Holding on by a Breath: Carbamazepine Overdose and Neurologic Dysfunction

Kurtz, S.; Hernandez, Adiac Espinosa; Kourouni, Ismini; Parekh, Karishma; Salonia, James

doi:10.1016/j.chest.2017.08.281

Cited by 3 publications

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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]<...>…”

Section: Resultsmentioning

confidence: 99%

“…Normal neuroimaging caused patients to fail brain death assessment prerequisites in 34 (60.7%) cases in this review, which highlights that neuroimaging is a key component in differentiating intoxication as a reversible cause of interrupted brainstem reflexes. Three notable cases in this review reported cerebral edema on neuroimaging: a single case of ethylene glycol [ 43 ], carbamazepine [ 45 ] and valproic acid toxicity [ 47 ]. In these instances, structural cerebral disease may have been the cause of, or contributed to, the loss of brainstem reflexes rather than the direct action of the xenobiotic.…”

Section: Discussionmentioning

confidence: 99%

“…Alternatively, the finding could have been suggestive of transient global edema, as may occur from causes such as hypercapnia, or an over-call by the radiologist, as may occur with younger patients with fuller brain tissue. Two of these patients made a full recovery [43,45] and the third was not specified, but was discharged from the intensive care unit [47]. Because of the additional cases of ethylene glycol and valproate toxicity that caused a patient to have features resembling brain death without cerebral edema, these xenobiotics may still be relevant to consider as toxicologic brain death confounders.…”

Section: Neuroimaging and Failed Prerequisitesmentioning

confidence: 99%

See 2 more Smart Citations

Toxicologic Confounders of Brain Death Determination: A Narrative Review

2020

View full text Add to dashboard Cite

The aim of this narrative review is to describe the toxicologic confounders of brain death currently reported in the literature to offer guidance for physicians assessing brain death after a toxic exposure. We established an a priori definition of a "brain death mimic" as an unresponsive, intubated patient missing some, but not all brainstem reflexes. We completed a review of the literature utilizing MEDLINE and EMBASE to find case reports of patients of all ages in English, French, and Spanish meeting the criteria and hand searched the references of the results. We recorded xenobiotic dose, duration of physical exam suggesting brain death, and how the cases failed to meet full brain death criteria, when available. Fifty-six cases representing 19 different substances met the a priori definition of brain death mimic. Xenobiotic toxicities included: snake envenomation (13), baclofen (11), tricyclic antidepressants (8), bupropion (7), alcohols (4), antiepileptic agents (3), barbiturates (2), antidysrhythmics (2), organophosphates (2), and one case each of magnesium, succinylcholine, tetrodotoxin, and zolpidem. All patients except one survived to discharge and the majority at their baseline physical health. The most common means by which the cases failed brain death examination prerequisites was via normal neuroimaging. The xenobiotics in this review should be considered in cases of poisoning resulting in loss of brainstem reflexes and addressed before brain death determination. Brain death diagnosis should not be pursued in the setting of normal cerebral imaging or incomplete evaluation of brain death prerequisites.

show abstract