Impact of co-ingestion of ethanol on the clinical symptomatology and severity of patients attended in the emergency department for recreational drug toxicity.

OBJECTIVE: Investigate whether there are differences in the drugs involved, symptomatology and severity of drug intoxication in patients with co-ingestion of alcohol attended in hospital emergency departments (ED). METHOD: Patients attended in 11 Spanish EDs due to drug intoxication were included. Sociodemographic and clinical characteristics were collected. A combined adverse event of cardiorespiratory arrest, need for intubation, and admission to intensive care or death was considered as the primary indicator of severity. The symptomatology and severity were compared adjusted for age, sex and type of drug based on whether or not ethanol had been co-ingested. RESULTS: 3925 patients (alcohol co-ingestion: 2290, 58.3%) with a mean age of 33 (±11) years were included, and 25% were women. Co-ingestion of alcohol was observed in younger patients, in EDs in areas with high leisure tourism, on holidays and during the early morning hours. It was also more frequent in individuals intoxicated by amphetamine derivatives (66.2%) and cocaine (65.7%), and was more frequently associated with a reduction in consciousness (odds ratio [OR] = 2.13, 95% confidence interval [CI] 1.69-2.67) and agitation/aggressiveness (OR = 1.22, 95% = 1.04-1.43). A combined adverse event was observed in 114 patients (2.9%) with no differences between individuals co-ingesting or not ethanol (3.1% vs. 2.7%; OR = 1.11, 95% CI = 0.74-1.65). CONCLUSION: Co-ingestion of alcohol is more frequent in individuals intoxicated by cocaine and amphetamines and predisposes a greater reduction in the level of consciousness or agitation, although there are no differences in the severity of the episodes of drug intoxication.

Epidemiology of acute poisoning by substances of abuse in the Emergency Department. Descriptive study in District IV of Asturias. / Epidemiología de las intoxicaciones agudas por sustancias de abuso en Urgencias. Estudio descriptivo en el área IV de Asturias.

The incidence of acute poisonings has increased in recent years and constitutes approximately 2% of the services provided by the Emergency Department currently. The objective of this study is to describe the frequency and characteristics of the intoxications treated at the Central University Hospital of Asturias during 2015 from biochemical-analytical, epidemiological and medical-legal perspectives. We conducted a retrospective study and a descriptive analysis of the clinical and sociodemographic variables included in the acute intoxication (AI) protocol at the national level. This hospital treated 2,478 cases of acute poisoning, representing 2.3% of the emergencies treated and corresponding to an incidence of 764 cases/100,000 inhabitants/year with an age ranging from under 1 year to over 80 years. The average age of the patients was 43.6 (SD = 16.6) years. Of these patients, 59.4% were males with an average age of 44 (SD = 16.8) years, and women represented 43.1% with an average age of 42.8 (SD = 16.5) years. These intoxications have a frequency of 47.2% during the weekend, while 37.4% occur between June and September. Acute voluntary intoxication is the most frequent intentionality, corresponding to 83.2% of the cases. We must point out that the medical records register 16.8% of the cases as suicide attempts. Ethanol and benzodiazepines are the most commonly-used toxics. These intoxications are treated in the Emergency Department without requiring hospitalization and have a very low mortality rate.

