Cut down (tried), Annoyed c people asking, Guilty, Eye opener. 2 or more=+
MEOS system induced in drinkers
6 to 24 hrs
Withdrawal (Rum Fits)-12-24 hours, short postictal periods (spin head unless history in past)
Direct Neurotoxic Effects
Decreases seizure med levels, and decreases threshold (downregs GABA)
If seizures are partial, always get head CT. Also c LOC, HA, Skull Fx
Disposition Discharge to a detoxification center is dependent on recovery of patients to baseline mental status and their ability to safely ambulate (52). Most patients with alcohol-related seizures that have been treated with appropriate doses of lorazepam, and in whom concurrent risk factors have been ruled out by history, physical examination and diagnostic testing, can be safely discharged after a 3-h period of observation (25). Patients are unlikely to develop further seizures if recurrent events do not develop within a 3-h window after initial benzodiazepine administration. The focus of patient management should be on promoting primary prevention by encouraging patients to seek help in a structured detoxification program. The patient should be referred to a detoxification unit, and receive treatment with longer acting benzodiazepines to prevent further sequelae of alcohol withdrawal including recurrent seizures. The occurrence of a new-onset seizure should be viewed as a major adverse consequence of alcohol dependence, and presents an opportunity for the physician to assess the patients readiness for change and to successfully link them to a treatment center (53, 54 and 55). References 1 G. Brathen, E. Brodtkorb, G. Helde, T. Sand and G. Bovim, The diversity of seizures related to alcohol use. A study of consecutive patients, Eur J Neurol 6 (1999), pp. 697703. Abstract-EMBASE | Abstract-Elsevier BIOBASE | Abstract + References in Scopus | Cited By in Scopus 2 N.K. Rathlev, A.S. Ulrich, S.S. Fish and G. DOnofrio, Clinical characteristics as predictors of recurrent alcohol-related seizures, Acad Emerg Med 7 (2000), pp. 886891. Abstract-EMBASE | Abstract-MEDLINE | Abstract + References in Scopus | Cited By in Scopus 3 N.K. Rathlev, A. Ulrich, T. Shieh, M. Callum, E. Bernstein and G. DOnofrio, Etiology and weekly occurrence of alcohol-related seizures, Acad Emerg Med 9 (2002), pp. 824828. Abstract-EMBASE | Abstract-MEDLINE | Full Text via CrossRef | Abstract + References in Scopus | Cited By in Scopus 4 M. Victor and C. Brausch, The role of abstinence in the genesis of alcoholic epilepsy, Epilepsia 8 (1967), pp. 120. Abstract-MEDLINE | Abstract + References in Scopus | Cited By in Scopus 5 B.K. Alldredge and D.H. Lowenstein, Status epilepticus related to alcohol abuse, Epilepsia 34 (1993), pp. 10331037. Abstract-MEDLINE | Abstract-EMBASE | Full Text via CrossRef | Abstract + References in Scopus | Cited By in Scopus 6 G. Brathen, Alcohol and epilepsy, Tidsskr Nor Laegeforen 123 (2003), pp. 15361538. Abstract + References in Scopus | Cited By in Scopus 7 I.P. Pieninkeroinen, T.M. Telakivi and M.E. Hillbom, Outcome in subjects with alcohol-provoked seizures, Alcohol Clin Exp Res 16 (1992), pp. 955959. Abstract-MEDLINE | Abstract-EMBASE | Full Text via CrossRef | Abstract + References in Scopus | Cited By in Scopus 8 J.A. Ewing, Detecting alcoholism the CAGE questionnaire, Jama 252 (1984), pp. 19051907. Abstract-EMBASE | Abstract-MEDLINE | Abstract + References in Scopus | Cited By in Scopus 9 C.J. Cherpitel, Analysis of cut points for screening instruments for alcohol problems in the emergency room, J Stud Alcohol 56 (1995), pp. 695700. