Alcoholic ketoacidosis: case report and review

3.5 out of 5 stars
A Patient with Alcoholic Ketoacidosis and Profound Lactemia. Gerrity RS et al. J Emerg Med 2016 Oct;51:447-449.
Abstract
This is a very good short case-based review of alcoholic ketoacidosis (AKA), and well-worth the 5 – 10 minutes reading time.
Some key points:

Development of AKA requires increased (binge) alcohol intake along with starvation (decreased food and water intake.)
The characteristic high anion gap metabolic acidosis with elevated lactate and β-hydroxybutyrate levels are the result of dehydration, decreased glycogen stores, increased reducing potential (increased NADH) and release of stress hormones (catecholamines, glucagon, cortisol, and growth hormone.)
The critical steps in treating AKA include fluid repletion along with administration of dextrose and parenteral thiamine, followed by feeding the patient as soon the clinical condition allows.
Although the differential diagnosis includes most conditions on the metabolic acidosis mnemonic, the key alternative diagnosis is usually toxic alcohol poisoning.

There are some parts of the discussion I wish the authors had expanded upon. The AKA patient in the case report remained hypotensive “despite fluid resuscitation,” was started on norepinephrine. The only fluids detailed in the report were 1 liter of D5NS bolus followed by 150 cc per hour. This is almost certainly grossly inadequate. AKA patients can be profoundly volume depleted from multiple factors such as prolonged de...

Source: The Poison Review - October 12, 2016 Category: Toxicology Authors: Leon Gussow Tags: Medical alcoholic ketoacidosis fluid repletion Review thiamine TUSH ultrasound Source Type: news