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Alcoholic Ketoacidosis

Alcoholic Ketoacidosis: Case Report And Review

Alcoholic Ketoacidosis: Case Report And Review

A Patient with Alcoholic Ketoacidosis and Profound Lactemia. Gerrity RS et al. J Emerg Med 2016 Oct;51:447-449. This is a very good short case-based review of alcoholic ketoacidosis (AKA), and well-worth the 5 – 10 minutes reading time. Some key points: Development of AKA requires increased (binge) alcohol intake along with starvation (decreased food and water intake.) The characteristic high anion gap metabolic acidosis with elevated lactate and β-hydroxybutyrate levels are the result of dehydration, decreased glycogen stores, increased reducing potential (increased NADH) and release of stress hormones (catecholamines, glucagon, cortisol, and growth hormone.) The critical steps in treating AKA include fluid repletion along with administration of dextrose and parenteral thiamine, followed by feeding the patient as soon the clinical condition allows. Although the differential diagnosis includes most conditions on the metabolic acidosis mnemonic, the key alternative diagnosis is usually toxic alcohol poisoning. There are some parts of the discussion I wish the authors had expanded upon. The AKA patient in the case report remained hypotensive “despite fluid resuscitation,” was started on norepinephrine. The only fluids detailed in the report were 1 liter of D5NS bolus followed by 150 cc per hour. This is almost certainly grossly inadequate. AKA patients can be profoundly volume depleted from multiple factors such as prolonged decreased fluid intake, vomiting, and the diuretic effect of ethanol. This would be an excellent indication for the Toxicologic Ultrasound in Shock and Hypotension (TUSH) exam, using bedside sonography to visualize collapsibility of the inferior vena cava to help guide fluid resuscitation. Since AKA patients as a rule have increased catecholami Continue reading >>

Does Alcohol Influence The Smell Of Perspiration? If So, How?

Does Alcohol Influence The Smell Of Perspiration? If So, How?

Yes alcohol influences the smell of perspiration. It does it in at least three ways. First you can smell the alcohol coming out in the sweat. Secondly you can smell the chemicals that are from the body metabolising the alcohol. Third is most people let their personal hygiene slip when they are drinking a lot. Some people metabolize alcohol differently than most people do and develop a very distinctive odour when they drink. If the drinking is severe and prolonged there could be damage to the liver and there will be a scent released from the skin related to the toxins from the liver. Alcoholic ketoacidosis is another condition sometimes seen in heavy drinkers where the body is failing to metabolize sugars and is metabolizing fats instead. You can smell the ketones that are produced. Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

• The characteristic example is an alcoholic person who abruptly abstains and has signs and symptoms such as vomiting, abdominal pain, malnutrition, and an anion gap metabolic acidosis, but no measurable alcohol levels. • A ratio of β-hydroxybutyrate to acetoacetate in excess of 10 : 1 is pathognomonic for alcoholic ketoacidosis, whereas a 3 : 1 ratio is more common in diabetic ketoacidosis. • Treatment emphasizes hydration with dextrose-containing solutions and thiamine; resolution of the acidosis usually occurs within 6 to 12 hours. The term alcoholic acidosis describes a syndrome of four types of metabolic acidosis that occur in alcoholics and vary in severity: ketoacidosis, lactic acidosis, acetic acidosis, and loss of bicarbonate in urine. AKA arises from a complicated interplay of the metabolic effects of alcohol in fasted, dehydrated alcoholics who abruptly stop their intake of ethanol.4 β-Hydroxybutyrate is the predominant ketoacid.5 Metabolism of ethanol to acetaldehyde is catalyzed by alcohol dehydrogenase in the liver and results in accumulation of the reduced form of nicotinamide adenine dinucleotide (NADH) relative to the oxidized form of nicotinamide adenine dinucleotide (NAD+). The altered ratio of NADH/NAD+ is the rate-limiting step in alcohol metabolism and favors the conversion of acetoacetate to β-hydroxybutyrate, as illustrated in Figure 161.1. Alcohol dehydrogenase in hepatocyte cytosol metabolizes ethanol to acetaldehyde, which is then transported into the mitochondria for metabolism to acetate. Acetate is activated by adenosine triphosphate (ATP), coenzyme A (CoA), and acetate thiokinase to form acetyl CoA, which can (1) be oxidized to carbon dioxide (CO2) by the citric acid cycle, (2) form ketone bodies, or (3) be converted to fat. Insul Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Abstract Alcoholic ketoacidosis is characterized by a metabolic acidosis with an elevated anion gap. It generally is seen in the chronic alcoholic patient who has recently gone on a 'binge' that was terminated because of complaints such as nausea, vomiting or abdominal pain. Caloric intake is diminished. Treatment includes volume repletion and glucose administration. Morbidity and mortality usually result from intercurrent illness. Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Go to: CHARACTERISATION In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic 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. Further case series by Levy et al, Cooperman et al, and Fulop et al were subsequently reported, with remarkably consistent features.3,4,5 All patients presented with a history of prolonged heavy alcohol misuse, preceding a bout of particularly excessive intake, which had been terminated several days earlier by nausea, severe vomiting, and abdominal pain. Clinical signs included tachypnoea, tachycardia, and hypotension. In 1974, Cooperman's series of seven ketoacidotic alcoholic patients all displayed diffuse epigastric tenderness on palpation.4 In contrast to patients with diabetic ketoacidosis, the patients were usually alert and lucid despite the severity of the acidosis and marked ketonaemia. When altered mental status occurred, this was clearly attributable to other causes. Laboratory results included absent blood alcohol with normal or low blood glucose level, no glycosuria, and a variably severe metabolic acidosis with a raised anion gap. This acidosis appeared to result from the accumulation in plasma of lactate and ketone bodies including beta‐hydroxybutyrate (BOHB) and acetoacetate (AcAc).3 Cooperman et al found that near patient testing for ketone bodies using nitroprusside test (Acetest, Ketostix) produced a low to moderate result in th Continue reading >>