La incidencia de las intoxicaciones agudas ha aumentado en los últimos años, y actualmente constituye aproximadamente el 2% de las atenciones sanitarias llevadas a cabo por los Servicios de Urgencias. El objetivo de este estudio es describir la frecuencia y características de las intoxicaciones atendidas en el Hospital Universitario Central de Asturias durante el año 2015 desde la perspectiva bioquímica-analítica, epidemiológica y médico-legal. Se realizó un estudio retrospectivo y un análisis descriptivo de las variables clínicas y sociodemográficas incluidas en el protocolo de intoxicación aguda a nivel nacional. Este hospital atendió 2478 casos de intoxicaciones agudas representando el 2,3% de las urgencias atendidas y que corresponde a una incidencia de 764 casos/100000 habitantes/año con un rango de edad de menores de 1 año a mayores de 80 años. La edad media de los pacientes atendidos fue de 43,6 (DE = 16,6) años. El 59,4% de los pacientes eran varones con una edad media de 44 (DE = 16,8) años, las mujeres representaban el 43,1% y su edad media era de 42,8 (DE = 16,5) años. El 47,2% de estas intoxicaciones ocurren durante el fin de semana y el 37,4% se dan entre junio y septiembre. La intencionalidad más frecuente es la intoxicación aguda voluntaria correspondiente al 83,2% de los casos. Cabe destacar que el 16,8% de los casos están referenciados en su historia clínica como intentos de suicidio. Los tóxicos más empleados son el etanol y las benzodiacepinas. Estas intoxicaciones son resueltas en el Servicio de Urgencias sin requerir ingreso hospitalario y poseen una tasa de mortalidad muy baja.

Sex differences in patients with suicidal intent that are managed by toxicologists: An analysis of the Toxicology Investigators' Consortium (ToxIC) Registry.

INTRODUCTION: The Toxicology Investigator's Consortium (ToxIC) maintains a prospective case registry of all patients that have been managed at the bedside by medical toxicologists. We set out to characterize the differences in toxicological suicide attempts between men and women among adult patients with poisonings managed by medical toxicologists. METHODS: ToxIC database consults for adults aged 19-65 whose primary reasons for encounter were classified as suicide attempt were used for this study (1/2010-12/2016). Data used for analysis included primary agents of toxic exposure, routes of administration, and complications. The statistical analysis was limited to descriptive methods. RESULTS: Out of 51,440 registry cases, 33,259 cases remained for analysis after applying the ages 19-65 and removing those without complete data. Of these, there were 4827 suicide attempts (14.5% of toxicological exposures) which were sub classified by gender. There were more females (F) than males (M) whose toxicology consults were due to suicidal attempts (57.6% versus 42.4%). We also found that more males used alcohol as their primary agent (2.8%M v 1.5%F) or a nonpharmaceutical (%7.4 M v %2.3 F). CONCLUSIONS: In our study, we found that there were more females than males who attempted suicide by self-poisoning; and more of them used pharmaceuticals than males. In contrast, a greater number of males used nonpharmaceuticals such as alcohol. We did not find large sex-differences in suicide completion rates, routes of administration, or subsequent symptomologies. In summary, sex-based differences were observed between adult patients with suicidal-intent exposures/ingestions managed at the bedside by medical toxicologists.

A comparison of blood toxicology in fatalities involving alcohol and other drugs in patients with an opioid use disorder treated with methadone, buprenorphine, and implant naltrexone.

Background: Methadone, buprenorphine, and implant naltrexone have comparable efficacy in preventing death from drug intoxication during treatment, but there may be differences between treatments in the specific drugs contributing to death and in the risk of death during different phases of treatment.Objective: The objective of this study was to compare concentrations of individual drugs in decedents for evidence that the three medications use to treat opioid use disorders differed in the protection they offered against fatal overdose.Methods: Fatalities with a primary or co-diagnosis of alcohol or other drug poisoning in patients treated with methadone (n = 66, 74.2% male), buprenorphine (n = 54, 74.1% male), or naltrexone (n = 28, 85.7% male) were identified by combining treatment (Monitoring of Drugs of Dependence System and clinical records) and mortality records (Western Australian Death Registry). Quantitative postmortem blood drug analysis data were obtained for drug-related deaths. The presence/absence of drugs were compared between the three medication groups and between phases of treatment (on-treatment/off-treatment).Results: Opioids (89.8%) and benzodiazepines (76.2%) were most commonly identified in postmortem blood. The three medication groups did not differ materially in the drugs present postmortem, except that alcohol was less prevalent in naltrexone-treated cases. Morphine or heroin intoxication was implicated in more patients dying off-treatment than on-treatment but levels of morphine and other drugs were comparable across the two phases.Conclusion: Comparisons of postmortem concentrations of specific drugs indicated that patients treated with methadone, buprenorphine, and implant naltrexone had comparable susceptibilities to lethal co-intoxication and that similar drug mixtures contributed to death.

