Brake fluid toxicity feigning brain death

Abstract

SummaryBrake fluid (glycol-based) toxicity is known to have a protean of central and peripheral nervous system manifestations. The principal component of this household poison is ethylene glycol. Toxic effect is generally attributed to peri-vascular deposition of calcium oxalate crystals in various tissues. However, clinical features resembling brain death have rarely been reported. We report a case of brake fluid toxicity simulating brain death in a 21-year-old healthy man who ingested it as a recreational agent. BACKGROUND

Toxicologic Confounders of Brain Death Determination: A Narrative Review

“…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][49]<...>…”

“…Considering all cases, ethylene glycol caused the longest duration of loss of brainstem reflexes, lasting 2 months in two of the cases [42,44]. The shortest duration of the physical exam suggesting brain death was ethanol at 40 min [41].…”

“…Because two of the cases demonstrated nerve injury later in their course, it may be more accurate to theorize that one of the metabolites of ethylene glycol causes direct injury to conduction pathways. Both cases reported nerve conduction studies displaying severe axonal polyneuropathy [42,44], and a sural nerve biopsy demonstrated oxalate crystal deposition in one case [42]. This would also explain why the case that received dialysis promptly had the shortest duration of a clinical brain death mimic, as dialysis removes both the parent alcohol and its metabolites.…”

“…None of the ethylene glycol cases reported confirmatory laboratory values. One case lost brainstem reflexes concurrently with acute inebriation, acidosis, and renal failure [43], while the remaining two cases exhibited neurotoxicity insidiously after developing renal failure and after the patients had recovered from the acute intoxicated state [42,44]. It remains unclear if ethylene glycol or its metabolites are responsible for the CNS toxicity displayed in these cases.…”

“…The change is likely secondary to separating intoxication from loss of reflexes caused by polyneuritis, infectious, and autoimmune causes, as many patients with severe poisoning can make a full recovery. In regards to the five cases reporting residual deficits, two cases of snake envenomation had residual muscular weakness [8,14], two cases of ethylene glycol poisoning had deafness and muscular weakness [42,44], and a lidocaine case had mild cognitive impairment [51].…”