Henry Ford Hospital Medical Journal Volume 34 Number 2 Article 4 6-1986 Management of Alcohol Withdrawal in the Critically Ill Patient: A Selected Review Rebecca B. Kantz H. Mathilda Horst Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Kantz, Rebecca B. and Horst, H. Mathilda (1986) "Management of Alcohol Withdrawal in the Critically Ill Patient: A Selected Review," Henry Ford Hospital Medical Journal : Vol. 34 : No. 2 , 87-89. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol34/iss2/4 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. IVIanagement of Alcohol Withdrawal in the Critically 111 Patient: X Selected Review I Rebecca B. Kantz, RPh,* and H. Mathilda Horst, MD* roper management of alcohol withdrawal represents a the critically ill patient) (1). Although withdrawal is thought to therapeutic challenge in the critically ill patient. The sever­ be a dose-dependent phenomenon, there is considerable indi­ Pity ofthe withdrawal syndrome varies with both the intensity and vidual variation in the amount of alcohol consumption necessary duration of the preceding alcohol exposure and may be compli­ to produce withdrawal. Furthermore, alcoholics are generally cated by other diseases such as traumatic injury, alcoholic gas­ unreliable in reporting their tme alcohol intake. Blood alcohol tritis, pancreatitis, liver failure, respiratory insufficiency, and/or concentrations may be used to detect tolerance; heavy imbibers malnutrition. These patients often cannot use the oral route for may show no symptoms of intoxication with blood alcohol lev­ therapy, and demonstrate considerable variability in response to els which would render a nontolerant person intoxicated (100 to treatment modalities. 250 mg%) or unconscious (350 to 500 mg%). Since tolerance to other CNS depressant dmgs (barbiturates, Diagnosis benzodiazepines, and other sedatives) occurs concurrently with Alcohol withdrawal may present a wide variety of clinical pat­ tolerance to alcohol (3), administration of a normally sedating terns ranging from mild self-limiting hyperadrenergic state, dose of medication (50 mg secobarbital or chlordiazepoxide) to tenned the common abstinence syndrome (CAS), to full-blown a tolerant individual may produce no sedation whatsoever This hallucinosis, grand mal seizures, and delirium tremens (DT's). method may provide the clinician with another clue as to which CAS is characterized by tremor, anxiety, and diaphoresis and patient is at risk for withdrawal. may occur as soon as six to eight hours after cessation of drink­ The theory behind pharmacologic treatment of alcohol with­ ing. Symptoms may occur alone or with auditory hallucinations drawal syndrome is that of substituting a sedative agent which is and/or convulsions. Peak symptoms are seen within ten to 30 cross-tolerant with alcohol, and then slowly weaning the patient hours and generally subside in 40 to 50 hours (1,2). Progression from that agent to prevent precipitation of symptoms. Numerous to DT's occurs in 1% to 10% of patients (1). Some authors feel pharmacologic agents have been used to treat alcohol with­ that aggressive treatment of early symptoms will minimize pro­ drawal syndrome, including phenothiazines, paraldehyde, ben­ gression to DT's; however, occasionally a patient will develop zodiazepines, barbiturates, antihistamines, butyrophenones, T's despite every preventive effort. beta-blockers, and ethanol (Table). Several studies have com­ DT's consist of profound disorientation associated with visual pared the efficacy of the first four dmgs in this list (5-10). In hallucinations and motor hyperactivity. The onset of DT's is 60 combining the results of five of these studies, Thompson (3) to 80 hours after the last drink. The average duration of DT's is found that patients treated with paraldehyde or benzodiaze­ two and one-half days, but symptoms may persist for a week or pines had the lowest incidence of DT's and seizures, while the more (1-3). use of phenothiazines was associated with a greater incidence of seizures. (Often deaths reported in the entire study popu­ Overlap in symptomatology may preclude a precise diagnosis lation of 978 patients, nine patients had been treated with in the critically ill patient (CAS versus DT's), although most au­ phenothiazines.) thors concur that symptoms are more easily controlled when agressively treated in the early stages (1). These studies were not controlled, and the dmg dosages em­ ployed varied widely. As there is no conclusive evidence as to which regimen is best, the choice of agent to control alcohol Tolerance withdrawal syndrome must therefore be based on efficacy, avail­ Alcohol, unlike other central nervous system (CNS) depres- ability, and lowest incidence of toxicity. Furthermore, the most santSj is metabolized primarily by the cytosolic liver enzyme appropriate regimen in the critically ill patient may be different alcohol dehydrogenase. Increased activity of this enzyme con- from that used to treat a patient with uncomplicated withdrawal tnbutes to the "tolerance" to alcohol displayed by heavy drink­ symptoms. ers (2). In theory, tolerance and physical dependence on ethanol 's a manifestation of compensatory neurophysiologic changes which offset the depressant effect of alcohol on neuronal excit­ ability, impulse conduction, and neurotransmitter release (4). Submitted for publication: May 9. 