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What Is Alcoholic Ketosis?

Alcoholic Ketosis: Prevalence, Determinants, And Ketohepatitis In Japanese Alcoholic Men

Alcoholic Ketosis: Prevalence, Determinants, And Ketohepatitis In Japanese Alcoholic Men

Alcoholic Ketosis: Prevalence, Determinants, and Ketohepatitis in Japanese Alcoholic Men National Hospital Organization Kurihama Medical and Addiction Center Corresponding author: National Hospital Organization Kurihama Medical and Addiction Center, 5-3-1 Nobi, Yokosuka, Kanagawa 239-0841, Japan. Tel.: +81-46-848-1550; Fax: + National Hospital Organization Kurihama Medical and Addiction Center National Hospital Organization Kurihama Medical and Addiction Center National Hospital Organization Kurihama Medical and Addiction Center National Hospital Organization Kurihama Medical and Addiction Center National Hospital Organization Kurihama Medical and Addiction Center National Hospital Organization Kurihama Medical and Addiction Center Alcohol and Alcoholism, Volume 49, Issue 6, 1 November 2014, Pages 618625, Akira Yokoyama, Tetsuji Yokoyama, Takeshi Mizukami, Toshifumi Matsui, Koichi Shiraishi, Mitsuru Kimura, Sachio Matsushita, Susumu Higuchi, Katsuya Maruyama; Alcoholic Ketosis: Prevalence, Determinants, and Ketohepatitis in Japanese Alcoholic Men, Alcohol and Alcoholism, Volume 49, Issue 6, 1 November 2014, Pages 618625, Aims: Alcoholic ketosis and ketoacidosis are metabolic abnormalities often diagnosed in alcoholics in emergency departments. We attempted to identify determinants or factors associated with alcoholic ketosis. Methods: The subjects of this cross-sectional survey were 1588 Japanese alcoholic men (40 years) who came to an addiction center within 14 days of their last drink. Results: The results of the dipstick urinalyses revealed a prevalence of ketosis of 34.0% (, 21.5%; +, 8.9%; and 2+/3+; 3.6%) in the alcoholics. Higher urine ketone levels were associated with higher serum total bilirubin, aspartate transaminase (AST), alanine transaminase and gamma-gl Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Author: George Ansstas, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... 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: An elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). The pathogenesis of AKA is complex. [ 7 ] Although the general physiological factors and mechanisms leading to AKA are understood, the precise factors have not been fully elucidated. The following are the 3 main predisposing events: Delay and decrease in insulin secretion and excess glucagon secretion, induced by starvation and counter-regulatory hormones Elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+) secondary to alcohol metabolism Volume depletion resulting from vomiting and poor oral intake of fluids During starvation there is decrease in insulin secretion and increases in production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth horm 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 >>

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment Of Alcoholic Ketoacidosis

Emergent Treatment of Alcoholic Ketoacidosis Author: Adam Blumenberg, MD, MA; Chief Editor: Erik D Schraga, MD more... Alcoholic ketoacidosis (AKA) is an acute metabolic acidosis seen in persons with a recent history of binge drinking and little or no nutritional intake. Alcoholic ketoacidosis is characterized by high serum ketone levels and an elevated anion gap (see the Anion Gap calculator). A concomitant metabolic alkalosis is also common, resulting from vomiting and volume depletion. Although AKA most commonly occurs in adults with alcoholism, alcoholic ketoacidosis has been reported in less-experienced drinkers of all ages. [ 1 , 2 ] Go to Alcoholic Ketoacidosis , Metabolic Alkalosis , and Pediatric Metabolic Alkalosis for complete information on these topics. Assess the patient's airway and manage as clinically indicated. Administer oxygen as indicated. Obtain intravenous access and administer fluid resuscitation for volume depletion and/or hypotension. Consider and treat hypoglycemia. [ 3 ] If the patient's mental status is diminished, consider administration of naloxone and thiamine . Note information about the patient's social situation and the presence of intoxicating agents besides alcohol. Suspect alcoholic ketoacidosis in any patient with recent binge drinking and an elevated anion gap. A history of alcoholism is not necessary for the development of alcoholic ketoacidosis. One episode of heavy alcohol intake combined with inadequate carbohydrate intake is sufficient to generate this disease state. Presenting symptoms may include nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension. [ 4 ] Urine tests for ketones may be falsely negative or only trace positive in alcoholic ketoacidosis. This is because 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 >>

