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What Is Alcoholic Ketoacidosis?

Alcoholic Ketoacidosis: Causes, Symptoms, Treatment, Prognosis

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

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

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

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

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 >>

Clinical Studies Of Alcoholic Ketoacidosis

Clinical Studies Of Alcoholic Ketoacidosis

Abstract Seven episodes of severe ketoacidosis in six nondiabetic patients were recognized at this hospital within an eighteen month period. All were women; one pregnant patient experienced two episodes at twenty-eight and thirty-two weeks' gestation. All patients admitted to heavy chronic alcohol intake and drinking binges. On admission, these patients were conscious and alert. Mean values were 143 mg./100 ml. for plasma glucose and 7.25 for arterial pH. Plasma bicarbonate was depressed with a mean anion gap of 18. Beta-hydroxybutyrate/acetoacetate ratio averaged 5.2. All patients had liver function abnormalities. Mean serum immunoreactive insulin was low, 5μU./ml. (n=2), while cortisol was markedly elevated at 76.5μg. per cent (n=3); mean growth hormone level was 14.1 ng./ml. (n=3). Free fatty acid concentration, measured on admission in one episode, was 1,945 mEq./L. Therapy with glucose, saline, and minimal amounts of alkali led to prompt recovery. Circulating levels of cortisol, insulin and growth hormone were measured serially in one patient during recovery; they quickly returned to normal. The dissociation of severe ketosis from glycosuria and hyperglycemia in these patients raises important questions concerning coupling of ketogenesis to gluconeogenesis. The striking preponderance of women, including one pregnant patient, reported with this condition also suggests a possible role for ovarian and placental hormones in its pathogenesis; fetal drain on carbohydrate reserves may further contribute to the tendency to ketosis. Alcoholic ketoacidosis may be relatively common, since we saw one case of this syndrome for about every four of diabetic ketoacidosis during this period. 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 >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

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

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

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 >>

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

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

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

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 >>

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 >>

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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