Alcohol: intoxication and poisoning – diagnosis and treatment

doi:10.1016/B978-0-444-62619-6.00007-0

Handbook of Clinical Neurology

Volume 125, 2014, Pages 115-121

https://doi.org/10.1016/B978-0-444-62619-6.00007-0 Get rights and content

Abstract

Alcohol intoxication refers to a clinically harmful condition induced by recent ingestion of alcohol, when alcohol and its metabolites accumulate in the blood stream faster than it can be metabolized by the liver. The major adverse effects of alcohol that gain clinical attention are the neurologic, gastrointestinal, and cardiovascular problems, which are usually related to blood alcohol concentration; however, the extent of acute alcohol intoxication also depends on several factors. Individuals who seek medical treatment for acute alcohol intoxication likely have additional medical problems related to chronic alcohol consumption or alcohol dependence. For this reason, additional investigations to identify potential problems needing particular attention should be considered, depending on the clinical features of the patient.

Introduction

Alcohol intoxication refers to a clinically harmful condition induced by recent ingestion of alcohol, when alcohol and its metabolites accumulate in the blood stream faster than they can be metabolized by the liver. Due to the long history and widespread use of alcohol as a recreational beverage, the clinical manifestations of alcohol intoxication are usually not taken seriously and considered to subside spontaneously with time; however, the adverse effects of alcohol at sufficiently high levels can cause coma and respiratory depression. In addition, individuals who seek medical treatment for acute alcohol intoxication likely have additional medical problems related to chronic alcohol consumption or alcohol dependence.

The aims of this chapter are to delineate and discuss: (1) the acute and chronic effects of ethanol on organ systems; (2) diagnostic criteria of alcohol intoxication; and (3) clinical conditions, which can accompany acute alcohol intoxication, especially those that are associated with chronic alcohol consumption (e.g., hepatic encephalopathy and Wernicke's encephalopathy); and (4) treatment.

Section snippets

The effects of ethanol on organ systems

Alcohol is absorbed primarily through the small intestine. Only 10% of consumed alcohol is absorbed from the stomach. Initial mucosal absorption begins within 10 minutes of consumption and serum peak blood alcohol concentration is reached between 30 and 90 minutes (Marco and Kelen, 1990). A standard single drink contains about 10–12 mg of ethanol, which is estimated to increase the blood alcohol concentration of a 70-kg (155-lb) man by 15–20 mg/dL. On the other hand, 90% of absorbed alcohol is

Diagnosis

The smell of alcohol on the patient's breath is the first cue that leads to the impression of alcohol intoxication. The diagnosis can usually be made based on history taking and physical examination. Intoxicated patients are likely to deny or understate their maladaptive pattern of alcohol use. Therefore, a thorough history of the individual's alcohol use should be taken from other informants if possible. The information about the time of the last drink is critical in order to prevent and

Differential diagnosis

In many cases, the intoxicated patient has comorbid medical conditions, which are usually related to chronic alcohol abuse. For this reason, additional investigations to identify potential problems needing particular attention should be considered, depending on the clinical features of the patient. Special attention should be paid to the changes of mental status, which might vary across a spectrum, comprising mild euphoria, disinhibition, lethargy, and coma. Mental statuses that are not

Treatment

The treatment of an intoxicated patient entails supportive and symptomatic care. Management starts with airway assessment and examination of the cardiac and respiratory function. The immediate steps include a complete assessment of the patient's medical status, including drinking history of alcohol or other possible substances that might interfere with clinical condition. The rapid absorption of alcohol through intestinal mucosa, which starts within 10 minutes, makes gastric lavage or activated

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Cited by (37)

