Treatment of Toxin-Related Status Epilepticus With Levetiracetam, Fosphenytoin, or Valproate in Patients Enrolled in the Established Status Epilepticus Treatment Trial.

STUDY OBJECTIVE: We describe a subset of patients with toxin-related precipitants of seizures/status epilepticus enrolled in the Established Status Epilepticus Treatment Trial (ESETT). METHODS: The ESETT was a prospective, double-blinded, adaptive trial evaluating levetiracetam, valproate, and fosphenytoin as second-line agents in benzodiazepine-refractory status epilepticus in adults and children. The primary outcome was the absence of seizures and improvement in the level of consciousness 1 hour after study drug administration. In this post hoc analysis, the safety and efficacy of second-line agents in a subset of patients with toxin-related seizures are described. RESULTS: A total of 249 adults and 229 children were enrolled in the ESETT. Toxin-related seizures occurred in 29 (11.6%) adults and 1 child (0.4%). In adults, men were more likely to have toxin-related seizures than women (25 of 145, 17.2% versus 4 of 104, 3.9%). The most common toxin-related precipitants were alcohol withdrawal and cocaine, 11(37%) of 30 patients each. Cocaine was used with other substances by most patients 10 (91%) of 11, most commonly with an opioid 7 (64%) of 11. For alcohol withdrawal-related seizures, treatment successes with levetiracetam, valproate, and fosphenytoin were 3 (100%) of 3, 3 (50%) of 6, and 1 (50%) of 2, respectively. For cocaine-related seizures, treatment success was 1 (14%) of 7 for levetiracetam, 0 (0%) of 1 for valproate, and 1 (33%) of 3 for fosphenytoin. One patient who used cocaine and an opioid received fosphenytoin and developed life-threatening hypotension. CONCLUSION: In the ESETT, approximately 1 in 10 adult patients with status epilepticus presented with a toxin-related seizure. Alcohol withdrawal and cocaine/opioid use were the most common toxin-related precipitants. Toxin-related benzodiazepine-refractory status epilepticus was successfully treated with a single dose of second-line antiseizure medication in 42% of the patients.

Systematic review on the use of activated charcoal for gastrointestinal decontamination following acute oral overdose.

