Acute ethanol poisoning and the ethanol withdrawal syndrome

B. Adinoff, G. H A Bone, M. Linnoila

Research output: Contribution to journalArticle

79 Citations (Scopus)

Abstract

Ethanol, a highly lipid-soluble compound, appears to exert its effect through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the γ-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolized at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology. The initial evaluation of ethanol withdrawal requires taking a history of ethanol intake, assessment of severity of past withdrawal episodes and other drug intake, and a physical examination to evaluate potential coexisting illnesses. As most patients in ethanol withdrawal do not require pharmacotherapy, a clinical evaluation, including measurement of the blood alcohol concentration and objective rating (i.e. CIWA-A scale) of withdrawal severity is indicated upon admission. Mild withdrawal symptoms may be treated with supportive care only (comfort, fluids, thiamine, multivitamins). Moderate withdrawal (tremors, agitation, diaphoresis) is generally well controlled with pharmacotherapy (oral diazepam 10 mg every 6 hours according to circumstances). A loading dose of diazepam (10 mg orally every hour) until symptoms subside, then every 6 hours when necessary is recommended for severe ethanol withdrawal (marked autonomic hyperactivity, severe distress, prodromal symptoms of delirium tremens). Other benzodiazepines or carbamazepine are also effective in the treatment of ethanol withdrawal. Other complications of the ethanol withdrawal syndrome should be treated as follows. Elevated blood pressure not responding to benzodiazepines, clonidine 0.2 mg every hour, then every 6 hours when necessary; arrhythmias, potassium and magnesium replacement, or more aggressive treatment as indicated; seizures, if history of withdrawal seizures, treat prophylactically. Following grand mal seizures, treat with benzodiazepines or carbamazepine. Other types of seizures require neurological evaluation for alternative aetiologies. Delirium tremens, exclude complicating illnesses; administer diazepam 10 mg intravenously every 30 to 60 minutes for sedation, haloperidol 5 mg intramuscularly every 6 hours for severe agitation, propranolol 1 mg intravenously every 5 minutes (up to 5 mg) for sympathetic hyperactivity. Fluid/electrolyte imbalance should be corrected as needed. All patients in ethanol withdrawal, if physically able, should partake in an alcohol treatment programme. Following resolution of the withdrawal syndrome, further inpatient or outpatient therapy, including Alcoholics Anonymous (AA), is required to maintain sobriety.

Original languageEnglish (US)
Pages (from-to)172-196
Number of pages25
JournalMedical Toxicology and Adverse Drug Experience
Volume3
Issue number3
StatePublished - 1988

Fingerprint

Poisoning
Ethanol
Alcohols
Benzodiazepines
Blood
Thiamine
Seizures
Diazepam
Coma
Alcohol Withdrawal Delirium
Drug therapy
Carbamazepine
Blood pressure
Tremor
Ataxia
Cell membranes
Stabilization
Alcoholics Anonymous
Cell Membrane
Prodromal Symptoms

ASJC Scopus subject areas

  • Toxicology

Cite this

Adinoff, B., Bone, G. H. A., & Linnoila, M. (1988). Acute ethanol poisoning and the ethanol withdrawal syndrome. Medical Toxicology and Adverse Drug Experience, 3(3), 172-196.

Acute ethanol poisoning and the ethanol withdrawal syndrome. / Adinoff, B.; Bone, G. H A; Linnoila, M.

In: Medical Toxicology and Adverse Drug Experience, Vol. 3, No. 3, 1988, p. 172-196.

