Alcohol intoxication

"Drunk" redirects here. For other uses, see Drunk (disambiguation).
Alcohol intoxication

The Drunkenness of Noah by Michelangelo
Classification and external resources
Specialty Toxicology
ICD-10 F10.0, T51
ICD-9-CM 305.0, 980
MedlinePlus 002644
MeSH D000435

Alcohol intoxication (also known as drunkenness or inebriation) is a physiological state (that may also include psychological alterations of consciousness) induced by the ingestion of ethanol (alcohol).

Alcohol intoxication is the result of alcohol entering the bloodstream faster than it can be metabolized by the liver, which breaks down the ethanol into non-intoxicating byproducts. Some effects of alcohol intoxication (such as euphoria and lowered social inhibitions) are central to alcohol's desirability as a beverage and its history as one of the world's most widespread recreational drugs. Despite this widespread use and alcohol's legality in most countries, many medical sources tend to describe any level of alcohol intoxication as a form of poisoning due to ethanol's damaging effects on the body in large doses; some religions consider alcohol intoxication to be a sin.

Symptoms of alcohol intoxication include euphoria, flushed skin and decreased social inhibition at lower doses, with larger doses producing progressively severe impairments of balance, muscle coordination (ataxia), and decision-making ability (potentially leading to violent or erratic behavior) as well as nausea or vomiting from alcohol's disruptive effect on the semicircular canals of the inner ear and chemical irritation of the gastric mucosa. Sufficiently high levels of blood-borne alcohol will cause coma and death from the depressive effects of alcohol upon the central nervous system.

Pathophysiology

Alcohol is metabolized by a normal liver at the rate of about 50 ml (1.7 US fl oz) of spirits (roughly a typical drink-size serving of beer, wine, or spirits) every 90 minutes. An "abnormal" liver with conditions such as hepatitis, cirrhosis, gall bladder disease, and cancer are likely to result in a slower rate of metabolism.

Ethanol is metabolised to acetaldehyde by alcohol dehydrogenase (ADH), which is found in many tissues, including the gastric mucosa. Acetaldehyde is metabolised to acetate by acetaldehyde dehydrogenase (ALDH), which is found predominantly in liver mitochondria. Acetate is used by the muscle cells to produce acetyl-CoA using the enzyme acetyl-CoA synthetase, and the acetyl-CoA is then used in the citric acid cycle.[1] It takes roughly 90 minutes for a healthy liver to metabolize a 30 ml (1.0 US fl oz) of pure ethanol, or approximately 24 minutes per British standard unit, which is 8 ml (0.27 US fl oz) of pure ethanol, or 42 min for a US standard drink, which is 14 grams 14 ml (0.47 US fl oz) of pure ethanol. One hour is often used as a safety allowance.

Wine is a Mocker by Dutch artist Jan Steen c. 1663

Ethanol's acute effects are due largely to its nature as a central nervous system depressant, and are dependent on blood alcohol concentrations:

As drinking increases, people become sleepy, or fall into a stupor. After a very high level of consumption, the respiratory system becomes depressed and the person will stop breathing. Comatose patients may aspirate their vomit (resulting in vomitus in the lungs, which may cause "drowning" and later pneumonia if survived). CNS depression and impaired motor co-ordination along with poor judgment increases the likelihood of accidental injury occurring.[3] It is estimated that about one-third of alcohol-related deaths are due to accidents and another 14% are from intentional injury.[4]

In addition to respiratory failure and accidents caused by effects on the central nervous system, alcohol causes significant metabolic derangements. Hypoglycaemia occurs due to ethanol's inhibition of gluconeogenesis, especially in children, and may cause lactic acidosis, ketoacidosis, and acute renal failure. Metabolic acidosis is compounded by respiratory failure. Patients may also present with hypothermia.

Pharmacology

In the past, alcohol was believed to be a non-specific pharmacological agent affecting many neurotransmitter systems in the brain.[5] However, molecular pharmacology studies have shown that alcohol has only a few primary targets. In some systems, these effects are facilitatory and in others inhibitory.