INTRODUCTION: The use of activated charcoal in poisoning remains both a pillar of modern toxicology and a source of debate. Following the publication of the joint position statements on the use of single-dose and multiple-dose activated charcoal by the American Academy of Clinical Toxicology and the European Association of Poison Centres and Clinical Toxicologists, the routine use of activated charcoal declined. Over subsequent years, many new pharmaceuticals became available in modified or alternative-release formulations and additional data on gastric emptying time in poisoning was published, challenging previous assumptions about absorption kinetics. The American Academy of Clinical Toxicology, the European Association of Poison Centres and Clinical Toxicologists and the Asia Pacific Association of Medical Toxicology founded the Clinical Toxicology Recommendations Collaborative to create a framework for evidence-based recommendations for the management of poisoned patients. The activated charcoal workgroup of the Clinical Toxicology Recommendations Collaborative was tasked with reviewing systematically the evidence pertaining to the use of activated charcoal in poisoning in order to update the previous recommendations. OBJECTIVES: The main objective was: Does oral activated charcoal given to adults or children prevent toxicity or improve clinical outcome and survival of poisoned patients compared to those who do not receive charcoal?  Secondary objectives were to evaluate pharmacokinetic outcomes, the role of cathartics, and adverse events to charcoal administration. This systematic review summarizes the available evidence on the efficacy of activated charcoal. METHODS: A medical librarian created a systematic search strategy for Medline (Ovid), subsequently translated for Embase (via Ovid), CINAHL (via EBSCO), BIOSIS Previews (via Ovid), Web of Science, Scopus, and the Cochrane Library/DARE. All databases were searched from inception to December 31, 2019. There were no language limitations.  One author screened all citations identified in the search based on predefined inclusion/exclusion criteria. Excluded citations were confirmed by an additional author and remaining articles were obtained in full text and evaluated by at least two authors for inclusion. All authors cross-referenced full-text articles to identify articles missed in the searches. Data from included articles were extracted by the authors on a standardized spreadsheet and two authors used the GRADE methodology to independently assess the quality and risk of bias of each included study. RESULTS: From 22,950 titles originally identified, the final data set consisted of 296 human studies, 118 animal studies, and 145 in vitro studies. Also included were 71 human and two animal studies that reported adverse events. The quality was judged to have a Low or Very Low GRADE in 469 (83%) of the studies. Ninety studies were judged to be of Moderate or High GRADE. The higher GRADE studies reported on the following drugs: paracetamol (acetaminophen), phenobarbital, carbamazepine, cardiac glycosides (digoxin and oleander), ethanol, iron, salicylates, theophylline, tricyclic antidepressants, and valproate. Data on newer pharmaceuticals not reviewed in the previous American Academy of Clinical Toxicology/European Association of Poison Centres and Clinical Toxicologists statements such as quetiapine, olanzapine, citalopram, and Factor Xa inhibitors were included. No studies on the optimal dosing for either single-dose or multiple-dose activated charcoal were found. In the reviewed clinical data, the time of administration of the first dose of charcoal was beyond one hour in 97% (n = 1006 individuals), beyond two hours in 36% (n = 491 individuals), and beyond 12 h in 4% (n = 43 individuals) whereas the timing of the first dose in controlled studies was within one hour of ingestion in 48% (n = 2359 individuals) and beyond two hours in 36% (n = 484) of individuals. CONCLUSIONS: This systematic review found heterogenous data. The higher GRADE data was focused on a few select poisonings, while studies that addressed patients with unknown and or mixed ingestions were hampered by low rates of clinically meaningful toxicity or death.  Despite these limitations, they reported a benefit of activated charcoal beyond one hour in many clinical scenarios.

Safety and effectiveness of physostigmine: a 10-year retrospective review.

BACKGROUND: Physostigmine has long been recognized as an antidote to reverse anticholinergic delirium. However, its effectiveness, safety profile, and dosing have been disputed. OBJECTIVES: To describe effectiveness, adverse events, and dosing associated with the use of physostigmine to reverse anticholinergic delirium. METHODS: A retrospective cohort study of hospitalized patients reported to a regional poison center system between 2003 and 2012 who received physostigmine to reverse an anticholinergic toxidrome. Data extraction of a priori defined variables were recorded with concurrence of investigators. The cases were stratified by the primary ingestant as the presumed causative agent and associations for response were performed using odds ratios (ORs), 95% confidence intervals (CI's), and p values. RESULTS: Of the 1422 cases identified, 191 met the inclusion criteria. Patients exposed to non-diphenhydramine antihistamines (n = 14), antipsychotics (n = 4), and tricyclic antidepressants (n = 3) had 100% response to physostigmine, whereas anticholinergic plants (n = 46/67; 68.7%, OR: 0.70; CI: 0.36-1.35), diphenhydramine (n = 43/56; 64.2%, OR: 1.30; CI: 0.63-2.68), and combination products (n = 8/10; 80%, OR: 1.48; CI: 0.30-7.24) had partial response rates. Of the included patients, 142 (74.3%) were treated with physostigmine alone, and 16 (8.4%) of these patients were discharged directly from the emergency department (ED). DISCUSSION: Most patients, 182 (95.3%), had no documented adverse effects. Four patients (2.1%) experienced emesis, two experienced QTc prolongation (1.0%), and two experienced seizures (1.0%). There was a single fatality 6 h after physostigmine administration. Average initial total doses of physostigmine ranged from 1.0 to 1.75 mg. Most patients were admitted to the ICU (n = 110; 57.6%), however, 36 (18.8%) patients were discharged directly from the ED. CONCLUSIONS: In this retrospective cohort study, physostigmine administration to reverse anticholinergic delirium had a good safety profile, and often improved or resolved anticholinergic delirium when administered in doses less than 2 mg.