Ethanol Intoxication Alleviates the Inflammatory Response of Remote Organs to Experimental Traumatic Brain Injury.

Traumatic brain injury (TBI) may cause damage to distant organs. Acute ethanol intoxication (EI) induces complex local and systemic anti-inflammatory effects and influences the early outcomes of traumatized patients. Here, we evaluated its effects on the BI-induced expression of local inflammatory mediators in the trauma-remote organs the lungs and liver. Male mice were exposed to ethanol as a single oral dose (5g·kg-1, 32%) before inducing a moderate blunt TBI. Sham groups underwent the same procedures without TBI. Ether 3 or 6h after the TBI, the lung and liver were collected. The gene expression of HMGB1, IL-6, MMP9, IL-1ß, and TNF as well as the homogenate protein levels of receptor for advanced glycation end products (RAGE), IL-6, IL-1ß, and IL-10 were analyzed. Liver samples were immunohistologically stained for HMGB1. EI decreased the gene expressions of the proinflammatory markers HMGB1, IL-6, and MMP9 in the liver upon TBI. In line with the reduced gene expression, the TBI-induced protein expression of IL-6 in liver tissue homogenates was significantly reduced by EI at 3h after TBI. While the histological HMGB1 expression was enhanced by TBI, the RAGE protein expression in the liver tissue homogenates was diminished after TBI. EI reduced the histological HMGB1 expression and enhanced the hepatic RAGE protein expression at 6h post TBI. With regard to the lungs, EI significantly reduced the gene expressions of HMGB1, IL-6, IL-1ß, and TNF upon TBI, without significantly affecting the protein expression levels of inflammatory markers (RAGE, IL-6, IL-1ß, and IL-10). At the early stage of TBI-induced inflammation, the gene expression of inflammatory mediators in both the lungs and liver is susceptible to ethanol-induced remote effects. Taken together, EI may alleviate the TBI-induced pro-inflammatory response in the trauma-distant organs, the lungs and liver, via the HMGB1-RAGE axis.

[Morphofunctional characteristic of the microvasculature of the lung tissue in acute fatal ethanol poisoning]. / Morfofunktsional'naya kharakteristika mikrotsirkulyatornogo rusla legochnoi tkani pri ostrom smertel'nom otravlenii etanolom.

The purpose of this work is an in-depth study of main morphological features and pathogenesis of acute lung injury in cases of acute fatal poisoning with ethanol; assessment of microcirculation disorders in the respiratory system; details of the mechanisms of development of non-cardiogenic pulmonary edema. An analysis of 160 deaths of men and women aged 19 to 85 years from acute ethanol poisoning was made. Histological preparations were colored with hematoxylin and eosin according to the Van Gieson method, elastic fibers - according to Weigert. It was established that the first reaction in response to the effect of ethanol is hemodynamic disorders, then interstitial and alveolar edema develops; pronounced changes occur in endothelial cells, which lead to plasmorrhagia and hyalinosis.

Ethanol and its metabolites: update on toxicity, benefits, and focus on immunomodulatory effects.