Alcohol use patterns and hypertension among adults in the United States: findings from the 2015–2016 NHANES data
2023, Public Health
This study assessed the association between alcohol use patterns and the prevalence of hypertension.
Data on alcohol use patterns and hypertension among 5918 adults from the 2015–2016 National Health and Nutrition Examination Survey was used for this study.
The association of alcohol use patterns; “ever-used alcohol”, “binge drinking”, “heavy drinking”, and “everyday alcohol use” with hypertension were assessed using multivariable-adjusted logistic regression to estimate the adjusted odds ratio (aOR) and 95% confidence interval (CI) at a two-sided P < 0.05.
Overall, the mean age of respondents was 48.3 ± 18.5 years, 50.9% (n = 3034) were women, and 44.6% (n = 2132) were hypertensive. Also, 85.9% (n = 4177) had used alcohol in their lifetime, 51.9% (n = 1764) were heavy drinkers, 25.1% (n = 370) engaged in binge drinking, and 17.7% (n = 721) reported everyday alcohol use. Compared to those that have never used alcohol, the aOR (95%CI) of stage II hypertension was 1.570 (1.565, 1.575) for overall alcohol use, 1.370 (1.367, 1.373) for everyday alcohol use, 1.127 (1.125, 1.129) for heavy drinking, and 1.092 (1.087, 1.098) for binge drinking. Among current active smokers, the aOR (95%CI) of stage II hypertension was aggravated for everyday alcohol use; 2.583 (2.576, 2.590).
Alcohol use patterns were associated with a higher prevalence of hypertension, particularly among smokers. A population-based longitudinal study should clarify whether these alcohol use phenotypes are predictive of hypertension at the population level in the United States.
Thermal antinociceptive responses to alcohol in DBA/2J and C57BL/6J inbred male and female mouse strains
2023, Behavioural Brain Research
Citation Excerpt :
The development of tolerance to alcohol analgesic effects may put patients at an increased risk of alcohol dependence [7] and prolonged use of alcohol can also induce hyperalgesia and exacerbate pain [8,9], perpetuating the cycle of pain and dependence. Ethanol is a small, water-soluble molecule that is mainly absorbed in the small intestine [10]. It is mainly metabolized in the liver by alcohol dehydrogenase in a concentration-dependent manner Le Daré et al. [11].
The phenomenon of alcohol analgesia and tolerance can facilitate misuse and lead to the development of alcohol use disorder (AUD). Numerous alcohol-induced behaviors are genetically influenced; however, it is unknown if alcohol analgesia has a genetic contribution. Rodent studies have shown that alcohol responses differ vastly between two widely studied inbred strains of mice, C57BL/6 J (B6) and DBA/2 J (D2). Here, we used B6 and D2 mice as an initial behavioral genetic analysis of acute alcohol-induced antinociception.
The antinociceptive effect of orally-administered alcohol was characterized using the hot plate test in B6 and D2 mice of both sexes. Using the opioid receptor antagonist naloxone, the involvement of the opioid system was assessed. Locomotor activity and blood alcohol concentrations were also measured. Ovariectomized mice were used to evaluate the influence of ovarian sex hormones on alcohol-induced antinociception.
Alcohol induced an antinociceptive effect in B6 and D2 male mice in a time- and dose-dependent manner. In addition, D2 male mice were more sensitive to the antinociceptive effect of alcohol than B6 male mice. However, locomotion is not impeded by the tested doses of alcohol in B6 mice. Female D2 and B6 mice failed to show significant antinociceptive effects in alcohol dose-response studies. In addition, alcohol-induced antinociception was still not evident in ovariectomized female mice. Male mice of both strains developed tolerance to this effect after repeated administration of alcohol. Strain differences were found in blood alcohol concentration. Finally, no difference was found in the blockade of alcohol antinociception by 2 mg/kg naloxone.
Our results indicate that the antinociceptive effects of alcohol in the hot plate test are influenced by strain and sex. These findings support further genetic analysis of alcohol-induced antinociception to identify operative mechanisms and better assess the contribution of this phenotype to AUD.
Clinician assessment of blood alcohol levels among emergency department patients
2023, American Journal of Emergency Medicine
Alcohol intoxication is a significant public health concern and is commonly seen among emergency department (ED) patients. This study was undertaken to identify the accuracy of clinician assessment of blood alcohol levels among emergency department patients.
This prospective survey study was conducted at a Level 1 Trauma Center. Eligible study participants included physicians, nurses, and medical students involved in the care of patients who had BAC. Clinicians estimated the BAC prior to results availability.
Among 243 clinicians, the mean difference between the estimated BAC and actual BAC was 17.4 (95% CI: 4.7 to 30.1). Providers tended to overestimate the actual BAC level. The accuracy between roles (attendings, residents, RNs, students) was not significant (ANOVA p-value 0.90). Accuracy was not correlated with age of the patient (Pearson correlation 0.04, p-value 0.54). Accuracy was not associated with the patient's gender (Student's t-test two-tailed p-value 0.90), ethnicity (White versus all others, t-test p-value 0.31), nor insurance (government versus not government, t-test p-value 0.81). The average accuracy value was associated with mode of arrival (t-test p-value 0.003). The average accuracy for walk-in subjects was −14.9 (CI: −32.8 to 3.1) compared to ambulance arrivals 28.3 (CI: 12.7 to 44.0). Providers underestimated BAC for walk-ins and overestimated BAC for ambulance arrivals.
Among 107 patients with a BAC of 0, clinician estimates ranged from 0 to 350. Clinicians estimated non-zero BAC levels in 17% of patients with BAC of 0 (N = 18).
Clinicians' estimates of BAC were often inaccurate, and often overestimated the BAC.
The protective effects and mechanisms of modified Lvdou Gancao decoction on acute alcohol intoxication in mice
2022, Journal of Ethnopharmacology
Acute alcohol intoxication (AAI) is a ubiquitous emergency worldwide, whereas the searching for both effective and safe drugs is still a task to be completed. Modified Lvdou Gancao decoction (MLG), a traditional Chinese medicine decoction, has been confirmed to be valid to alcohol-induced symptoms and hepatotoxicity clinically, whereas its protective mechanisms have not been determined.