Patients with acute poisoning presenting to an urban emergency department of a tertiary hospital in Tanzania.

BACKGROUND: Poisoning is a major public health concern in sub-Saharan Africa, affecting patients of all age groups. Poisoned patients often present to the emergency department (ED) and prompt evaluation and appropriate management are imperative to ensure optimal outcomes. Unfortunately, little is known about the specific presentations of poisoned patients in East Africa. We describe the clinical and epidemiological features of patients presenting to the Muhimbili National Hospital (MNH) ED with suspected toxicological syndromes. METHODS: This prospective study enrolled a consecutive sample of ED patients who presented with a suspected toxicological syndrome from March 2013 to June 2013. Trained investigators completed a structured case report form (CRF) for each eligible patient, documenting the suspected poison, demographic information, the clinical presentation, and the ED outcome and disposition. The study data were analyzed and summarized with descriptive statistics. RESULTS: Of 8827 patients, who presented to ED-MNH, 106 (1.2%) met inclusion criteria, and all were enrolled. Among those enrolled, the median age was 28 years (interquartile range [IQR] 16 years), and 81 (76.4%) were male. Overall 55 (52%) were single, and 28 (26.4%) had professional jobs. 60 (56.6%) patients were referred from district hospitals, 86.8% of which were in Dar es Salaam. Only 13 (12.3%) of patients presented to the ED within 2 h of the toxic exposure. The etiology of poisoning included alcohol in 42 (50%), a mixture of different medications in 12 (14.3%), and snakebite in 6 (11.3%). Most exposures were intentional (63 [59.4%]) and were via the oral route (88 [83%]). The most common abnormal physical findings were altered mental status (66 [62.3%]) and tachypnoea (68 [64.2%]). One patient died in the ED and 98 (92.5%) required hospital admission. CONCLUSIONS: Most patients presenting to the ED with a toxicological syndrome were adult males with intentional exposures. The most common toxic exposure was alcohol (ethanol) intoxication and the most common abnormal findings were altered mental status and tachypnoea. More than three-quarter of patients presented after 2 h of exposure. Almost all patients were admitted to the hospital.

Amanita phalloides Mushroom Poisonings - Northern California, December 2016.

Amanita phalloides, colloquially known as the "death cap," belongs to the Phalloideae section of the Amanita family of mushrooms and is responsible for most deaths following ingestion of foraged mushrooms worldwide (1). On November 28, 2016, members of the Bay Area Mycological Society notified personnel at the California Poison Control System (CPCS) of an unusually large A. phalloides bloom in the greater San Francisco Bay Area, coincident with the abundant rainfall and recent warm weather. Five days later, CPCS received notification of the first human A. phalloides poisoning of the season. Over the following 2 weeks, CPCS was notified of an additional 13 cases of hepatotoxicity resulting from A. phalloides ingestion. In the past few years before this outbreak, CPCS received reports of only a few mushroom poisoning cases per year. A summary of 14 reported cases is presented here. Data extracted from patient medical charts revealed a pattern of delayed gastrointestinal manifestations of intoxication leading to dehydration and hepatotoxicity. Three patients received liver transplants and all but one recovered completely. The morbidity and potential lethality associated with A. phalloides ingestion are serious public health concerns and warrant medical provider education and dissemination of information cautioning against consuming foraged wild mushrooms.

Fatal cardiac glycoside poisoning due to mistaking foxglove for comfrey.

