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Alcohol withdrawal syndrome

Revision as of 07:17, 18 May 2012 by SupaH12 (Message Wall | contribs) (→‎Background)
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Alcohol Withdrawal Syndrome
ICD-10 F103, F104
ICD-9 291.81
OMIM {{{OMIM}}}
DiseasesDB 3543
MedlinePlus 000764
eMedicine {{{eMedicineSubj}}}/{{{eMedicineTopic}}}
MeSH {{{MeshNumber}}}


Alcohol withdrawal syndrome is the set of symptoms seen when an individual reduces or stops alcohol consumption after prolonged periods of excessive alcohol intake. Excessive abuse of alcohol leads to tolerance, physical dependence, and an alcohol withdrawal syndrome. The withdrawal syndrome is largely due to the central nervous system being in a hyper-excitable state. Unlike most withdrawals from other drugs, alcohol withdrawal can be fatal. The withdrawal syndrome can include seizures and delirium tremens and may lead to excito-neurotoxicity.[1]

Background

Sedative-hypnotics such as alcohol are well known for their propensity to induce physiological dependence. Alcohol withdrawal occurs as a result of neuro-adaptation resulting from chronic exposure to alcohol. A withdrawal syndrome occurs upon declining blood levels of alcohol which can be alleviated by reintroduction of alcohol or a cross-tolerant agent. Alcohol withdrawal is characterized by neuropsychiatric excitability and autonomic disturbances similar to other sedative-hypnotic drugs. Dependence on other sedative-hypnotics increases the severity of the withdrawal syndrome.[2]

Signs and symptoms

The severity of the alcohol withdrawal syndrome can vary from mild symptoms such as mild sleep disturbances and mild anxiety to very severe and life threatening including delirium, particularly visual hallucinations in severe cases and convulsions (which may result in death).[3] These symptoms appear characteristically on waking, due to the fall in the blood alcohol concentration during sleep.[4] The severity of alcohol withdrawal depends on various factors including age, genetics, and, most importantly, degree of alcohol intake and length of time the individual has been misusing alcohol and number of previous detoxifications.[5][6]

Protracted withdrawal

See also: Protracted withdrawal syndrome

A protracted alcohol withdrawal syndrome occurs in many alcoholics where withdrawal symptoms continue beyond the acute withdrawal stage but usually at a subacute level of intensity and gradually decreasing with severity over time. This syndrome is also sometimes referred to as the post acute withdrawal syndrome. Some withdrawal symptoms can linger for at least a year after discontinuation of alcohol. Symptoms can include a craving for alcohol, inability to feel pleasure from normally pleasurable things (also known as anhedonia), clouding of sensorium, disorientation, nausea and vomiting or headache.[15] Insomnia is also a common protracted withdrawal symptom which persists after the acute withdrawal phase of alcohol. Insomnia has also been found to influence relapse rate. Studies have found that magnesium or trazodone can help treat the persisting withdrawal symptom of insomnia in recovering alcoholics. Insomnia can be difficult to treat in alcoholics because many of the traditional sleep aids (e.g. benzodiazepine receptor agonists and barbiturate receptor agonists) work via a GABAA receptor mechanism and are cross tolerant with alcohol. However, trazodone is not cross tolerant with alcohol.[16][17][18] The acute phase of the alcohol withdrawal syndrome can also occasionally be protracted. Protracted delirium tremens has been reported in the medical literature as a possible but unusual feature of alcohol withdrawal.[19]

Pathophysiology

Chronic use of alcohol leads to changes in brain chemistry especially in the GABAergic system. Various adaptations occur such as changes in gene expression and down regulation of GABAA receptors. During acute alcohol withdrawal, changes also occur such as upregulation of alpha4 containing GABAA receptors and down regulation of alpha1 and alpha3 containing GABAA receptors. Neurochemical changes occurring during alcohol withdrawal can be minimized with drugs which are used for acute detoxification. With abstinence from alcohol and cross tolerant drugs these changes in neurochemistry gradually return towards normal.[20][21] Adaptations to the NMDA system also occur as a result of repeated alcohol intoxication and are involved in the hyper-excitability of the central nervous system during the alcohol withdrawal syndrome. Homocysteine levels which are elevated during chronic drinking increase even further during the withdrawal state and may result in excito-neurotoxicity. Alterations in ECG, in particular an increase in QT interval, and EEG abnormalities including may occur during early withdrawal.[22]