Research output: Contribution to journalArticle

Adinoff, B, Bone, GHA & Linnoila, M 1988, 'Acute ethanol poisoning and the ethanol withdrawal syndrome', Medical Toxicology and Adverse Drug Experience, vol. 3, no. 3, pp. 172-196.
Adinoff, B. ; Bone, G. H A ; Linnoila, M. / Acute ethanol poisoning and the ethanol withdrawal syndrome. In: Medical Toxicology and Adverse Drug Experience. 1988 ; Vol. 3, No. 3. pp. 172-196.
@article{84f756b91c7e45e8931da364713b48a9,
title = "Acute ethanol poisoning and the ethanol withdrawal syndrome",
abstract = "Ethanol, a highly lipid-soluble compound, appears to exert its effect through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the γ-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg{\%} (250 mg{\%} = 250 mg/dl = 2.5 g/L = 0.250{\%}), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg{\%}, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg{\%}. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolized at the rate of approximately 15 mg{\%}/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg{\%}. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology. The initial evaluation of ethanol withdrawal requires taking a history of ethanol intake, assessment of severity of past withdrawal episodes and other drug intake, and a physical examination to evaluate potential coexisting illnesses. As most patients in ethanol withdrawal do not require pharmacotherapy, a clinical evaluation, including measurement of the blood alcohol concentration and objective rating (i.e. CIWA-A scale) of withdrawal severity is indicated upon admission. Mild withdrawal symptoms may be treated with supportive care only (comfort, fluids, thiamine, multivitamins). Moderate withdrawal (tremors, agitation, diaphoresis) is generally well controlled with pharmacotherapy (oral diazepam 10 mg every 6 hours according to circumstances). A loading dose of diazepam (10 mg orally every hour) until symptoms subside, then every 6 hours when necessary is recommended for severe ethanol withdrawal (marked autonomic hyperactivity, severe distress, prodromal symptoms of delirium tremens). Other benzodiazepines or carbamazepine are also effective in the treatment of ethanol withdrawal. Other complications of the ethanol withdrawal syndrome should be treated as follows. Elevated blood pressure not responding to benzodiazepines, clonidine 0.2 mg every hour, then every 6 hours when necessary; arrhythmias, potassium and magnesium replacement, or more aggressive treatment as indicated; seizures, if history of withdrawal seizures, treat prophylactically. Following grand mal seizures, treat with benzodiazepines or carbamazepine. Other types of seizures require neurological evaluation for alternative aetiologies. Delirium tremens, exclude complicating illnesses; administer diazepam 10 mg intravenously every 30 to 60 minutes for sedation, haloperidol 5 mg intramuscularly every 6 hours for severe agitation, propranolol 1 mg intravenously every 5 minutes (up to 5 mg) for sympathetic hyperactivity. Fluid/electrolyte imbalance should be corrected as needed. All patients in ethanol withdrawal, if physically able, should partake in an alcohol treatment programme. Following resolution of the withdrawal syndrome, further inpatient or outpatient therapy, including Alcoholics Anonymous (AA), is required to maintain sobriety.",
author = "B. Adinoff and Bone, {G. H A} and M. Linnoila",
year = "1988",
language = "English (US)",
volume = "3",
pages = "172--196",
journal = "Drug Safety",
issn = "0114-5916",
publisher = "Adis International Ltd",
number = "3",

}

TY - JOUR

T1 - Acute ethanol poisoning and the ethanol withdrawal syndrome

AU - Adinoff, B.

AU - Bone, G. H A

AU - Linnoila, M.