CONTEXT: Accidental ingestion of foxglove (Digitalis purpurea) can cause significant cardiac toxicity. We report a patient who ingested foxglove mistaking it for comfrey and developed refractory ventricular arrhythmias. The patient died despite treatment with digoxin-specific antibody fragments (DSFab) and veno-arterial extracorporeal membrane oxygenation (VA-ECMO). CASE DETAILS: A 55-year-old woman presented to the emergency department with nausea, vomiting and generalized weakness eight hours after drinking "comfrey" tea. She had bradycardia (54 beats/min) and hyperkalemia (7.6 mEq/L). Electrocardiogram revealed a first-degree atrioventricular conduction block with premature atrial contractions, followed by polymorphic ventricular tachycardia three hours after arrival. A serum digoxin level was 151.2 ng/mL. The patient developed ventricular fibrillation while waiting for Digibind infusion. Resuscitation was performed and an emergent VA-ECMO was set up. A total of eight vials of Digibind were given over the next 16 hours. She temporarily regained consciousness, but remained hemodynamically unstable and subsequently developed lower limb ischemia and multiple organ failure, and she expired on hospital day seven. A botanist confirmed that the plant was foxglove. CONCLUSIONS: The diagnosis of cardiac glycoside plant poisoning can be difficult in the absence of an accurate exposure history. In facilities where DSFab is unavailable or insufficient, early VA-ECMO might be considered in severely cardiotoxic patients unresponsive to conventional therapy.

Unintentional Pediatric Cocaine Exposures Result in Worse Outcomes than Other Unintentional Pediatric Poisonings.

BACKGROUND: Unintentional pediatric cocaine exposures are rare but concerning due to potentially serious complications such as seizures, dysrhythmias, and death. OBJECTIVES: The objectives were to assess the demographic and clinical characteristics of pediatric cocaine exposures reported to the California Poison Control System. METHODS: This is a retrospective study of all confirmed pediatric (< 6 years of age) cocaine exposures reported to the California Poison Control System from January 1, 1997-September 30, 2010. Case narratives were reviewed for patient demographics, exposure details, clinical effects, therapy, hospitalization, and final outcome. RESULTS: Of the 86 reported pediatric cocaine exposures, 36 had positive urine drug testing and were included in the study cohort. The median age at presentation was 18 months (range: 0-48 months), and 56% were male (n = 20). The most common clinical manifestations were tachycardia and seizures. The most common disposition was admission to an intensive care unit (n = 14; 39%). Eleven cases (31%) were classified as having a major effect as per American Association of Poison Control Centers case coding guidelines. One child presented in asystole with return of spontaneous circulation after cardiopulmonary resuscitation and multiple vasoactive medications. The proportion of cocaine exposures with serious (moderate or major) outcomes (66.7%; 95% confidence interval 50.3-79.8%) was higher than other pediatric poisonings reported to the American Association of Poison Control Centers during the study period (0.88%; 95% confidence interval 0.87-0.88). CONCLUSIONS: Although pediatric cocaine exposures are rare, they result in more severe outcomes than most unintentional pediatric poisonings. Practitioners need to be aware of the risk of recurrent seizures and cardiovascular collapse associated with cocaine poisoning.

Treatment of cocaine cardiovascular toxicity: a systematic review.

