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 >>
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 >>
Ketosis Vs. Ketoacidosis: What You Should Know
Despite the similarity in name, ketosis and ketoacidosis are two different things. Ketoacidosis refers to diabetic ketoacidosis (DKA) and is a complication of type 1 diabetes mellitus. It’s a life-threatening condition resulting from dangerously high levels of ketones and blood sugar. This combination makes your blood too acidic, which can change the normal functioning of internal organs like your liver and kidneys. It’s critical that you get prompt treatment. DKA can occur very quickly. It may develop in less than 24 hours. It mostly occurs in people with type 1 diabetes whose bodies do not produce any insulin. Several things can lead to DKA, including illness, improper diet, or not taking an adequate dose of insulin. DKA can also occur in individuals with type 2 diabetes who have little or no insulin production. Ketosis is the presence of ketones. It’s not harmful. You can be in ketosis if you’re on a low-carbohydrate diet or fasting, or if you’ve consumed too much alcohol. If you have ketosis, you have a higher than usual level of ketones in your blood or urine, but not high enough to cause acidosis. Ketones are a chemical your body produces when it burns stored fat. Some people choose a low-carb diet to help with weight loss. While there is some controversy over their safety, low-carb diets are generally fine. Talk to your doctor before beginning any extreme diet plan. DKA is the leading cause of death in people under 24 years old who have diabetes. The overall death rate for ketoacidosis is 2 to 5 percent. People under the age of 30 make up 36 percent of DKA cases. Twenty-seven percent of people with DKA are between the ages of 30 and 50, 23 percent are between the ages of 51 and 70, and 14 percent are over the age of 70. Ketosis may cause bad breath. Ket Continue reading >>
Starvation Ketoacidosis
Etiology xxx Physiology Accumulation of Ketones Generated by Metabolism of Free Fatty Acids Diagnosis Anion Gap: usually >20 Osmolal Gap: increased Serum Ketones: positive Serum Potassium: normal (ketoacidosis does not cause hyperkalemia) Clinical Manifestations Neurologic Manifestations xxxx Renal Manifestations Anion Gap Metabolic Acidosis (AGMA) (see Metabolic Acidosis-Elevated Anion Gap, [[Metabolic Acidosis-Elevated Anion Gap]]) Diagnosis Delta Gap/Delta Bicarbonate Ratio: usually 1.1 Ketoacidosis xxx Elevated Osmolal Gap (see Serum Osmolality, [[Serum Osmolality]]) Physiology: increased (due to presence of osmotically-active, acetone) Other Manifestations xxx xxx Treatment Nutritional Support References xxx Continue reading >>
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 >>
Diabetic Ketoacidosis: Evaluation And Treatment
Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>
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 >>
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 >>
Ketosis
Not to be confused with Ketoacidosis. Ketosis is a metabolic state in which some of the body's energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis in which blood glucose provides energy. Ketosis is a result of metabolizing fat to provide energy. Ketosis is a nutritional process characterised by serum concentrations of ketone bodies over 0.5 mM, with low and stable levels of insulin and blood glucose.[1][2] It is almost always generalized with hyperketonemia, that is, an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted (or from metabolising medium-chain triglycerides[3]). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate,[4] and the levels of ketone bodies are regulated mainly by insulin and glucagon.[5] Most cells in the body can use both glucose and ketone bodies for fuel, and during ketosis, free fatty acids and glucose synthesis (gluconeogenesis) fuel the remainder. Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet (ketogenic diet), and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes.[6] In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed.[5][7] For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.[8] Ketosis and ketoacidosis are similar, but ketoacidosis is an acute life-threatening state requiring prompt medical intervention while ketosis can be physiological. However, there are situations (such as treatment-resistant Continue reading >>
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 >>
Starvation Ketoacidosis In Pregnancy
Introduction: Starvation ketosis outside pregnancy is a rare phenomenon and is unlikely to cause a severe acidosis. Pregnancy is an insulin resistant state due to placental production of hormones including glucagon and human placental lactogen. Insulin resistance increases with advancing gestation and this confers a susceptibility to ketosis, particularly in the third trimester. Starvation ketoacidosis in pregnancy has been reported and is usually precipitated by a period of severe vomiting. Ketoacidosis has been associated with intrauterine death. Case report: A 22-year-old woman in her third pregnancy presented at 32 weeks gestation with a 24 h history of severe vomiting. She had been treated for an asthma exacerbation with prednisolone and erythromycin the day prior to presentation. She was unwell, hypertensive (145/70 mmHg) with a sinus tachycardia and Kussmaul breathing. Urinalysis showed ++++ ketones, + protein