SEVERE LACTIC ACIDOSIS SECONDARY TO ACUTE ALCOHOL INTOXICATION

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Alcoholic ketoacidosis is one of the several etiologies where serum lactate level rarely exceeds 3 mmol/L. We present to you an interesting case of severe lactic acidosis (24 mmol/L) in a patient with acute alcohol intoxication. CASE PRESENTATION: Patient is a 62-year male who presented with intractable abdominal pain for 2 days. Past medical history was significant for alcohol use disorder. On presentation, patient had tachycardia, tachypnea, was restless with slurred speech with mild abdominal tenderness. Laboratory findings were remarkable for leukocytosis of 22.7, serum bicarbonate of 4 mmol/L, serum glucose 104 mg/dL, serum lactate 24 mmol/L. ABG showed pH of < 7.00, pCO2 12 mmHg, HC03 4.6 mmol/L. Anion gap was 41.0. Serum ethanol level was elevated at 0.185 g/dl. Patient was started on bicarbonate infusion, IV thiamine with 5% dextrose fluid and CIWA protocol. Serum beta hydroxybutyrate was elevated at 2.9, serum osmolality was elevated at 344 with osmolar gap of 13. LFT was deranged with unremarkable liver ultrasound. Patient was admitted to the ICU. Serum isopropanol, methanol, and ethylene glycol were negative. Infectious workup including blood culture, urine culture, pneumonia workup were negative. Acetaminophen and salicylate levels were normal. Urine drug screen was unremarkable. No history of GI malabsorption (short-bowel syndrome), renal failure or recent phenobarbital administration. Lactic acidosis was therefore attributed to alcoholic ketoacidosis in a setting of alcoholic hepatitis. Patient gradually improved with final pH 7.38, lactate 1.80 and serum HC03 24.6 by day 2. DISCUSSION: Lactate level of > 4 mmol/L with arterial pH < 7.35 suggests lactic acidosis. Lactic acidosis is broadly classified into type A which occurs due to impaired systemic tissue oxygenation and type B due to toxin induced cellular metabolism impairment and regional ischemia, commonly in alcoholism, HIV, antiretroviral medications, beta adrenergic medications, D lactic acidosis (short-bowel syndrome), diabetes mellitus, metformin, malignancy. Alcoholic ketoacidosis remains important etiology as if missed may result in fatal consequences including sudden death. Occasionally, alcoholic ketoacidosis can be misdiagnosed as diabetic ketoacidosis with subsequent mismanagement resulting in increased morbidity and mortality. CONCLUSIONS: Alcoholic ketoacidosis typically presents with metabolic acidosis but rarely with lactate > 3mmol/L in absence of other contributing factors. Oftentimes, the diagnosis is missed or misdiagnosed as diabetic ketoacidosis resulting in mismanagement contributing to increased morbidity and mortality. REFERENCE #1: Adeva-Andany, M., et al. 'Comprehensive Review on Lactate Metabolism in Human Health'. Mitochondrion, vol. 17, July 2014, pp. 76–100. PubMed, doi:10.1016/j.mito.2014.05.007. REFERENCE #2: Kreisberg, R. A. 'Lactate Homeostasis and Lactic Acidosis'. Annals of Internal Medicine, vol. 92, no. 2 Pt 1, Feb. 1980, pp. 227–37. PubMed, doi:10.7326/0003-4819-92-2-227 REFERENCE #3: Madias, N. E. 'Lactic Acidosis'. Kidney International, vol. 29, no. 3, Mar. 1986, pp. 752–74. PubMed, doi:10.1038/ki.1986.62 DISCLOSURES: No relevant relationships by Luna Khanal, source=Web Response No relevant relationships by Adarsha Ojha, source=Web Response