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Alcoholic Ketoacidosis

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 >>

Alcoholic Ketoacidosis And Isopropyl Alcohol Intoxication

Alcoholic Ketoacidosis And Isopropyl Alcohol Intoxication

To the Editor.— The editorial entitled "Cyanide Poisoning—A Challenge" (Archives 137:993-994, 1977) contained a statement that "cyanide intoxication and diabetes mellitus (are) the only two major clinical situations with very high levels of serum acetone and acetone bodies." If indeed cyanide intoxication is a major clinical situation, then I would like to add two additional situations, ie, alcoholic ketoacidosis1 and isopropyl rubbing alcohol intoxication.2The syndrome of alcoholic ketoacidosis occurs in nondiabetic alcoholics, typically after a period of prolonged vomiting and decreased food intake. The fact that a mild ketosis may arise from starvation or prolonged vomiting is well known; the mechanism for the severe ketosis reported in nondiabetic alcoholics remains speculative. The syndrome is probably underdiagnosed because there tends to be an unusually high ratio of β-hydroxybutyrate to acetoacetate; only the latter is measured by the nitroprusside test (Acetest). Therefore, a metabolic acidosis with an apparently unexplained Continue reading >>

I Want To Quit Drinking And Smoking Altogether. However, As A Freshman In College, It's Hard Because Of The Constant Influence. Why Should I Quit?

I Want To Quit Drinking And Smoking Altogether. However, As A Freshman In College, It's Hard Because Of The Constant Influence. Why Should I Quit?

Peer pressure to join negative activities like smoking, drugs, drinking etc., is something every young man faces. The weak and feeble succumb while the strong and productive youngsters look for peer pressure on useful activities like debating clubs, public speaking, sports, running, community service etc., Many achievements (irony!) are possible. You can reach the heaven or hell sooner than many others. You can keep away many friends. You can annoy your spouse who may ask you to enjoy outdoor smoking. You can imbibe thousands of strange chemical molecules in the most micro size. You can leave your kids to grow up independently without interfering in their lives. You can use multiple machines to breathe at the later stages. You can use many ash trays which can alternate as crystal art pieces. You can outspend non-smokers on air-purifiers, exhaust fans, perfumes, mouth fresheners etc., You can set a great example to kids and youngsters to follow your “cool” personality. You can make a great contribution to Doctors and Pharma companies to bolster their bottom-line. And here is a successful method I used to quit smoking, Continue reading >>

Alcoholic Ketoacidosis—a Review

Alcoholic Ketoacidosis—a Review

Abstract Alcoholic ketoacidosis is a frequently encountered metabolic disturbance that follows a prolonged intake of ethanol. Following a brief duration of abstinence, patients typically present with vomiting, abdominal pain, and shortness of breath. Examination reveals Kussmaul breathing, variable volume loss, and coincident manifestations of chronic alcohol usage. Characteristic laboratory findings include anion-gap metabolic ketoacidosis, normal serum glucose, and zero ethanol levels. Phosphate measurements may be depressed, particularly after institution of therapy. Intravascular volume restitution, delivery of dextrose, attention to electrolytes, and discovery of alcohol-related illnesses are the mainstays of therapy. Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

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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 >>

Chapter 221. Alcoholic Ketoacidosis

Chapter 221. Alcoholic Ketoacidosis

Woods WA, Perina DG. Woods W.A., Perina D.G. Woods, William A., and Debra G. Perina.Chapter 221. Alcoholic Ketoacidosis. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. Tintinalli J.E., Stapczynski J, Ma O, Cline D.M., Cydulka R.K., Meckler G.D., T Eds. Judith E. Tintinalli, et al.eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e New York, NY: McGraw-Hill; 2011. Accessed March 27, 2018. Woods WA, Perina DG. Woods W.A., Perina D.G. Woods, William A., and Debra G. Perina.. "Chapter 221. Alcoholic Ketoacidosis." Tintinalli's Emergency Medicine: A Comprehensive Study Guide, 7e Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. Tintinalli J.E., Stapczynski J, Ma O, Cline D.M., Cydulka R.K., Meckler G.D., T Eds. Judith E. Tintinalli, et al. New York, NY: McGraw-Hill, 2011, Alcoholic ketoacidosis is a wide anion gap metabolic acidosis most often associated with acute cessation of alcohol consumption after chronic alcohol abuse and is typically associated with nausea, vomiting, and vague GI complaints. 1 Alcohol metabolism combined with little or no glycogen reserves results in elevated ketoacid levels. Although alcoholic ketoacidosis is usually seen in chronic alcoholics, it has been described in first-time binge drinkers. Repeated episodes can occur. 2 Although with proper treatment this illness is self limited, death has been reported from presumed excessive ketonemia. 24 Ethanol metabolism requires nicotinamide adenine dinucleotide (NAD) and the enzymes alcohol dehydrogenase and aldehyde dehydrogenase to convert ethanol to acetyl coenzyme A. Acetyl coenzyme A may be metabolized directly, resulting in ketoacid production, used as substrate for the Krebs cycle, or used for free fatty acid synthesis ( Figu 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

