Neonatal pharmacology, dose, interval, level

A former 26-week infant, now 36 weeks PMA in the NICU, has frequent regurgitation without apnea, desaturation or poor growth, and the team decides against metoclopramide. The main safety concern with this drug in infants is

1. Hepatotoxicity
   Liver injury is not the recognized risk of metoclopramide; the concern is its central dopamine blockade.
2. Pyloric stenosis
   Pyloric stenosis is linked to erythromycin or azithromycin in the first weeks of life, not to metoclopramide.
3. Extrapyramidal reactions
   Metoclopramide blocks dopamine receptors and carries a boxed warning for tardive dyskinesia; infants are prone to dystonia and other extrapyramidal effects, with little proof of benefit for reflux.

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A 5-day-old develops abdominal distension, ashen-gray color and cardiovascular collapse after starting an antibiotic. The most likely drug is

1. erythromycin
   Erythromycin in early infancy is linked to hypertrophic pyloric stenosis, which causes vomiting days to weeks later rather than collapse.
2. chloramphenicol
   Immature glucuronidation lets chloramphenicol accumulate, producing gray baby syndrome with distension, ashen color and circulatory collapse.
3. ceftriaxone
   Ceftriaxone's neonatal dangers are bilirubin displacement and precipitation with IV calcium, not a gray, collapsing infant.

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Erythromycin improves feeding intolerance in preterm infants by

1. inhibiting gastric acid secretion
   Acid suppression does not improve motility, and in preterm infants it raises the risk of NEC and infection.
2. stimulating 5-HT4 receptors
   5-HT4 agonism is how cisapride works, a different prokinetic withdrawn largely because of QT prolongation.
3. stimulating motilin receptors
   Erythromycin is a motilin receptor agonist that strengthens antral contractions and speeds gastric emptying, even at low doses.

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Early high-dose postnatal dexamethasone to prevent bronchopulmonary dysplasia is most strongly associated with which long-term adverse effect?

1. Cerebral palsy
   Early high-dose dexamethasone reduces BPD but increases cerebral palsy and neurodevelopmental impairment, which is why its use is now restricted.
2. Sensorineural hearing loss
   Hearing loss in preterm infants is tied to aminoglycosides, loop diuretics and hyperbilirubinemia, not to postnatal dexamethasone.
3. Necrotizing enterocolitis
   The gastrointestinal risk of early steroids is spontaneous intestinal perforation, especially with indomethacin, rather than NEC.

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An infant received a continuous fentanyl infusion for 12 days after surgery and is now extubated. The best strategy to prevent iatrogenic withdrawal is to

1. taper using enteral methadone
   After more than about 5 days of continuous opioid, the infant is dependent, so the daily dose is converted to enteral methadone and weaned gradually.
2. replace it with phenobarbital alone
   Phenobarbital sedates and may help as an adjunct, but alone it does not replace the opioid the infant depends on.
3. give naloxone to reverse tolerance
   Naloxone in an opioid-dependent infant precipitates acute withdrawal and can trigger seizures.

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A neonate on ECMO needs steadily increasing fentanyl doses to stay sedated. The main reason is

1. circuit drug sequestration
   Lipophilic, protein-bound drugs such as fentanyl adsorb to the oxygenator and tubing, and the circuit also enlarges the volume of distribution, so doses must rise.
2. rapid renal elimination
   Renal clearance is often reduced on ECMO, and fentanyl is cleared mainly by the liver.
3. decreased protein binding
   Lower protein binding would raise the free fraction and strengthen the effect, not create a growing dose requirement.

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GABA-agonist anticonvulsants are often less effective in neonates than in older children because, in immature neurons,

1. GABA receptors are absent
   GABA-A receptors are present early in development; the difference lies in the chloride gradient, not in missing receptors.
2. GABA depolarizes the cell
   Immature neurons hold high intracellular chloride (more NKCC1 than KCC2), so opening GABA-A channels lets chloride out and can excite rather than inhibit.
3. sodium channels are immature
   Sodium channel maturity affects drugs such as phenytoin, but it does not explain why GABA-enhancing drugs work less well.