Among the neurotransmitter systems with enhanced functions are: GABAA,[6] 5-HT3 receptor agonism[7] (responsible for GABAergic (GABAA receptor PAM), glycinergic, and cholinergic effects), nicotinic acetylcholine receptors.[8]

Among those that are inhibited are: NMDA,[7] dihydropyridine-sensitive L-type Ca2+ channels[9] and G-protein-activated inwardly rectifying K+ channels.[10]

The result of these direct effects is a wave of further indirect effects involving a variety of other neurotransmitter and neuropeptide systems, leading finally to the behavioural or symptomatic effects of alcohol intoxication.[5]

GABAA receptors

Ethanol binding to GABAA receptor

Many of the effects of activating GABAA receptors have the same effects as that of ethanol consumption. Some of these effects include anxiolytic, anticonvulsant, sedative and hypnotic effects, cognitive impairment, and motor incoordination.[11] This correlation between activating GABAA receptors and the effects of ethanol consumption has led to the study of ethanol and its effects on GABAA receptors. It has been shown that ethanol does in fact exhibit positive allosteric binding properties to GABAA receptors. However, binding is only limited to pentamers containing the δ-subunit rather than the γ-subunit.[12] GABAA receptors containing the δ-subunit have been shown to be located exterior to the synapse and are involved with tonic inhibition rather than its γ-subunit counterpart, which is involved in phasic inhibition.[11] The δ-subunit has been shown to be able to form the allosteric binding site which makes GABAA receptors containing the δ-subunit more sensitive to ethanol concentrations, even to moderate social ethanol consumption levels (30mM).[13] While it has been shown by Santhakumar et al. that GABAA receptors containing the δ-subunit are sensitive to ethanol modulation, depending on subunit combinations receptors, could be more or less sensitive to ethanol.[14] It has been shown that GABAA receptors that contain both δ and β3-subunits display increased sensitivity to ethanol.[12] One such receptor that exhibits ethanol insensitivity is α3-β6-δ GABAA.[14] It has also been shown that subunit combination is not the only thing that contributes to ethanol sensitivity. Location of GABAA receptors within the synapse may also contribute to ethanol sensitivity.[11]

Acute alcohol poisoning

"Acute alcohol poisoning" is a related medical term used to indicate a dangerously high concentration of alcohol in the blood, high enough to induce coma, respiratory depression, or even death. It is considered a medical emergency. The term is mostly used by healthcare providers. Toxicologists use the term "alcohol intoxication" to discriminate between alcohol and other toxins.

The signs and symptoms of acute alcohol poisoning include:

Diagnosis

Definitive diagnosis relies on a blood test for alcohol, usually performed as part of a toxicology screen.

Law enforcement officers often use breathalyzer units and field sobriety tests as more convenient and rapid alternatives to blood tests.

There are also various models of breathalyzer units that are available for consumer use. Because these may have varying reliability and may produce different results than the tests used for law-enforcement purposes, the results from such devices should be conservatively interpreted.

Many informal intoxication tests exist, which, in general, are unreliable and not recommended as deterrents to excessive intoxication or as indicators of the safety of activities such as motor vehicle driving, heavy equipment operation, machine tool use, etc.

For determining whether someone is intoxicated by alcohol by some means other than a blood-alcohol test, it is necessary to rule out other conditions such as hypoglycemia, stroke, usage of other intoxicants, mental health issues, and so on. It is best if his/her behavior has been observed while the subject is sober to establish a baseline. Several well-known criteria can be used to establish a probable diagnosis. For a physician in the acute-treatment setting, acute alcohol intoxication can mimic other acute neurological disorders, or is frequently combined with other recreational drugs that complicate diagnosis and treatment.

Management

Acute alcohol poisoning is a medical emergency due to the risk of death from respiratory depression and/or inhalation of vomit if emesis occurs while the patient is unconscious and unresponsive. Emergency treatment for acute alcohol poisoning strives to stabilize the patient and maintain a patent airway and respiration, while waiting for the alcohol to metabolize. This can be done by removal of any vomitus or, if patient is unconscious or has impaired gag reflex, intubation of the trachea using an endotracheal tube to maintain adequate airway:[17] Also:

Additional medication may be indicated for treatment of nausea, tremor, and anxiety.

Prognosis

A normal liver detoxifies the blood of alcohol over a period of time that depends on the initial level and the patient's overall physical condition. An abnormal liver will take longer but still succeeds, provided the alcohol does not cause liver failure.[18]

People having drunk heavily for several days or weeks may have withdrawal symptoms after the acute intoxication has subsided.[19]

A person consuming a dangerous amount of alcohol persistently can develop memory blackouts and idiosyncratic intoxication or pathological drunkenness symptoms.[20]

Long-term persistent consumption of excessive amounts of alcohol can cause liver damage and have other deleterious health effects.

