Emergency Medicine EOR practice questions

Why Observation and vascular risk factor control is correct

• An isolated CN VI palsy in an older patient with diabetes and hypertension and a normal MRI is most consistent with microvascular ischemic mononeuropathy
• The standard approach is conservative management with observation and tight control of blood pressure, glucose, and lipids; most cases resolve spontaneously within 3 months
• Symptomatic relief with a temporary eye patch or prism can be offered for diplopia

Why the others are wrong

• Systemic anticoagulation with intravenous heparin — anticoagulation treats cavernous sinus or cerebral venous sinus thrombosis, which would present with orbital pain, proptosis, chemosis, and multiple cranial neuropathies rather than a painless isolated abducens palsy
• Empiric intravenous acyclovir for viral neuropathy — empiric IV acyclovir would be appropriate if there were evidence of herpes zoster ophthalmicus or a viral cranial neuritis, but there is no rash, pain, or systemic infectious picture here
• High-dose intravenous methylprednisolone therapy — high-dose IV methylprednisolone is used for inflammatory or demyelinating optic neuropathy and in giant cell arteritis, not for an isolated ischemic abducens palsy

Why Sympathomimetic toxidrome is correct

• Sympathomimetic toxidrome: mydriasis (dilated reactive pupils), tachycardia, hypertension, hyperthermia, diaphoresis, and agitation — caused by cocaine, amphetamines, MDMA
• Key distinguishing feature from anticholinergic: sympathomimetic = wet (diaphoretic); anticholinergic = dry (no sweating, urinary retention, flushed)

Additional high-yield points

• Management: benzodiazepines (lorazepam) for agitation, hypertension, and seizures
• Avoid beta-blockers alone (unopposed alpha stimulation worsens hypertension)
• Cooling measures for hyperthermia
• Monitor for coronary vasospasm (cocaine)

Why the others are wrong

• Serotonin syndrome — Serotonin syndrome features neuromuscular hyperactivity (clonus, hyperreflexia, especially lower-extremity) and requires serotonergic exposure, which is not described (trap: overlapping hyperthermia and autonomic instability).
• Opioid toxidrome — Opioids cause miosis with respiratory and CNS depression, the opposite of this agitated, mydriatic, hypertensive, tachycardic patient (trap: default overdose assumption despite opposite findings).
• Anticholinergic toxidrome — Anticholinergic toxicity is "dry" (anhidrosis, flushed skin, urinary retention), whereas this patient is diaphoretic (wet); the wet-versus-dry skin distinguishes sympathomimetic from anticholinergic (trap: both cause mydriasis, agitation, and hyperthermia — the skin is the discriminator).

Why Intranasal or intravenous naloxone is correct

• The presentation is the classic opioid toxidrome: miosis (2 mm bilateral pinpoint pupils), respiratory depression (RR 6), bradycardia, hypotension, and decreased consciousness.
• Naloxone (Narcan) is an opioid receptor antagonist and the immediate treatment.
• Routes include IV (fastest onset), IM, or IN (intranasal — easy for bystanders).
• Dose: 0.4–2 mg IV; repeat every 2–3 minutes if no response; titrate to adequate respirations, not full reversal — avoid precipitating acute withdrawal and combative behavior.
• Supportive care includes supplemental oxygen and positioning.

Additional high-yield points

• The half-life of naloxone is shorter than most opioids — monitor for re-narcotization after initial response.

Why the others are wrong

• Immediate endotracheal intubation — Naloxone can reverse the respiratory depression noninvasively and often obviates intubation, which is reserved for failure to respond (trap: escalating to an invasive airway before the reversible antidote).
• Empiric intravenous flumazenil — Flumazenil reverses benzodiazepines, but pinpoint pupils with an RR of 6 define an opioid toxidrome, and flumazenil given for undifferentiated coma can precipitate seizures (trap: correct instinct to use an antidote, wrong receptor).
• Intravenous dextrose 50% — Dextrose treats hypoglycemia, which is not indicated by this classic opioid toxidrome, and does not address the respiratory depression (trap: reflexive coma-cocktail component without a glucose indication).

Why N-acetylcysteine infusion is correct

• The 4-hour acetaminophen level is 280 mcg/mL, which falls above the treatment line of the Rumack-Matthew nomogram (150 mcg/mL at 4 hours), so N-acetylcysteine (NAC) infusion is indicated.
• The patient is currently asymptomatic because hepatotoxicity peaks 72–96 hours after ingestion; normal initial labs do not exclude impending injury.
• NAC replenishes hepatic glutathione and detoxifies the reactive metabolite NAPQI.
• NAC is most effective when started within 8 hours; prompt initiation prevents fulminant hepatic failure.

Why the others are wrong

• Activated charcoal — Activated charcoal limits absorption only within roughly 1–2 hours of ingestion and would not treat a patient who already has a toxic 4-hour level.
• Observation with repeat liver enzymes in 24 hours — Dangerously delays the antidote in a patient whose level mandates treatment; normal initial enzymes are expected this early and do not exclude impending injury.
• Intermittent hemodialysis — Dialysis does clear acetaminophen but is reserved for massive ingestion with levels approaching 900 mcg/mL accompanied by coma, shock, or lactic acidosis; it has no role at a 280 mcg/mL 4-hour level in a hemodynamically normal patient and never substitutes for NAC.

Why Arthrocentesis with synovial fluid analysis is correct

• Arthrocentesis with synovial fluid analysis is the single most important next step for an acute, atraumatic, monoarticular effusion, especially when septic arthritis is a concern.
• Synovial fluid analysis distinguishes the underlying cause:
• WBC >50,000/µL with a polymorphonuclear (PMN) predominance suggests septic arthritis — a joint-threatening emergency.
• Positively or negatively birefringent crystals indicate pseudogout or gout.
• Bloody fluid (hemarthrosis) suggests coagulopathy or an occult intra-articular injury.
• Radiographs are already unremarkable here, so imaging has excluded fracture and the priority is to sample the joint before starting antibiotics.

Why the others are wrong

• Magnetic resonance imaging of the knee — MRI evaluates soft-tissue structures but does not identify infection or crystals and delays the definitive diagnostic tap.
• Empiric intravenous antibiotic therapy — Antibiotics should not be started before arthrocentesis in suspected septic arthritis because doing so lowers synovial culture yield.
• Measurement of the serum uric acid level — Serum uric acid is frequently normal during an acute gout flare and cannot confirm or exclude septic arthritis; joint aspiration is required.

Why Acute airway obstruction is correct

• The most feared and most common serious complication of recurrent respiratory papillomatosis is acute airway obstruction from papilloma growth in the larynx and trachea
• Children present with worsening stridor, retractions, and hypoxia
• May require urgent operative microlaryngoscopy and debulking; some need temporizing tracheostomy

Why the others are wrong

• Vocal cord scarring — scarring and web formation from repeated CO2 laser debulking cause chronic hoarseness and a breathy, weak voice over months rather than an abrupt hypoxic crisis with retractions
• Pulmonary parenchymal spread — distal seeding produces slowly enlarging cavitary nodules and gradual hypoxemia over months, and it would not generate biphasic stridor, which localizes to a fixed laryngotracheal lesion
• Malignant transformation — squamous cell carcinoma evolves over months to years in long-standing disease, usually with pulmonary involvement, and does not explain a deterioration over hours in a 5-year-old

Additional high-yield points

• About 1-3% of cases undergo malignant transformation to squamous cell carcinoma, typically when disease extends to the lungs, but this is a late complication, not an acute presentation