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Can Alcohol Cause Acidosis?

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a common reason for admission of alcohol dependent persons in hospitals emergency rooms. The term refers to a metabolic acidosis syndrome caused by increased ketone levels in serum . Glucose concentration is usually normal or a little lower. In 1940, Drs Edward S. Dillon, W. Wallace, and Leon S. Smelo, first described alcoholic ketoacidosis as a distinct syndrome . They stated that "because of the many and complex factors, both physiologic and pathologic , which influence the acid-base balance of the body, a multitude of processes may bring about the state of acidosis as an end result." [1] In the 1971, David W. Jenkins and colleagues described cases of three nondiabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis . This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. [2] Patients regularly report nausea , vomiting, and pain in abdomen which are the most commonly observed complaints. This syndrome is rapidly reversible and, if taken care of has a low mortality. Other patients present tachypnoea , tachycardia , and hypotension . [3] The main differences between patients with diabetic ketoacidosis is that patients with alcoholic ketoacidosis are usually alert and lucid despite the severity of the acidosis and marked ketonaemia. [4] However, there are cases where alcoholic ketoacidosis can cause death of the patient if not treated with administration of dextrose and saline solutions. [5] Dillon, E.; Dyer, W. Wallace; Smelo, L. S. (November 1940). "Ketone Acidosis in Nondiabetic Adults". Medical Clinics of North America. 24 (6): 18131822. doi : 10.1016/S0025-7125(16)36653-6 . Jenkins, David W.; Eckel, Robert E.; Craig, James W. Continue reading >>

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

1 A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2 The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a β- hydroxybutyrate dominated ketoacidosis. 3 Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4 The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5 The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6 The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7 It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recom mended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication. Continue reading >>

Metabolic Acidosis In The Alcoholic: A Pathophysiologic Approach.

Metabolic Acidosis In The Alcoholic: A Pathophysiologic Approach.

Metabolic acidosis in the alcoholic: a pathophysiologic approach. Halperin ML , Hammeke M , Josse RG , Jungas RL . The purpose of this paper is to review the acid-base abnormalities in patients presenting with metabolic acidosis due to acute ethanol ingestion and to review the theoretical constraints on ethanol metabolism in the liver. Alcohol-induced acidosis is a mixed acid-base disturbance. Metabolic acidosis is due to lactic acidosis, ketoacidosis and acetic acidosis but the degree of each varies from patient to patient. Metabolic alkalosis is frequently present due to ethanol-induced vomiting. However, it could be overlooked because of an indirect loss of sodium bicarbonate (as sodium B-hydroxybutyrate in the urine). Nevertheless, the accompanying reduction in ECF volume may play an important role in the pathogenesis of alcoholic acidosis because it could lead to a relative insulin deficiency. Treatment of alcohol acidosis should include sodium, chloride, potassium, phosphorus, magnesium and thiamine replacements along with attention to concomitant clinical problems. Unless hypoglycemia is present, glucose need not be given immediately. We feel that insulin should be withheld unless life-threatening acidemia is present or expected. Lastly, alcohol need not be detected on admission to make the diagnosis of this metabolic disturbance. However, when present, it could contribute directly to the lactic, acetic and B-hydroxybutyric acidoses. With respect to the theoretical constraints on ethanol metabolism, it appears that "overproduction" of NADH in the liver is best averted by converting ethanol to B-hydroxybutyric acid. Continue reading >>

Fasting Ketosis And Alcoholic Ketoacidosis

Fasting Ketosis And Alcoholic Ketoacidosis

INTRODUCTION Ketoacidosis is the term used for metabolic acidoses associated with an accumulation of ketone bodies. The most common cause of ketoacidosis is diabetic ketoacidosis. Two other causes are fasting ketosis and alcoholic ketoacidosis. Fasting ketosis and alcoholic ketoacidosis will be reviewed here. Issues related to diabetic ketoacidosis are discussed in detail elsewhere. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment".) PHYSIOLOGY OF KETONE BODIES There are three major ketone bodies, with the interrelationships shown in the figure (figure 1): Acetoacetic acid is the only true ketoacid. The more dominant acid in patients with ketoacidosis is beta-hydroxybutyric acid, which results from the reduction of acetoacetic acid by NADH. Beta-hydroxybutyric acid is a hydroxyacid, not a true ketoacid. Continue reading >>

