A Novel and Simple Method for a Differentiation of Alcohol Types.

BACKGROUND: Alcohol poisoning is a significant global problem that has become an epidemic. The determination of the alcohol type is hereby essential as it may affect the course of the treatment; however, there is no routine laboratory diagnostic method for alcohol types other than for ethanol. In this study, we aimed to define a simple method for alcohol type differentiation by utilizing a combination of breathalyzer and spectrophotometrically measured serum ethanol results. METHODS: A breathalyzer and spectrophotometry were used to measure four different types of alcohol: ethanol, isopropanol, methanol, and ethylene glycol. To conduct serum alcohol analysis, four serum pools were created, each containing a different type of alcohol. The pools were analyzed using the spectrophotometric method with an enzymatic ethanol test kit. An experiment was conducted to measure the different types of alcohol using impreg-nated cotton and a balloon, simulating a breathalyzer test. An algorithm was created based on the measurements. RESULTS: Based on the results, the substance consumed could be methanol or isopropanol if the breathalyzer test indicates a positive reading and if the blood ethanol measurement is negative. If both the breathalyzer and the blood measurements are negative, the substance in question may be ethylene glycol. CONCLUSIONS: This simple method may determine methanol or isopropanol intake. This straightforward and innovative approach could assist healthcare professionals in different fields with diagnosing alcohol intoxication and, more precisely, help reducing related morbidity and mortality.

Pathophysiology and Biomarker Potential of Fatty Acid Ethyl Ester Elevation During Alcoholic Pancreatitis.

BACKGROUND & AIMS: The role of fatty acid ethyl esters (FAEEs) during human alcoholic pancreatitis is unknown. We compared FAEEs levels with their nonesterified fatty acids (NEFAs) precursors during alcohol intoxication and clinical alcoholic pancreatitis. The pathophysiology underlying FAEEs increase and their role as diagnostic biomarkers for alcoholic pancreatitis was investigated. METHODS: A prospective blinded study compared FAEEs, NEFAs, and ethanol blood levels on hospitalization for alcoholic pancreatitis (n = 31), alcohol intoxication (n = 25), and in normal controls (n = 43). Serum FAEEs were measured at admission for nonalcoholic pancreatitis (n = 75). Mechanistic cell and animal studies were done. RESULTS: Median FAEEs were similarly elevated during alcohol intoxication (205 nmol/L; 95% confidence interval [CI], 71.8-515 nmol/L, P < .001) and alcoholic pancreatitis (103.1 nmol/L; 95% CI, 53-689 nmol/L, P < .001) vs controls (1.7 nmol/L; 95% CI, 0.02-4.3 nmol/L) or nonalcoholic pancreatitis (8 nmol/L; 95% CI, 1.1-11.5 nmol/L). Alcoholic pancreatitis increased serum NEFAs (1024 ± 710 µmol/L vs 307 ± 185 µmol/L in controls, P < .05). FAEEs comprised 0.1% to 2% of the parent NEFA concentrations. FAEES correlated strongly with NEFAs independent of ethanol levels in alcoholic pancreatitis but not during alcohol intoxication. On receiver operating characteristic curve analysis for diagnosing alcoholic pancreatitis, the area under the curve for serum FAEEs was 0.87 (95% CI, 0.78-0.95, P < .001). In mice and cells, alcohol administration transiently increased all FAEEs. Oleic acid ethyl ester was the only FAEE with a sustained increase up to 24 hours after intraperitoneal oleic acid plus ethanol administration. CONCLUSIONS: The sustained, alcohol-independent, large (20- to 50-fold) increase in circulating FAEEs during alcoholic pancreatitis results from their visceral release and mirrors the 2- to 4-fold increase in parent NEFA. The large areas under the curve of FAEEs on receiver operating characteristic curve analysis supports their role as alcoholic pancreatitis biomarkers.

Binge alcohol disrupts skeletal muscle core molecular clock independent of glucocorticoids.

