Clinical Reasoning: A 41-year-old comatose man with absent brainstem reflexes

Abstract

A 41-year-old obese man was stopped by the police for driving erratically. He was confused, dysarthric, ataxic, and vomited repeatedly before collapsing and becoming rapidly obtunded, eventually requiring rapid sequence intubation (RSI). He arrived at the emergency department (ED) with a Glasgow Coma Scale score of 3, hypothermia (35.3°C), and hypotension (78/38 mm Hg), with a heart rate of 80. He was treated with warm IV fluid boluses and warming blanket. He was examined by the attending and resident neurologists approximately 2.5 hours from the time of RSI. He was mechanically ventilated but had received no sedation since intubation. Nothing was known about his medical history and no collateral information was available.He did not respond to naloxone or thiamine. Clinical examination was performed with a temperature of 36°C and a blood pressure of 120/80 mm Hg. He remained mechanically ventilated without spontaneous respirations. No meningismus, external signs of trauma, needle puncture marks, or tongue or buccal lacerations were observed. Spontaneous movements were absent. He did not open his eyes, grimace, withdraw, or posture to noxious stimuli (nailbed and supraorbital pressure). Neuromuscular blockade was excluded with a train of 4 twitches with maximal ulnar nerve stimulation. His pupils were fixed at 2 mm and unreactive to light. Corneal and oculocephalic (vertical and horizontal) reflexes were absent. Irrigation of each ear canal with ice water produced no eye deviation. No gag or cough reflexes were elicited with posterior pharyngeal stimulation and tracheal suctioning respectively. His extremities were flaccid and areflexic. Babinski sign was absent. No gaze deviation, nystagmoid eye movements, facial twitching, or jerking movements were observed. Cardiovascular, lung, and abdominal examinations were unremarkable.

Toxicologic Confounders of Brain Death Determination: A Narrative Review

“…We grouped substances with greater than five cases into separate descriptive tables. Snake envenomation (Table 1) [7][8][9][10][11][12][13][14][15][16] was the most frequent cause of a brain death mimic, followed by baclofen (Table 2) [17][18][19][20][21][22][23][24][25][26][27], tricyclic antidepressants (TCA) ( Table 3) [28][29][30][31][32][33][34] and bupropion (Table 4) [5,6,[35][36][37][38][39][40]. We grouped all cases with three or fewer cases into Table 5 [41][42][43][44][45][46][47][48...…”

“…No response to painful stimulation. Flaccid tone Neuroimaging Normal CT Generalized slowing without reactivity to stimulation NR Extubated at 48 h; Recovery to baseline health [ 25 ] 41/M > 600 mg 10 h Fixed 2 mm pupils. Absent corneal, oculocephalic, cough, and gag reflex.…”

“…Baclofen is well-known to depress brainstem reflexes and is more frequently recognized as a brain death mimic [58]. It was the second most frequent cause of a brain death mimic in this review [17][18][19][20][21][22][23][24][25][26][27] (Table 3). The ability to interfere with reflexes is attributed to its mechanism as a γ-aminobutyric acid (GABA) type B receptor agonist, inhibiting calcium influx and preventing release of the excitatory neurotransmitters, glutamate and aspartate [27,58].…”

“…Diagnosis is typically through history alone, as there are no readily accessible rapid laboratory tests for identification. Despite the profound sedation seen in overdose, patients often make full recovery without permanent sequelae given appropriate supportive care and if no hypoxic-ischemic cerebral injury has occurred [25,58].…”