Alcoholic Ketoacidosis: A Case Report And Review Of The Literature

Alcoholic Ketoacidosis: A Case Report And Review Of The Literature

Alcoholic ketoacidosis (AKA) is a condition that presents with a significant metabolic acidosis in patients with a history of alcohol excess. The diagnosis is often delayed or missed, and this can have potentially fatal consequences. There are a variety of non-specific clinical manifestations that contribute to these diagnostic difficulties. In particular, cases of AKA can be misdiagnosed as diabetic ketoacidosis (DKA). Subsequent mismanagement can lead to increasing morbidity and mortality for patients. AKA typically presents with a severe metabolic acidosis with a raised anion gap and electrolyte abnormalities, which are treatable if recognized early and appropriate management instituted. Given the increasing epidemic of alcohol-related healthcare admissions, this is an important condition to recognize and we aim to offer guidance on how to approach similar cases for the practising clinician. We present a 64-year-old female who presented with generalized abdominal pain, nausea, vomiting and shortness of breath. Arterial blood gas analysis showed significant acidaemia with a pH of 7.10, bicarbonate of 2.9 mmol/l and lactate of 11.7 mmol/l. Serum ketones were raised at 5.5 mmol/l. Capillary blood glucose was noted to 5.8 mmol/l. The anion gap was calculated and was elevated at 25 mmol/l. The diagnosis of DKA was queried after initial triage. However, following senior medical review, given a recent history of drinking alcohol to excess, the diagnosis of AKA was felt more likely. Whilst a decreased conscious level may have been expected, our patient was lucid enough to report drinking one to two bottles of wine per day for the past 30 years, with a recent binge the day prior to admission. Subsequent fluid resuscitation and monitoring were instituted. Further biochemical i Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Background In 1940, Dillon and colleagues first described alcoholic ketoacidosis (AKA) as a distinct syndrome. AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration. [1, 2] Although AKA most commonly occurs in adults with alcoholism, it has been reported in less-experienced drinkers of all ages. Patients typically have a recent history of binge drinking, little or no food intake, and persistent vomiting. [3, 4, 5] A concomitant metabolic alkalosis is common, secondary to vomiting and volume depletion (see Workup). [6] Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are: This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>

Metabolic Abnormalities In Alcoholic Patients: Focus On Acid Base Andelectrolyte Disorders

Metabolic Abnormalities In Alcoholic Patients: Focus On Acid Base Andelectrolyte Disorders

E-mail: [emailprotected] , [emailprotected] Received Date: December 20, 2014; Accepted Date: January 24, 2015; Published Date: 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 3:185. 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. 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 m Continue reading >>