PY - 1988

Y1 - 1988

N2 - Ethanol, a highly lipid-soluble compound, appears to exert its effect through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the γ-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolized at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology. The initial evaluation of ethanol withdrawal requires taking a history of ethanol intake, assessment of severity of past withdrawal episodes and other drug intake, and a physical examination to evaluate potential coexisting illnesses. As most patients in ethanol withdrawal do not require pharmacotherapy, a clinical evaluation, including measurement of the blood alcohol concentration and objective rating (i.e. CIWA-A scale) of withdrawal severity is indicated upon admission. Mild withdrawal symptoms may be treated with supportive care only (comfort, fluids, thiamine, multivitamins). Moderate withdrawal (tremors, agitation, diaphoresis) is generally well controlled with pharmacotherapy (oral diazepam 10 mg every 6 hours according to circumstances). A loading dose of diazepam (10 mg orally every hour) until symptoms subside, then every 6 hours when necessary is recommended for severe ethanol withdrawal (marked autonomic hyperactivity, severe distress, prodromal symptoms of delirium tremens). Other benzodiazepines or carbamazepine are also effective in the treatment of ethanol withdrawal. Other complications of the ethanol withdrawal syndrome should be treated as follows. Elevated blood pressure not responding to benzodiazepines, clonidine 0.2 mg every hour, then every 6 hours when necessary; arrhythmias, potassium and magnesium replacement, or more aggressive treatment as indicated; seizures, if history of withdrawal seizures, treat prophylactically. Following grand mal seizures, treat with benzodiazepines or carbamazepine. Other types of seizures require neurological evaluation for alternative aetiologies. Delirium tremens, exclude complicating illnesses; administer diazepam 10 mg intravenously every 30 to 60 minutes for sedation, haloperidol 5 mg intramuscularly every 6 hours for severe agitation, propranolol 1 mg intravenously every 5 minutes (up to 5 mg) for sympathetic hyperactivity. Fluid/electrolyte imbalance should be corrected as needed. All patients in ethanol withdrawal, if physically able, should partake in an alcohol treatment programme. Following resolution of the withdrawal syndrome, further inpatient or outpatient therapy, including Alcoholics Anonymous (AA), is required to maintain sobriety.

AB - Ethanol, a highly lipid-soluble compound, appears to exert its effect through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the γ-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolized at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology. The initial evaluation of ethanol withdrawal requires taking a history of ethanol intake, assessment of severity of past withdrawal episodes and other drug intake, and a physical examination to evaluate potential coexisting illnesses. As most patients in ethanol withdrawal do not require pharmacotherapy, a clinical evaluation, including measurement of the blood alcohol concentration and objective rating (i.e. CIWA-A scale) of withdrawal severity is indicated upon admission. Mild withdrawal symptoms may be treated with supportive care only (comfort, fluids, thiamine, multivitamins). Moderate withdrawal (tremors, agitation, diaphoresis) is generally well controlled with pharmacotherapy (oral diazepam 10 mg every 6 hours according to circumstances). A loading dose of diazepam (10 mg orally every hour) until symptoms subside, then every 6 hours when necessary is recommended for severe ethanol withdrawal (marked autonomic hyperactivity, severe distress, prodromal symptoms of delirium tremens). Other benzodiazepines or carbamazepine are also effective in the treatment of ethanol withdrawal. Other complications of the ethanol withdrawal syndrome should be treated as follows. Elevated blood pressure not responding to benzodiazepines, clonidine 0.2 mg every hour, then every 6 hours when necessary; arrhythmias, potassium and magnesium replacement, or more aggressive treatment as indicated; seizures, if history of withdrawal seizures, treat prophylactically. Following grand mal seizures, treat with benzodiazepines or carbamazepine. Other types of seizures require neurological evaluation for alternative aetiologies. Delirium tremens, exclude complicating illnesses; administer diazepam 10 mg intravenously every 30 to 60 minutes for sedation, haloperidol 5 mg intramuscularly every 6 hours for severe agitation, propranolol 1 mg intravenously every 5 minutes (up to 5 mg) for sympathetic hyperactivity. Fluid/electrolyte imbalance should be corrected as needed. All patients in ethanol withdrawal, if physically able, should partake in an alcohol treatment programme. Following resolution of the withdrawal syndrome, further inpatient or outpatient therapy, including Alcoholics Anonymous (AA), is required to maintain sobriety.

UR - http://www.scopus.com/inward/record.url?scp=0023898420&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023898420&partnerID=8YFLogxK

M3 - Article

C2 - 3041244

AN - SCOPUS:0023898420

VL - 3

SP - 172

EP - 196

JO - Drug Safety

JF - Drug Safety

SN - 0114-5916

IS - 3

ER -