Circadian rhythms are central to optimal physiological function, as disruption contributes to the development of several chronic diseases. Alcohol (EtOH) intoxication disrupts circadian rhythms within liver, brain, and intestines, but it is unknown whether alcohol also disrupts components of the core clock in skeletal muscle. Female C57BL/6Hsd mice were randomized to receive either saline (control) or alcohol (EtOH) (5 g/kg) via intraperitoneal injection at the start of the dark cycle [Zeitgeber time (ZT12)], and gastrocnemius was collected every 4 h from control and EtOH-treated mice for the next 48 h following isoflurane anesthetization. In addition, metyrapone was administered before alcohol intoxication in separate mice to determine whether the alcohol-induced increase in serum corticosterone contributed to circadian gene regulation. Finally, synchronized C2C12 myotubes were treated with alcohol (100 mM) to assess the influence of centrally or peripherally mediated effects of alcohol on the muscle clock. Alcohol significantly disrupted mRNA expression of Bmal1, Per1/2, and Cry1/2 in addition to perturbing the circadian pattern of clock-controlled genes, Myod1, Dbp, Tef, and Bhlhe40 (P < 0.05), in muscle. Alcohol increased serum corticosterone levels and glucocorticoid target gene, Redd1, in muscle. Metyrapone prevented the EtOH-mediated increase in serum corticosterone but did not normalize the EtOH-induced change in Per1, Cry1 and Cry2, and Myod1 mRNA expression. Core clock gene expression (Bmal, Per1/2, and Cry1/2) was not changed following 4, 8, or 12 h of alcohol treatment on synchronized C2C12 myotubes. Therefore, binge alcohol disrupted genes of the core molecular clock independently of elevated serum corticosterone or direct effects of EtOH on the muscle.NEW & NOTEWORTHY Alcohol is a myotoxin that impairs skeletal muscle metabolism and function following either chronic consumption or acute binge drinking; however, mechanisms underlying alcohol-related myotoxicity have not been fully elucidated. Herein, we demonstrate that alcohol acutely interrupts oscillation of skeletal muscle core clock genes, and this is neither a direct effect of ethanol on the skeletal muscle, nor an effect of elevated serum corticosterone, a major clock regulator.

An Adolescent Porcine Model of Voluntary Alcohol Consumption Exhibits Binge Drinking and Motor Deficits in a Two Bottle Choice Test.

AIMS: Alcohol is the most commonly abused substance leading to significant economic and medical burdens. Pigs are an attractive model for studying alcohol abuse disorder due to the comparable alcohol metabolism and consumption behavior, which are in stark contrast to rodent models. This study investigates the usage of a porcine model for voluntary binge drinking (BD) and a detailed analysis of gait changes due to motor function deficits during alcohol intoxication. METHODS: Adolescent pigs were trained to drink increasing concentration (0-8%) of alcohol mixed in a 0.2% saccharin solution for 1 h in a two bottle choice test for 2 weeks. The training period was followed by a 3-week alcohol testing period, where animals were given free access to 8% alcohol in 0.2% saccharin solution and 0.2% saccharin water solution. Blood alcohol levels were tested and gait analysis was performed pre-alcohol consumption, last day of training, and Day 5 of each testing period. RESULTS: Pigs voluntarily consumed alcohol to intoxication at all timepoints with blood alcohol concentration (BAL) ≥80 mg/dl. Spatiotemporal gait parameters including velocity, cadence, cycle time, swing time, stance time, step time, and stride length were perturbed as a result of intoxication. The stratification of the gait data based on BAL revealed that the gait parameters were affected in a dose-dependent manner. CONCLUSION: This novel adolescent BD porcine model with inherent anatomical and physiological similarities to humans display similar consumption and intoxication behavior that is likely to yield results that are translatable to human patients.

The utility of S100B level in detecting mild traumatic brain injury in intoxicated patients.

BACKGROUND: S100B is a serum protein known to elevate in patients with brain injury, but it is unknown whether it can predict intracranial pathology in intoxicated patients following mild traumatic brain injury (MTBI). We performed a systematic review and meta-analysis of the English language literature to address this question. MAIN OUTCOMES AND RESULTS: Four prospective cohort trials of serum S100B levels on acutely intoxicated patients with MTBI were included in this meta-analysis. Prevalence of intracranial pathology in the pooled cohort of the intoxicated MTBI patients was 10%, lower than the 15-30% reported in the literature for the general MTBI population. Standard mean difference of serum S100B levels between patients with and without intracranial pathology on CT was 0.73 µg/L (Z = 18.33, P < 0.001). Following sensitivity analysis and hierarchical summary receiver-operating characteristic models, three remaining articles were used for pooled estimates that found that S100B had a sensitivity of 0.96 (95% CI: 0.84-1.00, I2 = 0%) and specificity of 0.63 (95% CI: 0.58-0.68, I2 = 86.8%) with a high negative predictive value (100%, 95% CI: 95.14-100, I2 = 0%) and a negative LR of 0.06 (95% CI: 0.01-0.31). CONCLUSIONS: Serum S100B levels may have utility in ruling out intracranial pathology in intoxicated patients, however more study and comparison with other serum biomarkers of brain injury are necessary before this becomes the accepted standard of care.