Society and culture

Alcohol intoxication is a risk factor in some cases of catastrophic injury, in particular for unsupervised recreational activity. A study in the province of Ontario based on epidemiological data from 1986, 1989, 1992, and 1995 states that 79.2% of the 2,154 catastrophic injuries recorded for the study were preventable, of which 346 involved alcohol consumption.[21] The activities most commonly associated with alcohol-related catastrophic injury were snowmobiling (124), fishing (41), diving (40), boating (31) and canoeing (7), swimming (31), riding an all-terrain vehicle (24), and cycling (23).[21] These events are often associated with unsupervised young males, often inexperienced in the activity, and many result in drowning.[21]

Legal issues

A drunk-driving simulator in Montreal.

Laws on drunkenness vary. In the United States, it is a criminal offence for a person to be drunk while driving a motorized vehicle, except in Wisconsin, where it is only a fine for the first offence.[22] It is also a criminal offence to fly an aircraft or (in some American states) to assemble or operate an amusement park ride while drunk.[23] Similar laws also exist in the United Kingdom and most other countries.

In some countries, it is also an offence to serve alcohol to an already-intoxicated person,[24] and, often, alcohol can be sold only by persons qualified to serve responsibly through alcohol server training.

The blood alcohol content (BAC) for legal operation of a vehicle is typically measured as a percentage of a unit volume of blood. This percentage ranges from 0.00% in Romania and the United Arab Emirates; to 0.05% in Australia, South Africa, Germany and Scotland; to 0.08% in England and Wales, the United States, Canada, and New Zealand.[25]

The United States Federal Aviation Administration prohibits crew members from performing their duties with a BAC greater than 0.04% within eight hours of consuming an alcoholic beverage, or while under the influence of alcohol.[26][27]

In the United States, the United Kingdom, and Australia, people are arrested for public intoxication, called "being drunk and disorderly" or "being drunk and incapable."[28]

In some countries, there are special facilities, sometimes known as "drunk tanks", for the temporary detention of persons found to be drunk.

Religious views

Some religious groups permit the consumption of alcohol. Some permit consumption but prohibit intoxication, while others prohibit alcohol consumption altogether. Most Christian denominations such as Catholic and Orthodox use wine as a part of the Eucharist and permit the drinking of alcohol but consider it sinful to become intoxicated.

In the Qur'an,[29][30][31] there is a prohibition on the consumption of grape-based alcoholic beverages, and intoxication is considered as an abomination in the Hadith. Islamic schools of law (Madh'hab) have interpreted this as a strict prohibition of the consumption of all types of alcohol and declared it to be haraam ("forbidden"), although other uses may be permitted.[32]

Some Protestant Christian denominations prohibit the drinking of alcohol[33] based upon Biblical passages that condemn drunkenness (such as Proverbs 23:21,[34] Isaiah 28:1,[35] Habakkuk 2:15[36]), but others allow moderate use of alcohol.[37] While Proverbs 31:4, warns against kings and rulers drinking wine and strong drink, Proverbs 31:6–7 promotes giving strong drink to the perishing and wine to those whose lives are bitter, to forget their poverty and troubles.[38] In some Christian groups, a small amount of wine is part of the rite of communion. In The Church of Jesus Christ of Latter-day Saints, alcohol consumption is forbidden,[39] and teetotalism has become a distinguishing feature of its members. Jehovah's Witnesses allow moderate alcohol consumption among its members.

In Buddhism, in general, the consumption of intoxicants is discouraged for both monastics and lay followers. Many followers of Buddhism observe a code of conduct known as the Five Precepts, of which the fifth precept is an undertaking to refrain from the consumption of intoxicating substances (except for medical reasons). In the Bodhisattva Vows of the Brahma Net Sutra, observed by some monastic communities and some lay followers, distribution of intoxicants is likewise discouraged as well as consumption.

In the branch of Hinduism known as Gaudiya Vaishnavism, one of the four regulative principles forbids the taking of intoxicants, including alcohol.

In Judaism, the Babylonian Talmud says in Megillah 7b that "Rava said: A person is obligated to become intoxicated on Purim until he is unaware of the difference between 'Cursed be Haman' and 'Blessed be Mordechai.'" This is taken to mean that on the Jewish festival of Purim one is commanded to drink alcohol to the point of intoxication.[40] During all other times of year, though, Judaism stresses moderation—not cutting out alcohol entirely, but not getting too drunk either.[41]