INTRODUCTION: Cocaine abuse is a major worldwide health problem. Patients with acute cocaine toxicity presenting to the emergency department may require urgent treatment for tachycardia, dysrhythmia, hypertension, and coronary vasospasm, leading to pathological sequelae such as acute coronary syndrome, stroke, and death. OBJECTIVE: The objective of this study is to review the current evidence for pharmacological treatment of cardiovascular toxicity resulting from cocaine abuse. METHODS: MEDLINE, PsycINFO, Database of Abstracts of Reviews of Effects (DARE), OpenGrey, Google Scholar, and the Cochrane Library were searched from inception to November 2015. Articles on pharmacological treatment involving human subjects and cocaine were selected and reviewed. Evidence was graded using Oxford Centre for Evidence-Based Medicine guidelines. Treatment recommendations were compared to current American College of Cardiology/American Heart Association guidelines. Special attention was given to adverse drug events or treatment failure. The search resulted in 2376 articles with 120 eligible involving 2358 human subjects. Benzodiazepines and other GABA-active agents: There were five high-quality (CEBM Level I/II) studies, three retrospective (Level III), and 25 case series/reports (Level IV/V) supporting the use of benzodiazepines and other GABA-active agents in 234 subjects with eight treatment failures. Benzodiazepines may not always effectively mitigate tachycardia, hypertension, and vasospasm from cocaine toxicity. Calcium channel blockers: There were seven Level I/II, one Level III, and seven Level IV/V studies involving 107 subjects and one treatment failure. Calcium channel blockers may decrease hypertension and coronary vasospasm, but not necessarily tachycardia. Nitric oxide-mediated vasodilators: There were six Level I/II, one Level III, and 25 Level IV/V studies conducted in 246 subjects with 11 treatment failures and two adverse drug events. Nitroglycerin may lead to severe hypotension and reflex tachycardia. Alpha-adrenoceptor blocking drugs: There were two Level I studies and three case reports. Alpha-1 blockers may improve hypertension and vasospasm, but not tachycardia, although evidence is limited. Alpha-2-adrenoceptor agonists: There were two high-quality studies and one case report detailing the successful use of dexmedetomidine. Beta-blockers and ß/α-blockers: There were nine Level I/II, seven Level III, and 34 Level IV/V studies of ß-blockers, with 1744 subjects, seven adverse drug events, and three treatment failures. No adverse events were reported for use of combined ß/α-blockers such as labetalol and carvedilol, which were effective in attenuating both hypertension and tachycardia. Antipsychotics: Seven Level I/II studies, three Level III studies, and seven Level IV/V case series and reports involving 168 subjects have been published. Antipsychotics may improve agitation and psychosis, but with inconsistent reduction in tachycardia and hypertension and risk of extrapyramidal adverse effects. Other agents: There was only one high level study of morphine, which reversed cocaine-induced coronary vasoconstriction but increased heart rate. Other agents reviewed included lidocaine, sodium bicarbonate, amiodarone, procainamide, propofol, intravenous lipid emulsion, propofol, and ketamine. CONCLUSIONS: High-quality evidence for pharmacological treatment of cocaine cardiovascular toxicity is limited but can guide acute management of associated tachycardia, dysrhythmia, hypertension, and coronary vasospasm. Future randomized prospective trials are needed to evaluate new agents and further define optimal treatment of cocaine-toxic patients.

Treatment of drug-induced seizures.

Seizures are a common complication of drug intoxication, and up to 9% of status epilepticus cases are caused by a drug or poison. While the specific drugs associated with drug-induced seizures may vary by geography and change over time, common reported causes include antidepressants, stimulants and antihistamines. Seizures occur generally as a result of inadequate inhibitory influences (e.g., gamma aminobutyric acid, GABA) or excessive excitatory stimulation (e.g. glutamate) although many other neurotransmitters play a role. Most drug-induced seizures are self-limited. However, status epilepticus occurs in up to 10% of cases. Prolonged or recurrent seizures can lead to serious complications and require vigorous supportive care and anticonvulsant drugs. Benzodiazepines are generally accepted as the first line anticonvulsant therapy for drug-induced seizures. If benzodiazepines fail to halt seizures promptly, second line drugs include barbiturates and propofol. If isoniazid poisoning is a possibility, pyridoxine is given. Continuous infusion of one or more anticonvulsants may be required in refractory status epilepticus. There is no role for phenytoin in the treatment of drug-induced seizures. The potential role of ketamine and levetiracetam is promising but not established.

Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review.