AAI mice model was established by alcohol gavage (13.25 mL/kg) and MLG (5, 10, 20 g/kg BW) was administered to mice 2 h before and 30 min after the alcohol exposure. Assay kits for alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), glutamine transferase (GGT), total superoxide dismutase (T-SOD), malondialdehyde (MDA), nitric oxide (NO), and glutathione peroxidase (GSH-Px), as well as histopathology were used to explore the effects of MLG on acute alcohol-induced intoxication and hepatotoxicity. Mechanisms of MLG on oxidative stress and inflammatory were evaluated with RT-qPCR and Western Blot.
MLG remarkably decreased the drunkenness rate, prolonged the tolerance time and shortened the sober-up time of AAI mice. After acute alcohol exposure, MLG treatment induced significant increment of ADH, ALDH, T-SOD and GSH-Px activities in liver, while serum ALT, AST, GGT and NO levels as well as hepatic MDA activity were reduced, in a dose-dependent manner. In contrast to the model group, the mRNA expression of TNFα, IL-1β and NF-κB in the MLG treated groups had a downward trend while the Nrf-2 showed an upward trend simultaneously. Furthermore, the protein levels of p65, p-p65, p-IκBα in the MLG treated groups were considerably diminished, with HO-1 and Nrf2 elevated. To sum up, our results suggested that MLG could efficaciously ameliorate AAI via accelerating the metabolism of alcohol, alleviating acute hepatotoxicity, and weakening the oxidative stress coupled with inflammation response, which might be attributed to the inhibition of the NF-κB signaling pathway and the activation of the Nrf2/HO-1 signaling pathway.
Taken together, our present study verified the protective effect and mechanisms of MLG to AAI mice, and we further conclude that MLG may be a potent and reliable candidate for the prevention and treatment of AAI.
Liver-specific Nrf2 deficiency accelerates ethanol-induced lethality and hepatic injury in vivo
2021, Toxicology and Applied Pharmacology
Alcoholic liver disease (ALD) is a major cause of morbidity and mortality from liver disorders. Various mechanisms, including oxidative stress and impaired lipid metabolism, have been implicated in the pathogenesis of ALD. Our previous studies showed that nuclear factor erythroid-derived 2-like 2 (Nrf2) is a master regulator of adaptive antioxidant response and lipid metabolism by using a liver-specific Nrf2 knockout (Nrf2(L)-KO) mouse model. In the current study, an ALD model was developed by a Lieber-DeCarli liquid-based ethanol diet given to this Nrf2(L)-KO mouse strain. We found that Nrf2(L)-KO mice were quite sensitive to lethality from 6.3% ethanol diet. We thus decreased the ethanol concentration to 4.2% to obtain tissues to analyze the role of hepatic Nrf2 in the development of ALD. We found that mild hepatic steatosis occurred with both liquid control and 4.2% ethanol diet feeding, which contain 35% fat. Both the fatty acid β-oxidation marker peroxisome proliferators-activated receptor α (PPARα), and lipogenesis regulator PPARγ were reduced with ethanol feeding in Nrf2(L)-KO mice, compared to Nrf2 floxed control mice (Nrf2-LoxP). However, Nrf2(L)-KO livers showed more cell injury than the livers of Nrf2-LoxP mice. Consistent with these data, there was increased proportion of apoptotic cells in the liver of ethanol-fed Nrf2(L)-KO mice comparing Nrf2-LoxP controls. Mechanistically, Nrf2 mediated expression of ethanol detoxification enzymes, such as alcohol dehydrogenase 1 and aldehyde dehydrogenase1a1, likely contributed to the sensitivity to ethanol toxicity. In conclusion, hepatic Nrf2 is critical to the development of ALD, particularly the morbidity and liver injury.
Consistency between self-reported alcohol consumption and biological markers among patients with alcohol use disorder – A systematic review
2021, Neuroscience and Biobehavioral Reviews
Citation Excerpt :
Although self-report measures of alcohol consumption have sound psychometric properties and are accepted in the research community, they have mostly been validated against other self-report measures. This may be problematic since several factors may impact self-reported alcohol consumption, e.g. poor episodic memory, other cognitive impairments, social desirability, potential or imagined consequences of reported consumption etc. (Jung and Namkoong, 2014; Le Berre et al., 2017; Welte and Russell, 1993). Further, even when applying collateral reports there is a risk that family members and staff may not be aware of the patient’s drinking pattern, due to e.g. lack of continuous monitoring etc. (Connors and Maisto, 2003).
No systematic review has yet examined the consistency between self-reports of alcohol consumption and alcohol biomarkers among patients in treatment for alcohol use disorders (AUD). Therefore, we aimed to provide an overview of the consistency between self-reported alcohol intake and biomarkers among patients in treatment for AUD.
The electronical databases MEDLINE, PsycINFO, EMBASE, Cochrane Database of Systematic Reviews (CDSR) and CENTRAL were searched for all original studies that examined the validity of self-reported alcohol consumption using a biological marker in samples of patients with AUD. Eligible studies were included in a qualitative synthesis of the outcomes. Quality assessment was conducted with the quality assessment tool for Observational Cohort and Cross-sectional studies, developed by The National Heart, Lung and Blood Institute.
The search identified 7672 hits, and 11 papers comprising 13 eligible studies were included. All the identified studies revealed inconsistencies between self-reporting and biomarkers. Under-reporting was the most common type of inconsistency across short-, intermediate- and long-term biomarkers. For short-term markers, under-reporting was indicated in 7 studies (n = 15–585) in a range from 5.5%–56.0% of the patients, and over-reporting in 2 studies (n = 34–65) in a range from 5.9%–74.1%. Only under-reporting was reported for intermediate-term, direct markers and was indicated in 2 studies (n = 18–54) in a range from 5.0%–50.0% of the patients. Although the results for long-term biomarkers were not reported consistently across the studies, under-reporting was indicated in 3 studies (n = 73–1580) in a range from 0.1%–40.0% of the patients, and over-reporting in 2 studies (n = 15–1580) in a range from 13.0%–70.6%. Correlations between self-reported alcohol consumption and biological markers were strongest for the intermediate-term direct markers, ranging from moderate to strong. For short-term and long-term markers, the correlations were mostly weak. Most of the studies were quality rated as fair.
The findings indicate that inconsistency between self-reported alcohol consumption and biomarkers may occur in a considerable proportion of patients with AUD. However, further studies applying more sensitive, specific, and easily assessable biological markers are warranted to confirm this preliminary synthesis.
PROSPERO registration no.: CRD42018105308