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus 10 S. Bleich, D. Degner, N. von Ahsen, E. Ruther and J. Kornhuber, Plasma homocysteine is a predictor of alcohol withdrawal seizures, Neuroreport 11 (2000), pp. 27492752. Abstract-EMBASE | Abstract-MEDLINE | Abstract-Elsevier BIOBASE | Abstract + References in Scopus | Cited By in Scopus 11 S.K.C. Ng, W.A. Hauser, J.C.M. Brust and M. Susser, Alcohol withdrawal and consumption in new-onset seizures, N Engl J Med 319 (1988), pp. 666673. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus 12 M.P. Earnest, Etiologies of acute alcohol-related seizures. In: R.J. Porter, R.H. Mattson, J.A. Cramer and I. Diamond, Editors, Alcohol and seizures basic mechanisms and clinical concepts, FA Davis Company, Philadelphia, PA (1990), pp. 197205. 13 M.E. Hillbom, Occurrence of cerebral seizures provoked by alcohol abuse, Epilepsia 21 (1980), pp. 459466. Abstract-EMBASE | Abstract-MEDLINE | Abstract + References in Scopus | Cited By in Scopus 14 A.W. Chan, Alcoholism and epilepsy, Epilepsia 26 (1985), pp. 323333. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus 15 R.H. Mattson, M.L. Fay, J.K. Sturman, J.A. Cramer, J.D. Wallace and E.M. Mattson, The effect of various patterns of alcohol use on seizures in patients with epilepsy. In: R.J. Porter, R.H. Mattson, J.A. Cramer and I. Diamond, Editors, Alcohol and seizures basic mechanisms and clinical concepts, FA Davis Company, Philadelphia, PA (1990), pp. 233240. 16 J.F. Annegers, A. Hauser, S.P. Coan and W. Rocca, A population-based study of seizures after traumatic brain injuries, N Engl J Med 338 (1998), pp. 2024. Abstract-EMBASE | Abstract-MEDLINE | Full Text via CrossRef | Abstract + References in Scopus | Cited By in Scopus 17 P. Davidson, J. Koziol-McLain, L. Harrison, D. Timken and S.R. Lowenstein, Intoxicated ED patients a 5-year follow-up of morbidity and mortality, Ann Emerg Med 30 (1997), pp. 593597. SummaryPlus | Full Text + Links | PDF (470 K) | Abstract + References in Scopus | Cited By in Scopus 18 K. Skullerud, S.N. Andersen and J. Lundevall, Cerebral lesions and causes of death in male alcoholics a forensic autopsy study, Int J Legal Med 104 (1991), pp. 209213. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus 19 K. Seppa and P. Sillanaukee, Binge drinking and ambulatory blood pressure, Hypertension 33 (1999), pp. 7982. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus 20 A.L. Klatsky, M.A. Armstrong, S. Sidney and G.D. Friedman, Alcohol drinking and the risk of hemorrhagic stroke, Am J Cardiol 88 (2001), pp. 703706. SummaryPlus | Full Text + Links | PDF (81 K) | Abstract + References in Scopus | Cited By in Scopus 21 G. Mazzaglia, A.R. Britton, D.R. Altman and L. Chenet, Exploring the relationship between alcohol consumption and non-fatal and fatal stroke a systematic review, Addiction 96 (2001), pp. 17431756. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus 22 J.S. Gill, M.J. Shipley and S.A. Tsementzis et al., Alcohol consumptiona risk factor for hemorrhagic and non-hemorrhagic stroke, Am J Med 90 (1991), pp. 489497. SummaryPlus | Full Text + Links | PDF (984 K) | Abstract + References in Scopus | Cited By in Scopus 23 W.A. Hauser and L.T. Kurland, The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967, Epilepsia 16 (1975), pp. 166. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus 24 N.K. Rathlev, G. DOnofrio and S.S. Fish et al., The efficacy of phenytoin in the prevention of recurrent alcohol withdrawal seizures, Ann Emerg Med 23 (1994), pp. 513518. Abstract-MEDLINE | Abstract-EMBASE | Abstract + References in Scopus | Cited By in Scopus 25 G. DOnofrio, N.K. Rathlev, A.S. Ulrich, S.S. Fish and E.S. Freedland, Lorazepam for the prevention of recurrent seizures related to alcohol, N Engl J Med 340 (1999), pp. 915919. Go to source: ScienceDirect – Journal of Emergency Medicine : Alcohol-related seizures