Kindling

See also: Kindling (substance withdrawal)

Kindling is the phenomenon where repeated alcohol detoxifications lead to an increased severity of the withdrawal syndrome. For example, binge drinkers may initially experience no withdrawal symptoms but with each period of resumption of drinking followed by abstinence their withdrawal symptoms intensify in severity and may eventually result in full blown delirium tremens with convulsive seizures. Alcoholics who experience seizures during hospital detoxification have been found to be much more likely to have experienced more previous alcohol detoxification episodes than alcoholics who did not have seizures. Those experiencing previous detoxification are more likely to have more medically complicated alcohol withdrawal symptoms. Kindling can cause complications and may increase the risk of relapse, alcohol related brain damage and cognitive deficits. Chronic alcohol misuse and kindling via multiple alcohol withdrawals may lead to permanent alterations in the GABAA receptors.[23]

The mechanism behind kindling is sensitization of some neuronal systems and desensitization of other neuronal systems which leads to increasingly gross neurochemical imbalances. This in turn leads to more profound withdrawal symptoms including anxiety, convulsions and neurotoxicity.[6]

Binge drinking is associated with increased impulsivity, impairments in spatial working memory and impaired emotional learning. These adverse effects are believed to be due to the neurotoxic effects of repeated withdrawal from alcohol on aberrant neuronal plasticity and cortical damage. Repeated periods of acute intoxication followed by acute detoxification has profound effects on the brain and is associated with an increased risk of seizures as well as cognitive deficits. The effects on the brain are similar to those seen in alcoholics who have been detoxified multiple times but not as severe as in alcoholics who have no history of prior detox. Thus the acute withdrawal syndrome appears to be the most important factor in causing damage or impairment to brain function. The brain regions most sensitive to harm from binge drinking are the amygdala and prefrontal cortex.[24]

People in adolescence who experience multiple withdrawals from binge drinking show impairments of long-term nonverbal memory. Alcoholics who have had two or more alcohol withdrawals show more frontal lobe cognitive dysfunction than alcoholics who have experienced one or no prior withdrawals. Kindling of neurons is the proposed cause of withdrawal related cognitive damage. Kindling from multiple withdrawals leads to accumulating neuroadaptational changes. Kindling may also be the reason for cognitive damage seen in binge drinkers.[25]

Diagnosis

Many hospitals use the Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol in order to assess the level of withdrawal present and therefore the amount medication needed.[7] When overuse of alcohol is suspected but drinking history is unclear, testing for elevated values of carbohydrate-deficient transferrin and/or gammaglutamyl transferase can help make the diagnosis of alcohol overuse and dependence more clear.

Treatment

Benzodiazepines are effective for the management of symptoms as well as the prevention of seizures.[26]

Treatment of alcohol withdrawal syndrome can be managed with various pharmaceutical medications including barbiturates and clonidine. Certain vitamins are also an important part of the management of alcohol withdrawal syndrome.

Benzodiazepines

Benzodiazepines such as diazepam or lorazepam, are the most commonly used drug for the treatment of alcohol withdrawal and are generally safe and effective in suppressing alcohol withdrawal signs. Chlordiazepoxide and diazepam are the benzodiazepines most commonly used in alcohol detoxification.[27] Benzodiazepines can be life saving, particularly if delirium tremens appears during alcohol withdrawal.[28] Benzodiazepines should only be used short term in alcoholics who aren't already dependent on benzodiazepines as benzodiazepines share cross tolerance with ethanol and there is a risk of replacing the addiction with a benzodiazepine dependence or worse still adding an additional addiction. Furthermore, disrupted GABA benzodiazepine receptor function is part of alcohol dependence and chronic benzodiazepines may prevent full recovery from alcohol induced mental effects.[29][30] Benzodiazepines have the problem of increasing cravings for alcohol in problem alcohol consumers and they also increase the volume of alcohol consumed by problem drinkers.[31] The combination of benzodiazepines and alcohol can amplify the adverse psychological effects of each other causing enhanced depressive effects on mood and increase suicidal actions and are generally contraindicated except for alcohol withdrawal.[32]