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The main reason chlorothiazide is chosen over furosemide for long-term diuresis in bronchopulmonary dysplasia is that chlorothiazide

1. reduces urinary calcium loss
   Thiazides lower urinary calcium excretion, whereas long-term furosemide causes hypercalciuria, nephrocalcinosis and bone demineralization.
2. improves lung compliance more
   Any short-term gain in lung mechanics is similar with both diuretics; compliance is not why thiazides are preferred for long-term use.
3. has a longer duration of action
   Duration of action is a minor difference; the clinical reason for the switch is calcium handling.

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The standard ibuprofen lysine regimen for closing a PDA is

1. 10, 10, 10 mg/kg q12h
   Repeating the loading dose every 12 hours roughly triples the exposure and adds renal and bleeding risk.
2. 15 mg/kg q6h for 3 days
   Fifteen milligrams per kilogram every 6 hours is the acetaminophen regimen used when NSAIDs are contraindicated.
3. 10, 5, 5 mg/kg q24h
   Ibuprofen lysine is given as a 10 mg/kg loading dose followed by two 5 mg/kg doses 24 hours apart.

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A 2-week-old with symptomatic congenital CMV (microcephaly, hearing loss) is started on antiviral therapy. The recommended regimen is

1. IV acyclovir for 21 days
   A 21-day IV acyclovir course treats HSV CNS disease; acyclovir is not active enough against CMV.
2. CMV immune globulin alone
   CMV immune globulin has been studied in pregnancy but is not an established treatment for an infected newborn.
3. valganciclovir for 6 months
   For moderate-to-severe symptomatic congenital CMV, 6 months of oral valganciclovir started in the first month improves hearing and developmental outcomes more than 6 weeks.

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A newborn of a mother with untreated syphilis has hepatosplenomegaly and a nontreponemal titer fourfold higher than the mother's. The correct treatment is

1. oral azithromycin for 5 days
   Azithromycin is not an accepted treatment for syphilis at any age in the newborn, and resistance is common.
2. IV aqueous penicillin G for 10 days
   Proven or highly probable congenital syphilis, with abnormal findings and a titer fourfold above the mother's, needs 10 days of aqueous crystalline penicillin G.
3. single-dose IM benzathine penicillin
   A single benzathine dose is only for low-risk infants with a normal exam whose mothers were adequately treated; it does not reach the CSF reliably.

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Levetiracetam dosing must be adjusted in a neonate with acute kidney injury because it is eliminated mainly by

1. hepatic CYP450 oxidation
   Levetiracetam's lack of CYP metabolism is why it has few drug interactions, unlike phenytoin and phenobarbital.
2. renal excretion
   About two-thirds of levetiracetam leaves unchanged in the urine, so clearance tracks GFR and doses are reduced or spaced in kidney injury.
3. glucuronidation
   Glucuronidation matters for drugs such as morphine, not for levetiracetam, which is excreted largely unchanged.

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The 'gasping syndrome' of metabolic acidosis and death in preterm infants was traced to which drug excipient?

1. propylene glycol
   Propylene glycol can cause hyperosmolality and lactic acidosis, but it was not the cause of the gasping syndrome.
2. polysorbate 80
   Polysorbate 80 in an IV vitamin E product (E-Ferol) caused liver failure and thrombocytopenia, a different excipient disaster.
3. benzyl alcohol
   Benzyl alcohol, once a preservative in flush solutions, accumulated in preterm infants and caused gasping respirations, metabolic acidosis and death, so preservative-free products are now used.

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A neonate on a vasopressin infusion for refractory shock should be monitored closely for

1. hyperkalemia
   Vasopressin does not block potassium excretion, so hyperkalemia is not its expected effect.
2. polyuria
   Polyuria is the picture of vasopressin deficiency, diabetes insipidus, the opposite state.
3. hyponatremia
   Vasopressin is antidiuretic hormone, so besides vasoconstriction it retains free water and can cause dilutional hyponatremia with low urine output.

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Caffeine citrate can be given once daily to preterm infants MAINLY because

1. high protein binding prolongs its effect
   Caffeine is only modestly protein-bound, so binding does not explain its long dosing interval.
2. slow hepatic metabolism prolongs its half-life
   Preterm infants have very little CYP1A2 activity, so caffeine is excreted mostly unchanged with a half-life near 100 hours, allowing once-daily dosing.
3. it is rapidly glucuronidated
   Rapid glucuronidation would shorten the half-life and require more frequent doses, the opposite of what happens in preterm infants.

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