Alcoholic Keto Acidosis and Mixed Disorders

Alcoholic patients commonly develop a variety of acid-base and electrolyte disturbances. The aim of this review is to describe the most commonly encountered abnormalities and their significant role in the patients’ morbidity and mortality. Physicians should be aware of these clinically important disturbances caused by alcohol abuse and their underlying pathophysiological mechanisms involved for their appropriate management. Alcoholic Keto Acidosis (AKA) is a medical emergency is more common than previously thought and is characterized by an increased anion gap metabolic acidosis. However, in AKA mixed acid-base disorders are commonly observed. Alcoholic patients also exhibit severe electrolyte derangements. Multifactorial origin hypomagnesaemia is the most common electrolyte abnormality observed. Hypocalcaemia is also a frequent electrolyte disturbance and is commonly associated with hypomagnesaemia. Hypokalemia is occasionally encountered in these patients, while multifactorial origin hypophosphatemia is the second common electrolyte abnormality found. Hyponatremia is also a common electrolyte derangement and may occur subsequent to several mechanisms mediated by alcohol toxicity. Of special interest is the so-called beer potomania syndrome in poor nourished patients who consume a large amount of water with beer leading to hyponatremia. Chronic alcoholism and its comorbidities are a predisposing factor for the development of Central Pontine Myelinolisis during rapid correction of hyponatremia. Occasionally, alcoholic patients could be presented with alcohol-related intoxication mainly due to simultaneous methanol or ethylene glycol intoxication. In these cases the determination of the serum osmolal gap is used as a screening tool to identify potential toxins. fluid volume depletion, and c) Nicotinamide Adenine Dinucleotide hydogenase(NADH)/Nicotinamide Adenine Dinucleotide(NAD) ratio elevation secondary to alcohol metabolism by alcohol dehydrogenase [3]. In alcoholic patient’s dehydration and acute starvation suppress insulin, increase ketogenesis and the secretion of counter regulatory hormones, such as catecholamine’s, cortisol, growth hormone and glucagon. The latest can increase the release of fatty acids which are metabolized to beta-hydroxybutyrate and acetoacetic acid. The raised ketoacids resulted in an increased anion gap metabolic acidosis. Clinical symptoms, such as nausea, intractable vomiting, abdominal pain, and altered mental status are by far the most common manifestations in AKA. Likewise, the most frequent physical findings include tachycardia, tachypnea and abdominal tenderness [3,4]. On the other hand signs of significant abdominal distention, decreased bowel sounds, ascites or rebound tenderness are rarely reported. In AKA altered mental status, abnormalities in *Corresponding author: Moses Elisaf, Professor of Internal Medicine, Department of Medicine, Medical School, University of Ioannina 451 10 Ioannina, Greece, Tel: +302651007509; Fax: +302651007016; E-mail: [email protected], [email protected] Received: December 20, 2014; Accepted: January 24, 2015; Published: January 27, 2015 Citation: Moses Elisaf MD, Rigas Kalaitzidis MD (2015) Metabolic Abnormalities in Alcoholic Patients: Focus on Acid Base and Electrolyte Disorders. J Alcohol Drug Depend 2: 185. doi: 10.4172/2329-6488.1000185 Copyright: © 2015 Moses Elisaf MD, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Citation: Moses Elisaf MD, Rigas Kalaitzidis MD (2015) Metabolic Abnormalities in Alcoholic Patients: Focus on Acid Base and Electrolyte Disorders. J Alcohol Drug Depend 2: 185. doi: 10.4172/2329-6488.1000185