SAT160 Alcoholic Ketoacidosis : An Endocrine Emergency

Abstract

Abstract Disclosure: L.E. Tiu: None. T.D. Crisostomo: None. Background: Alcoholic Ketoacidosis is a complex metabolic condition frequently confused with Diabetic Ketoacidosis. Currently, there remains an undefined consensus guideline in the diagnosis and management of this disorder that leads to unreported cases. Clinical Case: A 47-year-old male presented with 2-day history of poor dietary intake due to abdominal pain and vomiting after an alcoholic binge drinking. He is a chronic alcoholic beverage drinker (2 liters of beer per day for 10 years). He has family history of Type 2 Diabetes Mellitus but has no known co-morbidities. Upon admission, vital signs were normal, but he was drowsy and incoherent with signs of dehydration and epigastric tenderness. Initial capillary blood glucose was 52 mg/dL. D50W 50ml intravenously was given with repeat CBG of 222 mg/dL. Arterial blood gas (ABG) showed high anion gap metabolic acidosis (pH 7.0 and anion gap of 42) with undetectable bicarbonate and elevated lactate at 17mmol/L. Serum ketones were elevated at 6mmol/L but Hba1c was normal at 4.6 %. Thus, Alcoholic Ketoacidosis was highly considered. Intravenous hydration with saline solution was instituted then shifted to D10W 125mL/hour to allow insulin infusion therapy at initial rate of 2units/hour. Sodium bicarbonate 100 mEqs was given intravenously with recovery of sensorium thereafter. Oral Vitamin B supplement was started, and two doses of Thiamine 100 mg/IV were given. Other tests showed hyperkalemia (5.28meq/L), hypochloridemia (89.7meq/L), hyperuricemia (12.74mg/dL), and hyperphosphatemia (5.8mg/dL). Serial monitoring and correction of electrolytes were done. Moreover, management integrated simultaneous referrals to other subspecialties to rule out other causes of encephalopathy, to evaluate and manage Hypertriglyceridemic Pancreatitis and Alcoholic Liver Disease, and to facilitate nutritional, psychosocial support and rehabilitation. On 2nd hour, repeat ABG showed improvement of pH to 7.3 and HCO3 to 9.80mmol/L. Lactate decreased to 12.70mmol/L. On the 17th hour, ABG showed metabolic alkalosis with resolution of ketosis hence insulin was discontinued. CBG levels for the next 24-48 hours were within normal limits. Oral feeding was supplemented with parenteral nutrition due to decreased appetite. On 48th hour, he displayed combative behavior with visual hallucinations, but there was no consent for psychiatric referral. On 72nd hour, there was spontaneous marked improvement in his behavior. He was discharged clinically stable. Conclusion: Early recognition of Alcoholic Ketoacidosis is imperative. This is an unrecognized endocrine emergency that portends good outcome with timely diagnosis and management. Treatment includes 1. adequate fluid resuscitation 2. thiamine 3. judicious use of insulin and bicarbonate 4. correction of electrolytes 5. multidisciplinary team management. Presentation: Saturday, June 17, 2023