1986. Two methods have been suggested to aid the clinician in iden­ Accepted for publication: June 20, 1986. *Division of Trauma Surgery. Henry Ford Hospital. tifying the patient at risk of withdrawal (in addition to a positive Address correspondence to Ms Kantz, Division of Trauma Surgery, Henry Ford Hospital, history for withdrawal or DT's, which may not be elicited from 2799 W Grand Blvd. Detroit. Ml 48202. '^"ry Ford Hosp Med J- -Vol -'i4. No 2, 1986 Alcohol Withdrawal in Critically 111—Kantz et al 87 Table TVeatment of Alcohol Withdrawal in the Critically III Maximal Recommended Dose Reported Drug Route* Dose Frequency Dose Reference Chlordiazepoxide PO,lM,IVP 50 to 100 mg Every 6 hrs 1600 mg/day 1 Diazapam PO,lM,lVP Sto 10 mg IV Every 5 min until calm then 5 to 15 mg every 2 to 6 hrs l536 mg/48 hrs li Lorazepam PO,lM,lVP 2 to 8 mg Every 2 to 4 hrs Not available quire less i Haloperidol PO,lM,lVP 0.5 to 5 mg Every 2 to 6 hrs Not available 4,9,11,12 Paraldehyde P0,1V, 10 to 170 mL Every 6 hrs 436 mU24 hrs 13 Metabolisi rectal rectally Clinical Secobarbital IM 200 mg initially Every 6 hrs Not available 4,18,19 torydepres then 100 to 200 mg Propranolol PO 40 mg Every 6 hrs Not available 16,17 accumulati IV 0.5 mg Every 6 hrs tensive wi •PO = orally, IM = intramuscular, IV = intravenous, and IVP = intravenous pu.sh. half-life ol to diazepa to active i glucuronic Phenothiazines are not widely recommended in the treatment with bronchospastic disease, heart failure, and insulin-depen­ Further of alcohol withdrawal syndrome since they have not been shown dent diabetes. Efficacy studies of these agents in critically ill pa­ influencec to be superior to other agents. In addition, phenothiazines lower tients are lacking. biotransfo seizure threshold, cause sedation, and may potentiate the hyper­ Barbiturates are effective, inexpensive agents for alcohol ide may b thermia seen in withdrawal (4,5,7-9). Antihistamines are con­ withdrawal, provide sedation and anticonvulsant activity, and by coadm traindicated for this purpose and have anticholinergic effects can be given intravenously (4,18,19). Pentobarbital and secobar­ the half-l that can cause tachycardia, somnolence, and hallucinations bital have been used in doses of 200 mg IM initially, then 100 to these san (4,9,11). 200 mg IM every six hours. Despite favorable effects in control­ enced by Haloperidol, a butyrophenone and major tranquilizer, has ling withdrawal, barbiturates have largely been replaced by In dosi been shown to be effective in controlling agitation, hallucina­ newer agents. Phenobarbital (normal half-life two to five days) severaln tions, and DT's with minimal side-effects (12). However, the metabolism may be impaired in hepatic disease. Furthermore, diazepox ability ofthis dmg to lower seizure threshold is worrisome. For combining phenobarbital with narcotic analgesics can poten­ six hours the treatment of withdrawal, haloperidol is recommended in in­ tially cause oversedation in the critically ill patient (20,21). employei tramuscular (IM) doses of 0.5 to 2 mg every one to two hours The administration of intravenous ethanol has been used as a Thorn until satisfactory response is achieved, then 2 to 5 mg IM every 5% solution in 5% dextrose at 150 mL/hr to prevent withdrawal required four to six hours (4,9,11,12). symptoms (22). The drug has a narrow therapeutic index, a short than pat Paraldehyde is one of the classic dmgs used for alcohol with­ half-life, and may perpetuate metabolic disturbances. Its use is creatitis. drawal. Paraldehyde is a short-acting sedative-hypnotic that has not widely recommended (4). tially ca employe cross-tolerance with alcohol. It also has anticonvulsant activity Many clinicians consider the benzodiazepines to be the Thomps which prevents progression to seizures or DT's when used early agents of choice for the treatment of withdrawal due to their IV push in withdrawal (3,5,8). Paraldehyde is not without its attendant efficacy as well as their safety. These dmgs produce adequate (If agit;i problems, such as being erratically absorbed from the oral and sedation, anticonvulsant activity, and fewer side-effects than bled.) N rectal routes and causing sterile abscess formation with repeated other agents. While control of withdrawal symptoms may be two to s IM injections.