Alcoholic ketoacidosis

Alcoholic ketoacidosis is a common reason for admission of alcohol dependent persons in hospitals emergency rooms. The term refers to a metabolic acidosis syndrome caused by increased ketone levels in serum. Glucose concentration is usually normal or a little lower.

In 1940, Drs Edward S. Dillon, W. Wallace, and Leon S. Smelo, first described alcoholic ketoacidosis as a distinct syndrome. They stated that "because of the many and complex factors, both physiologic and pathologic, which influence the acid-base balance of the body, a multitude of processes may bring about the state of acidosis as an end result."[1]

In 1971, David W. Jenkins and colleagues described cases of three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis.[2]

Patients regularly report nausea, vomiting, and pain in abdomen which are the most commonly observed complaints. This syndrome is rapidly reversible and, if taken care of has a low mortality. Other patients present tachypnoea, tachycardia, and hypotension.[3]

The main differences between patients with diabetic ketoacidosis is that patients with alcoholic ketoacidosis are usually alert and lucid despite the severity of the acidosis and marked ketonaemia.[4]

However, there are cases where alcoholic ketoacidosis can cause death of the patient if not treated with administration of dextrose and saline solutions.[5]

Alcoholic ketoacidosis
SpecialtyInternal medicine


  1. ^ Dillon, E.; Dyer, W. Wallace; Smelo, L. S. (November 1940). "Ketone Acidosis in Nondiabetic Adults". Medical Clinics of North America. 24 (6): 1813–1822. doi:10.1016/S0025-7125(16)36653-6.
  2. ^ Jenkins, David W.; Eckel, Robert E.; Craig, James W. (12 July 1971). "Alcoholic Ketoacidosis". JAMA: The Journal of the American Medical Association. 217 (2): 177. doi:10.1001/jama.1971.03190020037007.
  3. ^ Wrenn, KD; Slovis, CM; Minion, GE; Rutkowski, R (August 1991). "The syndrome of alcoholic ketoacidosis". The American Journal of Medicine. 91 (2): 119–28. PMID 1867237.
  4. ^ McGuire, L C (1 June 2006). "Alcoholic ketoacidosis". Emergency Medicine Journal. 23 (6): 417–420. doi:10.1136/emj.2004.017590. PMC 2564331. PMID 16714496.
  5. ^ Brutsaert, Erika F. "Alcoholic Ketoacidosis". Merck Manual. Merck Sharp & Dohme Corp. Retrieved 2 February 2018.

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Alcoholism, also known as alcohol use disorder (AUD), is a broad term for any drinking of alcohol that results in mental or physical health problems. The disorder was previously divided into two types: alcohol abuse and alcohol dependence. In a medical context, alcoholism is said to exist when two or more of the following conditions are present: a person drinks large amounts of alcohol over a long time period, has difficulty cutting down, acquiring and drinking alcohol takes up a great deal of time, alcohol is strongly desired, usage results in not fulfilling responsibilities, usage results in social problems, usage results in health problems, usage results in risky situations, withdrawal occurs when stopping, and alcohol tolerance has occurred with use. Risky situations include drinking and driving or having unsafe sex, among other things. Alcohol use can affect all parts of the body, but it particularly affects the brain, heart, liver, pancreas and immune system. This can result in mental illness, Wernicke–Korsakoff syndrome, irregular heartbeat, an impaired immune response, liver cirrhosis and increased cancer risk, among other diseases. Drinking during pregnancy can cause damage to the baby resulting in fetal alcohol spectrum disorders. Women are generally more sensitive than men to the harmful physical and mental effects of alcohol.Environmental factors and genetics are two components associated with alcoholism, with about half the risk attributed to each. Someone with a parent or sibling with alcoholism is three to four times more likely to become an alcoholic themselves. Environmental factors include social, cultural and behavioral influences. High stress levels and anxiety, as well as alcohol's inexpensive cost and easy accessibility, increase the risk. People may continue to drink partly to prevent or improve symptoms of withdrawal. After a person stops drinking alcohol, they may experience a low level of withdrawal lasting for months. Medically, alcoholism is considered both a physical and mental illness. Questionnaires and certain blood tests may both detect people with possible alcoholism. Further information is then collected to confirm the diagnosis.Prevention of alcoholism may be attempted by regulating and limiting the sale of alcohol, taxing alcohol to increase its cost, and providing inexpensive treatment. Treatment may take several steps. Due to medical problems that can occur during withdrawal, alcohol detoxification should be carefully controlled. One common method involves the use of benzodiazepine medications, such as diazepam. These can be either given while admitted to a health care institution or occasionally while a person remains in the community with close supervision. Mental illness or other addictions may complicate treatment. After detoxification, support such as group therapy or support groups are used to help keep a person from returning to drinking. One commonly used form of support is the group Alcoholics Anonymous. The medications acamprosate, disulfiram or naltrexone may also be used to help prevent further drinking.The World Health Organization estimates that as of 2010 there were 208 million people with alcoholism worldwide (4.1% of the population over 15 years of age). In the United States, about 17 million (7%) of adults and 0.7 million (2.8%) of those age 12 to 17 years of age are affected. It is more common among males and young adults, becoming less common in middle and old age. It is the least common in Africa, at 1.1%, and has the highest rates in Eastern Europe, at 11%. Alcoholism directly resulted in 139,000 deaths in 2013, up from 112,000 deaths in 1990. A total of 3.3 million deaths (5.9% of all deaths) are believed to be due to alcohol. It often reduces a person's life expectancy by around ten years. In the United States, it resulted in economic costs of US$224 billion in 2006. Many terms, some insulting and others informal, have been used to refer to people affected by alcoholism; the expressions include tippler, drunkard, dipsomaniac and souse. In 1979, the World Health Organization discouraged the use of "alcoholism" due to its inexact meaning, preferring "alcohol dependence syndrome".