This article summarizes recent experimental and epidemiological data on the toxic and beneficial effects of ethanol and its metabolites (acetaldehyde), and focuses on their immunomodulatory effects. The section dealing with the toxic effects of alcohol focuses on its chronic toxicity (liver disorders, carcinogenic effects, cardiovascular disorders, neuropsychic disorders, addiction and withdrawal syndrome, hematologic disorders, reprotoxicity, osteoporosis) although acute toxicity is considered. The role of oxidative metabolism of ethanol by alcohol dehydrogenase, cytochrome P450 2E1, and aldehyde dehydrogenase, as well as the impact of genetic polymorphism in its physiopathology are also highlighted. The section dealing with the beneficial effects of low to moderate alcohol consumption (on cardiovascular system, diabetes, the nervous system and sensory organs, autoimmune diseases, and rheumatology) highlights the importance of anti-inflammatory and immunomodulatory effects in these observations. This knowledge, enriched by a focus on the immunomodulatory effects of ethanol and its metabolites, in particular on the NLRP3 inflammasome pathway, might facilitate the development of treatments that can reduce ethanol's harmful effects or accentuate its beneficial effects.

The Role of Drugs in Alcohol Poisoning and Blackout Events: A Latent Class Analysis of a Residential Treatment Sample.

BACKGROUND: Alcohol can lead to fatal and nonfatal overdose (OD) through its neurobiological inhibitory effects when used alone or with other drugs. Little research has examined alcohol OD characteristics in the context of concomitant drug use. METHODS: This study utilized alcohol OD data (defined as alcohol poisoning, passing out, or blacking out) collected in a large residential addiction treatment facility (N = 660). Latent class analysis identified classes of alcohol OD events based on concomitant drug use at the time of OD. We evaluated correlates of alcohol OD classes, including depression, emergency medical services, and hospitalization, using latent class regression. RESULTS: Only 20% of alcohol ODs involved alcohol alone. Marijuana was the most commonly used drug during the most recent alcohol OD (43.2%), followed by sedatives (27.9%), cocaine or crack (25.9%), prescription opioids (26.1%), and heroin (20%). The final latent class model included 3 classes: no/low drug involvement (61%), moderate drug involvement (33%), and high drug involvement (6%). Relative to the no/low drug involvement class, participants admitted to the hospital were 6.4-fold more likely to be in the high drug involvement class (95% CI: 2.4 to 16.6) and 2.9-fold more likely to be in the moderate drug involvement class (95% CI: 1.2 to 7.2). Participants receiving emergency medical services were more likely to be in the high drug involvement class (aOR: 2.2, 95% CI: 2.2, 1.1 to 4.5) and less likely to be in the moderate drug involvement class (aOR 0.39, 95% CI: 0.2 to 0.96). CONCLUSIONS: Combining drug classes with alcohol prior to OD was common and associated with a higher likelihood of hospitalization. Overdose prevention efforts should address acute risks of alcohol ingestion with other drugs.

Historical Persistence of Alcohol-Induced Mortality in the Russian Federations: Legacy of Early Industrialization.

AIMS: The study aims to investigate insofar regional differences in alcohol-induced mortality in Russia, which emerged during the early industrialization of the country, persisted over a prolonged period of time (from late nineteenth to early twenty-first century), surviving fundamental political and social changes Russia experienced. METHODS: Multivariate regression models with historical and contemporary data on alcohol-induced mortality in Russian regions were estimated to document the persistence of spatial patterns of mortality, as well as to identify the possible mediating variables. Numerous robustness checks were used to corroborate the results. RESULTS: Alcohol-induced male mortality in Russian regions in 1880s-1890s is significantly and strongly correlated with male mortality due to accidental alcohol poisoning in Russian regions in 2010-2012. For female mortality, no robust correlation was established. The results for male mortality do not change if one controls for a variety of other determinants of alcohol-induced mortality and are not driven by outlier regions. Consumption of strong alcohol (in particular vodka) appears to be the mediator variable explaining this persistence. CONCLUSIONS: Hazardous drinking behavioral patterns, once they emerge and crystalize during the periods of fragmentation of the traditional society and the early onsets of modernization and urbanization, can be extremely persistent. Even highly intrusive policy interventions at a later stage (like those of the Soviet government) may turn out to be insufficient to change the path-dependent outcomes.

