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Starvation Ketosis Lab Findings

Starvation Ketoacidosis

Starvation Ketoacidosis

Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis. When insulin levels are low and glucagon levels are high (such as in a fasting state), long chain fatty acids and glycerol from triglycerides are released from peripheral fat stores and are transported to the liver. The fatty acids undergo beta-oxidation and generate acetyl-CoA. However, with excessive amounts of acetyl-CoA, the Krebs cycle may become oversaturated, and instead the acetyl-CoA enter the ketogenic pathway resulting in production of ketone bodies. Mild ketosis (1mmol/L) results after fasting for approximately 12 to 14 hours. However, the ketoacid concentration rises with continued fasting and will peak after 20 to 30 days (8-10mmol/L). Clinical Features Nausea and vomiting Abdominal pain Dehydration Altered mental status Fatigue Kussmaul breathing Differential Diagnosis Evaluation Serum chemistry (elevated anion gap) Glucose (usually euglycemic or hypoglycemic) Urinalysis (ketonuria) Serum beta-hydroxybutyrate Lactate Salicylate level (if overdose suspected) Serum osmolality (if toxic alcohol ingestion suspected) Management Dextrose and saline solutions Dextrose Will cause increase in insulin and decrease in glucagon secretion, which will reduce ketone production and increase ketone metabolism Beta-hydroxybutyrate and acetoacetate will regenerate bicarbonate, causing partial correction of metabolic acidosis Saline or lactated ringer Will provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis) Considerations Rate of infusion dependent on volume status If hypokalemic, need to correct before administering glucose (as glucose stimulate Continue reading >>

Alcoholic Ketoacidosis Workup

Alcoholic Ketoacidosis Workup

Approach Considerations Diagnosis of alcoholic ketoacidosis (AKA) requires arterial blood gas (ABG) measurement and serum chemistry assays. Usual laboratory findings include the following [19] : Continue reading >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Copyright © 2014 Nupur Sinha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as “accelerated starvation.” Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. 1. Introduction A relative insulin deficient state has been well described in pregnancy. This is due to placentally derived hormones including glucagon, cortisol, and human placental lactogen which are increased in periods of stress [1]. The insulin resistance increases with gestational age Continue reading >>

Reference Range

Reference Range

Acetoacetate, beta-hydroxybutyrate, and acetone are ketone bodies. In carbohydrate-deficient states, fatty-acid metabolism spurs acetoacetate accumulation. The reduction of acetoacetate in the mitochondria results in beta-hydroxybutyrate production. Beta-hydroxybutyrate and acetoacetate, the predominant ketone bodies, are rich in energy. Beta-hydroxybutyrate and acetoacetate transport energy from the liver to other tissues. Acetone forms from the spontaneous decarboxylation of acetoacetate. Acetone is the cause of the sweet odor on the breath in persons with ketoacidosis. [1, 2] Ketone bodies fuel the brain with an alternative source of energy (close to two thirds of its needs) during periods of prolonged fasting or starvation, when the brain cannot use fatty acids for energy. The reference range for ketone is a negative value, at less than 1 mg/dL (< 0.1 mmol/L). [3] 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 >>

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 >>

An Unusual Cause For Ketoacidosis

An Unusual Cause For Ketoacidosis

Abstract Introduction In our continuing series on the application of principles of integrative physiology at the bedside, once again the central figure is an imaginary consultant, the renal and metabolic physiologist, Professor McCance, who deals with data from a real case. On this occasion his colleague Sir Hans Krebs, an expert in the field of glucose and energy metabolism, assists him in the analysis. Their emphasis is on concepts that depend on an understanding of physiology that crosses subspecialty boundaries. To avoid overwhelming the reader with details, key facts are provided, but only when necessary. The overall objective of this teaching exercise is to demonstrate how application of simple principles of integrative physiology at the bedside can be extremely helpful for clinical decision-making (Table 1). Principle Comment 1. A high H+ concentration per se is seldom life-threatening The threat to survival is usually due to the cause for the acidosis rather than the pH per se 2. Finding a new anion means a new acid was added Look in plasma (anion gap) and urine (net charge) to identify the new anions 3. Identify the acid by thinking of the properties of the anion Rate of production, rapidity of clearance from plasma, and unique toxic effects may all provide clues 4. Metabolic acidosis develops when the kidney fails to add new HCO3 to the body The kidney generates HCO3− by excreting NH4+, (usually with Cl−), in the urine 5. Ketoacids are brain fuels, produced when there is a prolonged lack of insulin The usual causes are diabetic ketoacidosis, alcoholic ketoacidosis, starvation or hypoglycemia-induced ketoacidosis, or that associated with salicylate overdose 6. Ketoacids are produced in the liver from acetyl-CoA, usually derived from fatty acids A low net in 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 >>