Alcoholic Ketoacidosisunderrecognized Cause Of Metabolic Acidosis In The Elderly

Alcoholic Ketoacidosisunderrecognized Cause Of Metabolic Acidosis In The Elderly

Alcoholic KetoacidosisUnderrecognized Cause of Metabolic Acidosis in the Elderly The Substance Abuse & Mental Health Services Administration (SAMHSA) reported that substance abuse among adults age 60 years and older is a rapidly growing health problem. The report also stated that in 2000, 17% of Americans age 65 and older had problems with prescription drug and alcohol abuse.1 Most elderly people with alcohol abuse problems have a history of early-life alcohol abuse. However, a significant proportion start drinking later in life in response to traumatic life events such as the death of a loved one, loneliness, pain, insomnia, and retirement. This subset often experiences periods of binge drinking with little or no food intake. Alcoholic ketoacidosis (AKA) is an acute anion gap metabolic acidosis that typically occurs in people with a recent history of binge drinking and little or no nutritional intake. Some patients with AKA also have intractable vomiting and dehydration, and in these cases there is a concomitant metabolic alkalosis. An 86-year-old female, who had been a widow for the past 20 years, presented to the hospital with complaints of nausea, epigastric discomfort, and breathlessness for 2 days. She confessed to a history of alcohol abuse starting shortly after her husbands death and to regularly consuming a pint of hard liquor each day. She had been on an alcohol binge for 4-5 days without eating any food, but she had stopped consuming alcohol because of nausea for 2 days prior to presentation. Although the patient was depressed and admitted to suicidal ideation, she denied ingestion of antifreeze, methanol-containing solvents, rubbing alcohol, or salicylates. Physical examination was remarkable for only signs of dehydration and epigastric tenderness. Fundosc Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis Damian Baalmann, 2nd year EM resident A 45-year-old male presents to your emergency department with abdominal pain. He is conscious, lucid and as the nurses are hooking up the monitors, he explains to you that he began experiencing abdominal pain, nausea, vomiting about 2 days ago. Exam reveals a poorly groomed male with dry mucous membranes, diffusely tender abdomen with voluntary guarding. He is tachycardic, tachypneic but normotensive. A quick review of the chart reveals a prolonged history of alcohol abuse and after some questioning, the patient admits to a recent binge. Pertinent labs reveal slightly elevated anion-gap metabolic acidosis, normal glucose, ethanol level of 0, normal lipase and no ketones in the urine. What are your next steps in management? Alcoholic Ketoacidosis (AKA): What is it? Ketones are a form of energy made by the liver by free fatty acids released by adipose tissues. Normally, ketones are in small quantity (<0.1 mmol/L), but sometimes the body is forced to increase its production of these ketones. Ketones are strong acids and when they accumulate in large numbers, their presence leads to an acidosis. In alcoholics, a combination or reduced nutrient intake, hepatic oxidation of ethanol, and dehydration can lead to ketoacidosis. Alcoholics tend to rely on ethanol for their nutrient intake and when the liver metabolizes ethanol it generates NADH. This NADH further promotes ketone formation in the liver. Furthermore, ethanol promotes diuresis which leads to dehydration and subsequently impairs ketone excretion in the urine. Alcoholic Ketoacidosis: How do I recognize it? Typical history involves a chronic alcohol abuser who went on a recent binge that was terminated by severe nausea, vomiting, and abdominal pain. These folk Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Increased production of ketone bodies due to: Dehydration (nausea/vomiting, ADH inhibition) leads to increased stress hormone production leading to ketone formation Depleted glycogen stores in the liver (malnutrition/decrease carbohydrate intake) Elevated ratio of NADH/NAD due to ethanol metabolism Increased free fatty acid production Elevated NADH/NAD ratio leads to the predominate production of β–hydroxybutyrate (BHB) over acetoacetate (AcAc) Dehydration Fever absent unless there is an underlying infection Tachycardia (common) due to: Dehydration with associated orthostatic changes Concurrent alcohol withdrawal Tachypnea: Common Deep, rapid, Kussmaul respirations frequently present Nausea and vomiting Abdominal pain (nausea, vomiting, and abdominal pain are the most common symptoms): Usually diffuse with nonspecific tenderness Epigastric pain common Rebound tenderness, abdominal distension, hypoactive bowel sounds uncommon Mandates a search for an alternative, coexistent illness Decreased urinary output from hypovolemia Mental status: Minimally altered as a result of hypovolemia and possibly intoxication Altered mental status mandates a search for other associated conditions such as: Head injury, cerebrovascular accident (CVA), or intracranial hemorrhage Hypoglycemia Alcohol withdrawal Encephalopathy Toxins Visual disturbances: Reports of isolated visual disturbances with AKA common History Chronic alcohol use: Recent binge Abrupt cessation Physical Exam Findings of dehydration most common May have ketotic odor Kussmaul respirations Palmar erythema (alcoholism) Lab Acid–base disturbance: Increased anion gap metabolic acidosis hallmark Mixed acid–base disturbance common: Respiratory alkalosis Metabolic alkalosis secondary to vomiting and dehydration Hyperchlorem Continue reading >>