Alcohol-related seizures occur 6 – 48 hrs after the last drink. When multiple seizures occur, the interval between the first and the last seizure is usually less than 6 hrs. (Journal of Emergency Medicine, August, 2006, pg. 158). (emedhome)
etoh worse than benzos for prophylaxis of withdrawl (J Trauma 2008;64:99)
>Prophylactic Lorazepam in the ED for Alcohol-Related Seizures > > > >Benzodiazepines should be given not only for the >treatment of active alcohol-withdrawal >convulsions in the ED, but also for short-term >prophylaxis within the 6- to 12-h window in >which patients are at high risk for recurrent >alcohol-related seizures. This is particularly >true for patients who are at high risk because >of a prior history of epilepsy, alcohol-related >seizures, or multiple previous detoxifications (1,2). > >Lorazepam appears to be an ideal agent for the >treatment of patients with alcohol-related >seizures and should be given within the 6- to >12-h period when recurrent seizures typically >occur. It has minimal depressant effects on >respirations and the circulation and has a >shorter half-life than diazepam with no active >metabolites. It controls seizures longer than >diazepam due to favorable pharmacokinetics >(1,3). Lorazepam has the additional advantage >that it can be administered intramuscularly with >good effect if IV access is not available. > >Lorazepam has been demonstrated to be an >extremely effective agent for the prevention of >recurrent seizures in patients who present >following an initial alcohol-related seizure >(1,4). In one study, among patients receiving >lorazepam, 3% had a second seizure during a 6-h >observation period, compared with 24% in the >placebo group (4). Lorazepam should therefore be >administered routinely upon presentation to the >ED, unless contraindicated because of heavy >sedation due to intoxication, head injury, etc. > >Discharge to a detoxification center: Most >patients with alcohol-related seizures that have >been treated with appropriate doses of >lorazepam, and in whom concurrent risk factors >have been ruled out by history, physical >examination and diagnostic testing, can be >safely discharged after a 3-h period of >observation (4). Patients are unlikely to >develop further seizures if recurrent events do >not develop within a 3-h window after initial benzodiazepine administration. > > > >References: > >(1) Rathlev NK, et al. Alcohol-related >seizures J of Emerg Med 2006; 31:157-163. > >(2) Morton WA, et al. A prediction model for >identifying alcohol withdrawal seizures Am J >Drug Alcohol Abuse 1994;20:75Â86. > >(3) Alldredge BK et al. Status epilepticus >related to alcohol abuse Epilepsia 1993;34:1033Â1037. > >(4) DÂOnofrio G, et al. Lorazepam for the >prevention of recurrent seizures related to >alcohol N Engl J Med 1999;340:915Â919. > >(5) White >SR. ><http://www.emedhome.com/features_archive_detail.cfm?FID=1698>Withdrawal >Syndromes in the Emergency Department www.EMedHome.com May 1, 2004.
Baclofen may have a role in this first RCT I have seen (J Hosp Med. 2011;6(8):474-9 )
Phenobarb (American Journal of Emergency Medicine (2011) 29, 382–385)Back to top
ETOH Induced Hypotension
Emergency Medicine Journal 2007;24:e7; doi:10.1136/emj.2006.041590 Severe hypotension and hypothermia caused by acute ethanol toxicityBack to top
Delirium Tremens (DTs)
initial treatment with Benzos
Give Valium to 200 mg, if still with symptoms, intubate and give propofol.