Critical Evaluation of the Association Between Elevated Mean Corpuscular Volume and Alcohol-Related Traffic Accidents: A Retrospective Study on 6244 Car Crash Cases.

BACKGROUND: Erythrocyte mean corpuscular volume (MCV) has been used for decades as a biomarker of chronic alcohol abuse and in the treatment of alcohol dependence. More recently, it has also been adopted to investigate the fitness of subjects to hold the driving license to prevent traffic accidents. So far, however, the studies on the association of MCV with an increased risk of alcohol-associated car accidents are extremely scarce, if not totally absent. To the best of our knowledge, the present work is the first specifically aimed at studying a plausible association between elevated MCV and crash accidents correlated with alcohol abuse. METHODS: A total of 6,244 drivers involved in traffic accidents underwent mandatory laboratory analyses including blood alcohol concentration (BAC) determination and MCV analysis. BAC and MCV determinations were performed by headspace gas chromatography and complete blood count, respectively. RESULTS: The chi-square test evaluating the proportions of subjects with elevated MCVs (>95 fl) yielded a highly significant result (χ2  = 68.0; p < 0.001) in the blood samples where the BAC was above the legal limit (i.e., >0.5 g/l). However, when considering only drivers showing BACs in the range of 0.51 to 1.5 g/l, the frequencies of elevated MCV values are fairly comparable (χ2  = 0.062, p = 0.80). In contrast, limiting the evaluation to BACs > 1.5 g/l, the frequency of elevated MCVs raised to 19.1% (χ2  = 58.9, p value < 0.001 vs. the group with BAC within the legal limits). CONCLUSIONS: The present observations show that MCV increases are typically associated with drivers involved in accidents only if driving under severe alcohol intoxication, leading to a preliminary conclusion that, in the context of the certification of the fitness to the driving license, MCV fails to reveal individuals at risk who tend to drive in a condition of low-to-moderate alcohol intoxication.

Alcohol Intoxication as a Stroke Mimic and the Incidence of Acute Alcohol Intoxication in Stroke.

BACKGROUND AND AIM: Alcohol intoxication can be a posterior circulation stroke mimic as they share symptoms such as dysarthria, gait disturbances and nystagmus. We describe alcohol intoxication as a stroke mimic and the frequency of acute alcohol intoxication among stroke patients. METHODS: Prospective observational single-center study (2014-2017, Haga Ziekenhuis, the Hague). In all patients older than 16 years presenting as possible acute stroke less than 6 hours of onset, blood ethanol was measured; greater than 0.1 blood alcohol concentration (BAC) was considered elevated. RESULTS: In total 974 patients were included: 60 (6%) had elevated blood ethanol (mean: 1.3 BAC). In 180 of 974 patients (18%) a stroke mimic was diagnosed: 12 were due to alcohol intoxication (1% of total cohort, 7% of stroke mimic, mean ethanol level: 2.2 BAC). Half of these patients denied or downplayed their alcohol consumption. Stroke and concurrent alcohol intoxication occurred in 38 of 794 strokes (5%, mean ethanol level: 1.1 BAC). Compared to other stroke patients, these 38 patients presented more often after working hours (mean 6.38pm versus 2.23pm) and received alteplase and endovascular therapy less often (24% versus 43%, P = .018 and 3% versus 10%, P = .241, respectively). CONCLUSIONS: Of all patients presenting as possible acute stroke, 6% also drank alcohol. 18% of the whole cohort was diagnosed with a stroke mimic. Acute alcohol intoxication as sole diagnosis was diagnosed in 1% of the total cohort and 7% of stroke mimics, 50% denied or downplayed their alcohol consumption. 5% of all stroke patients also drank alcohol, they were significantly less likely to receive alteplase or endovascular treatment.

Effects of Phyllanthus amarus PHYLLPROTM leaves on hangover symptoms: a randomized, double-blind, placebo-controlled crossover study.