Antipsychotics

Antipsychotic agents such as haloperidol are sometimes used for alcohol withdrawal as an add-on to first-line measures such as benzodiazepines to control agitation or psychosis.[7] Antipsychotics may potentially worsen alcohol withdrawal effects (or other CNS depressant withdrawal states) as they lower the seizure threshold and can worsen withdrawal effects. Clozapine, olanzapine or low potency phenothiazines (e.g. chlorpromazine) are particularly risky; if used, extreme caution is required.[33] There is also concern for this class of drugs prolonging the QT interval, sometimes leading to fatal heart dysrhthmias.

Anticonvulsants

Some evidence indicates that topiramate[22] carbamazepine and other anticonvulsants are effective in the treatment of alcohol withdrawal however, research is limited.[22][34] A Cochrane review similarly reported that the evidence to support the role of anticonvulsants over benzodiazepines in the treatment of alcohol withdrawal is not statistically significant and noted significant weaknesses in the studies available and recommended further research. The Cochrane Review did note however, that paraldehyde combined with chloral hydrate showed superiority over chlordiazepoxide with regard to incidence of life threatening side effects and also noted that carbamazapine may have advantages for certain symptoms.[35] The advantages of carbamazapine demonstrated in one trial are less rebound withdrawal symptoms and appears to have a higher success rate for abstinence from alcohol post detoxification compared to benzodiazepines.[36]

Baclofen

Baclofen has been shown to be as effective as diazepam in uncomplicated alcohol withdrawal syndrome.[37]

Barbiturates

Barbiturates are superior to diazepam in the treatment of severe alcohol withdrawal syndromes such as delirium tremens but equally effective in milder cases of alcohol withdrawal.[38]

Clomethiazole

Clomethiazole (Heminevrin) is a non-benzodiazepine sedative-hypnotic with anticonvulsant effects which is active on the barbiturate site of the GABA-A receptor. Clomethiazole also inhibits the enzyme alcohol dehydrogenase, which is responsible for breaking down alcohol in the body. This slows the rate of elimination of alcohol from the body, which helps to relieve the sudden effects of alcohol withdrawal in alcoholics.

Clonidine

Clonidine has demonstrated superior clinical effects in the suppression of alcohol withdrawal symptoms in a head to head comparison study with the benzodiazepine drug chlordiazepoxide.[39][40][41]

Ethanol

Alcohol (ethanol) itself at low doses has been found to be superior to chlordiazepoxide in the detoxification of alcohol dependent patients. Low dose ethanol as a means of weaning alcoholics off of alcohol was found to produce less profound sleep disturbances during withdrawal.[42] Low dose ethanol has been found to reduce treatment time, improve the failure rate from 20% down to 7% and increase retention in treatment centers with an increased rate of alcoholics attending substance misuse clinics after detoxification.[43]

Flumazenil

Flumazenil, which has shown some promise in the management of the benzodiazepine withdrawal syndrome has also demonstrated benefit in a research study in reducing anxiety withdrawal related symptomatology during alcohol withdrawal.[44]

Trazodone

Trazodone has demonstrated efficacy in the treatment of the alcohol withdrawal syndrome. It may have particular use in withdrawal symptoms, especially insomnia, persisting beyond the acute withdrawal phase.[17][18][45]

Magnesium

Magnesium appears to be effective in the treatment of alcohol withdrawal related cardiac arrhythmias. It is ineffective in controlling other symptoms of alcohol withdrawal.[46]

