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Difficulty: MediumSubstance-Related and Addictive Disorders

An internal medicine rapid response team is called to evaluate a 25-year-old hospitalized man for acute-onset severe agitation and chest discomfort. The patient was admitted yesterday for a soft tissue infection of the right arm and has been receiving intravenous cefazolin. When the physician arrives, the patient is pacing the room, visibly sweating, and shouting at the nursing staff. Vital signs are temperature 37.9°C (100.2°F), blood pressure 178/112 mm Hg, pulse 132/min, and respirations 24/min. Physical examination reveals bilateral mydriasis and significant diaphoresis. A friend who was visiting the patient abruptly left the room right before the episode started. An ECG demonstrates sinus tachycardia with no ST-segment changes. Which of the following is the most appropriate initial step in the pharmacologic management of this patient?

  1. Intravenous lorazepamAnswer
  2. B
    Intravenous metoprolol
  3. C
    Intramuscular haloperidol
  4. D
    Intravenous naloxone
  5. E
    Intravenous flumazenil

Answer

The most appropriate initial step is to administer intravenous lorazepam.
The correct answer is intravenous lorazepam. This patient's presentation of acute severe agitation, hypertension, tachycardia, diaphoresis, and mydriasis shortly after a visitor left strongly suggests acute stimulant intoxication (e.g., cocaine or methamphetamine) acquired during his hospitalization. Benzodiazepines are the first-line pharmacotherapy for stimulant toxicity. They enhance GABA-A receptor activity, which decreases central nervous system sympathetic outflow. This effectively treats the agitation, lowers blood pressure and heart rate, and raises the seizure threshold, thereby addressing both the symptoms and the major life-threatening complications of stimulant overdose.

Step-by-Step Solution

1
Identify the patient's clinical toxidrome based on vital signs and physical examination.
The patient exhibits severe agitation, hypertension, tachycardia, hyperthermia, diaphoresis, and mydriasis.
Recognizing the toxidrome is essential to narrow down the differential diagnosis of acute agitation and hemodynamic instability.
2
Correlate the toxidrome with the clinical context to establish the most likely diagnosis.
The acute onset of a sympathomimetic toxidrome immediately following a visit from a friend strongly points to acute illicit stimulant intoxication (e.g., cocaine or methamphetamine) acquired while in the hospital.
The context helps confirm the etiology, distinguishing it from other causes of agitation such as delirium or medication adverse effects.
3
Determine the most appropriate initial pharmacological intervention for stimulant toxicity.
Benzodiazepines, such as intravenous lorazepam, are selected to decrease central sympathetic outflow, thereby controlling agitation, lowering blood pressure and heart rate, and preventing seizures.
First-line management of stimulant intoxication relies on GABA-ergic medications to safely counteract the hyperadrenergic state without risking unopposed alpha-receptor stimulation.

Key Concept

The initial management of acute stimulant (e.g., cocaine, methamphetamine) intoxication is centered on the administration of benzodiazepines to reduce central sympathetic outflow, while strictly avoiding beta-blockers due to the risk of unopposed alpha-adrenergic stimulation.
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Topics

Substance-Related and Addictive Disorders

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