CONTEXT: Phyllanthus amarus Schumach. and Thonn. (Euphorbiaceae) is traditionally known to improve general liver health. However, its effect on hangover is unknown. OBJECTIVE: This study evaluated PHYLLPRO™, a standardized ethanol extract of P. amarus leaves for protection against oxidative stress and recovery from hangover symptoms. MATERIAL AND METHODS: Ten days daily oral supplementation of 750 mg/day followed by intoxication was evaluated in a randomized placebo-controlled (containing only excipient), crossover study in 15 subjects (21-50 years old), for oxidative stress, liver damage, alleviating hangover symptoms (Hangover Severity Score: HSS) and mood improvement (Profile-of-Mood-Scores: POMS). RESULTS: PHYLLPRO™ was able to remove blood alcohol in the active group while the placebo group still had 0.05% at 12 h post-intoxication (p < 0.0001). For HSS, the active group showed reduced hangover symptoms while there were higher levels of nausea, headache, anorexia, tremulousness, diarrhoea and dizziness in the placebo group (p < 0.05) at hour 10 post-intoxication. Increased fatigue at hour 2 and tension (p > 0.05) from baseline to hour 22 was reported in the placebo group using POMS. Significant anti-inflammatory group effect favouring the active group, by the upregulation of cytokines IL-8 (p = 0.0014) and IL-10 (p = 0.0492) and immunomodulatory effects via IL-12p70 (p = 0.0304) were observed. The incidence of adverse events was similar between groups indicating the safety of PHYLLPRO™. DISCUSSION AND CONCLUSION: Preliminary findings of PHYLLPRO™ in managing hangover, inflammation and liver functions following intoxication, is demonstrated. Future studies on PHYLLPRO™ in protecting against oxidative stress and hangover in larger populations is warranted.

Unsuspected Critical Illness Among Emergency Department Patients Presenting for Acute Alcohol Intoxication.

STUDY OBJECTIVE: Emergency department (ED) visits for acute alcohol intoxication are common, but this population is at risk for decompensation and occult critical illness. The purpose of this study is to describe the incidence and predictors of unsuspected critical illness among patients with acute alcohol intoxication. METHODS: This was a retrospective observational study of ED patients from 2011 to 2016 with acute alcohol intoxication. The study cohort included patients presenting for alcohol intoxication, whose initial assessment was uncomplicated alcohol intoxication without any other active acute medical or traumatic complaints. The primary outcome was defined as the unanticipated subsequent use of critical care resources during the encounter or admission to an ICU. We investigated potential predictors for this outcome with generalized estimating equations. RESULTS: We identified 31,364 eligible patient encounters (median age 38 years; 71% men; median breath alcohol concentration 234 mg/dL); 325 encounters (1%) used critical care resources. The most common diagnoses per 1,000 ED encounters were acute hypoxic respiratory failure (3.1), alcohol withdrawal (1.7), sepsis or infection (1.1), and intracranial hemorrhage (1.0). Three patients sustained a cardiac arrest. Presence of the following had an increased adjusted odds ratio (aOR) of developing critical illness: hypoglycemia (aOR 9.2), hypotension (aOR 3.8), tachycardia (aOR 1.8), fever (aOR 7.6), hypoxia (aOR 3.8), hypothermia (aOR 4.2), and parenteral sedation (aOR 2.4). The initial blood alcohol concentration aOR was 1.0. CONCLUSION: Critical care resources were used for 1% of ED patients with alcohol intoxication who were initially assessed by physicians to have low risk. Abnormal vital signs, hypoglycemia, and chemical sedation were associated with increased odds of critical illness.

Susceptibility to Alcohol Hangovers: Not Just a Matter of Being Resilient.

INTRODUCTION: Although most drinkers have experienced a hangover the day following heavy alcohol consumption, a minority claims to be hangover resistant despite consuming the same large quantities of alcohol as those reporting alcohol hangover. The aim of the current study was to examine if susceptibility to experiencing hangovers is related to a drinker's interpretation of wellbeing and psychological assets to bounce back. METHODS: A survey was conducted among 2295 Dutch students assessing their past month alcohol consumption patterns, and measuring mental resilience and wellbeing. Estimated peak blood alcohol concentration (e-pBAC) for their heaviest drinking occasion in the past month was computed for each participant. Data from participants who reported a past month hangover, i.e. hangover sensitive drinkers, were compared with hangover resistant drinkers. The analyses were conducted for (a) all participants reaching an e-pBAC ≥ 0.11% (N = 986, of which 24.6% claimed to be hangover resistant) and (b) participants reaching an e-pBAC ≥ 0.18% (N = 480, of which 16.7% claimed to be hangover resistant). RESULTS: For both e-pBAC cut-off values, no significant differences between hangover sensitive and hangover resistant drinkers were found for mental resilience and wellbeing. CONCLUSION: The current findings suggest that having a hangover is not simply an expression of poor psychological coping with the next-day consequences of heavy alcohol consumption.