Aarp's Health Tools

Aarp's Health Tools

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 shorttime. Without insulin, your cells wont be able to use the glucose you consumefor energy. To get the energy you need, your body will start to burn fat. When your body burns fat for energy, byproducts known as ketonebodies are produced. If your body is not producing insulin, ketone bodies willbegin to build up in your bloodstream. This buildup of ketones can produce alife-threatening condition known as ketoacidosis. Ketoacidosis, ormetabolic acidosis, occurs when you ingest something that is metabolized orturned into an acid. This condition has a number of causes, including: In addition to general ketoacidosis, there are several specifictypes. These types include: alcoholic ketoacidosis, which is caused by excessive consumptionof alcohol diabetic ketoacidosis (DKA), which mostly develops in peoplewith type 1 diabetes starvation ketoacidosis, which occurs most often in women whoare 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 breakdownof fat cells and the production of ketones. Alcoholic ketoacidosis can develop when you drink excessive amountsof alcohol for a long period of time. Excessive alcohol consumption often causesmalnourishment (not enough nutrients for the body to function well). People who drink large quantities of alcohol may not eatregularly. They may also vomit as a result of drinking too much. Not eatingenough or vomiting can lead to periods of starvation. This further reduces t 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 >>

Postmortem Diagnosis Of Alcoholic Ketoacidosis | Alcohol And Alcoholism | Oxford Academic

Postmortem Diagnosis Of Alcoholic Ketoacidosis | Alcohol And Alcoholism | Oxford Academic

Aims: The aim of this article is to review the forensic literature covering the postmortem investigations that are associated with alcoholic ketoacidosis fatalities and report the results of our own analyses. Methods: Eight cases of suspected alcoholic ketoacidosis that had undergone medico-legal investigations in our facility from 2011 to 2013 were retrospectively selected. A series of laboratory parameters were measured in whole femoral blood, postmortem serum from femoral blood, urine and vitreous humor in order to obtain a more general overview on the biochemical and metabolic changes that occur during alcoholic ketoacidosis. Most of the tested parameters were chosen among those that had been described in clinical and forensic literature associated with alcoholic ketoacidosis and its complications. Results: Ketone bodies and carbohydrate-deficient transferrin levels were increased in all cases. Biochemical markers of generalized inflammation, volume depletion and undernourishment showed higher levels. Adaptive endocrine reactions involving insulin, glucagon, cortisol and triiodothyronine were also observed. Conclusions: Metabolic and biochemical disturbances characterizing alcoholic ketoacidosis can be reliably identified in the postmortem setting. The correlation of medical history, autopsy findings and biochemical results proves therefore decisive in identifying pre-existing disorders, excluding alternative causes of death and diagnosing alcoholic ketoacidosis as the cause of death. Alcoholic ketoacidosis: definition and clinical features The entity of alcoholic ketoacidosis, sometimes called alcoholic acidosis in the literature, was first described by Dillon et al. in 1940. In this report, the authors described a series of nine patients who had episodes of sever Continue reading >>

Ketoacidosis

Ketoacidosis

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate. Ketoacidosis is a pathological metabolic state marked by extreme and uncontrolled ketosis. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased. In extreme cases ketoacidosis can be fatal.[1] Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct by-product of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover.[2] Ketosis may also give off an odor, but the odor is usually more subtle due to lower concentrations of acetone. Treatment consists most simply of correcting blood sugar and insulin levels, which will halt ketone production. If the severity of the case warrants more aggressive measures, intravenous sodium bicarbonate infusion can be given to raise blood pH back to an acceptable range. However, serious caution must be exercised with IV sodium bicarbonate to avoid the risk of equally life-threatening hypernatremia. Cause[edit] Three common causes of ketoacidosis are alcohol, starvation, and diabetes, resulting in alcoholic ketoacidosis, starvation ketoacidosis, and diabetic ketoacidosis respectively.[3] In diabetic ketoacidosis, a high concentration of ketone bodies is usually accomp 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 >>

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

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 >>

Alcohol And Ketosis | Alcohol And Ketosis Diet And Weight Loss

Alcohol And Ketosis | Alcohol And Ketosis Diet And Weight Loss

There’s something called a ketogenic diet that a lot more people are relying on as a way to lose weight, particularly recently. So what is the ketogenic diet, what is ketosis, and what is the relationship between alcohol and the ketosis diet and weight loss? Below are some of the things to know about the ketogenic diet and alcohol and ketosis. Before looking at the specifics of alcohol and ketosis, what is ketosis in general? Ketosis is a term that refers to a metabolic process that your body regularly goes through. When you don’t have the glucose you need to fuel your body with energy, you’ll instead go into a mode where you’re burning stored fats. When this happens, ketones, which are a build-up of acids, are in the body. The belief with the ketogenic diet is that you can encourage your body to go into that state of ketosis or fat-burning by following a certain diet, which is low-carb. You’re basically forcing your body to eliminate fat because that’s what it’s using for energy instead of carbs. The state of ketosis frequently occurs in people with diabetes, and while it’s a normal process, some extremes are possible. If you have extreme ketosis, you’re more likely to have type 1 diabetes, as an example. If your ketone levels rise too much, it can cause your acid level in your blood to similarly rise, which can cause a condition called ketoacidosis. This can be deadly. Your body typically primarily uses glucose as energy, such as from sugary or starchy foods, but if there’s not enough of this glucose your body will then go to breaking down your stores of fat. The ketogenic diet is also called a low-carb diet, or a keto diet. It’s based on a concept of eating primarily fats, and a reduced amount of carbohydrates. While it’s relatively popular, t Continue reading >>

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 >>

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