Vitamins

The prophylactic administration of thiamine intravenously is recommended before starting any carbohydrate containing fluids or food. Alcoholics are often deficient in various nutrients which can cause severe complications during alcohol withdrawal such as the development of Wernicke syndrome. The vitamins of most importance in alcohol withdrawal are thiamine and folic acid. To help to prevent Wernicke syndrome alcoholics should be administered a multivitamin preparation with sufficient quantities of thiamine and folic acid. Vitamins should always be administered before any glucose is administered otherwise Wernicke syndrome can be precipitated.[47]

Prevention of brain damage

It has been proposed that brain damage due to alcohol withdrawal may be prevented by the administration of NMDA antagonists, calcium antagonists, and glucocorticoid antagonists.[48] The NMDA antagonist acamprosate reduces excessive glutamate rebound thereby suppressing excitotoxicity and potential withdrawal related neurotoxicity.[49]

Substances impairing recovery

Continued use of benzodiazepines may impair recovery from psychomotor and cognitive impairments from alcohol.[50] Cigarette smoking may slow down or interfere with recovery of brain pathways in recovering alcoholics.[51]

See also

References

  1. ↑ Hughes JR (February 2009). Alcohol withdrawal seizures. Epilepsy Behav 15 (2): 92–7.
  2. ↑ (1 December 2003) Medical Toxicology, 3rd, 139–140, USA: Lippincott Williams & Wilkins.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 Harada K (1993). Emotional condition in alcohol withdrawal acute psychosis. Seishin Shinkeigaku Zasshi 95 (7): 523–9.
  4. ↑ Gelder et al,2005 p188. Psychiatry 3rd Ed. oxford:New York.
  5. ↑ Liskow BI, Rinck C, Campbell J, DeSouza C (September 1989). Alcohol withdrawal in the elderly. J Stud Alcohol 50 (5): 414–21.
  6. ↑ 6.0 6.1 Howard C. Becker (1998). Kindling in Alcohol Withdrawal. Alcohol Health & Research World 22 (1).
  7. ↑ 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 7.11 7.12 7.13 7.14 7.15 7.16 Bayard M, McIntyre J, Hill KR, Woodside J (March 2004). Alcohol withdrawal syndrome. Am Fam Physician 69 (6): 1443–50.
  8. ↑ Cowley DS (January 24, 1992). Alcohol abuse, substance abuse, and panic disorder. Am J Med 92 (1A): 41S–48S.
  9. ↑ Muralidharan K, Rajkumar RP, Ananthapadmanabha Rao S, Benegal V (2007). Catatonia as a Presenting Feature of Alcohol Withdrawal: A Case Report. Prim Care Companion J Clin Psychiatry 9 (6).
  10. ↑ Burov YV, Treskov VG, Vedernikova NN, Shevelyova OS (May 1986). Types of alcohol withdrawal syndrome and dexamethasone suppression test. Drug Alcohol Depend 17 (1): 81–8.
  11. ↑ Abitan J, Sigrist O (8-15). [Treatment of alcohol withdrawal symptoms: a clinical study (author's transl)]. Sem Hop 55 (21–22): 1105–7.
  12. ↑ Peppers MP (January–February 1996). Benzodiazepines for alcohol withdrawal in the elderly and in patients with liver disease. Pharmacotherapy 16 (1): 49–57.
  13. ↑ Fruensgaard K (February 1976). Withdrawal psychosis: a study of 30 consecutive cases. Acta Psychiatr Scand 53 (2): 105–18.
  14. ↑ Gann H, Feige B, Hohagen F, van Calker D, Geiss D, Dieter R (September 1, 2001). Sleep and the cholinergic rapid eye movement sleep induction test in patients with primary alcohol dependence. Biol Psychiatry 50 (5): 383–90.