BACKGROUND: Overdose of amphetamine, related derivatives, and analogues (ARDA) continues to be a serious worldwide health problem. Patients frequently present to the hospital and require treatment for agitation, psychosis, and hyperadrenegic symptoms leading to pathologic sequelae and mortality. OBJECTIVE: To review the pharmacologic treatment of agitation, psychosis, and the hyperadrenergic state resulting from ARDA toxicity. METHODS: MEDLINE, PsycINFO, and the Cochrane Library were searched from inception to September 2014. Articles on pharmacologic treatment of ARDA-induced agitation, psychosis, and hyperadrenergic symptoms were selected. Evidence was graded using Oxford CEBM. Treatment recommendations were compared to current ACCF/AHA guidelines. RESULTS: The search resulted in 6082 articles with 81 eligible treatment involving 835 human subjects. There were 6 high-quality studies supporting the use of antipsychotics and benzodiazepines for control of agitation and psychosis. There were several case reports detailing the successful use of dexmedetomidine for this indication. There were 9 high-quality studies reporting the overall safety and efficacy of ß-blockers for control of hypertension and tachycardia associated with ARDA. There were 3 high-quality studies of calcium channel blockers. There were 2 level I studies of α-blockers and a small number of case reports for nitric oxide-mediated vasodilators. CONCLUSIONS: High-quality evidence for pharmacologic treatment of overdose from ARDA is limited but can help guide management of acute agitation, psychosis, tachycardia, and hypertension. The use of butyrophenone and later-generation antipsychotics, benzodiazepines, and ß-blockers is recommended based on existing evidence. Future randomized prospective trials are needed to evaluate new agents and further define treatment of these patients.

Ventricular dysrhythmias associated with poisoning and drug overdose: a 10-year review of statewide poison control center data from California.

BACKGROUND: Ventricular dysrhythmias are a serious consequence associated with drug overdose and chemical poisoning. The risk factors for the type of ventricular dysrhythmia and the outcomes by drug class are not well documented. OBJECTIVE: The aim of this study was to determine the most common drugs and chemicals associated with ventricular dysrhythmias and their outcomes. METHODS: We reviewed all human exposures reported to a statewide poison control system between 2002 and 2011 that had a documented ventricular dysrhythmia. Cases were differentiated into two groups by type of arrhythmia: (1) ventricular fibrillation and/or tachycardia (VT/VF); and (2) torsade de pointes (TdP). RESULTS: Among the 300 potential cases identified, 148 cases met the inclusion criteria. Of these, 132 cases (89%) experienced an episode of VT or VF, while the remaining 16 cases (11%) had an episode of TdP. The most commonly involved therapeutic classes of drugs associated with VT/VF were antidepressants (33/132, 25%), stimulants (33/132, 25%), and diphenhydramine (16/132, 12.1%). Those associated with TdP were antidepressants (4/16, 25%), methadone (4/16, 25%), and antiarrhythmics (3/16, 18.75%). Drug exposures with the greatest risk of death in association with VT/VF were antidepressant exposure [odds ratio (OR) 1.71; 95% confidence interval (CI) 0.705-4.181] and antiarrhythmic exposure (OR 1.75; 95% CI 0.304-10.05), but neither association was statistically significant. Drug exposures with a statistically significant risk for TdP included methadone and antiarrhythmic drugs. CONCLUSIONS: Antidepressants and stimulants were the most common drugs associated with ventricular dysrhythmias. Patients with suspected poisonings by medications with a high risk of ventricular dysrhythmia warrant prompt ECG monitoring.

Symptomatic Exposures Among California Inmates 2011-2013.

