Alcohol Related Ketoacidosis (AKA)

Alcoholic ketoacidosis is often associated with acute cessation of alcohol consumption after long term consumption. Few cases have been described in binge drinkers as well. It shows up as a high anion gap metabolic acidosis (HAGMA) on blood gas and is typically associated with nausea, vomiting, and GI complaints. Metabolism of alcohol combined with poor glycogen reserves results in elevated ketoacid levels. Death can occur from excessive ketonemia and thus treatment is focused on fluid and electrolytes management. βHB is the pre- dominant ketone product formed in AKA. 

Clinical Presentation

Classically presents with history of heavy drinking followed by vomiting and an acute decrease in alcohol consumption. Common symptoms are nausea, vomiting, and nonspecific abdominal pain. AKA can present with concomitant gastritis or pancreatitis, hypoglycemia, alcohol-withdrawal seizures, GI Bleed, Hepatitis, Sepsis or unrecognized head injury. 


Diagnosis (AKA is a diagnosis of exclusion)

• Low, normal, or slightly elevated serum glucose 
• Binge drinking ending in nausea, vomiting, and decreased intake 
• High anion gap metabolic acidosis
• Positive serum ketones
• Wide anion gap metabolic acidosis without alternate explanation

BHB Ketosis

Normally, the ratio of  Beta HB (beta hydroxybutyric acid) to acetoacetate to 1:1 but in alcoholic ketoacidosis, the ratio can go up to 7:1. Ketone production can be further stimulated in malnourished, vomiting patients. The nitroprusside reagent used to measure urine and serum ketones measures acetoacetate, acetone is only weakly reactive and βHB is not detected at all. Therefore, initial ketone levels may be low or negative in AKA. Mild lactic acidosis may be present due to a shift to pyruvate metabolism toward lactate

In AKA, the average ratio of beta hydroxybutyric acid to acetoacetic acid (5:1) tends to be higher than that which occurs in diabetic ketoacidosis (3:1). With initial therapy, ketone formation shifts toward the production of acetoacetic acid. Thus measured ketone levels rise with initial treatment, although β-OH levels decrease.

   

Differential Diagnosis

• Lactic Acidosis
• Toxic Alcohol Ingestion
• Sepsis
• DKA
• Renal Failure 
• Alcohol Withdrawal 

Treatment

• Dextrose Normal Saline is the initial fluid of choice (to correct hypoglycaemia and acidosis)
• Supplement Electrolytes (Mg, K
• Supplement Multivitamins  (Pabrinex)

• Acidosis usually settles with fluids and bicarbonate use is recommended if pH remains <7.0 despite fluid resuscitation 

Indications for admission

• Persisting Acidosis despite fluid resuscitation
• Unable to tolerate orally
• Other concerning concomitant diagnosis (GI Bleed, Sepsis, Pancreatitis etc)

Take Home

• AKA is diagnosis of exclusion. Rule out other causes of HAGMA (MUDPILES)
• Treatment is focused on Fluid and electrolyte management 

  
References:

1. McGuire, LC, Cruickshank AM, Munro PT: Alcoholic ketoacidosis. Emerg Med J 23: 417, 2006.
   
2. Wrenn KD, Slovis CM, Minion GE, Rutkowski R: The syndrome of alcoholic ketoaci- dosis. Am J Med 91: 119, 1991.
3. Iten PX, Meier M: Beta-hydroxybutyric acid: An indicator for an alcoholic ketoacidosis as cause of death in deceased alcohol abusers. J Forens Sci 45: 624, 2000.
   
   
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        Lakshay Chanana

        

        Speciality Doctor

        Northwick Park Hospital

        Department of Emergency Medicine

        England

   
   

        @EMDidactic