  15. ↑ Martinotti G, Nicola MD, Reina D, Andreoli S, Focà F, Cunniff A, Tonioni F, Bria P, Janiri L (2008). Alcohol protracted withdrawal syndrome: the role of anhedonia. Subst Use Misuse 43 (3–4): 271–84.
  16. ↑ Hornyak M, Haas P, Veit J, Gann H, Riemann D (November 2004). Magnesium treatment of primary alcohol-dependent patients during subacute withdrawal: an open pilot study with polysomnography. Alcohol Clin Exp Res 28 (11): 1702–9.
  17. ↑ 17.0 17.1 Le Bon O, Murphy JR, Staner L, Hoffmann G, Kormoss N, Kentos M, Dupont P, Lion K, Pelc I, Verbanck P (August 2003). Double-blind, placebo-controlled study of the efficacy of trazodone in alcohol post-withdrawal syndrome: polysomnographic and clinical evaluations. J Clin Psychopharmacol 23 (4): 377–83.
  18. ↑ 18.0 18.1 Borras L, de Timary P, Constant EL, Huguelet P, Eytan A (November 2006). Successful treatment of alcohol withdrawal with trazodone. Pharmacopsychiatry 39 (6).
  19. ↑ Miller FT (Mar-April 1994). Protracted alcohol withdrawal delirium. J Subst Abuse Treat 11 (2): 127–30.
  20. ↑ Sanna, E; Mostallino, Mc; Busonero, F; Talani, G; Tranquilli, S; Mameli, M; Spiga, S; Follesa, P; Biggio, G (December 17, 2003). Changes in GABA(A) receptor gene expression associated with selective alterations in receptor function and pharmacology after ethanol withdrawal. Journal of Neuroscience 23 (37): 11711–24.
  21. ↑ Idemudia SO, Bhadra S, Lal H (June 1989). The pentylenetetrazol-like interoceptive stimulus produced by ethanol withdrawal is potentiated by bicuculline and picrotoxinin. Neuropsychopharmacology 2 (2): 115–22.
  22. ↑ 22.0 22.1 22.2 (Jun 2009). Alcohol withdrawal seizures. Epilepsy Behav 15 (2): 92–7.
  23. ↑ Malcolm RJ (2003). GABA systems, benzodiazepines, and substance dependence. J Clin Psychiatry 64 Suppl 3: 36–40.
  24. ↑ (Oct 2008). Cognitive and emotional consequences of binge drinking: role of amygdala and prefrontal cortex. Philos Trans R Soc Lond B Biol Sci 363 (1507): 3169–79.
  25. ↑ (Jan 2009). Binge Drinking in Young Adults: Data, Definitions, and Determinants. Psychol Bull 135 (1): 142–56.
  26. ↑ Amato L, Minozzi S, Vecchi S, Davoli M (2010). Benzodiazepines for alcohol withdrawal. Cochrane Database Syst Rev 3 (3): CD005063.
  27. ↑ Ebell MH (April 2006). Benzodiazepines for alcohol withdrawal. Am Fam Physician 73 (7).[dead link]
  28. ↑ Wolf KM, Shaughnessy AF, Middleton DB (1993). Prolonged delirium tremens requiring massive doses of medication. J Am Board Fam Pract 6 (5): 502–4.
  29. ↑ Toki S, Saito T, Nabeshima A, Hatta S, Watanabe M, Takahata N (February 1996). Changes in GABAA receptor function and cross-tolerance to ethanol in diazepam-dependent rats. Alcohol. Clin. Exp. Res. 20 (1 Suppl): 40A–44A.
  30. ↑ Rassnick S, Krechman J, Koob GF (April 1993). Chronic ethanol produces a decreased sensitivity to the response-disruptive effects of GABA receptor complex antagonists. Pharmacol. Biochem. Behav. 44 (4): 943–50.
  31. ↑ Ziegler PP (August 2007). Alcohol use and anxiety. Am J Psychiatry 164 (8): 1270; author reply 1270–1.
  32. ↑ (23 October 2007) "Alphabetical presentation of drugs" Desk Reference for Clinical Pharmacology, 2nd, USA: CRC Press.
  33. ↑ Prince V, Turpin KR (June 1, 2008). Treatment of alcohol withdrawal syndrome with carbamazepine, gabapentin, and nitrous oxide. Am J Health Syst Pharm 65 (11): 1039–47.