Diabetic, Alcoholic And Starvation Ketoacidosis

Diabetic, Alcoholic And Starvation Ketoacidosis

Copious amounts of ketones which are generated in insulin-deficient or insulin-unresponsive patients will give rise to a high anion gap metabolic acidosis. Ketones are anions, and they form the high anion gap. Management of DKA and HONK is discussed elsewhere. Meet the ketones Chemically speaking, a ketone is anything with a carbonyl group between a bunch of other carbon atoms. The above are your three typical ketoacidosis-associated ketone bodies. The biochemistry nerds among us will hasten to add that the beta-hydroxybutyrate is in fact not a ketone but a carboxylic acid, but - because it is associated with ketoacidosis, we will continue to refer to it as a ketone for the remainder of this chapter, in the spirit of convention. In the same spirit, we can suspend our objections to acetone being included in a discussion of ketoacidosis, which (though a true ketone) is in fact not acidic or basic, as it does not ionise at physiological pH (its pKa is 20 or so). So really, the only serious ketone acid is acetoacetate, which has a pKa of 3.77. However, beta-hydroxybutyrate is the prevalent ketone in ketoacidosis; the normal ratio of beta-hydroxybutyrate and acetoacetate is 3:1, and it can rise to 10:1 in diabetic ketoacidosis. Acetone is the least abundant. The metabolic origin of ketones The generation of ketones is a normal response to fasting, which follows the depletion of hepatic glycogen stores. Let us discuss normal physiology for a change. You, a healthy adult without serious alcohol problems, are fasting from midnight for a routine elective hernia repair. You will go to be after dinner with a few nice lumps of undigested food in your intestine, as well as about 75g of hepatic glycogen. As you sleep, you gradually digest the food and dip into the glycogen store. At 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 >>

Ketoacidosis

Ketoacidosis

GENERAL ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. CAUSES The three major types of ketosis are: (i) Starvation ketosis (ii) Alcoholic ketoacidosis (iii) Diabetic ketoacidosis STARVATION KETOSIS when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. patients are usually not diabetic. ALCOHOLIC KETOSIS Presentation a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or Continue reading >>

Ketoacidosis

Ketoacidosis

Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition), 2017 Introduction Although ketoacidosis is a form of metabolic acidosis because of the addition of acids, it is discussed separately in this chapter to emphasize the metabolic and biochemical issues required to understand the clinical aspects of this disorder (see margin note). We discuss the metabolic setting that is required to allow for the formation of ketoacids in the liver at a high rate and what sets the limit on the rate of production. Removal of ketoacids occurs mainly in the brain and kidneys. We examine what sets the limit on the rate of removal of ketoacids by these organs. We believe that understanding the biochemical and metabolic aspects of ketoacidsis provides the clinician with a better understanding of this disorder and allows for a better design of therapy in the individual patient with ketoacidosis. Relevant to the pathophysiology of this case, the soft drinks the patient consumed contained a large quantity of glucose, fructose, and caffeine. Ketoacids • A ketone is an organic compound that has a keto group (C=O) on an internal carbon atom. • Acetone is a ketone but not an acid. • Only acetoacetic acid is a ketoacid. β-Hydroxybutyric acid has a hydroxyl group (C–OH) on its internal carbon, so it is a hydroxy acid and not a ketoacid. Abbreviations β-HB, beta hydroxybutyrate anion AcAc, acetoacetate anion ADP, adenosine diphosphate ATP, adenosine triphosphate NAD+, nicotinamide adenine dinucleotide NADH,H+, reduced form of NAD+ FAD, flavin adenine dinucleotide FADH2, hydroxyquinone form of FAD EABV, effective arterial blood volume PAnion gap, plasma anion gap PGlucose, concentration of glucose in plasma POsmolal gap, plasm Continue reading >>

