Category: Other - Ketoacidosis

Monitor: 1


Friday, Apr 26
11:30 AM – 12:00 PM

Objective :

Alcoholic Ketoacidosis (AKA) is a distinct cause of anion gap metabolic acidosis (AGMA) that typically occurs in adults with chronic alcoholism.  Due to electrolyte derangement and potential arrythmias and shock, AKA can be fatal. Distinguishing this AKA from other life-threatening causes of metabolic acidosis is crucial for appropriate management but can be difficult due to overlap of clinical and biochemical features with other metabolic causes of AGMA, namely diabetic ketoacidosis (DKA).   We present a challenging case of AKA notable for a markedly elevated BHB level beyond what is traditionally reported in this condition.  


Methods :

A 24-year-old healthy African American female presents to the emergency department with 12 hours of progressive nausea, vomiting and abdominal pain.  Initial findings were significant AGMA 34 (Na 138 mmol/L, Cl 96mmol/L, HC03 8mmol/L, Potassium 5.6 mmol/L) with pH 7.13 as well as glucose 175 mg/dL, creatinine 1 mg/dL, plasma BHB 91.3mg/dL (0.2-2.8mg/dl). The patient was treated for suspected euglycemic DKA, although no known diabetes, with intravenous insulin. Despite resolution of acidosis, symptoms persisted following transition to subcutaneous insulin and carb-limited diet.  At this point, the patient admitted to days of significant alcohol intake and minimal food consumption overlying one year of binge drinking; thus, leading to diagnosis of AKA.   Supporting this results of ALT 111 Iu/L (<30), AST 124 Iu/L (7-35), HgbA1c 4.6% and negative GAD-65 antibodies.  After liberalization to full-carb diet, the BHB again cleared with resolution of symptoms and return to usual health. 


Results : NA

Discussion : AKA shares clinical features with DKA such as vomiting, abdominal pain, hemodynamic instability but can be differentiated by relevant history of alcoholism, low/normal blood glucose levels and lack of obtundation.  As is seen in this case of AKA, glucose can be modestly elevated and ketosis, measured by serum BHB, can be profound.  The pathophysiology of AKA is complex.  Alcohol ingestion with decreased caloric intake can lead to starvation-related hypo-insulinemia, lipolysis with free fatty acid formation, oxidation of alcohols and excess glucagon secretion, all of which contribute to formation of ketones.  During alcohol ingestion, high amounts of NAD+ is reduced to NADH; the imbalance of which leads to preferential formation of BHB over other ketones and inhibition of hepatic gluconeogenesis. Unlike our case, AKA typically has a lower anion gap and less severe acidosis than in DKA with bicarbonate levels above 18 and pH above 7.30.  Standard therapy focuses on aggressive fluid, carbohydrate and electrolyte repletion as well as withdrawal monitoring.

Conclusion : NA


KImberly K. Lessard

Fellow, PGY4
Thomas Jefferson University Hospital

Current first-year endocrinology fellow at Thomas Jefferson University Hospital in Philadelphia and former internal medicine resident and chief resident at Einstein Medical Center, Philadelphia, PA.

Serge Jabbour

Professor of Medicine, Director - Division of Endocrinology
Thomas Jefferson University Hospital
philadelphia, Pennsylvania

Jabbour is Professor of Medicine and Director of the Division of Endocrinology, Diabetes, and Metabolic Diseases in the Department of Medicine at Sidney Kimmel Medical College of Thomas Jefferson University in Philadelphia, Pennsylvania. He is also Director of the Jefferson Diabetes Center.
Dr Jabbour completed his training in Endocrinology, Diabetes, and Metabolic Diseases at Thomas Jefferson University in Philadelphia.