  34. ↑ (2010). Anticonvulsants for alcohol withdrawal. Cochrane Database Syst Rev 3 (3): CD005064.
  35. ↑ Malcolm R, Myrick H, Roberts J, Wang W, Anton RF, Ballenger JC (May 2002). The Effects of Carbamazepine and Lorazepam on Single versus Multiple Previous Alcohol Withdrawals in an Outpatient Randomized Trial. J Gen Intern Med 17 (5): 349–55.
  36. ↑ Addolorato G, Leggio L, Abenavoli L, Agabio R, Caputo F, Capristo E, Colombo G, Gessa GL, Gasbarrini G (March 2006). Baclofen in the treatment of alcohol withdrawal syndrome: a comparative study vs diazepam. Am J Med 119 (3): 276.e13–8.
  37. ↑ Kramp P, Rafaelsen OJ (August 1978). Delirium tremens: a double-blind comparison of diazepam and barbital treatment. Acta Psychiatr Scand 58 (2): 174–90.
  38. ↑ Baumgartner GR (January 1988). Clonidine versus chlordiazepoxide in acute alcohol withdrawal: a preliminary report. South Med J 81 (1): 56–60.
  39. ↑ Baumgartner GR, Rowen RC (July 1987). Clonidine vs chlordiazepoxide in the management of acute alcohol withdrawal syndrome. Arch Intern Med 147 (7): 1223–6.
  40. ↑ Björkqvist SE (October 1975). Clonidine in alcohol withdrawal. Acta Psychiatr Scand 52 (4): 256–63.
  41. ↑ Funderburk FR, Allen RP, Wagman AM (March 1978). Residual effects of ethanol and chlordiazepoxide treatments for alcohol withdrawal. J Nerv Ment Dis 166 (3): 195–203.
  42. ↑ Dissanaike S, Halldorsson A, Frezza EE, Griswold J (August 2006). An ethanol protocol to prevent alcohol withdrawal syndrome. J Am Coll Surg 203 (2): 186–91.
  43. ↑ Little HJ (July 1991). The benzodiazepines: anxiolytic and withdrawal effects. Neuropeptides 19 Suppl: 11–4.
  44. ↑ Roccatagliata G, Albano C, Maffini M, Farelli S (1980). Alcohol withdrawal syndrome: treatment with trazodone. Int Pharmacopsychiatry 15 (2): 105–10.
  45. ↑ Wilson A, Vulcano B (1984). A double-blind, placebo-controlled trial of magnesium sulfate in the ethanol withdrawal syndrome. Alcohol. Clin. Exp. Res. 8 (6): 542–5.
  46. ↑ Hugh Myrick, Raymond F Anton (1998). Treatment of Alcohol Withdrawal. Alcohol Health & Research World 22 (1).
  47. ↑ (November–December 1993). Are binge drinkers more at risk of developing brain damage?. Alcohol 10 (6): 559–61.
  48. ↑ De Witte P, Littleton J, Parot P, Koob G (2005). Neuroprotective and abstinence-promoting effects of acamprosate: elucidating the mechanism of action. CNS Drugs 19 (6): 517–37.
  49. ↑ (1 October 2006) Substance Use Disorders: A Practical Guide, 2nd, 95–96, USA: Lippincott Williams and Wilkins.
  50. ↑ Durazzo TC, Meyerhoff DJ (2007). Neurobiological and neurocognitive effects of chronic cigarette smoking and alcoholism. Front. Biosci. 12 (8–12): 4079–100.


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Psychoactive substance-related disorder (F10–F19, 291–292; 303–305)
General

SID (Substance intoxication/Drug overdose, Withdrawal, Substance-induced psychosis) · SUD (Substance abuse, Physical dependence/Substance dependence)

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SID (Alcohol intoxication/Acute, Alcohol withdrawal, Delirium tremens, Alcoholic hallucinosis, Korsakoff's syndrome) · Alcoholism/SUD (Alcohol abuse, Alcohol dependence)

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SID (Opioid overdose) · SUD (Opioid dependence)

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