Effects of acute ethanol intoxication in an ovine peritonitis model.

BACKGROUND: Acute ethanol intoxication has been shown to have contrasting effects on outcomes in sepsis. The aim of this study was to explore the effects of acute ethanol intoxication on hemodynamics, renal function, brain perfusion and lactate/pyruvate in an ovine sepsis model. METHODS: Anesthetized, mechanically ventilated female sheep were randomized to an ethanol group (n = 7), which received 1 g/kg ethanol diluted in intravenous (i.v.) saline infusion or a control group (n = 7), which received the same volume of i.v. saline. Both groups received the treatment for a period of 2 h prior to induction of sepsis by intraperitoneal injection of feces. Other treatment included fluid resuscitation but no vasopressors or antibiotics. Global hemodynamics, renal blood flow, brain cortex laser Doppler flowmetry and microdialysis analyses were recorded hourly. RESULTS: In the ethanol group, blood ethanol concentrations were 137 ± 29 mg/dL at the time of feces injection and decreased to become undetectable by 12 h. Arterial hypotension occurred earlier in the ethanol than in the control group (8 [7-12] vs. 14 [11-20] hours, p = 0.03). Lactate levels increased to > 2 mmol/L earlier in the ethanol group. Renal dysfunction (9 [6-13] vs. 13 [12-15] hours, p = 0.05) and oliguria (urine output < 0.5 mL/kg/h; 10 [7-12] vs. 13 [12, 13] hours, p = 0.01) developed earlier in the ethanol than in the control group. Brain blood flow and lactate/pyruvate were unaffected. There was no significant difference in survival time. CONCLUSIONS: Acute ethanol intoxication in this model of peritonitis resulted in earlier development of shock and renal dysfunction but did not alter brain perfusion and metabolism or short-term survival.

Acute alcohol intoxication among adolescents-the role of the context of drinking.

This study aims (1) to describe the context of drinking among adolescents with acute alcohol intoxication (AAI) by gender, (2) to explore temporal changes in the context of drinking and (3) to analyse the association between the context of drinking and blood alcohol concentration (BAC). A retrospective chart review of 12- to 17-year-old inpatients with AAI (n = 1441) of the years 2000 to 2006 has been conducted in five participating hospitals in Germany. Gender differences in the context of drinking were tested with t test and chi2 test. Differences over time were analysed using logistic regressions. Multivariate linear regression was used to predict BAC. Girls and boys differed in admission time, drinking situation, drinking occasion and admission context. No temporal changes in drinking situation and in admission to hospital from public locations or places were found. Higher BAC coincided with male gender and age. Moreover, BAC was higher among patients admitted to hospital from public places and lower among patients who drank for coping. CONCLUSION: The results suggest gender differences in the context of drinking. The context of drinking needs to be considered in the development and implementation of target group-specific prevention and intervention measures. What is known: • The context of drinking, e.g. when, where, why and with whom is associated with episodic heavy drinking among adolescents. What is new: • Male and female inpatients with acute alcohol intoxication differ with regards to the context of drinking, i.e. in admission time, drinking situation, drinking occasion and admission context. • Being admitted to hospital from public places is associated with higher blood alcohol concentration.

Acute Alcohol Intoxication Exacerbates Rhabdomyolysis-Induced Acute Renal Failure in Rats.