Ketoacidosis During A Low-carbohydrate Diet

Ketoacidosis During A Low-carbohydrate Diet

To the Editor: It is believed that low-carbohydrate diets work best in reducing weight when producing ketosis.1 We report on a 51-year-old white woman who does not have diabetes but had ketoacidosis while consuming a “no-carbohydrate” diet. There was no family history of diabetes, and she was not currently taking any medications. While adhering to a regimen of carbohydrate restriction, she reached a stable weight of 59.1 kg, a decrease from 72.7 kg. After several months of stable weight, she was admitted to the hospital four times with vomiting but without abdominal pain. On each occasion, she reported no alcohol use. Her body-mass index (the weight in kilograms divided by the square of the height in meters) was 26.7 before the weight loss and 21.7 afterward. Laboratory evaluation showed anion-gap acidosis, ketonuria, and elevated plasma glucose concentrations on three of the four occasions (Table 1). She had normal concentrations of plasma lactate and glycosylated hemoglobin. Screening for drugs, including ethyl alcohol and ethylene glycol, was negative. Abdominal ultrasonography showed hepatic steatosis. On each occasion, the patient recovered after administration of intravenous fluids and insulin, was prescribed insulin injections on discharge, and gradually reduced the use of insulin and then discontinued it while remaining euglycemic for six months or more between episodes. Testing for antibodies against glutamic acid decarboxylase and antinuclear antibodies was negative. Values on lipid studies were as follows: serum triglycerides, 102 mg per deciliter; high-density lipoprotein (HDL) cholesterol, 50 mg per deciliter; and calculated low-density lipoprotein (LDL) cholesterol, 189 mg per deciliter. The patient strictly adhered to a low-carbohydrate diet for four Continue reading >>

Starvation Ketoacidosis As A Cause Of Unexplained Metabolic Acidosis In The Perioperative Period

Starvation Ketoacidosis As A Cause Of Unexplained Metabolic Acidosis In The Perioperative Period

Go to: Abstract Patient: Female, 24 Final Diagnosis: Starvation ketoacidosis Symptoms: None Medication: — Clinical Procedure: Lumbar laminectomy Specialty: Orthopedics and Traumatology Besides providing anesthesia for surgery, the anesthesiologist’s role is to optimize the patient for surgery and for post-surgical recovery. This involves timely identification and treatment of medical comorbidities and abnormal laboratory values that could complicate the patient’s perioperative course. There are several potential causes of anion and non-anion gap metabolic acidosis in surgical patients, most of which could profoundly affect a patient’s surgical outcome. Thus, the presence of an acute acid-base disturbance requires a thorough workup, the results of which will influence the patient’s anesthetic management. An otherwise-healthy 24-year-old female presented for elective spine surgery and was found to have metabolic acidosis, hypotension, and polyuria intraoperatively. Common causes of acute metabolic acidosis were investigated and systematically ruled out, including lactic acidosis, diabetic ketoacidosis, drug-induced ketoacidosis, ingestion of toxic alcohols (e.g., methanol, ethylene glycol), uremia, and acute renal failure. Laboratory workup was remarkable only for elevated serum and urinary ketone levels, believed to be secondary to starvation ketoacidosis. Due to the patient’s unexplained acid-base disturbance, she was kept intubated postoperatively to allow for further workup and management. Starvation ketoacidosis is not widely recognized as a perioperative entity, and it is not well described in the medical literature. Lack of anesthesiologist awareness about this disorder may complicate the differential diagnosis for acute intraoperative metabolic acidosi Continue reading >>

Emdocs.net Emergency Medicine Educationtoxcards: Alcoholic Ketoacidosis - Emdocs.net - Emergency Medicine Education

Emdocs.net Emergency Medicine Educationtoxcards: Alcoholic Ketoacidosis - Emdocs.net - Emergency Medicine Education

Author: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit) A 45 year old male presents intoxicated, smelling of alcohol and appears disheveled with vomit on his clothes. He is sleepy but arousable to noxious stimuli. His serum ethanol level is 143 mg/dL. Na 135, K 3.9, Cl 97, CO2 20, BUN 33, Cr 1.1. Lactate 3.1. pH 7.35, CO2 28, HCO3 15. His urine is negative for ketones. His vitals are HR 103, RR 30, BP 115/65, O2 98% RA. Could these laboratory results be consistent with alcohol ketoacidosis (AKA)? The classic laboratory findings in patients with AKA include an elevated anion gap metabolic acidosis and an elevated lactate. Early in AKA patients may be negative for ketones when the nitroprusside test is used because it does not detect beta-hydroxybutyrate. As patients recover, the nitroprusside test will become positive as beta-hydroxybutyrate gets converted to acetone and acetate. Patients with AKA typically have elevated anion gap metabolic acidosis. However, vomiting may cause a primary metabolic alkalosis and a compensatory respiratory alkalosis which may result in a normal or even elevated pH. AKA patients, as compared to DKA patients, typically have higher pH, lower K and Cl, and higher HCO3 in their blood tests. As ethanol is metabolized by ADH and ALDH to acetaldehyde and acetate, respectively, an increased amount of NADH forms which causes a high redox state and excess of reducing potential (increased NADH:NAD+ ratio). Increased lactate due to pyruvate shunting: Reduced caloric intake, decreased glycogen stores, and thiamine depletion results in amino acids being c Continue reading >>

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