Cirrhosis of the liver can cause exhaustion, leg swelling, and nausea. The prevalence of AKA in a given community correlates with the incidence and distribution of alcohol abuse in that community. The metabolism of alcohol itself is a probable contributor to the ketotic state. Alcohol dehydrogenase alcoholic ketoacidosis (ADH), a cytosolic enzyme, metabolizes alcohol to acetaldehyde in hepatocytes. Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase. Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH).
Metabolism of ethanol
- Hormone-sensitive lipase is normally inhibited by insulin, and, when insulin levels fall, lipolysis is up-regulated, causing release of free fatty acids from peripheral adipose tissue.
- Exclude other causes of autonomic hyperactivity and altered mental status.
- The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body.
In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis. The clinical and biochemical features of AKA are summarised in boxes 1 and 2. The classical presentation is of an alcoholic patient with abdominal pain and intractable vomiting following a significant period of increased alcohol intake and starvation. There may be a history of previous episodes requiring brief admissions with labels of “query pancreatitis” or “alcoholic gastritis”.
History and Physical
- The decreased insulin-to-glucagon ratio that occurs in starvation indirectly reduces the inhibition on CAT activity, thereby allowing more free fatty acids to undergo oxidation and ketone body formation.
- Growth hormone can enhance precursor fatty acid release and ketogenesis during insulin deficiency.
- Glucose comes from the food you eat, and insulin is produced by the pancreas.
- This drop in blood sugar causes your body to decrease the amount of insulin it produces.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. Dehydration and volume constriction directly decrease the ability of the kidneys to excrete ketoacids. Profound dehydration can culminate in circulatory collapse and/or lactic acidosis. If indicated, provide follow-up with AKA patients to assess the problem of alcohol abuse. Consider referral to a counselor at an alcohol treatment center. This drop in blood sugar causes your body to decrease the amount of insulin it produces.
An evidence-based narrative review of the emergency department evaluation and management of rhabdomyolysis
In the series from Fulop and Hoberman, seven patients were alkalaemic. In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. 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. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid.
BOX 1 PRESENTING FEATURES OF AKA
Metabolic acidosis in the alcoholic: a pathophysiologic approach
Alcoholic Ketoacidosis Treatment & Management