Can ethanol intoxication secondary to docetaxel be predicted based on dose administered using a point-of-care saliva ethanol test?

BACKGROUND: The Food and Drug Administration issued a drug safety alert highlighting the potential association of docetaxel infusion with signs and symptoms of alcohol intoxication. This concern is significant because patients treated with docetaxel often have comorbidities and are prescribed concomitant centrally active medications. As a result, these patients may be at risk for iatrogenic events. OBJECTIVE: The objective of this study was to identify a correlation with docetaxel infusion and saliva ethanol concentration using a point-of-care ethanol test. METHODS: In this pilot study, ethanol concentrations were measured using a validated saliva ethanol test in patients receiving intravenous docetaxel as part of their chemotherapy regimen. Both ethanol dose and infusion rate were calculated based on the amount of the specific docetaxel product administered. Saliva ethanol concentrations were measured at baseline, immediately after infusion completion, and at 30 and 60 min postinfusion. RESULTS: A total of 17 patients were included in the analysis. The mean ethanol dose administered was 2.6 ± 0.5 g of ethanol per infusion of docetaxel with a mean infusion rate of 3.2 ± 0.7 ml of ethanol per hour. At baseline, immediately after infusion, and 30 and 60 min postinfusion, all patients had a saliva ethanol test result of 0 mg/dl. CONCLUSION: Based on this small pilot study, the prediction of patients who will experience ethanol intoxication using a point-of-care saliva ethanol test based on the docetaxel dose administered is challenging. This observation requires confirmation in larger and more heterogeneous populations.

Ethanol Intoxication of Young Children.

Ethanol intoxication of infants and young children can be a challenging diagnosis in the pediatric emergency department, and features of the poisoning may differ in comparison with adolescents. The sources of ethanol exposures in this age are varied and include unintentional, malicious, and iatrogenic etiologies. Young children exposed to ethanol often present with mixed clinical signs and symptoms that may not fit the traditional ethanol or sedative-hypnotic toxidrome. Pediatric ethanol intoxications are often managed supportively, and recovery is usually rapid. The purpose of this review is to describe the sources of ethanol poisoning among children 6 years and younger, highlight presenting symptoms and pharmacokinetic considerations unique to this age group, and review management strategies. In addition, published cases of ethanol poisoning due to ingestion among young infants are compiled for presentation.

Validation of the Poisoning Severity Score (PSS) in suicidal behavior by self-poisoning.

Intentional self-poisoning is the leading method of suicidal behavior leading to medical attention worldwide. The medical severity of self-poisoning events has major treatment, prognostic, and medico-legal implications, yet measures of severity are limited. The Poisoning Severity Score (PSS) is a widely used scale but validation data are limited, particularly in the study of suicidal behavior per se. The sample was a consecutive series of intentional self-poisoning patients aged 13 to 65 treated at a large university medical center (n = 673). PSS scores, with a range 0 (none) to 4 (death), were calculated along with other structured clinical data and analyzed in a series of linear regressions adjusted for age and sex. Higher PSS scores were consistently associated with greater medical morbidity and more intensive acute medical treatments, and nearly all effect sizes were large. Results support the validity of the PSS in hospital-treated self-poisoning patients.

[Morphological markers of liver function in alcohol intoxication]. / Morfologicheskie markery funktsional'noi aktivnosti pecheni pri alkogol'noi intoksikatsii.

The aim of this study was to find additional diagnostic markers characterizing the functional state of the liver to substantiate the cause of death from ethanol poisoning. A total of 95 deaths from acute ethanol poisoning and 15 deaths from craniocerebral injury were studied. Signs of steatosis, chronic hepatitis or cirrhosis were taken into account in histological examination of the liver. The histochemical activity of ethano-locking enzymes was determined in structurally functional zones of the acini: portal pathways (Zone 1), liver beams (Zone 2) and central veins (Zone 3). Quantitative indices characterizing functional-metabolic activity of the liver during acute ethanol poisoning were obtained.