Seen in patients with recent history of binge drinking with little/no nutritional intake Anion gap metabolic acidosis associated with acute cessation of ETOH consumption after chronic abuse Characterized by high serum ketone levels and an elevated AG Consider other causes of elevated AG, as well as co-ingestants Concomitant metabolic alkalosis can occur from dehydration (volume depletion) and emesis Ethanol metabolism depletes NAD stores[1] Results in inhibition of Krebs cycle, depletion of glycogen stores, and ketone formation High NADH:NAD also results in increased lactate production Acetoacetate is metabolized to acetone so elevated osmolal gap may also be seen Differential Diagnosis Starvation Ketosis Binge drinking ending in nausea, vomiting, and decreased intake Positive serum ketones Wide anion gap metabolic acidosis without alternate explanation Urine ketones may be falsely negative or low Lab measured ketone is acetoacetate May miss beta-hydroxybutyrate Consider associated diseases (ie pancreatitis, rhabdomyolysis, hepatitis, infections) Oral nutrition if able to tolerate Consider bicarb if life-threatening acidosis (pH <7.1) unresponsive to fluid therapy Discharge home after treatment if able to tolerate POs and acidosis resolved Consider admission for those with severe volume depletion and/or acidosis Hypoglycemia is poor prognostic feature, indicating depleted glycogen stores See Also 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 – A Case Report

Alcoholic Ketoacidosis – A Case Report

Summarized from Noor N, Basavaraju K, Sharpstone D. Alcoholic ketoacidosis: a case report and review of the literature. Oxford Medical Case Reports 2016; 3: 31-33 Three parameters generated during blood gas analysis, pH, pCO2 and bicarbonate, provide the means for assessment of patient acid-base status, which is frequently disturbed in the acutely/critically ill. Four broad classes of acid-base disturbance are recognized: metabolic acidosis, respiratory acidosis, metabolic alkalosis and respiratory alkalosis. Metabolic acidosis, which is characterized by primary reduction in pH and bicarbonate, and secondary (compensatory) decrease in pCO2, has many possible causes including the abnormal accumulation of the keto-acids, β-hydroxybutyrate and acetoacetate. This particular form of metabolic acidosis, called ketoacidosis, has three etiologies giving rise to three quite separate conditions with common biochemical features: diabetes (diabetic ketoacidosis); excessive alcohol ingestion (alcoholic ketoacidosis) and severe starvation (starvation ketoacidosis). Diabetic ketoacidosis, which is the most common of the three, is the subject of a recent review (discussed below) whilst alcoholic ketoacidosis is the focus of this recent case study report. The case concerns a 64-year-old lady who presented to the emergency department of her local hospital with acute-onset abdominal pain, nausea, vomiting and shortness of breath. Blood gas results (pH 7.10, bicarbonate 2.9 mmol/L) confirmed metabolic acidosis, and the presence of raised ketones (serum ketones 5.5 mmol/L) allowed a diagnosis of ketoacidosis. Initially, doctors caring for the patient entertained the possibility that the lady was suffering diabetic ketoacidosis, but her normal blood glucose concentration (5.8 mmol/L) and pr Continue reading >>

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment Of Alcoholic Ketoacidosis

Exenatide extended-release causes an increased incidence in thyroid C-cell tumors at clinically relevant exposures in rats compared to controls. It is unknown whether BYDUREON BCise causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of exenatide extended-release-induced rodent thyroid C-cell tumors has not been determined BYDUREON BCise is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with the use of BYDUREON BCise and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for detection of MTC in patients treated with BYDUREON BCise Acute Pancreatitis including fatal and non-fatal hemorrhagic or necrotizing pancreatitis has been reported. After initiation, observe patients carefully for symptoms of pancreatitis. If suspected, discontinue promptly and do not restart if confirmed. Consider other antidiabetic therapies in patients with a history of pancreatitis Acute Kidney Injury and Impairment of Renal Function Altered renal function, including increased serum creatinine, renal impairment, worsened chronic renal failure, and acute renal failure, sometimes requiring hemodialysis and kidney transplantation have been reported. Not recommended in patients with severe renal impairment or end-stage renal disease. Use caution in patients with renal transplantation or moderate renal impairment Gastrointestinal Disease Because exenatide is commonly associated with gastrointestinal adverse reactions, not recommended in patients with sev 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 >>

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 >>

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