Epinephrine is the first-line therapy for anaphylaxis, and intramuscular (IM) administration at recommended doses is essential to prevent progression to airway compromise, circulatory collapse, and death. However, epinephrine is a potent sympathomimetic that can provoke severe cardiovascular responses in susceptible patients. We report the case of a 50-year-old African-American male with a history of long-standing hypertension, end-stage renal disease on intermittent hemodialysis with poor adherence, type two diabetes mellitus, and chronic hepatitis C, who developed acute neurological deterioration shortly after receiving two doses of 0.5 mg IM epinephrine for suspected anaphylaxis. Blood pressure measurements were unobtainable in the prehospital setting. In the emergency department, the patient was noted to have severe hypertension with an initial recorded blood pressure of 213/110 mmHg prior to intubation. Due to difficulty obtaining reliable noninvasive measurements thereafter, a radial arterial line was placed, revealing a blood pressure of 326/101 mmHg. Computed tomography (CT) of the brain demonstrated a large acute intraparenchymal hemorrhage involving the pons and midbrain with intraventricular extension. CT angiography excluded aneurysm or vascular malformation. Despite intensive care management and blood pressure control, the patient had limited neurological recovery and required prolonged ventilatory support, tracheostomy, and transfer to a long-term acute care hospital. This case highlights a rare but severe complication temporally associated with epinephrine, particularly in patients with underlying cerebrovascular risk factors. This case also underscores the importance of vigilant hemodynamic monitoring after epinephrine administration and early recognition of neurological deterioration.
Liang et al. (Mon,) studied this question.