Alcohol Toxicity - The Clinical Advisor

Alcohol Toxicity - The Clinical Advisor

Alcohol toxicity or poisoning is caused by drinking large quantities of alcohol in a short period of time. According to Centers for Disease Control (CDC) data released January 2015, an average of 6 people died of alcohol poisoning each day in the US from 2010-2012. Seventy-six percent of alcohol poisoning deaths are among adults ages 35-64 years old, the majority of whom are men and non-Hispanic whites. While alcohol dependence was identified as a factor in 30% of alcohol poisoning deaths, binge drinking (defined as more than 5 drinks on an occasion for men or 4 or more drinks on an occasion for women) can also lead to death from alcohol poisoning. A standard drink in the US is considered either 12 ounces (oz) of beer (5% alcohol), 8 oz of malt liquor (7% alcohol), 5 oz of wine (12% alcohol), or 1.5 oz of distilled spirits (40% alcohol; 80 proof). The current Dietary Guidelines for Americans recommend not to exceed 1 drink a day for women or 2 drinks a day for men. Any alcohol can be toxic if ingested in large enough quantities. While alcohol toxicity most commonly results from the abuse of ethanol ("drinking alcohol") found in alcoholic beverages, it can also result from the ingestion of isopropanol (rubbing alcohol) and the toxic alcohols which include methanol (found in commercially available products such as solvents, windshield washing fluids and paint removers) and ethylene glycol (the primary ingredient in anti-freeze). Toxic alcohols share the characteristic of the parent compounds causing inebriation with little toxicity while their active metabolites have the potential to cause metabolic acidosis and significant end organ damage. Toxic alcohol poisoning is far less prevalent than ethanol abuse, with most exposures in the US resulting from unintentional ingest Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

What is alcoholic ketoacidosis? Cells need glucose (sugar) and insulin to function properly. Glucose comes from the food you eat, and insulin is produced by the pancreas. When you drink alcohol, your pancreas may stop producing insulin for a short time. Without insulin, your cells won’t be able to use the glucose you consume for energy. To get the energy you need, your body will start to burn fat. When your body burns fat for energy, byproducts known as ketone bodies are produced. If your body is not producing insulin, ketone bodies will begin to build up in your bloodstream. This buildup of ketones can produce a life-threatening condition known as ketoacidosis. Ketoacidosis, or metabolic acidosis, occurs when you ingest something that is metabolized or turned into an acid. This condition has a number of causes, including: shock kidney disease abnormal metabolism In addition to general ketoacidosis, there are several specific types. These types include: alcoholic ketoacidosis, which is caused by excessive consumption of alcohol diabetic ketoacidosis (DKA), which mostly develops in people with type 1 diabetes starvation ketoacidosis, which occurs most often in women who are pregnant, in their third trimester, and experiencing excessive vomiting Each of these situations increases the amount of acid in the system. They can also reduce the amount of insulin your body produces, leading to the breakdown of fat cells and the production of ketones. Alcoholic ketoacidosis can develop when you drink excessive amounts of alcohol for a long period of time. Excessive alcohol consumption often causes malnourishment (not enough nutrients for the body to function well). People who drink large quantities of alcohol may not eat regularly. They may also vomit as a result of drinking too Continue reading >>

Metabolic Acidosis In The Alcoholic: A Pathophysiologic Approach - Sciencedirect

Metabolic Acidosis In The Alcoholic: A Pathophysiologic Approach - Sciencedirect

Volume 32, Issue 3 , March 1983, Pages 308-315 Metabolic acidosis in the alcoholic: A pathophysiologic approach Author links open overlay panel M.L.Halperin Get rights and content The purpose of this paper is to review the acid-base abnormalities in patients presenting with metabolic acidosis due to acute ethanol ingestion and to review the theoretical constraints on ethanol metabolism in the liver. Alcohol-induced acidosis is a mixed acid-base disturbance. Metabolic acidosis is due to lactic acidosis, ketoacidosis and acetic acidosis but the degree of each varies from patient to patient. Metabolic alkalosis is frequently present due to ethanol-induced vomiting. However, it could be overlooked because of an indirect loss of sodium bicarbonate (as sodium B-hydroxybutyrate in the urine). Nevertheless, the accompanying reduction in ECF volume may play an important role in the pathogenesis of alcoholic acidosis because it could lead to a relative insulin deficiency. Treatment of alcohol acidosis should include sodium, chloride, potassium, phosphorus, magnesium and thiamine replacements slong with attention to concomitant clinical problems. Unless hypoglycemia is present, glucose need not be given immediately. We feel that insulin should be withheld unless life-threatening acidemia is present or expected. Lastly, alcohol need not be detected on admission to make the diagnosis of this metabolic disturbance. However, when present, it could contribute directly to the lactic, acetic and B-hydroxybutyric acidoses. With respect to the theoretical constraints on ethanol metabolism, it appears that overproduction of NADH in the liver is best averted by converting ethanol to B-hydroxybutyric acid. Continue reading >>

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