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.
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 decreased fluid intake, vomiting, and the diuretic effect of ethanol. This would be an excellent indication for the Toxicologic Ultrasound in Shock and Hypotension (TUSH) exam, using bedside sonography to visualize collapsibility of the inferior vena cava to help guide fluid resuscitation. Since AKA patients as a rule have increased catecholamine release, giving additional exogenous pressors may not be beneficial, especially if the patient’s tank is not full.
An interesting but ultimately unconvincing accompanying editorial by Cynthia Koh, Alicia Minns and Peter Rosen argues that these patients can often be treated without obtaining any lab tests except a bedside fingerstick glucose and urine pH. Again, the authors of the editorial make no mention of bedside ultrasound.