Alcoholic ketoacidosis

Arterial blood gas and biochemistry studies reveal a raised anion gap metabolic acidosis without evidence of lactic or diabetic ketoacidosis. Lactic acidosis occurs when ethanol metabolism what is alcoholism results in a high hepatic NADH/NAD ratio, diverting pyruvate metabolism towards lactate and inhibiting gluconeogenesis. In peripheral tissues, where NADH levels are lower, this lactate may be converted to pyruvate for metabolic needs.

Alcoholic ketoacidosis

• Both cause abdominal pain, with marked central nervous system depression, but methanol toxicity results in visual impairment, while ethylene glycol toxicity results in crystalluria, oliguria, and renal failure.
• The classical presentation is of an alcoholic patient with abdominal pain and intractable vomiting following a significant period of increased alcohol intake and starvation.
• Alcoholic ketoacidosis (AKA) is a common reason for investigation and admission of alcohol dependent patients in UK emergency departments.
• This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis.
• Management is based around exclusion of serious pathology and specific treatment for AKA where it is present.
• This is why diagnosis and subsequent treatment can sometimes be challenging, but it’s crucial to receive a proper and timely diagnosis to obtain the correct treatment.

Larger studies by Fulop and Hoberman5 and Wrenn et al6 (24 and 74 patients, respectively) clarified the alcoholic ketoacidosis underlying acid base disturbance. Although many patients had a significant ketosis with high plasma BOHB levels (5.2–14.2 mmol/l), severe acidaemia was uncommon. Elevated cortisol levels can increase fatty acid mobilization and ketogenesis. Growth hormone can enhance precursor fatty acid release and ketogenesis during insulin deficiency. Catecholamines, particularly epinephrine, increase fatty acid release and enhance the rate of hepatic ketogenesis.

Ethanol metabolism

Several mechanisms are responsible for dehydration, including protracted vomiting, decreased fluid intake, and inhibition of antidiuretic hormone secretion by ethanol. Volume depletion is a strong stimulus to the sympathetic nervous system and is responsible for elevated cortisol and growth hormone levels. The greatest threats to patients with alcoholic ketoacidosis are marked contraction in extracellular fluid volume (resulting in shock), hypokalaemia, hypoglycaemia, and acidosis.

BOX 2 BIOCHEMICAL FEATURES OF AKA

• 7 Under conditions of starvation, the liver increases the production of ketones from fatty acids to supply the brain, kidney, and other peripheral tissues with a metabolic fuel that can replace glucose.
• Prolonged vomiting leads to dehydration, which decreases renal perfusion, thereby limiting urinary excretion of ketoacids.
• The metabolism of alcohol itself is a probable contributor to the ketotic state.
• Alcoholic ketoacidosis most commonly happens in people who have alcohol use disorder and chronically drink a lot of alcohol.

This review covers definition, pathophysiology, clinical manifestations, diagnostic approach and treatment. Usually, patients respond well and quickly to treatment, if it is started early in the course. Take our free, 5-minute alcohol abuse self-assessment below if you think you or someone you love might be struggling with alcohol abuse.

Clinicians underestimate the degree of ketonemia if they rely solely on the results of laboratory testing. Alcoholic ketoacidosis is usually triggered by an episode of heavy drinking. If you can’t eat for a day or more, your liver will use up its stored-up glucose, which is a type of sugar.

When your liver uses up its stored glucose and you aren’t eating anything to provide more, your blood sugar levels will drop. The hallmark of AKA is ketoacidosis without marked hyperglycemia; the serum glucose level may be low, normal, or slightly elevated. 4 This finding can help to distinguish AKA from diabetic ketoacidosis (DKA). Alcoholic ketoacidosis is a relatively rare condition, which may have a lethal outcome if left untreated.

• Support groups can be a valuable source of support and can be combined with medication and therapy.
• 1, 2, 3  The diagnosis of AKA requires arterial blood gas (ABG) measurement and serum chemistry assays.
• It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis.
• Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH).
• But it can happen after an episode of binge drinking in people who do not chronically abuse alcohol.

Infection or other illnesses such as pancreatitis can also trigger alcoholic ketoacidosis in people with alcohol use disorder. Alcoholic ketoacidosis is a recognised acute complication in alcohol dependent patients. Given the frequency with which the condition is seen in other countries, the possibility exists that many cases may be unrecognised and misdiagnosed in UK EDs. AKA should be included in the differential diagnosis of alcohol dependent patients presenting with acute illness. Management is based around exclusion of serious pathology and specific treatment for AKA where it is present.

All chronic alcohol misusers attending the ED should receive intravenous B vitamins as recommended by The Royal College of Physicians.23 Strenuous efforts must be made to exclude concomitant pathology. The prevalence of AKA in a given community correlates with the incidence and distribution of alcohol abuse in that community. With timely and aggressive intervention, the prognosis for a patient with AKA is good. The long-term prognosis for the patient is influenced more strongly by recovery from alcoholism. Meetings are widely available at little-to-no cost in most communities. Support groups can be a valuable source of support and can be combined with medication and therapy.