The Coma Cocktail: Indications, Contraindications, Adverse Effects, Proper Dose, and Proper Route

Bartlett, Dana

doi:10.1016/j.jen.2004.09.002

Cited by 10 publications

(6 citation statements)

References 1 publication

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“…Flumazenil competitively inhibits ligand binding at the BZD binding site inside the GABA A channel [7]. Expectedly, use of flumazenil may predispose patients to increased sensitivity to seizures or necessitate resedation [8, 9]. …”

Section: Introductionmentioning

confidence: 99%

Inhibition of Soluble Epoxide Hydrolase as a Novel Approach to High Dose Diazepam Induced Hypotension

et al. 2016

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Context Hypotension is one of the dose limiting side effects of benzodiazepines (BZDs), in particular of diazepam (DZP) which is still widely used in the clinic. Currently, only one FDA approved antidote exists for BZD overdose and novel approaches are needed to improve management of DZP overdose, dependency and withdrawal. Objective Here, we hypothesized that increasing bioactive lipid mediators termed epoxy fatty acids (EpFAs) will prevent hypotension, as was shown previously in a murine model of LPS-induced hypotension. Therefore, we first characterized the time and dose dependent profile of DZP induced hypotension in mice, and then investigated the reversal of the hypotensive effect by inhibiting the soluble epoxide hydrolase (sEH), an enzyme that regulates the levels of EpFAs. Materials and methods Following baseline systolic BP recording using tail cuffs, mice were administered a sEH inhibitor (TPPU) before DZP and BP was monitored. Blood and brain levels of DZP and TPPU were quantified to examine distribution and metabolism. Plasma EpFAs levels were quantified to determine TPPU target engagement. Results In this murine model, DZP induced dose dependent hypotension which was more severe than midazolam. The temporal profile was consistent with the reported pharmacokinetics/pharmacodynamics of DZP. Treatment with TPPU reversed the hypotension resulting from high doses of DZP and decreased the sEH metabolites of EpFAs in the plasma demonstrating target engagement. Discussion and conclusion Overall, these findings demonstrate the similarity of a murine model of DZP induced hypotension to clinical observations in humans. Furthermore, we demonstrate that stabilization of EpFAs by inhibiting sEH is a novel approach to overcome DZP-induced hypotension and this beneficial effect can be enhanced by an omega three diet probably acting through epoxide metabolites of the fatty acids.

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Section: Introductionmentioning

confidence: 99%

Inhibition of Soluble Epoxide Hydrolase as a Novel Approach to High Dose Diazepam Induced Hypotension

et al. 2016

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“…Sometimes, "coma cocktail" (dextrose, naloxone, thiamine, and oxygen) is empirically administered to the comatose patient, and it is nearly safe. 10 Due to the high prevalence of drug abuse in this population, a urine multi‐drug assessment should be obtained. Also, there are some main metabolic causes of LOC such as hypoglycemia, hyponatremia, hypoxia, and hyperventilation that need to be ruled out.…”

Section: Discussionmentioning

confidence: 99%

Heavy head lice infestation in an adolescent girl following benzodiazepine poisoning

Moghimi

Nekoukar

Sharifpour

et al. 2022

Clinical Case Reports

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“…Smaller dosages have been used in controlled settings (during anesthesiology) with sufficient response. Starting with a dose of 0.1 mg and increasing the dose slowly if needed may be the solution to prevent iatrogenic acute opiate withdrawal and therefore VT/VF in these patients [ 11 ]. Another solution could be to abandon administration of naloxone in opiate addicts, therefore acute withdrawal syndrome cannot take place, and have them intubated until awoken.…”

Section: Discussionmentioning

confidence: 99%

Ventricular Tachycardia After Naloxone Administration: a Drug Related Complication? Case Report and Literature Review

Lameijer

Azizi

Ligtenberg

et al. 2014

Drug Saf - Case Rep

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ObjectiveTo present a case of ventricular tachycardia following naloxone administration and to review current literature concerning ventricular tachycardia associated with naloxone.MethodsWe present a case and review the literature concerning ventricular tachycardia (VT) as a complication of naloxone administration.ResultsIn our patient, a 44-year old male intoxicated multi-drug user, VT presented on the electrocardiogram shortly after naloxone (twice 0.4 mg intra-osseous) administration for suspected methadone overdose. After initial medical treatment he was treated with electro cardioversion because of hemodynamic instability. Our patient was subsequently stabilized and admitted to our intensive care unit (ICU). Eight comparable cases concerning VT after administration of naloxone were found in the literature, both in multi-drug uses as in patients receiving opiates for elective surgery.ConclusionWe suggest VT as a possible, but rarely reported serious complication of naloxone administration (Naranjo scale possible to probable). Patients who are multi-drug users or receive opiates in high doses may be prone to VT/VF due to acute (iatrogenic) opiate withdrawal or reduction of sympathetic suppression and therefore overstimulation. Also, antagonism of the protective mechanism of opioids against sympathetic excess (due to substance abuse, cardiac disease or hypoxia, as seen in all cases) may induce VT/VF. We suggest the use of small dosages (0.1 mg vs 0.4 mg), cardiac monitoring, and to have defibrillation devices stand-by.

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The Coma Cocktail: Indications, Contraindications, Adverse Effects, Proper Dose, and Proper Route

Cited by 10 publications

References 1 publication

Inhibition of Soluble Epoxide Hydrolase as a Novel Approach to High Dose Diazepam Induced Hypotension

Inhibition of Soluble Epoxide Hydrolase as a Novel Approach to High Dose Diazepam Induced Hypotension

Heavy head lice infestation in an adolescent girl following benzodiazepine poisoning

Ventricular Tachycardia After Naloxone Administration: a Drug Related Complication? Case Report and Literature Review

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