Traumatic and nontraumatic rhabdomyolysis can lead to acute renal failure (ARF), and acute alcohol intoxication can lead to multiple abnormalities of the renal tubules. We examined the effect of acute alcohol intoxication in a rat model of rhabdomyolysis and ARF. Intravenous injections of 5 g/kg ethanol were given to rats over 3 h, followed by glycerol-induced rhabdomyolysis. Biochemical parameters, including blood urea nitrogen (BUN), creatinine (Cre), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and creatine phosphokinase (CPK), were measured before and after induction of rhabdomyolysis. Renal tissue injury score, renal tubular cell expression of E-cadherin, nuclear factor-κB (NF-κB), and inducible nitric oxide synthase (iNOS) were determined. Relative to rats in the vehicle group, rats in the glycerol-induced rhabdomyolysis group had significantly increased serum levels of BUN, Cre, GOT, GPT, and CPK, elevated renal tissue injury scores, increased expression of NF-κB and iNOS, and decreased expression of E-cadherin. Ethanol exacerbated all of these pathological responses. Our results suggest that acute alcohol intoxication exacerbates rhabdomyolysis-induced ARF through its pro-oxidant and inflammatory effects.

Developing a standardized measurement of alcohol intoxication.

INTRODUCTION: We assessed multiple examinations and assessment tools to develop a standardized measurement of alcohol intoxication to aid medical decision making in the Emergency Department. METHODS: Volunteers underwent an alcohol challenge. Pre- and post-alcohol challenge, subjects were videotaped performing three standardized clinical examinations: (1) Standardized Field Sobriety Test (SFST) examination, (2) Hack's Impairment Index (HII) examination, and (3) Cincinnati Intoxication Examination (CIE). Emergency clinicians evaluated the level of intoxication using five standardized assessment tools in a blinded and randomized fashion: (1) SFST assessment tool (range 0-18), (2) HII assessment tool (range 0-1), (3) St. Elizabeth Alcohol Intoxication Scale (STE, range 0-17), (4) a Visual Analog Scale (VAS, range 0-100), and (5) a Binary Intoxication Question (BIQ). Construct validity was assessed along with inter- and intra-rater reliability. RESULTS: Median scores pre- and post-alcohol challenge were: SFST 6 (interquartile range 5) and 11 (3), respectively; HII 0 (0.05), 0.1 (0.1); STE 0 (1), 1 (2); VAS 10 (22), 33 (31). For BIQ, 59% and 91% indicated intoxication, respectively. Inter-rater reliability scores were: SFST 0.71 (95% confidence interval 0.48-0.86) to 0.93 (0.88-0.97) depending on examination component; HII 0.90 (0.82-0.95); STE 0.86 (0.75-0.93); VAS 0.92 (0.88-0.94); BIQ 0.3. Intra-rater reliability scores were: SFST 0.74 (0.64-0.82) to 0.87 (0.81-0.91); HII 0.85 (0.79-0.90); STE 0.78 (0.68-0.85); VAS 0.82 (0.74-0.87); BIQ 0.71. VAS reliability was best when paired with the HII and SFST examinations. CONCLUSIONS: HII examination, paired with either a VAS or HII assessment tool, yielded valid and reliable measurements of alcohol intoxication.

[Injuries under the influence of alcohol]. / Verletzungen unter Alkoholeinfluss.

BACKGROUND: In Germany, an average of 9.5 L of pure alcohol is consumed per capita per year. Alcohol is known to negatively influence psychomotor abilities. The aim of this study was to evaluate injuries that lead to hospital admission with and without prior intake of alcohol. PATIENTS AND METHODS: Over a 7-month period, all 1317 patients who were admitted to the hospital because of an injury were evaluated with respect to their blood-alcohol level. Patient data of both groups (139 injuries under alcohol influence and 1178 injuries without alcohol influence) were compared with respect to the mechanism and type of injury, patient demographics, and treatment costs. RESULTS: At the time of presentation, 11 % (n = 139) of all admitted patients had detectable blood-alcohol levels of more than 0.1 g/L with an average blood-alcohol level of 2.21 g/L. Female patients had an average of 1.96 g/L and males an average of 2.28 g/L (N.S.). Almost every fifth male patient (109 out of 570, 19 %) had a detectable blood-alcohol level, compared to only 4 % of all admitted female patients. Among the patients admitted between 11:00 p.m. and 5:00 a.m., 35 % had detectable blood-alcohol levels and among the 20- to 30-year-old patients, 24 % had detectable blood-alcohol levels. The leading mechanisms of injury among intoxicated patients were falls (50 %, n = 70) and physical violence (18 %, n = 25). The latter was recorded significantly (p = 0.01) less among sober patients (0.17 %, n = 2). The most frequent diagnosis was a mild concussion in both intoxicated (60%, n = 84) and sober (34 %, n = 402) patients (p = 0.04). The time to discharge averaged 4.3 days for intoxicated and 5.6 days for sober patients. CONCLUSIONS: Injuries that occur while under the influence of alcohol that lead to hospital admission are particularly frequent in male patients aged between 20 and 30 years. They do not necessarily lead to more severe injuries.