Barbs (open GABA Cl channel without GABA binding)-Phenobarbital 5 mg/kg then ½ that Q 30 minutes
Propofol is better
McCowan C, Marik P. Refractory delirium tremens treated with propofol: a case series. Crit Care Med. 2000 Jun;28(6):1781-4. Cooms TR, Smith SW Successful use of propofol in refractory delirium tremens. Ann Emerg Med. 1997 Dec;30(6):825-8. Prolonged Propofol Sedation in the Critical Care Unit. Critical Care Medicine. 23(7):1304-1305, July 1995. Mirenda, Joseph MD This may be the cite you are looking for from Pitt: Propofol: therapeutic indications and side-effects by Marik PE. Professor of Critical Care, Department of Critical Care, University of Pittsburgh, 640A Scaife Hall, 3550 Terrace Street, Pittsburgh, PA, 15261, USA. firstname.lastname@example.org. Curr Pharm Des. 2004;10(29):3639-49 ABSTRACT Propofol (2, 6-diisopropylphenol) is a potent intravenous hypnotic agent which is widely used for the induction and maintenance of anesthesia and for sedation in the intensive care unit. Propofol is an oil at room temperature and insoluble in aqueous solution. Present formulations consists of 1% or 2% (w/v) propofol, 10% soyabean oil, 2.25% glycerol, and 1.2% egg phosphatide. Disodium edetate (EDTA) or metabisulfite is added to retard bacterial and fungal growth. Propofol is a global central nervous system depressant. It directly activates GABA(A) receptors. In addition, propofol inhibits the NMDA receptor and modulates calcium influx through slow calcium ion channels. Propofol has a rapid onset of action with a dose-related hypnotic effect. Recovery is rapid even after prolonged use. Propofol decreases cerebral oxygen consumption, reduces intracranial pressure and has potent anti-convulsant properties. It is a potent antioxidant, has anti-inflammatory properties and is a bronchodilator. As a consequence of these properties propofol is being increasingly used in the management of traumatic head injury, status epilepticus, delirium tremens, status asthmaticus and in critically ill septic patients. Propofol has a remarkable safety profile. Dose dependent hypotension is the commonest complication; particularly in volume depleted patients. Hypertriglyceridemia and pancreatitis are uncommon complications. Allergic complications, which may include bronchospasm, have been reported with the formulation containing metabisulfite. In addition, this formulation has been demonstrated to result in the generation of oxygen free radicals. High dose propofol infusions have been associated with the “propofol syndrome”; this is a potentially fatal complication characterized by severe metabolic acidosis and circulatory collapse. This is a rare complication first reported in pediatric patients and believed to be due to decreased transmembrane electrical potential and alteration of electron transport across the inner mitochondrial membrane.
Study from the Bellevue Folks on valium and phenobarb to avoid having to intubate (Crit Care Med 2007;35:724)Back to top
best review (Emerg Med J 2006;23:417)
ketonuria c normal glucose, partially due to increased NADH blocking sugar path. Can have impressive abd pain, vomiting.
A. Fib or V. Tach
Saturday Night Palsy
wrist drop from nerve compression
ETOH + Cocaine
Forms cocaethylene, cocaine like effects, but lasts much longer and more cardiotoxic
Oculomotor (Nystagmus or Ocular Palsy)/Confusion/Ataxia
two of the following four signs must be present:
1. Dietary deficiencies judged by a body mass index less than two standard deviations below normal, a history of grossly impaired dietary intake, or an abnormal thiamine assay.