[The use of biochemical characteristics of cadaveric blood in the forensic diagnosis of lethal poisoning]. / Ispol'zovanie nekotorykh sudebno-biokhimicheskikh pokazatelei trupnoi krovi pri diagnostike letal'nykh otravlenii.

The purpose of the work is the development of mathematical models in the forensic diagnosis of poisonings by the main groups of toxicologically important substances, on the basis of biochemical characteristics of blood. The most informative forensic and biochemical indicators of cadaveric blood used to detect lethal poisoning are the urea content, total protein content, and the ratio of urea to creatinine. Mathematical models of poisoning can be used to diagnose poisoning with narcotic drugs, psychotropic substances and substitutes of ethyl alcohol.

[Analysis of fatal cases of psychoactive drug overdoses in the Crimean Republic between 1993-2017]. / Analiz smertel'nykh otravlenii psikhoaktivnymi veshchestvami v Respublike Krym za 1993-2017 gg.

An analysis of fatal drug overdoses in the population of the Crimean Republic between 1993-2017 was conducted. The epidemiological characteristics of these drug overdoses were determined. Deaths from drug overdoses occurs mainly in male population during the most active years of drug use (21-30 years). The most frequent cause of death is opioid drug overdose and combined alcohol-opioid intoxication.

Prenatal Ethanol Exposure Persistently Alters Endocannabinoid Signaling and Endocannabinoid-Mediated Excitatory Synaptic Plasticity in Ventral Tegmental Area Dopamine Neurons.

Prenatal ethanol exposure (PE) leads to increased addiction risk which could be mediated by enhanced excitatory synaptic strength in ventral tegmental area (VTA) dopamine (DA) neurons. Previous studies have shown that PE enhances excitatory synaptic strength by facilitating an anti-Hebbian form of long-term potentiation (LTP). In this study, we investigated the effect of PE on endocannabinoid-mediated long-term depression (eCB-LTD) in VTA DA neurons. Rats were exposed to moderate (3 g/kg/d) or high (6 g/kg/d) levels of ethanol during gestation. Whole-cell recordings were conducted in male offspring between 4 and 10 weeks old.We found that PE led to increased amphetamine self-administration. Both moderate and high levels of PE persistently reduced low-frequency stimulation-induced eCB-LTD. Furthermore, action potential-independent glutamate release was regulated by tonic eCB signaling in PE animals. Mechanistic studies for impaired eCB-LTD revealed that PE downregulated CB1 receptor function. Interestingly, eCB-LTD in PE animals was rescued by metabotropic glutamate receptor I activation, suggesting that PE did not impair the synthesis/release of eCBs. In contrast, eCB-LTD in PE animals was not rescued by increasing presynaptic activity, which actually led to LTP in PE animals, whereas LTD was still observed in controls. This result shows that the regulation of excitatory synaptic plasticity is fundamentally altered in PE animals. Together, PE leads to impaired eCB-LTD at the excitatory synapses of VTA DA neurons primarily due to CB1 receptor downregulation. This effect could contribute to enhanced LTP and the maintenance of augmented excitatory synaptic strength in VTA DA neurons and increased addiction risk after PE.SIGNIFICANCE STATEMENT Prenatal ethanol exposure (PE) is among many adverse developmental factors known to increase drug addiction risk. Increased excitatory synaptic strength in VTA DA neurons is a critical cellular mechanism for addiction risk. Our results show that PE persistently alters eCB signaling and impairs eCB-LTD at the excitatory synapses, an important synaptic plasticity that weakens synaptic strength. These effects combined with PE-induced anti-Hebbian long-term potentiation reported in a previous study could result in the maintenance of enhanced excitatory synaptic strength in VTA DA neurons, which in turn contributes to PE-induced increase in addiction risk. Our findings also suggest that restoring normal eCB signaling in VTA DA neurons could be a useful strategy for treating behavioral symptoms caused by PE.

