pierre Robin sequence, the glossoptosis (posterior displacement of the tongue) is the primary mechanism of obstruction. The lateral decubitus (or prone) position uses gravity to displace the tongue anteriorly, relieving the obstruction — this is the safest first-line maneuver before any instrumentation or drug administration. Prone positioning is classically recommended for neonates with PRS; in an older, agitated child, lateral decubitus with simultaneous jaw thrust is the most feasible combination. Inserting a nasopharyngeal airway (option B) requires a cooperative child and risks bleeding from adenoidal tissue. Immediate supraglottic airway insertion (option C) risks complete airway loss if placement fails, and should not be the first step before positional maneuvers.

A term neonate undergoing repair of a large omphalocele suddenly develops oxygen saturations of 72% in the right hand and 89% in the left foot immediately after abdominal closure. Ventilation parameters are unchanged. What is the MOST likely mechanism?

Answer: Re-opening of the ductus arteriosus with right-to-left shunting at ductal level

The key to this question is the differential cyanosis pattern: low pre-ductal saturation (right hand) with higher post-ductal saturation (left foot) is the hallmark of ductal-level right-to-left shunting — i.e., deoxygenated blood enters the aorta distal to the ductus. Abdominal closure sharply increases intra-abdominal and intrathoracic pressure, triggering a surge in pulmonary vascular resistance (PVR). In neonates, the ductus arteriosus can re-open (or fail to close) in response to hypoxia and elevated PVR, resulting in right-to-left ductal shunting. The pre-ductal right hand receives oxygenated blood from the left ventricle directly, while the post-ductal left foot receives mixed (desaturated) blood via the ductus. This is a critical distinction: the right hand should be MORE saturated than the foot in ductal right-to-left shunting — the question reversal makes option A the correct interpretation.

You are managing a 3-month-old (5.2 kg) undergoing elective pyloromyotomy for hypertrophic pyloric stenosis. After a rapid-sequence induction, endotracheal intubation is confirmed, and you note the following ABG: pH 7.51, PaCO2 38 mmHg, HCO3 30 mEq/L, Na 138, Cl 88, K 2.9. Your MOST appropriate initial ventilatory strategy is:

Answer: Maintain normoventilation and rely on renal correction of the alkalosis postoperatively

Hypertrophic pyloric stenosis causes a hypochloremic, hypokalemic metabolic alkalosis from vomiting of gastric HCl. The ABG confirms a primary metabolic alkalosis with appropriate respiratory compensation (PaCO2 38 is appropriate — the lung will not over-ventilate to correct a metabolic alkalosis beyond a certain point). Crucially, this alkalosis should NOT be corrected by deliberate hypercapnia intraoperatively. The correct preoperative management is fluid resuscitation with normal saline to restore chloride and correct hypokalemia BEFORE surgery. If the child has been adequately resuscitated (as implied by this elective setting), the residual mild alkalosis will self-correct postoperatively through renal bicarbonate excretion once chloride is repleted. Inducing hypercapnia (options C and D) risks cardiovascular depression and neonatal acidosis. The kidneys — not the ventilator — are the appropriate organ to correct this disorder.

A 6-year-old (22 kg) with a known G6PD deficiency is scheduled for tonsillectomy and adenoidectomy. Which of the following anesthetic agents carries the greatest risk of precipitating a hemolytic crisis in this patient?

Answer: Propofol infusion at 200 mcg/kg/min for TIVA

G6PD deficiency impairs the hexose monophosphate shunt, reducing NADPH availability and the cell's capacity to regenerate glutathione — leaving erythrocytes vulnerable to oxidative stress. Propofol (2,6-diisopropylphenol) is a known oxidative stressor to red blood cells; at infusion rates used for TIVA (particularly prolonged or high-dose), it can generate sufficient oxidative load to precipitate hemolysis in G6PD-deficient patients. Case reports of hemolytic anemia following propofol TIVA in G6PD-deficient patients exist in the literature. Nitrous oxide does not cause direct oxidative hemolysis (its risk in G6PD is not established). Ranitidine at clinical doses has not been shown to cause hemolysis. Acetaminophen in standard dosing is generally considered safe in G6PD deficiency, though historically questioned — current evidence supports its use at therapeutic doses. Of the listed options, high-dose propofol infusion presents the most clinically relevant oxidative threat.

During emergence from halogenated anesthetic-based general anesthesia for a 9-year-old undergoing appendectomy, the patient develops a temperature of 39.8°C, masseter rigidity on jaw opening, and a mixed respiratory and metabolic acidosis. CK is pending. You administer dantrolene 2.5 mg/kg IV. Which of the following is the MOST important concurrent intervention to prevent acute renal failure in the next 30 minutes?

Answer: High-volume isotonic crystalloid infusion targeting urine output >1 mL/kg/hr

In malignant hyperthermia (MH), massive rhabdomyolysis releases myoglobin, which precipitates in renal tubules — particularly in an acidic, concentrated urine. The most critical renal protection strategy is aggressive isotonic crystalloid resuscitation (Lactated Ringer's or normal saline) targeting a urine output of at least 1 mL/kg/hr (ideally 2–3 mL/kg/hr) to dilute myoglobin and flush it through the tubules. While urinary alkalinization (option A) is often discussed, it is NOT the primary or mandatory intervention in MH protocols — the MHAUS guidelines emphasize urine output via volume first. Calcium gluconate (option C) is contraindicated in MH as calcium is the intracellular trigger for the hypermetabolic crisis — giving calcium worsens the condition. Inserting a catheter (option D) is useful for monitoring but not itself a protective intervention. The Ringer's lactate infusion is the first-line renal protection concurrent with dantrolene.