Beta-Hydroxybutyric acid

β-Hydroxybutyric acid, also known as 3-hydroxybutyric acid, is an organic compound and a beta hydroxy acid with the chemical formula CH3CH(OH)CH2CO2H; its conjugate base is β-hydroxybutyrate, also known as 3-hydroxybutyrate. β-Hydroxybutyric acid is a chiral compound with two enantiomers: D-β-hydroxybutyric acid and L-β-hydroxybutyric acid. Its oxidized and polymeric derivatives occur widely in nature. In humans, D-β-hydroxybutyric acid is one of two primary endogenous agonists of hydroxycarboxylic acid receptor 2 (HCA2), a Gi/o-coupled G protein-coupled receptor (GPCR).

Binge drinking

Binge drinking, or heavy episodic drinking, is a modern epithet for drinking alcoholic beverages with an intention of becoming intoxicated by heavy consumption of alcohol over a short period of time, but definitions (see below) vary considerably.Binge drinking is a style of drinking that is popular in several countries worldwide, and overlaps somewhat with social drinking since it is often done in groups. The degree of intoxication, however, varies between and within various cultures that engage in this practice. A binge on alcohol can occur over hours, last up to several days, or in the event of extended abuse, even weeks. Due to the long-term effects of alcohol misuse, binge drinking is considered to be a major public health issue.Binge drinking is associated with a profound social harm, economic costs as well as increased disease burden. Binge drinking is more common in males, during adolescence and young adulthood. Heavy regular binge drinking is associated with adverse effects on neurologic, cardiac, gastrointestinal, hematologic, immune, musculoskeletal organ systems as well as increasing the risk of alcohol induced psychiatric disorders. A US-based review of the literature found that up to one-third of adolescents binge-drink, with 6% reaching the threshold of having an alcohol-related substance use disorder. Approximately one in 25 women binge-drinks during pregnancy, which can lead to fetal alcohol syndrome and fetal alcohol spectrum disorders. Binge drinking during adolescence is associated with traffic accidents and other types of accidents, violent behavior as well as suicide. The more often a child or adolescent binge drinks and the younger they are the more likely that they will develop an alcohol use disorder including alcoholism. A large number of adolescents who binge-drink also consume other psychotropic substances.

