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 >>
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: 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
What is alcoholic ketoacidosis? Cells need glucose (sugar) and insulin to function properly. Glucose comes from the food you eat, and insulin is produced by the pancreas. When you drink alcohol, your pancreas may stop producing insulin for a short time. Without insulin, your cells won’t be able to use the glucose you consume for energy. To get the energy you need, your body will start to burn fat. When your body burns fat for energy, byproducts known as ketone bodies are produced. If your body is not producing insulin, ketone bodies will begin to build up in your bloodstream. This buildup of ketones can produce a life-threatening condition known as ketoacidosis. Ketoacidosis, or metabolic acidosis, occurs when you ingest something that is metabolized or turned into an acid. This condition has a number of causes, including: shock kidney disease abnormal metabolism In addition to general ketoacidosis, there are several specific types. These types include: alcoholic ketoacidosis, which is caused by excessive consumption of alcohol diabetic ketoacidosis (DKA), which mostly develops in people with type 1 diabetes starvation ketoacidosis, which occurs most often in women who are pregnant, in their third trimester, and experiencing excessive vomiting Each of these situations increases the amount of acid in the system. They can also reduce the amount of insulin your body produces, leading to the breakdown of fat cells and the production of ketones. Alcoholic ketoacidosis can develop when you drink excessive amounts of alcohol for a long period of time. Excessive alcohol consumption often causes malnourishment (not enough nutrients for the body to function well). People who drink large quantities of alcohol may not eat regularly. They may also vomit as a result of drinking too Continue reading >>
Alcoholic Ketoacidosis – 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 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 >>
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 >>
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
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
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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 >>
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
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
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
Glucose or sugar is the preferred source of fuel for the body. If the body’s cells get insufficient glucose, fat is used as the alternative source of energy. When fat is used as a source of energy, it produces ketones, which are acidic chemicals. A buildup of ketones causes the blood to become too acidic. This leads to chemical derangements called ketoacidosis. Ketoacidosis comes in two different forms - diabetic ketoacidosis and alcoholic ketoacidosis. Here is more information about alcoholic ketoacidosis. What Is Alcoholic Ketoacidosis? Alcoholic Ketoacidosis (AKA) is a condition that develops in people who drink too much alcohol. This condition results in the increase of Ketones. AKA is common in adults who have a history with alcoholism. Any person showing signs of AKA needs to seek immediate medical attention because it is a potentially fatal condition. If you consume alcoholic beverages excessively without eating a balanced diet, the acidic levels of your blood might rise, causing health complications. Drinking alcoholic beverages in moderation or drinking as you eat can help reduce the likelihood of getting AKA. When the body’s fat cells breakdown after they have been consumed, ketones are formed. Consequently, the amount of acid in the blood dramatically increases and the blood’s pH (potenz Hydrogen) balance drops. While people who drink lots of alcoholic drinks and do not eat sufficient nutrients, or a balanced diet are likely to develop AKA, they are not the only ones. Inexperienced drinkers who binge drink can also develop this condition. What Are the Symptoms of Alcoholic Ketoacidosis? AKA symptoms vary based on the amount of alcohol you consume. Symptoms also depend on the amount of ketones you have in the bloodstream. If any of the following symptoms Continue reading >>
