Alcololic ketoacidisos (AKA)

This is the most recent free full text general topic review I have been able to find.

Key points about AKA:

It is not as benign as popularly believed. It may be a cause of unexplained sudden death in alcoholics.

Acidosis may be severe but if altered LOC occurs suspect another cause.

The treatment is general supportive care and dextrose containing IV fluids (thiamine to go with that, please, and give it first).

The pathophysiology of AKA defies complete understanding. Dr. Daniel Foster, Professor of Endocrinology at UT Southwestern Medical School, believes that AKA is idiosyncratic, with most patients never developing it while a few patients do so repeatedly. A history of recurrent episodes is characteristic. The nature of the idiosyncratic susceptibility is unclear.

Alcohol is metabolized to acetate via sequential steps mediated by alcohol dehydrogenase, and the acetate thus formed can produce acetoacetate. However, the major source of ketone bodies produced in AKA, like DKA, is the catabolic sequence in which free fatty acids (FFA) are released from adipocytes and undergo beta oxidation in the liver mitochondria.

A state of semistarvation (leading to low insulin levels) prevails in patients with AKA in whom alcohol has been their major source of caloric intake. Alcohol intake is often markedly reduced around the time of development of AKA thus accentuating caloric deprivation. If an individual has working beta cells (i.e. does not have DM-1) starvation ketosis is limited and does not progress to ketoacidosis. This is due to a feedback mechanism in which ketones and FFAs feed back on the pancreas, causing it to secrete a small trickle of insulin. In this way, during starvation, the body produces ketones as fuel for the brain (ketones are the brain’s only alternative to glucose) while avoiding fatal ketoacidosis. This regulatory mechanism appears to be ineffective in certain unusual clinical states of which AKA appears to be one. In AKA ketosis continues unfettered. FFAs are much higher than in ordinary starvation ketosis and counter-regulatory hormones are high. Dextrose is therapeutic because it ends the catabolic sequence and shuts off ketosis.