2. Oculomotor abnormalities including opthalmoplegia, nystagmus, or a gaze palsy.
3. Cerebellar dysfunction, including ataxia, past pointing, dysdiadokinesia, or impaired heel-shin testing.
4. Altered mental status or mild memory impairment, judged as inability to recall two or more items in the four-item memory test or impairment on more elaborate neuropsychological tests of memory function.
review of wernicke’s (Annals EM 2007;50:715)
give thiamine asap after glucose, but don’t wait to treat hypoglycemia in order to get thiamine (The Journal of Emergency MedicineVolume 42, Issue 4, April 2012, Pages 488–494)
Confabulation, Amnesia, Apathy
ETOH is risk factor for embolic stroke and Tb
Can cause hypoglycemia in kiddies
Accucheck, UA (Rhabdo rule out)
If you get ETOH levels- Metabolize 25 mg/dl/hr at zero order kinetics
Banana Bag-500 cc D51/2NS @ 125 cc hr c 20 meq KCl, 100 mg thiamine (never give rapid IVP), 2 grams Mg, 20 meq K-Phos, 5cc MVI, 1 mg Folate
Rx of Withdrawal
Ativan 2-4 mg, then 2-4 mg Q 20 minutes until elimination of sx
Do not use phenothiazines or butyrophenones
Symptom triggered rather than fixed dose benzos utilize far less drugs with the assumption of lower risks (Arch Intern Med 162:1117, 2002)
Metadoxine (Pyridoxol) 900 mg IV bolus hastens recovery and elimination of ETOH (Alcoholism: Clin Exp Res 26 (3):340 2002)
PHARMACOLOGICAL MANAGEMENT OF ALCOHOL WITHDRAWAL: (JAMA, July 9, 1997 – Vol. 278, No. 2)
Clonidine decreases sympathetic outflow through its alpha-2 receptor agonism in the locus coeruleus. The overall intensity of withdrawal associated with clonidine treatment is similar to that with methadone treatment, but symptoms resolve more quickly with use of clonidine . Clonidine is associated with more adverse effects than methadone. These effects rarely include drowsiness, fatigue, lethargy, dry mouth and very rarely hypotension. Typical doses include 0.1 mg every 8 hours, although higher doses have been used in the inpatient setting with close blood pressure monitoring . There are many outpatient studies examining the use of clonidine in this setting and treatment duration varies from 3-10 days, with a typical maximum daily dose up to 1.0 mg. Some employ a taper, some do not. The following statement appropriately summarizes the issue: Generally, clonidine treatment for three-five days is adequate for the treatment of heroin withdrawal. Tapering can be considered in patients prescribed clonidine for more than a few days or at high doses. With regard to the necessity for tapering, it should be noted that regimens in the literature for the use of clonidine and other alpha-2 agonists focus mainly on the outpatient rehab setting where longer courses and much higher doses are typically used. The goal here is not just to treat withdrawal symptoms, but to promote abstinence. In the ED, the goal is simply to provide symptomatic improvement in those already withdrawing, so tapering is generally not necessary.
Signs of long standing etoh use
rhinophyma, palmar erythema, spider angiomata, hepatomegaly, and/or testicular atrophy. Other findings may include “chipmunk cheeks” (parotid enlargement), gynecomastia, acne rosacea, and Dupuytrens contractures of the hands
ALCOHOL WITHDRAWAL/CULTURAL DIVERSITY Emergency Medicine | Volume 18, Issue 15 | August 7, 2001 The following is an abstracted summary, not a verbatim transcript, of the lectures/discussions on this audio program. To continue to Step 4, click here. ALCOHOL WITHDRAWAL/CULTURAL DIVERSITY ALCOHOL WITHDRAWALRobert S. Hoffman, MD, Director, New York City Poison Control Center, New York City Incidence: third largest health problem in United States; hundreds of thousands of known deaths related to alcohol use; health care costs $60 billion in 1984; patients admitted for alcoholism predominantly men Definitions: toleranceconsuming same amount of alcohol every day results in less effect or person must consume more alcohol on successive days to get same effect; alcoholics have physiologic tolerance (change in receptors), pharmacologic tolerance (change in metabolism), and cross-tolerance, ie, tolerance to alcohol confers tolerance to benzodiazepines, barbiturates, and a whole host of other things; dependencewithdrawal symptoms occur when alcoholic does not drink; addictiondiffers in magnitude