Alcohol decreases baseline brain glucose metabolism more in heavy drinkers than controls but has no effect on stimulation-induced metabolic increases.

During alcohol intoxication, the human brain increases metabolism of acetate and decreases metabolism of glucose as energy substrate. Here we hypothesized that chronic heavy drinking facilitates this energy substrate shift both for baseline and stimulation conditions. To test this hypothesis, we compared the effects of alcohol intoxication (0.75 g/kg alcohol vs placebo) on brain glucose metabolism during video stimulation (VS) versus when given with no stimulation (NS), in 25 heavy drinkers (HDs) and 23 healthy controls, each of whom underwent four PET-(18)FDG scans. We showed that resting whole-brain glucose metabolism (placebo-NS) was lower in HD than controls (13%, p = 0.04); that alcohol (compared with placebo) decreased metabolism more in HD (20 ± 13%) than controls (9 ± 11%, p = 0.005) and in proportion to daily alcohol consumption (r = 0.36, p = 0.01) but found that alcohol did not reduce the metabolic increases in visual cortex from VS in either group. Instead, VS reduced alcohol-induced decreases in whole-brain glucose metabolism (10 ± 12%) compared with NS in both groups (15 ± 13%, p = 0.04), consistent with stimulation-related glucose metabolism enhancement. These findings corroborate our hypothesis that heavy alcohol consumption facilitates use of alternative energy substrates (i.e., acetate) for resting activity during intoxication, which might persist through early sobriety, but indicate that glucose is still favored as energy substrate during brain stimulation. Our findings are consistent with reduced reliance on glucose as the main energy substrate for resting brain metabolism during intoxication (presumably shifting to acetate or other ketones) and a priming of this shift in HDs, which might make them vulnerable to energy deficits during withdrawal.

Alcohol level and injury severity: is the floppy patient myth true?

BACKGROUND: The impact of inebriation on severity of injury is unclear. The few studies to date on this topic are limited to a particular mechanism of injury (MOI), injury pattern, or blood alcohol level (BAL). Therefore, we sought to determine the impact of BAL on injury pattern and severity across all MOI. We hypothesize that there is no relationship between BAL and injury severity when controlling for MOI. MATERIALS AND METHODS: After institutional review board approval, a retrospective study was performed at an adult trauma center from January 1, 2012-December 31, 2012. All MOI were included. Injury severity was assessed using the injury severity score (ISS). Chi square and analysis of variance were used to examine the relationship between BAL, injury pattern, and ISS within each MOI. Multivariate regression analysis examined the BAL-ISS association adjusting for MOI, gender, and age. RESULTS: Of 1397 patients, the mean age was 44 ± 19, ISS was 7.5 ± 6.8, BAL was 93 ± 130 mg/dL, and 70% were male. Rib fracture (P = 0.002) and hemothorax and/or pneumothorax (P = 0.0009) were negatively associated with BAL, whereas concussion and soft tissue injury had a positive association with BAL (P < 0.0001). An increasing BAL had a negative correlation with ISS after fall from standing (P < 0.001), whereas bicycle collisions had a positive association (P = 0.027). Across all MOI, there was no significant association between BAL and ISS. CONCLUSIONS: BAL is associated with ISS, in specific MOI; however, across all MOI, there was no significant association between BAL and ISS. Inebriated patients should be triaged with the same clinical index of suspicion for injury as sober patients.

[PROGNOSTIC SIGNIFICANCE OF CHANGES OF BLOOD GLUCOSE LEVEL IN PATIENTS WITH THORACOABDOMINAL INJURIES.]

