Alcoholic ketoacidosis

Template:Infobox medical condition (new) Alcoholic ketoacidosis (AKA) is a specific group of symptoms and metabolic state related to alcohol use.<ref name=All2014/> Symptoms often include abdominal pain, vomiting, agitation, a fast respiratory rate, and a specific "fruity" smell.<ref name=Stat2019/> Consciousness is generally normal.<ref name=BMJ2006/> Complications may include sudden death.<ref name=BMJ2006>Template:Cite journal</ref>

AKA most commonly occurs in long term alcoholics and less commonly in those who binge drink.<ref name=Stat2019>Template:Cite book</ref> Onset is generally after a decreased ability to eat for a few days.<ref name=Stat2019/> Diagnosis is generally based on symptoms.<ref name=Stat2019/> Blood sugar levels are often normal or only mildly increased.<ref name=Stat2019/> Other conditions that may present similarly include other causes of high anion gap metabolic acidosis including diabetic ketoacidosis.<ref name=Stat2019/>

Treatment is generally with intravenous normal saline and intravenous sugar solution.<ref name=Stat2019/> Thiamine and measures to prevent alcohol withdrawal are also recommended.<ref name=Stat2019/> Treatment of low blood potassium may also be required.<ref name=Stat2019/> Those who are affected are most frequently between the ages of 20 and 60.<ref name=Stat2019/> The condition was initially recognized in 1940 and named in 1971.<ref name=All2014>Template:Cite journal</ref>

Signs and symptoms

Nausea, vomiting, and abdominal pain are commonly present and people may also have tachypnea, tachycardia, and hypotension.<ref>Template:Cite journal</ref> In contrast to diabetic ketoacidosis, people with alcoholic ketoacidosis are usually alert and lucid despite the severity of the acidosis.<ref name=BMJ2006/>

Causes

Alcoholic ketoacidosis is caused by complex physiology that is the result of prolonged and heavy alcohol intake, usually in the setting of poor nutrition. Chronic alcohol use can cause depleted hepatic glycogen stores and ethanol metabolism further impairs gluconeogenesis. This can reduce glucose availability and lead to hypoglycemia and increased reliance on fatty acid and ketone metabolism.<ref name=BMJ2006/><ref name=Cart2012>Template:Cite journal</ref> An additional stressor such as vomiting or dehydration can cause an increase in counterregulatory hormones such as glucagon, cortisol and growth hormone which may further increase free fatty acid release and ketone production. Ethanol metabolism can also increase blood lactic acid levels (lactic acidosis), due to pseudohypoxia, which may also contribute to a metabolic acidosis.<ref name=Hoj2017>Template:Cite journal</ref>

Diagnosis

Diagnosis is generally based on symptoms.<ref name=Stat2019/> An elevated anion gap metabolic acidosis and ketosis is the classic present.<ref name=All2014/> However, a mixed acid-base disorder may be present especially if vomiting is contributing to a hypochloremic alkalosis.<ref name=Stat2019/> The ketone which is present is mostly beta-hydroxybutyrate rather than acetoacetate resulting in only a weakly positive nitroprusside test.<ref name=Stat2019/> People usually do not present with high blood sugar or sugar in the urine.<ref name=Stat2019/> This can cause false negative results when testing urine ketones as they only measure acetoacetate. Ethanol level are often low or negative despite a chronic alcohol use history.<ref name=Hoj2017 /> Electrolyte disturbances may include hypokalemia or hypomagnesemia may also be present.<ref name=Stat2019/>

Differential diagnosis

Other conditions that may present similarly include other causes of high anion gap metabolic acidosis such as diabetic ketoacidosis, toxic alcohol ingestion, and starvation ketosis.<ref name=Stat2019/> Toxic alcohol ingestion includes methanol and ethylene glycol poisoning.<ref name=Hoj2017 /> Pancreatitis, alcoholic hepatitis, and gastritis may also result in similar symptoms.<ref name=All2014/> The ratio of beta-hydroxybutryate to acetoacetate is usually higher in AKA (8:1) in contrast to diabetic ketoacidosis (3:1).<ref name=Stat2019/>

Management

Treatment includes administration of intravenous saline to rehydrate and 5% dextrose to turn off gluconeogenesis. Electrolyte imbalances, specifically hypokalaemia, should be corrected. Thiamine supplementation is often included to prevent Wernicke encephalopathy. Insulin is generally not used due to risk of hypoglycemia.<ref name=Cart2012/> Other potential causes of the symptoms should be ruled out.<ref name=Hoj2017 />

Prognosis

Outcomes are generally favorable with treatment but up to 10% may develop cardiac arrest.<ref name=Cart2012/> It is proposed that alcoholic ketoacidosis is a significant cause of death among people with chronic alcoholism although the true prevalence is unknown. Estimation of prevalence and outcomes of this population is limited by difficulty in diagnosing the condition and the presence of multiple disorders at presentation.<ref name=Hoj2017 />

History

In 1940, 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".<ref>Template:Cite journal</ref>

In 1971, David W. Jenkins and colleagues described cases of three non-diabetic people 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.<ref>Template:Cite journal</ref>