and sociologically from dependence; socially inappropriate dependence, ie, drinker resorts to inappropriate activities in order to maintain dependence Identifying alcoholics: enlarged parotid glands (chipmunk cheeks); chronic hyperamylasemia from overactive salivary glands; acne rosacea; spider hemangiomata; gynecomastia; female sexual hair patterns in men; cirrhosis; testicular atrophy; Dupuytrens contracture; serum aspartate transaminase (AST) level twice that of alanine transaminase (ALT); unexplained macrocytic anemia; commentfeatures neither sensitive nor specific; must talk to patients to determine alcoholism CAGE questionnaire: looks at how patient relates to own alcohol use; consists of 4 questions; have you ever tried to Cut down? do you get Annoyed when people talk to you about your drinking? do you feel Guilty about your alcohol use? do you need an Eye-opener in the morning? greater than or equal to 2 Yes answers define patient as alcoholic; questions must be slipped in during regular history and physical examination Michigan Alcohol Screening Test (MAST): addresses how patients alcohol use affects life events; questions gauged by point system; have you lost your job and/or spouse? have you been cited for driving while intoxicated (DWI)? have you ever attended Alcoholics Anonymous? have you ever asked anyone for help? have you ever been hospitalized for your drinking? Mechanism of addiction: dopamineuse of addictive substance (eg, nicotine, opioids, alcohol) stimulates release in frontal cortex, and you feel happy; withdrawal of dopamine stimulation disrupts reward pathway; gamma-aminobutyric acid (GABA)inhibitory neurotransmitter; alcoholics have decreased sensitivity; less inhibition produces more excitation, which produces alcohol withdrawal when not drinking, normal behavior when drinking; N -methyl-d-aspartate (NMDA) channelintracellular calcium channel that moves calcium into cell, causing excitation; alcohol inhibits excitation; chronic alcohol consumption enhances inhibition and impairs excitation; withdrawal of alcohol produces agitation due to impaired inhibition and enhanced excitation Four separate disorders (study by Victor and Adams) Alcoholic tremulousness: alcohol withdrawal; early manifestation; 8-12 hr after last drink; symptoms include mild hypertension and tachycardia, tremor, fasciculations of tongue, diaphoresis, agitation, discomfort, craving; normal orientation Alcoholic hallucinosis: normal vital signs and orientation; transient persecutory visual and auditory hallucinations; occurs soon after last drink; not necessarily associated with tremulousness; crossover between functional and organic hallucinations Rum fits: seizure without other manifestations of alcohol abstinence; generalized tonic-clonic seizure; usually single, can be multiple, status epilepticus uncommon (if present, suspect underlying idiopathic epilepsy); characteristic short postictal period; if untreated, 33% of patients progress to delirium tremens Delirium tremens (DT): same manifestations as alcoholic tremulousness but with disorientation; fatality rate less than or equal to 15%; death usually due to infection contracted before withdrawal, (illness makes patient stop drinking) or after withdrawal (due to aspiration during sedation or seizure); in older people, protracted tachycardia may exacerbate preexisting cardiovascular problems, resulting in myocardial infarction; occurs 1-3 days later than other syndromes; takes 3-5 days for successful treatment of uncomplicated DT, approximately 1 wk for severe cases; no one should ever be given the diagnosis of delirium tremens without a head CT (computed tomography) and an LP (lumbar puncture) on their chart to detect trauma or infection that caused patient to stop drinking Management of uncomplicated withdrawal: take care of them with common sense items, food and water and support; intravenous (IV) fluids containing glucose, thiamine, and water-soluble vitamins; electrocardiography (ECG) to screen for electrolyte abnormalities, especially potassium and magnesium; always look for occult infection; benzodiazepines medication of choice; use parenteral route in sick patients to ensure they got it now; speaker favors diazepam for its long-acting metabolites and rapid onset; lorazepam has no active metabolites, peaks 