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Chapter 7 - Alcohol: intoxication and poisoning – diagnosis and treatment

Abstract

Introduction

Section snippets

The effects of ethanol on organ systems

Diagnosis

Differential diagnosis

Treatment

Am J Gastroenterol

Neurochem Int

Clin Liver Dis

Med Clin North Am

Emerg Med Clin North Am

Am J Med

Ann Emerg Med

Lancet Neurol

Curr Opin Neurobiol

Gastroenterology

Pharmacol Biochem Behav

Eur J Intern Med

Metadoxine in the treatment of acute and chronic alcoholism: a review

Int J Immunopathol Pharmacol

Acute ethanol poisoning and the ethanol withdrawal syndrome

Med Toxicol Adverse Drug Exp

Diagnostic and statistical manual of mental disorders

The relationship between alcohol consumption and cortisol secretion in an aging cohort

J Clin Endocrinol Metab

Current concepts in the assessment and treatment of hepatic encephalopathy

Q J Med

Activation of aldehyde dehydrogenase-2 reduces ischemic damage to the heart

Science

ALDH2, ADH1B, and ADH1C genotypes in Asians: a literature review

Alcohol Res Health

The effects of moderate alcohol consumption on female hormone levels and reproductive function

Alcohol Alcohol

Alcohol amnesia

Addiction

Clinical signs in the Wernicke–Korsakoff complex: a retrospective analysis of 131 cases diagnosed at necropsy

J Neurol Neurosurg Psychiatry

Pathological intoxication – is there such an entity?

J Clin Psychiatry

Alcohol, snoring and sleep apnea

J Neurol Neurosurg Psychiatry

Serum vs. breath alcohol levels and accidental injury: analysis among US Army personnel in an emergency room setting

Mil Med

Current state of knowledge about the mechanisms of alcohol tolerance

Addict Biol

Acute alcohol use among patients with acute hip fractures: a descriptive incidence study in southeastern Finland

Alcohol Alcohol