Carbon monoxide poisoning

Carbon monoxide poisoning typically occurs from breathing in carbon monoxide (CO) at excessive levels. Symptoms are often described as "flu-like" and commonly include headache, dizziness, weakness, vomiting, chest pain, and confusion. Large exposures can result in loss of consciousness, arrhythmias, seizures, or death. The classically described "cherry red skin" rarely occurs. Long term complications may include feeling tired, trouble with memory, and movement problems. In those exposed to smoke, cyanide toxicity should also be considered.Carbon monoxide poisoning can occur accidentally or as an attempt to end one's life. CO is a colorless and odorless gas which is initially non-irritating. It is produced during incomplete burning of organic matter. This can occur from motor vehicles, heaters, or cooking equipment that run on carbon-based fuels. It can also occur from exposure to methylene chloride. Carbon monoxide primarily causes adverse effects by combining with hemoglobin to form carboxyhemoglobin (HbCO) preventing the blood from carrying oxygen. Additionally, myoglobin and mitochondrial cytochrome oxidase are affected. Diagnosis is based on a HbCO level of more than 3% among nonsmokers and more than 10% among smokers.Efforts to prevent poisoning include carbon monoxide detectors, proper venting of gas appliances, keeping chimneys clean, and keeping exhaust systems of vehicles in good repair. Treatment of poisoning generally consists of giving 100% oxygen along with supportive care. This should generally be carried out until symptoms are no longer present and the HbCO level is less than 10%. While hyperbaric oxygen therapy is used for severe poisonings, the benefit over standard oxygen delivery is unclear. The risk of death among those affected is between 1 and 30%.Carbon monoxide poisoning is relatively common, resulting in more than 20,000 emergency department visits a year in the United States. It is the most common type of fatal poisoning in many countries. In the United States non-fire related cases results in more than 400 deaths a year. Poisonings occur more often in the winter, particularly from the use of portable generators during power outages. The toxic effects of CO have been known since ancient history. The realization that hemoglobin was affected by CO was determined in 1857.

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. A person's breath may develop a specific smell. Onset of symptoms is usually rapid. In some cases, people may not realize they previously had diabetes.DKA happens most often in those with type 1 diabetes but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke and certain medications such as steroids. DKA results from a shortage of insulin; in response, the body switches to burning fatty acids, which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH and ketoacids in either the blood or urine.The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually, potassium is also needed to prevent the development of low blood potassium. Throughout treatment, blood sugar and potassium levels should be regularly checked. Antibiotics may be required in those with an underlying infection. In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.Rates of DKA vary around the world. In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% of type-1 diabetics a year. DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost universally fatal. The risk of death with adequate and timely treatment is around 1–4%.

Ethylene glycol poisoning

Ethylene glycol poisoning is poisoning caused by drinking ethylene glycol. Early symptoms include intoxication, vomiting and abdominal pain. Later symptoms may include a decreased level of consciousness, headache, and seizures. Long term outcomes may include kidney failure and brain damage. Toxicity and death may occur after drinking even a small amount.Ethylene glycol is a colorless, odorless, sweet liquid, commonly found in antifreeze. It may be drunk accidentally or intentionally in an attempt to cause death. When broken down by the body it results in glycolic acid and oxalic acid which cause most of the toxicity. The diagnosis may be suspected when calcium oxalate crystals are seen in the urine or when acidosis or an increased osmol gap is present in the blood. Diagnosis may be confirmed by measuring ethylene glycol levels in the blood; however, many hospitals do not have the ability to perform this test.Early treatment increases the chance of a good outcome. Treatment consists of stabilizing the person, followed by the use of an antidote. The preferred antidote is fomepizole with ethanol used if this is not available. Hemodialysis may also be used in those where there is organ damage or a high degree of acidosis. Other treatments may include sodium bicarbonate, thiamine, and magnesium.More than 5000 cases of poisoning occur in the United States each year. Those affected are often adults and male. Deaths from ethylene glycol have been reported as early as 1930. An outbreak of deaths in 1937 due to a medication mixed in a similar compound, diethylene glycol, resulted in the Food, Drug, and Cosmetic Act of 1938 in the United States which mandated evidence of safety before new medications could be sold. Antifreeze products sometimes have a substance to make it bitter added to discourage drinking by children and other animals but this has not been found to be effective.

High anion gap metabolic acidosis

High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap (a medical value based on the concentrations of ions in a patient's serum). Metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing enough acid from the body. Several types of metabolic acidosis occur, grouped by their influence on the anion gap.

The anion gap can be increased due to relatively low levels of cations other than sodium and potassium (e.g. calcium or magnesium). An anion gap is usually considered to be high if it is over 12 mEq/L.