See also

References

  1. ↑ Smith, C., Marks, Allan D., Lieberman, Michael, 2005, Marks' Basic Medical Biochemistry: A Clinical Approach, 2nd Edtn, Lippincott Williams & Williams, USA, p. 458
  2. ↑ "Alcohol & Public Health: Fact Sheets - Binge Drinking". Centers for Disease Control and Prevention. 7 November 2012. Retrieved 7 June 2013.
  3. ↑ McArdle P (2004). "Substance abuse by children and young people". Arch. Dis. Child 89: 701–704. doi:10.1136/adc.2003.040584.
  4. ↑ The World Health Organisation (2007) Alcohol and Injury in Emergency Departments
  5. 1 2 Vengeliene, V. Bilbao, A., Molander, A. & Spangel, R., V; Bilbao, A; Molander, A; Spanagel, R (2008). "Neuropharmacology of alcohol addiction". British Journal of Pharmacology 154 (2): 299–315. doi:10.1038/bjp.2008.30. PMC 2442440. PMID 18311194.
  6. ↑ Mihic, S. John; Ye, Qing; Wick, Marilee J.; Koltchine, Vladimir V.; Krasowski, Matthew D.; Finn, Suzanne E.; Mascia, Maria Paola; Valenzuela, C. Fernando; et al. (1997). "Sites of alcohol and volatile anaesthetic action on GABA(A) and glycine receptors". Nature 389 (6649): 385–389. doi:10.1038/38738. PMID 9311780.
  7. 1 2 Lovinger, D. M., David M (1999). "5-HT3 receptors and the neural action of alcohols: An increasingly exciting topic". Neurochemistry International 35 (2): 125–130. doi:10.1016/S0197-0186(99)00054-6. PMID 10405996.
  8. ↑ Narahashi, T., Aistrup, G. L., Marszalec, W. & Nagata, K., Toshio; Aistrup, Gary L; Marszalec, William; Nagata, Keiichi (1999). "Neuronal nicotinic acetylcholine receptors: A new target site of ethanol". Neurochemistry International 35 (2): 131–141. doi:10.1016/S0197-0186(99)00055-8. PMID 10405997.
  9. ↑ Wang, X., Wang, G., Lemos, J. R. & Treistman, S. N., X; Wang, G; Lemos, JR; Treistman, SN (1994). "Ethanol directly modulates gating of a dihydropyridine-sensitive Ca2+ channel in neurohypophysial terminals". The Journal of Neuroscience 14 (9): 5453–5460. PMID 7521910.
  10. ↑ Kobayashi, T., Ikeda, K., Kojima, H., Niki, H., Yano R.,Yoshioka, T., & Kumanishi, T., Toru; Ikeda, Kazutaka; Kojima, Hiroshi; Niki, Hiroaki; Yano, Ryoji; Yoshioka, Tohru; Kumanishi, Toshiro (1999). "Ethanol opens G-protein activated inwardly rectifying K+ channels". Nature Neuroscience 2 (12): 1091–1097. doi:10.1038/16019. PMID 10570486.
  11. 1 2 3 Kumar, Sandeep; Porcu, Patrizia; Werner, David; Matthews, Douglas; Diaz-Granados, Jamie; Helfand, Rebecca; Morrow, Leslie (2009). "The role of GABAA receptors in the acute and chronic effects of ethanol: a decade of progress". Psychopharmacology 205 (4): 529–64. doi:10.1007/s00213-009-1562-z. PMC 2814770. PMID 19455309.
  12. 1 2 Santhakumar, Vijayalakshmi; Wallner, Martin; Otis, Thomas (2007). "Ethanol acts directly on extrasynaptic subtypes of GABAA receptors to increase tonic inhibition". Alcohol 41 (3): 211–221. doi:10.1016/j.alcohol.2007.04.011. PMC 2040048. PMID 17591544.
  13. ↑ Wallner, Martin; Hanchar, Jacob; Olsen, Richard (2003). "Ethanol enhances alpha 4 beta 3 delta and alpha 6 beta 3 delta gamma-aminobutyric acid type A receptors at low concentrations known to affect humans". Proceedings of the National Academy of Sciences of the United States of America 100 (25): 15218–15223. doi:10.1073/pnas.2435171100.
  14. 1 2 Baur, Roland; Kaur, Kuldeep; Sigel, Erwin (2009). "Structure of α6β3δ GABAA receptors and their lack of ethanol sensitivity". Journal of Neurochemistry 111 (5): 1172–1181. doi:10.1111/j.1471-4159.2009.06387.x.