AntogomiR-451 protects human gastric epithelial cells from ethanol via activating AMPK signaling.

The prevention and treatment efficiency of ethanol-induced gastric epithelial injury are not satisfied. We have previously shown that AMP-activated protein kinase (AMPK) activation exerts a pro-survival function in human gastric epithelial cells (GECs). miroRNA-451 ("miR-451")'s inhibitor, antagomiR-451, can activate AMPK signaling. In the present study, we show that forced-expression of antagomiR-451 via a lentiviral vector depleted miR-451, leading to AMPK activation in established GES-1 cells and primary human GECs. AntagomiR-451 efficiently protected GES-1 cells and primary human GECs from ethanol-induced viability reduction and apoptosis. AMPK activation is required for antagomiR-451-induced GEC protection. AMPKα1 knockdown (by targeted-shRNAs) or knockout (by CRISPR-Cas-9 KO plasmid) blocked antagomiR-451-induced AMPK activation, and GEC protection against ethanol. Further experimental results show that antagomiR-451 significantly attenuated ethanol-induced reactive oxygen species (ROS) production, lipid peroxidation and DNA damage. Collectively, antagomiR-451 protects human GECs from ethanol via activating AMPK signaling.

Surrogate Alcohol or Nonbeverage Alcohol Consumption: The Surrogate Alcohol Questionnaire (SAQ).

BACKGROUND: Diagnosis and treatment of alcohol use disorders and their sequelae are common clinical questions for the consultation-liaison psychiatrist. At an urban, academic medical center, the authors consulted on several patients whose consumption of alcohol included nonbeverage forms of alcohol, (described in the literature as surrogate alcohols, nonbeverage alcohols, e.g., mouthwash). METHODS: The authors describe 4 patients who presented with surrogate alcohol consumption. The authors review the clinical issues and literature related to surrogate alcohol use. The authors describe the array of substances, which either contain ethanol, but are not intended for drinking, or which contain other intoxicating alcohols (e.g., methanol), that are consumed in lieu of traditional beverage alcohol. Furthermore, the authors discuss standard medical treatment interventions for ethanol and non-ethanol based alcohols. The authors propose a screening tool, the surrogate alcohol questionnaire, a tool to facilitate better recognition of surrogate alcohol use.

Etiologies of altered mental status in patients with presumed ethanol intoxication.

BACKGROUND: Altered mental status is a commonly evaluated problem in the ED. Ethanol intoxication is common, and prehospital history may bias emergency physicians to suspect this as the cause of altered mental status. Quantitative ethanol measurement can rapidly confirm the diagnosis, or if negative, prompt further evaluation. Our objective was to identify the etiologies of altered mental status in ED patients initially presumed to be intoxicated with ethanol but found to have negative quantitative ethanol levels. METHODS: This was a 5-year (2012-2016) electronic medical record review of ED patients presenting with altered mental status. Patients were included if they presented with presumed ethanol intoxication and had an initial ethanol concentration of zero. Etiologies of altered mental status were categorized into medical, traumatic, psychiatric, and drug-related causes. RESULTS: 29,322 patients presented during the study period with presumed alcohol intoxication, 1875 patients had negative ethanol levels. The etiology of altered mental status was due to illicit substances in 1337 patients (71%), psychiatric causes in 354 patients (19%), medical causes in 166 patients (9%) and trauma in 18 patients (1%). A total of 179 patients (10%) were admitted to the hospital; 19 patients (1%) to the ICU. CONCLUSIONS: The presumptive diagnosis of ethanol intoxication in patients presenting to the ED with altered mental status was inaccurate in 5% of patients. The etiology of altered mental status was serious and required hospitalization in 10% of the cohort. Rapid assessment of quantitative ethanol levels should be performed, breathalyzers may be preferred over serum testing.