High anion gap metabolic acidosis is typically caused by acid produced by the body. More rarely, it may be caused by ingesting methanol or overdosing on aspirin. The Delta Ratio is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether mixed acid base disorder (metabolic acidosis) is present. The list of agents that cause high anion gap metabolic acidosis is similar to but broader than the list of agents that cause a serum osmolal gap.


Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate.


Ketogenesis is the biochemical process through which organisms produce ketone bodies through breakdown of fatty acids and ketogenic amino acids. This process supplies energy under circumstances such as fasting or caloric restriction to certain organs, particularly the brain, heart and skeletal muscle. Insufficient gluconeogenesis can cause hypoglycemia and excessive production of ketone bodies, ultimately leading to a life-threatening condition known as ketoacidosis.

Ketone bodies

Ketone bodies are three water-soluble molecules (acetoacetate, beta-hydroxybutyrate, and the spontaneous breakdown product of acetoacetate, acetone) containing the ketone group that are produced by the liver from fatty acids during periods of low food intake (fasting), carbohydrate restrictive diets, starvation, prolonged intense exercise, alcoholism or in untreated (or inadequately treated) type 1 diabetes mellitus. Ketone bodies are readily transported into tissues outside the liver and converted into acetyl-CoA, which then enters the citric acid cycle and is oxidized in the mitochondria for energy. In the brain, ketone bodies are also used to make acetyl-CoA into long-chain fatty acids.

Ketone bodies are produced by the liver under the circumstances listed above (i.e. fasting, starving, low carbohydrate diets, prolonged exercise and untreated type 1 diabetes mellitus) as a result of intense gluconeogenesis, which is the production of glucose from non-carbohydrate sources (not including fatty acids). They are therefore always released into the blood by the liver together with newly produced glucose after the liver glycogen stores have been depleted (these glycogen stores are depleted within the first 24 hours of fasting).When two acetyl-CoA molecules lose their -CoAs, (or Co-enzyme A groups) they can form a (covalent) dimer called acetoacetate. Beta-hydroxybutyrate is a reduced form of acetoacetate, in which the ketone group is converted into an alcohol (or hydroxyl) group (see illustration on the right). Both are 4-carbon molecules, that can readily be converted back into acetyl-CoA by most tissues of the body, with the notable exception of the liver. Acetone is the decarboxylated form of acetoacetate which cannot be converted back into acetyl-CoA except via detoxification in the liver where it is converted into lactic acid, which can, in turn, be oxidized into pyruvic acid, and only then into acetyl-CoA.

Ketone bodies have a characteristic smell, which can easily be detected in the breath of persons in ketosis and ketoacidosis. It is often described as fruity or like nail polish remover (which usually contains acetone or ethyl acetate).

Apart from the three endogenous ketone bodies, acetone, acetoacetic acid, and beta-hydroxybutyric acid, other ketone bodies like beta-ketopentanoate and beta-hydroxypentanoate may be created as a result of the metabolism of synthetic triglycerides, such as triheptanoin.


Ketosis is a metabolic state in which some of the body's energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis in which blood glucose provides energy. Generally, ketosis occurs when the body is metabolizing fat at a high rate and converting fatty acids into ketones.

Ketosis is a nutritional process characterised by serum concentrations of ketone bodies over 0.5 mM, with low and stable levels of insulin and blood glucose. It is almost always generalized with hyperketonemia, that is, an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted (or from metabolising medium-chain triglycerides). Ketones can also be consumed in exogenous ketone foods and supplements.

The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate, and the levels of ketone bodies are regulated mainly by insulin and glucagon. Most cells in the body can use both glucose and ketone bodies for fuel, and during ketosis, free fatty acids and glucose synthesis (gluconeogenesis) fuel the remainder.

Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet (ketogenic diet), and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes. In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed. For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.The difference between ketosis and ketoacidosis is the level of ketones in the blood. Ketosis is a physiological adaptation to a low carbohydrate environment like fasting or a ketogenic diet. There are situations (such as treatment-resistant epilepsy) where ketosis can be beneficial to health. Ketoacidosis is an acute life-threatening state requiring prompt medical intervention; its most common form is diabetic ketoacidosis where both glucose and ketone levels are significantly elevated.

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