  15. ↑ Hales, Dianne (2010). An invitation to health (Brief [ed]., 2010–2011 ed.). Belmont, CA: Wadsworth Cengage Learning. p. 344. ISBN 978-0-495-39192-0.
  16. ↑ "Alcohol poisoning - NHS Choices". www.nhs.uk.
  17. ↑ Devi G., Castro V. J., Huitink J., Buitelaar D., Kosten T., O'Connor P. (2003). "Management of Drug and Alcohol Withdrawal". NEJM 349: 405–407. doi:10.1056/NEJM200307243490420. PMID 12878752.
  18. ↑ "Management of alcoholic hepatitis". Drug and Therapeutics Bulletin 41: 49–52. 2003. doi:10.1136/dtb.2003.41749.
  19. ↑ DeBellis R., Smith B. S., Choi S., Malloy M. (2005). "Management of Delirium Tremens". J Intensive Care Med 20: 164–173. doi:10.1177/0885066605275353.
  20. ↑ Gelder, M., Mayou, R. and Geddes, J. 2005. Psychiatry. 3rd ed. New York: Oxford. pp. 186.
  21. 1 2 3 Tator, Charles H., ed. (2008). Catastrophic Injuries in Sports and Recreation: Causes and Prevention: A Canadian Study (2 ed.). University of Toronto Press. ISBN 9780802089670.
  22. ↑ "Wisconsin Legislature: Chapter 346". wisconsin.gov.
  23. ↑ Texas Penal Code § 49.065
  24. ↑ "Camden Council: Booze license suspended after selling alcohol to drunk customers". camden.gov.uk.
  25. ↑ "Drinking and Driving". icap.org.
  26. ↑ "Federal Aviation Regulation Sec. 1.1 - General definitions.". risingup.com.
  27. ↑ "FAR Part 91 Sec. 91.17 effective as of 07/21/2006". faa.gov.
  28. ↑ "Licensing Act 1872". Acts of the United Kingdom Parliament 1872. 1872-08-10. Retrieved 2010-05-08.
  29. ↑ "Qur'an: 4:43". Usc.edu. Archived from the original on 4 December 2010. Retrieved 2010-12-04.
  30. ↑ "Qur'an: 2:19". Usc.edu. Archived from the original on 4 December 2010. Retrieved 2010-12-04.
  31. ↑ "Cmje". usc.edu.
  32. ↑ Yilmaz, Ihsan (2004) [2005-01-31]. "Post-Modern Muslim Legality and its Consequences". Muslim Laws, Politics And Society In Modern Nation States: Dynamic Legal Pluralisms In England, Turkey And Pakistan. Ashgate Publishing. p. 158. ISBN 978-0-7546-4389-0.
  33. ↑ "On Alcohol Use in America". SBC Resolutions. Southern Baptist Convention. June 2006. Retrieved 7 June 2013.
  34. ↑ "Proverbs 23:21". Net.bible.org. Retrieved 2009-11-03.
  35. ↑ "Isaiah 28:1". Net.bible.org. Retrieved 2009-11-03.
  36. ↑ "Habakkuk 2:15". Net.bible.org. Retrieved 2009-11-03.
  37. ↑ "Frequently Asked Questions: Alcohol". LCMS Views – Contemporary Issues. Lutheran Church–Missouri Synod. p. 3. Retrieved 7 June 2013.
  38. ↑ "Proverbs 31: 4-7 NASB - It is not for kings, O Lemuel, It is - Bible Gateway". Bible Gateway.
  39. ↑ "Doctrine and Covenants 89".
  40. ↑ Yanki Tauber: Are Jews actually supposed to get drunk on Purim? Chabad.org (referring to the Talmudic tractate Megillah (7b).
  41. ↑ Menachem Posner: What is Judaism's take on alcohol consumption? on Chabad.org

Bibliography

  • Bales, Robert F. "Attitudes toward Drinking in the Irish Culture". In: Pittman, David J. and Snyder, Charles R. (Eds.) Society, Culture and Drinking Patterns. New York: Wiley, 1962, pp. 157–187.
  • Gentry, Kenneth L., Jr., God Gave Wine: What the Bible Says about Alcohol. Lincoln, Calif.: Oakdown, 2001.
  • Rorabaugh, W.J. "The Alcoholic Republic," Chapter 2 & 5, Oxford University Press.
  • Sigmund, Paul. St. Thomas Aquinas On Politics and Ethics. W.W. Norton & Company, Inc, 1988, p. 77.
  • Walton, Stuart. Out of It. A Cultural History of Intoxication. Penguin Books, 2002. ISBN 0-14-027977-6.

External links

Wikisource has the text of the 1911 Encyclopædia Britannica article Drunkenness.
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