Alcoholic Ketoacidosis
OVERVIEW rare small proportion of chronic ethanol abusers relatively benign if patients given IV dextrose and fluids unclear aetiology ? starvation, dehydration, excess acetate production, altered redox state, hormonal imbalances, genetic predisposition HISTORY alcohol binge -> when blood alcohol level declining + not eating anorexia nausea epigastric pain vomiting EXAMINATION clear sensorium acetone odour tachypnoea or Kussmaul respiration (if marked acidaemia) tachycardia volume depletion INVESTIGATIONS ABG: metabolic acidosis, ketonaemia, ketonuria (may have metabolic alkalosis if has severe vomiting) normal, low or slightly high blood glucose ratio of beta-hydroxybutyerate to acetoacetate seen in alcoholic is higher than seen in DKA MANAGEMENT exclude other causes for metabolic acidosis (AKA is a diagnosis of exclusion) give fluid + dextrose monitor closely for refeeding syndrome Continue reading >>
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 >>
Alcoholic Ketoacidosis: A Case Report And Review Of The Literature
Alcoholic ketoacidosis: a case report and review of the literature Corresponding address. Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK. Tel: +441223-762322; Fax: + Oxford Medical Case Reports, Volume 2016, Issue 3, 1 March 2016, Pages 3133, Nurulamin M. Noor, Krishna Basavaraju, Dan Sharpstone; Alcoholic ketoacidosis: a case report and review of the literature, Oxford Medical Case Reports, Volume 2016, Issue 3, 1 March 2016, Pages 3133, Alcoholic ketoacidosis (AKA) is a cause of severe metabolic acidosis usually occurring in malnourished patients with a history of recent alcoholic binge, often on a background of alcohol dependency. AKA can be fatal due to associated electrolyte abnormalities and subsequent development of cardiac arrhythmias. This is a diagnosis that is often delayed or missed, in patients who present with a severe lactic and ketoacidosis. Here we report the case of a 64-year-old female who presented with generalized abdominal pain, nausea and shortness of breath. 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. The diagnosis of AKA was suspected, and subsequent aggressive fluid resuscitation, management and monitoring were instituted. Given the early recognition of AKA and appropriate multidisciplinary team management, our patient had a good outcome and was discharged home without any complication. 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 Continue reading >>
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 >>
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 >>
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 >>
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 >>
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 >>
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: Another Risk Of Chronic Alcohol Abuse
Alcoholic Ketoacidosis: Another Risk ofChronic Alcohol acts like poison within the human body. It enters the bloodstream and affects every part of the body, making the drinker vulnerable to serious health consequences. Chronic alcohol abuse exposes the central nervous, digestive, circulatory, immune, skeletal, and muscle systems to severe and long-lasting damage. Alcoholic ketoacidosis (AKA) is a disease that develops from drinking too much alcohol. Learn about this harmful condition and what you can do to prevent it. Alcoholic ketoacidosis occurs when there is an unhealthy buildup of ketones in the body. Ketones are a byproduct of the body burning fat instead of glucose for energy. Cells need glucose and insulin to function properly. The pancreas produces insulin, and glucose comes from the foods you eat. Consuming too much alcohol regularly, combined with a poor diet, can lead to the pancreas failing to produce insulin for a short time. This leads to your body burning fat for energy instead of using the glucose you consume. Without the production of insulin, ketones build up in the bloodstream, causing the life-threatening condition of AKA. Ketoacidosis occurs when the body digests something that gets turned into acid. Alcoholic ketoacidosis happens when excessive amounts of alcohol cause digestive problems. Failure to follow a holistic approach , such as eating a balanced diet, combined with excessive drinking and/or vomiting, leads to blood that is too acidic. Alcoholic ketoacidosis can be fatal, and requires treatment right away. Knowing how to identify AKA will help you recognize this condition in yourself or loved ones early on, giving you the best chance of recovery. This condition is treatable, but only with swift action to stop excessive alcohol consumption, Continue reading >>
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: Causes, Symptoms, Treatment, Prognosis
Ketoacidosis is a medical condition in which the food that is ingested by an individual is either metabolized or converted into acid. Alcoholic Ketoacidosis is a condition in which there is development of Ketoacidosis as a result of excessive alcohol intake for a long period of time and less ingestion of food resulting in malnutrition. Drinking excessive alcohol causes the individual to be able to eat less food. Additionally, if excess alcohol is ingested then it may lead to vomiting which further worsens the nutritional status of the individual which results in formation of excess acids resulting in Alcoholic Ketoacidosis. The symptoms caused by Alcoholic Ketoacidosis include abdominal pain, excessive fatigue, persistent vomiting, and the individual getting dehydrated due to frequent vomiting episodes and less fluid intake. If an individual has a history of alcohol abuse and experiences the above mentioned symptoms then it is advised that the individual goes to the nearest emergency room to get evaluated and if diagnosed treated for Alcoholic Ketoacidosis. As stated above, the root cause of Alcoholic Ketoacidosis is drinking excessive amounts of alcohol for a prolonged period of time. When an individual indulges in binge drinking he or she is not able to take in enough food that is required by the body to function. This eventually results in malnourishment. Additionally, vomiting caused by excessive drinking also results in loss of vital nutrients and electrolytes from the body such that the body is not able to function normally. This results in the insulin that is being produced by the body becoming less and less. All of these ultimately results in the development of Alcoholic Ketoacidosis. An individual may develop symptoms within a day after binge drinking, dependin Continue reading >>
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 >>
Alcoholic Ketoacidosis Treatment & Management
Approach Considerations Treatment of alcoholic ketoacidosis (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. [4] Carbohydrate and fluid replacement reverse the pathophysiologic derangements that lead to AKA by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones. Dextrose stimulates the oxidation of NADH and aids in normalizing the NADH/NAD+ ratio. Fluids alone do not correct AKA as quickly as do fluids and carbohydrates together. Indeed, evidence-based guidelines by Flannery et al, on the management of intensive care unit patients with a chronic alcohol disorder, including symptoms that mimic or mask Wernicke encephalopathy, recommend that in cases of suspected AKA, dextrose-containing fluids be used in place of normal saline during the first day of admission. [23] In alcoholics, thiamine (100 mg IV or IM) should be administered prior to any glucose-containing solutions. This will decrease the risk of precipitating Wernicke encephalopathy or Korsakoff syndrome. [13] Phosphate depletion is also common in alcoholics. The plasma phosphate concentration may be normal on admission; however, it typically falls to low levels with therapy as insulin drives phosphate into the cells. When present, severe hypophosphatemia may be associated with marked and possibly life-threatening complications, such as myocardial dysfunction, in these patients. Institute appropriate treatment for serious, coexisting, acute illnesses. These may include pancreatitis, hepatitis, heart failure, or infection. Prevention of AKA involves the treatment of chronic alcohol abuse. Transfer considerations Pati Continue reading >>
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Alcoholic Ketoacidosis
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