The Syndrome Of Alcoholic Ketoacidosis

The Syndrome Of Alcoholic Ketoacidosis

Abstract purpose: To further elucidate the clinical spectrum of alcoholic ketoacidosis (AKA). patients and methods: A case series of 74 patients with AKA defined as a wide anion gap metabolic acidosis unexplained by any other disorder or toxin, including any patient with a history of chronic alcohol abuse. The setting was the Medical Emergency Department at Grady Memorial Hospital in Atlanta, Georgia, a university-affiliated inner-city hospital. results: AKA is a common disorder in the emergency department, more common than previously thought. The acid-base abnormalities are more diverse than just a wide-gap metabolic acidosis and often include a concomitant metabolic alkalosis, hyperchloremic acidosis, or respiratory alkalosis. Lactic acidosis is also common. Semiquantitative serum acetoacetate levels were positive in 96% of patients. Elevated blood alcohol levels were present in two thirds of patients in whom alcohol levels were determined, and levels consistent with intoxication were seen in 40% of these patients. Electrolyte disorders including hyponatremia, hypokalemia, hypophosphatemia, hyperglycemia, hypocalcemia, and hypomagnesemia were common on presentation. The most common symptoms were nausea, vomiting, and abdominal pain. The most common physical findings were tachycardia, tachypnea, and abdominal tenderness. Altered mental status, fever, hypothermia, or other abnormal findings were uncommon and reflected other underlying processes. conclusions: AKA is a common disorder in chronic malnourished alcoholic persons. The acid-base abnormalities reflect not only the ketoacidosis, but also associated extracellular fluid volume depletion, alcohol withdrawal, pain, sepsis, or severe liver disease. Although the pathophysiology is complex, the syndrome is rapidly reve 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 >>

Alcoholic Ketoacidosis Presenting With Extreme Hypoglycemia

Alcoholic Ketoacidosis Presenting With Extreme Hypoglycemia

Abstract A 66-year-old man with a history of chronic alcoholism presented with Kussmaul respirations following several days of fasting accompanied by vomiting, in the presence of continued ethanol intake. He was subsequently found to have a serum glucose level of <20 mg/dL and an anion gap of 36. Despite his profound hypoglycemia, he was fully alert with no obvious neurological deficits. He recovered without incident with intravenous saline, dextrose, thiamine, and antibiotics for a bacteremic pneumonia. He had no evidence of hypoxemia, hypotension, or other features of sepsis. Alcoholic ketoacidosis in the setting of hypoglycemia is discussed. If the serum glucose level is less than the anion gap, the diagnosis of alcoholic ketoacidosis should be considered. Continue reading >>

Characteristics Of Severe Alcoholic Ketoacidosis With A Reversible Visual Disturbance

Characteristics Of Severe Alcoholic Ketoacidosis With A Reversible Visual Disturbance