20 min after parenteral administration; speaker prefers administration prn vs standing orders; diazepam for patients who need parenteral medication, chlordiazepoxide (Librium) for patients who need po medication; give it until they are where you want them to be (speaker has given 2 g diazepam in <24 hr) Ethanol levels: predict possible complications; after initial treatment, patients with high ethanol levels go to intensive care unit (ICU) for close observation during next 8-12 hr Librium taper: an excuse to not look at your patients; oversedates some patients, undersedates others; not evidence-based Benzodiazepines: open chloride channels and increase GABA, hyperpolarizing cell; if treatment insufficient, add barbiturates Barbiturates: synergistic effect when combined with benzodiazepines; speaker preferred pentobarbital or thiopental (vs phenobarbital or amobarbital), now uses propofol; sedate patient, intubate to protect airway, maintain on barbiturate drip until stable; propofol when discontinued, patient awakens immediately, vs 3 days with pentobarbital; excitatory amino acid antagonist; attacks that other part of ethanol and ethanol withdrawal that heretofore weve been unable to get at Magnesium: alcoholics do not consume or absorb magnesium and have renal tubular magnesium wasting, leading to hypomagnesemia; hypomagnesemia has appearance of ethanol withdrawal (ie, tremulousness and hyperreflexia) because magnesium is excitatory amino acid antagonist, blocks what ethanol withdrawal enhances; no demonstrated evidence that magnesium efficacious for alcohol withdrawal without hypomagnesemia; speaker gives to any patient with documented hypomagnesemia, reassesses after first dose; be sure renal function normal before giving multiple doses Neuroleptics: demonstrated to be bad; enhance mortality in alcohol withdrawal Wernickes encephalopathy: caused by thiamine deficiency; associated with low-carbohydrate diet, sedentary lifestyle, and northern European descent; hemorrhage into mamillary bodies and central structures of brain produces triad of ataxia, ophthalmoplegia (nystagmus or palsy of sixth cranial nerve), and altered mental status; decreased deep tendon reflexes, hypothermia, metabolic acidosis, and hypotension; can be prevented with parenteral thiamine (approximately 100 mg daily); standing order for thiamine 100 mg po qd ineffective because alcohol prevents absorption from gut Conclusion: minority of chronic alcoholics recognizable (disheveled, alcohol on breath, without home, job, family, and health care coverage); majority of alcoholics moderately functional, get sicker after hospitalization (due to undetected alcoholism); suspect alcohol withdrawal in patients with unexplained seizure day after admission, psychomotor agitation, tremulousness, craving, and desire to flee; patients do well if treated early and aggressively; prevent infection, replace sedation, offer program for alcohol abstinence (5% of alcoholics achieve long-term sobriety)
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Differential of Alcoholism-Induced Encephalopathy
from Leon Gussow’s Poison Review
- Marchiafava-Bignami disease
Alcoholic ketoacidosis coincides with acute Marchiafava-Bignami disease — a case report. Chen MH, Cheng C. Am J Emerg Med 2012 Feb 3 [Epub ahead of print]
Yeah, I didn’t know what Marchiafava-Bignami disease (MBD) is either. Discovered by two Italian pathologists (let’s call them Dr. M and Dr. B) in 1903, MBD is rare but can occur in chronic drinkers. The crucial lesion involves demyelination and necrosis of the corpus callosum. The exact cause is not known. Characteristic presenting manifestations include altered mental status, coma, stupor, and pyramidal-tract signs.
This case report — from Taiwan — describes a 53-year-old chronic alcohol abuser who had recently been binge drinking. He presented with alcoholic ketoacidosis, but also neurological impairment including semi-coma, rigidity, and bilateral positive Babinski signs. Magnetic resonance imaging showed characteristic lesions.
The authors note that the differential diagnosis of alcohol-related acute encephalopathy includes:
- Wernicke encephalopathy
- osmotic demyelination syndromes (such as central pontine myelinolysis)
- alcohol withdrawal syndrome (delirium tremens)
- hepatic encephalopathy