Background Currently, one of the causes of high morbidity and mortality is injuries. Predict the outcome of injuries - it is an important task of the treating physician. Trauma is a stress factor so to predict the outcome, you can use markers of stress, the most accessible ofwhich is blood glucose. THE AIM: to reveal the dynamics of the relationship between blood glucose levels and the outlook for the life ofpatients with thoracoabdominal injuries. MATERIALS AND METHODS: A retrospective analysis of medical records of hospitalized patients were divided into two groups, depending on the outlook for the life of (favorable or unfavorable), and each of the groups - into two subgroups according to the presence or absence of signs of intoxication at admission. The subgroups were calculated and compared the mean blood glucose levels at different hours of hospital treatment. RESULTS: It was found that the average blood glucose levels at various hours of hospital stay were significantly higher in patients with poor outcome. The most noticeable was the difference in the first days of hospital treatment. Signs of intoxication was associated with lower values of glucose and a tendency to hypoglycaemia. In addition, among patients with high blood glucose ( 8 mg / dL) was observed over deaths in the first day of hospital stay. CONCLUSION: High blood glucose levels ( 8,0 mmol / L) in the first day of hospital treatment is a predictor ofpoor outcome in patients with thoracoabdominal injuries.

First objective association between elevated carbohydrate-deficient transferrin concentrations and alcohol-related traffic accidents.

BACKGROUND: Carbohydrate-deficient transferrin (CDT) is a well-recognized highly specific marker of chronic alcohol abuse. The association of CDT with alcohol-related traffic accidents was evaluated to objectively validate the use of this marker for certifying the physical fitness for driving license regranting after its confiscation for drunk driving. METHODS: The study was carried out on 468 injured drivers (InjDr), who underwent mandatory blood alcohol concentration (BAC) and drug analysis in biological fluids. The InjDr group was divided into 2 subgroups on the basis of BAC legal limit adopted in Italy (BAC ≤ 0.5 g/l: InjDr1 ; BAC >0.5 g/l: InjDr2 ). The control group (CntDr) included 236 subjects holding safety-sensitive job positions and undergoing mandatory toxicological analyses. The determination of BAC in blood and CDT in serum were performed using validated analytical methods based on head-space gas chromatography and high-performance liquid chromatography, respectively. RESULTS: The evaluation of CDT distribution in the 3 groups (CntDr, InjDr1 , InjDr2 ) showed that CDT distribution in the InjDr1 group was similar to that observed in the CntDr group (p = 0.159) and different from that observed in the InjDr2 group (p < 0.001). Partitioning the CDT data of each group into "CDT positives" and "CDT negatives" on the basis of the cut off (1.90%), it was possible to calculate the odds of the 3 groups and then the odds ratios. The odds ratio of InjDr1 versus CntDr was 4.56 (p = 0.158), whereas the odds ratio of InjDr2 versus CntDr was 132 (p < 0.001). Furthermore, a dose-response effect was found only when comparing InjDr2 with CntDr. CONCLUSIONS: The data of the present study strongly support the use of the CDT test to evaluate the risk of a subject to be involved in a road accident while driving under the influence of alcohol.

Histone Deacetylase Gene Expression Following Binge Alcohol Consumption in Rats and Humans.

BACKGROUND: Alcohol binge drinking is one of the most common patterns of excessive alcohol use and recent data would suggest that histone deacetylases (HDACs) gene expression profiling could be useful as a biomarker for psychiatric disorders. METHODS: This study aimed to characterize the gene expression patterns of Hdac 1-11 in samples of rat peripheral blood, liver, heart, prefrontal cortex, and amygdala following repeated binge alcohol consumption and to determine the parallelism of Hdac gene expression between rats and humans in peripheral blood. To accomplish this goal, we examined Hdac gene expression following 1, 4, or 8 alcohol binges (3 g/kg, orally) in the rat, in patients who were admitted to the hospital emergency department for acute alcohol intoxication, and in rats trained in daily operant alcohol self-administration. RESULTS: We primarily found that acute alcohol binging reduced gene expression (Hdac1-10) in the peripheral blood of alcohol-naïve rats and that this effect was attenuated following repeated alcohol binges. There was also a reduction of Hdac gene expression in the liver (Hdac2,4,5), whereas there was increased expression in the heart (Hdac1,7,8) and amygdala (Hdac1,2,5). Additionally, increased blood alcohol concentrations were measured in rat blood at 1 to 4 hours following repeated alcohol binging, and the only group that developed hepatic steotosis (fatty liver) were those animals exposed to 8 alcohol binge events. Finally, both binge consumption of alcohol in humans and daily operant alcohol self-administration in rats increased Hdac gene expression in peripheral blood. CONCLUSIONS: Our results suggest that increases in HDAC gene expression within the peripheral blood are associated with chronic alcohol consumption, whereas HDAC gene expression is reduced following initial exposure to alcohol.