No. Age Sex Alcohol intake Alcoho history Conscious Level Pupil diameter Light reflex Systolic BP unit year g/day year mm mmHg 1 66 Male ? 24 Alert 4 none 82 2 53 Male 100 20 Semicoma 6 none 90 3 63 Male ? ? Alert ? ? 90 4 44 Male 200 over 5 Alert 7 none 80 5 59 Male 170 40 Alert 4 sluggish 73 6 48 Male 180 over 8 Semicoma 7 none 87 7 61 Male ? ? Disoriented 5 ? 65 8 49 Male ? ? Alert ? ? 73 9 48 Female over 110 ? Disoriented ? sluggish 134 10 68 Male ? ? Disoriented 3.5 none 150 11 56 Male ? ? Disoriented 5 none 79 12 49 Female ? ? Alert 3 none 130 13 43 Male 180 over 10 Disoriented ? ? 80 14 57 Female ? ? Alert Dilated sluggish 120 No. pH PCO2 PO2 HCO3 Base excess Lactate Glucose Alcohol BHBA AAA Thiamine deficiency Require of_IC Arrest DH Outcome unit mmHg mmHg mmHg mg/dl mg/dl mmol/l mmol/l mg/dl μmol/l μmol/l 1 6.855 13.9 190.5 2.5 -31.4 ? 69 45.8 140 14 no yes no survival 2 6.497 51 ? 3.8 -29 ? ? 8 1190 332 no yes yes survival 3 6.612 14 ? 1.5 -28 ? ? not exam 6360 261 no yes yes survival 4 6.707 13.6 272.8 1.6 -30 ? 91 0 245 11 no yes yes death 5 6.748 13 134 1.7 -33 270 70 not exam 2160 220 no yes no survival 6 6.748 20.3 151 2.6 -33.9 297 85 27.4 ? ? not exam yes no survival 7 6.623 35.0 231 3.5 -34 ? ? ? 2960 460 no yes yes death 8 6.78 15.5 118 2.3 -31 ? ? ? ? ? no no no survival 9 6.64 8.3 159 ? -37.5 109 153 not exam 823 272 no yes yes survival 10 6.79 11.8 137.2 1.8 -33 ? 38 not exam 4825 210 not exam yes no survival 11 6.55 44.4 198 3.7 -29.4 ? 20 not exam not exam not exam not exam yes no survival 12 6.79 8 196 ? ? 90 ? 68 ? 8.82 no ? no survival Arrest No-Arrest p-value n=6 n=8 Age 52.0 + 3.4 56.5 + 2.7 n.s. Sex (Male/Female) 5/1 6/2 n.s. Consciousness (number of alert) 2 5 n.s. Systolic blood pressure (mmHg) 89.8 + 9.5 99.2 + 10.5 n.s. pH 6.637 + 0.0 Continue reading >>

Emdocs.net Emergency Medicine Educationtoxcards: Alcoholic Ketoacidosis - Emdocs.net - Emergency Medicine Education

Emdocs.net Emergency Medicine Educationtoxcards: Alcoholic Ketoacidosis - Emdocs.net - Emergency Medicine Education

Author: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit) A 45 year old male presents intoxicated, smelling of alcohol and appears disheveled with vomit on his clothes. He is sleepy but arousable to noxious stimuli. His serum ethanol level is 143 mg/dL. Na 135, K 3.9, Cl 97, CO2 20, BUN 33, Cr 1.1. Lactate 3.1. pH 7.35, CO2 28, HCO3 15. His urine is negative for ketones. His vitals are HR 103, RR 30, BP 115/65, O2 98% RA. Could these laboratory results be consistent with alcohol ketoacidosis (AKA)? The classic laboratory findings in patients with AKA include an elevated anion gap metabolic acidosis and an elevated lactate. Early in AKA patients may be negative for ketones when the nitroprusside test is used because it does not detect beta-hydroxybutyrate. As patients recover, the nitroprusside test will become positive as beta-hydroxybutyrate gets converted to acetone and acetate. Patients with AKA typically have elevated anion gap metabolic acidosis. However, vomiting may cause a primary metabolic alkalosis and a compensatory respiratory alkalosis which may result in a normal or even elevated pH. AKA patients, as compared to DKA patients, typically have higher pH, lower K and Cl, and higher HCO3 in their blood tests. As ethanol is metabolized by ADH and ALDH to acetaldehyde and acetate, respectively, an increased amount of NADH forms which causes a high redox state and excess of reducing potential (increased NADH:NAD+ ratio). Increased lactate due to pyruvate shunting: Reduced caloric intake, decreased glycogen stores, and thiamine depletion results in amino acids being c Continue reading >>

Definition

Definition

Alcoholic ketoacidosis is the buildup of ketones in the blood. Ketones are a type of acid that form when the body breaks down fat for energy. The condition is an acute form of metabolic acidosis. Alternative Names Ketoacidosis – alcoholic Causes Alcoholic ketoacidosis is caused by excessive alcohol use. It is most often seen in a malnourished person who drinks large amounts of alcohol every day. Symptoms Abdominal pain Agitation Changed level of alertness, which may lead to coma Confusion Fatigue Slow, sluggish, lethargic movement Irregular deep, rapid breathing (Kussmaul’s sign) Loss of appetite Nausea and vomiting Symptoms of dehydration, such as dizziness, light-headedness, and thirst Exams and Tests Arterial blood gases (measure the acid/base balance and oxygen level in blood) Blood alcohol level Blood chemistries, and liver function tests, such as CHEM-20 CBC (complete blood count, measures red and whilte blood cells, and platelets, which help blood to clot) Prothrombin time (PT, a different measure of blood clotting, often abnormal from liver disease) Toxicology (poison) screening Urine ketones Treatment Treatment may involve fluids (salt and sugar solution) given through a vein. You may need to have your blood taken often. You may get vitamin supplements to treat nutritional deficiencies caused by excess alcohol use. People with this condition are admitted to the hospital, often to the intensive care unit (ICU). Additional medications may be given to prevent alcohol withdrawal. Outlook (Prognosis) Prompt medical attention improves the overall outlook. How severe the alcoholism is, and the presence of liver disease or other complications also affect the outlook. Possible Complications This can be a life-threatening disorder. Complications can include: Coma and Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

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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

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 >>

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 >>

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