In sepsis patients, etomidate has become an increasingly controversial agent secondary to its transient cortisol suppression.¹⁰ Further, increased mortality has been observed in sepsis patients relative to the degree of adrenal dysfunction.¹¹ Although etomidate is known to suppress cortisol, outcome trials in sepsis syndrome are still lacking, and a cause-effect relationship has yet to be determined.^12,13 Currently, no guidelines state that etomidate is a contraindicated agent in sepsis, but the emergency physician may consider another induction agent in this clinical scenario.

Ketamine is a phencyclidine derivate dosed at 1.5 mg/kg IV; the time of onset is 45-60 seconds, and the duration of action is approximately 10-20 minutes.¹ Ketamine acts as an amnestic, anesthetic, and analgesic agent. Also, ketamine possesses unique bronchodilatory properties that make it the induction agent of choice in patients with reactive airway disease.^14,15 Ketamine also produces a catecholamine surge that increases heart rate and mean arterial pressure. This characteristic makes ketamine a viable alternative to etomidate, especially in sepsis management. Recently, a randomized, controlled trial published in Lancet comparing induction with etomidate versus ketamine in acutely ill patients demonstrated no difference in outcomes, while showing higher rates of adrenal insufficiency in the etomidate arm.¹⁶ However, because of this catecholamine release, ketamine remains relatively contraindicated in normo- or hypertensive patients who have underlying ischemic cardiac disease.¹

Medical dogma previously dictated that ketamine is contraindicated in patients who have the potential for increased ICP. The traditional theories suggested that ketamine causes a further rise in ICP; however, emerging literature has begun to discount prior teachings. While ketamine is not the drug of choice for the head-injured patient, this agent may no longer be absolutely contraindicated in this patient population.^17,18,19

Propofol is an alkylphenol derivate dosed at 1.5 mg/kg IV; the time of onset is 15-45 seconds, and the duration of action is approximately 5-10 minutes.¹ Propofol is an appropriate agent for induction for the hemodynamically stable seizure patient, as this medication potentiates GABA activity. This agent also has bronchodilatory properties and can be considered for patients with reactive airway disease.²⁰ However, propofol can cause profound hypotension and must be used judiciously.

Thiopental is a barbiturate dosed at 3 mg/kg IV; the onset of action is 30 seconds, and the duration of action is approximately 5-10 minutes. The pharmacologic profile of thiopental is similar to that of propofol, as both agents decrease ICP at the expense of cerebral perfusion pressure and possess GABA-enhancing activity. As with all barbiturates, thiopental causes myocardial depression and venodilation. Expert recommendation is to decrease the dose of thiopental to 1-2 mg/kg IV in hypotension, but avoidance of this agent in this scenario would be preferable. Thiopental must also be avoided in patients with reactive airway disease, as barbiturates will cause a secondary histamine release.¹