July 27th, 2015

Alcoholic Ketoacidosis

By Damian Baalmann, M.D.

SugarPoison

Alcoholic Ketoacidosis

Damian Baalmann, 2nd year EM resident

 

A 45-year-old male presents to your emergency department with abdominal pain. He is conscious, lucid and as the nurses are hooking up the monitors, he explains to you that he began experiencing abdominal pain, nausea, vomiting about 2 days ago. Exam reveals a poorly groomed male with dry mucous membranes, diffusely tender abdomen with voluntary guarding. He is tachycardic, tachypneic but normotensive. A quick review of the chart reveals a prolonged history of alcohol abuse and after some questioning, the patient admits to a recent binge. Pertinent labs reveal slightly elevated anion-gap metabolic acidosis, normal glucose, ethanol level of 0, normal lipase and no ketones in the urine. What are your next steps in management?

 

Alcoholic Ketoacidosis (AKA): What is it?

 

Ketones are a form of energy made by the liver by free fatty acids released by adipose tissues. Normally, ketones are in small quantity (<0.1 mmol/L), but sometimes the body is forced to increase its production of these ketones. Ketones are strong acids and when they accumulate in large numbers, their presence leads to an acidosis. In alcoholics, a combination or reduced nutrient intake, hepatic oxidation of ethanol, and dehydration can lead to ketoacidosis. Alcoholics tend to rely on ethanol for their nutrient intake and when the liver metabolizes ethanol it generates NADH. This NADH further promotes ketone formation in the liver. Furthermore, ethanol promotes diuresis which leads to dehydration and subsequently impairs ketone excretion in the urine.

 

Alcoholic Ketoacidosis: How do I recognize it?

 

Typical history involves a chronic alcohol abuser who went on a recent binge that was terminated by severe nausea, vomiting, and abdominal pain. These folks often have tender abdomens with no other specific abdominal findings. Unlike DKA, they often have minimal alteration of conscious level despite a marked metabolic acidosis. The diagnosis should be in the differential of such a patient; as well as the common players in alcoholics such as pancreatitis, liver etiologies, biliary etiologies, ulcerative disease, and other bowel etiologies. The most consistent finding is a raised anion gap metabolic acidosis which may be confounded with a lactic acidosis as well but can be differentiated by the fact that the lactate insufficiently high to explain extent of acidosis. Unlike DKA, blood glucose is typically normal or even low. Ethanol levels are usually low because the patient likely had to stop their binge because of the symptoms. Ketones are usually positive on urine/serum analysis, but their absence does not exclude AKA. This is because ketones are often detected using a nitroprusside test which is able to detect the ketone: acetoacetate. However, because of the high levels of NADH, acetoacetate is preferably converted to another form of a ketone: hydroxybutyrate which is not detected on nitroprusside test. In fact, hydroxybutyrate: acetoacetate = 8:1 compared to DKA where the ratio is 3:1.

 

Alcoholic Ketoacidosis: How do I treat it?

 

Consider the following points in management of AKA:

  • Intravenous Thiamine (before dextrose)
    • 100-mg; (can also be given IM)
    • theoretically alcohol patients have a thiamine deficiency secondary to poor nutrient intake and thus administration of glucose can precipitate Wernicke’s Encephalopathy. However, this phenomenon has not been well demonstrated clinically
  • Intravenous Rehydration with 5% dextrose
    • typically 1-2L bolus
    • Increases insulin secretion/decreases glucagon secretion leading to decrease ketone production
    • must be careful with severe hypokalemia because dextrose pushes potassium into cells
  • Intravenous Hydration with Normal Saline
    • may paradoxically worsen acidosis initially
    • increasing intravascular volume decreases catecholamine secretion which decreases ketogenesis
  • Replace Potassium, Magnesium, and Phosphorus as needed
  • Beware of concurrent pathology: pancreatitis, sepsis, withdrawal….

 

References

 

●Kitabchi, A. (2012, June 26). Treatment of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults. Treatment of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults. Retrieved June 10, 2014, from http://www.uptodate.com/contents/treatment-of-diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults?source=search_result&search=diabetic+ketoacidosis&selectedTitle=1~150

●Marino, P. L., & Sutin, K. M. (2007). Acid Base Disorders. The ICU book (3rd ed., ). Philadelphia: Lippincott Williams & Wilkins.

●Mehta, A. (2014, April 16). Fasting ketosis and alcoholic ketoacidosis. Fasting ketosis and alcoholic ketoacidosis. Retrieved June 10, 2014, from http://www.uptodate.com/contents/fasting-ketosis-and-alcoholic-ketoacidosis?source=search_result&search=ketoacidosis&selectedTitle=1~150

●McGuire, L., Cruickshank, A., & Munro, P. Alcoholic Ketoacidosis. Emerg Med J, 417-420.

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