Prisoners have a high prevalence of substance misuse and abuse, but few studies have examined symptomatic exposures among incarcerated populations. We sought to further characterize the nature of these exposures among this population using the California Poison Control System data. Keyword searches identified inmate cases in 2011-2013 for patients 20+ years old exposed to a single substance and taken to hospital from jail, prison, or police custody. Comparisons were made with non-inmate cases during the same period, using similar limitations. Body stuffers and body packers were analyzed as a subgroup. Seven hundred four inmate cases were compared to 106,260 non-inmate cases. Inmates were more likely to be younger, male, and to have engaged in drug misuse or abuse. They most commonly ingested methamphetamine, heroin, acetaminophen, and anticonvulsants. Inmates were more likely to receive activated charcoal (OR 9.87, 8.20-11.88), whole bowel irrigation (OR 44.50, 33.83-58.54), undergo endotracheal intubation (OR 4.09, 2.91-5.73), and to experience a major clinical outcome or death (OR 1.41, 1.05-1.89). When body stuffers and packers were removed, clinical findings were similar, though the odds of a major outcome or death became statistically non-significant. Body stuffers and body packers primarily used methamphetamine and heroin, and compared with other inmates had significantly higher odds of both adverse clinical effects and poor outcome. This large series provides a profile of symptomatic exposures among inmates, a little-studied population. The potential for high morbidity among body stuffers and packers suggests that a high index of suspicion of such ingestions be maintained when evaluating patients prior to incarceration.

Massive naproxen overdose with serial serum levels.

CONTEXT: Massive naproxen overdose is not commonly reported. Severe metabolic acidosis and seizure have been described, but the use of renal replacement therapy has not been studied in the context of overdose. CASE DETAILS: A 28-year-old man ingested 70 g of naproxen along with an unknown amount of alcohol in a suicidal attempt. On examination in the emergency department 90 min later, he was drowsy but had normal vital signs apart from sinus tachycardia. Serum naproxen level 90 min after ingestion was 1,580 mg/L (therapeutic range 25-75 mg/L). He developed metabolic acidosis requiring renal replacement therapy using sustained low efficiency dialysis (SLED) and continuous venovenous hemofiltration (CVVH) and had recurrent seizure activity requiring intubation within 4 h from ingestion. He recovered after 48 h. DISCUSSION: Massive naproxen overdose can present with serious toxicity including seizures, altered mental status, and metabolic acidosis. CONCLUSION: Hemodialysis and renal replacement therapy may correct the acid base disturbance and provide support in cases of renal impairment in context of naproxen overdose, but further studies are needed to determine the extraction of naproxen.

Predictors of Death and Prolonged Renal Insufficiency in Ethylene Glycol Poisoning.

BACKGROUND: We assessed the predictive value of selected factors on the outcomes of death and prolonged renal insufficiency (RI) from ethylene glycol poisoning. METHODS: Retrospective, observational California Poison Control System study, over a 10-year period (1999-2008). We compared 2 groups. The first group (D/RI) included 59 patients who died (9 patients) or had prolonged RI (50 patients). Prolonged RI was defined as kidney injury in which dialysis was required for greater than 3 days after presentation. The second group (RECOV) of 62 patients had an uncomplicated recovery. Secondarily, we evaluated the association of time to antidote (ethanol and/or fomepizole) and time to dialysis with these outcomes. RESULTS: The D/RI group was more likely than the RECOV group to present comatose, have seizures, and require intubation. The D/RI group had a lower mean initial arterial pH of 7.03 (standard deviation [SD] 0.20), compared to 7.27 (SD 0.14) for the RECOV group. The D/RI group had a higher initial creatinine (1.7 mg/dL, SD 0.71) than that of the RECOV group (1.0 mg/dL, SD 0.33). Patients with a time to antidote greater than 6 hours had a higher odds of dying or having prolonged RI (OR 3.34, 95% CI : 1.21-9.26) Patients with a time to dialysis greater than 6 hours had a lower odds of dying or having prolonged RI (OR 0.36, 95% CI : 0.15-0.87). CONCLUSION: Compared to survivors with an uncomplicated recovery, patients poisoned with ethylene glycol who died or had prolonged RI were more likely to exhibit clinical signs such as coma, seizures, and acidosis. Antidote administration within 6 hours is associated with better outcomes, unlike earlier time to dialysis.