and pH 5. Fingerprick glucose was 4 mmol/l and ketones were 4.0 mmol/l. Arterial blood gas showed pH 7.27, PaCO2 1.1 kPa, base excess −23, bicarbonate 8.6 mmol/l and lactate 0.6 mmol/l. The anion gap was 20. Serum ethanol, salicylates and paracetamol levels were undetectable. She was fluid resuscitated but her biochemical parameters did not improve. She was intubated and underwent emergency caesarean section. A healthy boy was delivered and her acidosis resolved over the subsequent 8 h. Discussion: We believe this case is explained by starvation ketoacidosis. There was no evidence of diabetes mellitus or other causes of a metabolic acidosis. In view of the hypertension, proteinuria and raised urate the differential diagnosis was an atypical presentation of pre-eclampsia. This case illustrates the metabolic stress imposed by the feto-placental unit. It als Continue reading >>
Ketosis: Symptoms, Signs & More
Every cell in your body needs energy to survive. Most of the time, you create energy from the sugar (glucose) in your bloodstream. Insulin helps regulate glucose levels in the blood and stimulate the absorption of glucose by the cells in your body. If you don’t have enough glucose or insufficient insulin to get the job done, your body will break down fat instead for energy. This supply of fat is an alternative energy source that keeps you from starvation. When you break down fat, you produce a compound called a ketone body. This process is called ketosis. Insulin is required by your cells in order to use the glucose in your blood, but ketones do not require insulin. The ketones that don’t get used for energy pass through your kidneys and out through your urine. Ketosis is most likely to occur in people who have diabetes, a condition in which the body produces little or no insulin. Ketosis and Ketoacidosis: What You Need To Know Ketosis simply means that your body is producing ketone bodies. You’re burning fat instead of glucose. Ketosis isn’t necessarily harmful to your health. If you don’t have diabetes and you maintain a healthy diet, it’s unlikely to be a problem. While ketosis itself isn’t particularly dangerous, it’s definitely something to keep an eye on, especially if you have diabetes. Ketosis can be a precursor to ketoacidosis, also known as diabetic ketoacidosis. Ketoacidosis is a condition in which you have both high glucose and high ketone levels. Having ketoacidosis results in your blood becoming too acidic. It’s more common for those with type 1 diabetes rather than type 2. Once symptoms of ketoacidosis begin, they can escalate very quickly. Symptoms include: breath that smells fruity or like nail polish or nail polish remover rapid breat Continue reading >>
Why Dka & Nutritional Ketosis Are Not The Same
There’s a very common misconception and general misunderstanding around ketones. Specifically, the misunderstandings lie in the areas of: ketones that are produced in low-carb diets of generally less than 50 grams of carbs per day, which is low enough to put a person in a state of “nutritional ketosis” ketones that are produced when a diabetic is in a state of “diabetic ketoacidosis” (DKA) and lastly, there are “starvation ketones” and “illness-induced ketones” The fact is they are very different. DKA is a dangerous state of ketosis that can easily land a diabetic in the hospital and is life-threatening. Meanwhile, “nutritional ketosis” is the result of a nutritional approach that both non-diabetics and diabetics can safely achieve through low-carb nutrition. Diabetic Ketoacidosis vs. Nutritional Ketosis Ryan Attar (soon to be Ryan Attar, ND) helps explain the science and actual human physiology behind these different types of ketone production. Ryan is currently studying to become a Doctor of Naturopathic Medicine in Connecticut and also pursuing a Masters Degree in Human Nutrition. He has interned under the supervision of the very well-known diabetes doc, Dr. Bernstein. Ryan explains: Diabetic Ketoacidosis: “Diabetic Ketoacidosis (DKA), is a very dangerous state where an individual with uncontrolled diabetes is effectively starving due to lack of insulin. Insulin brings glucose into our cells and without it the body switches to ketones. Our brain can function off either glucose or fat and ketones. Ketones are a breakdown of fat and amino acids that can travel through the blood to various tissues to be utilized for fuel.” “In normal individuals, or those with well controlled diabetes, insulin acts to cancel the feedback loop and slow and sto Continue reading >>
Starvation Ketoacidosis: Treatment Pitfalls
Dear Editor, Yeow et al.1 describe a case of non-diabetic euglycaemic acidosis resulting from post op dysphagia and poor intake of approximately six weeks duration. We have seen a similar case of ‘starvation ketoacidosis’ in a patient undergoing percutaneous endoscopic gastrostomy feeding tube replacement. We think that intravenous (IV) glucose should be the initial treatment, with the addition of insulin only if required. The correspondence from Frise and Mackillop2 states this strategy is effective for treating ketoacidosis in pregnancy; however, there are also some other pitfalls in treatment of starvation ketoacidosis which must be considered, and some overlap with alcoholic ketoacidosis. Unlike patients with diabetic ketoacidosis, patients with starvation ketosis release insulin when carbohydrate is administered. They are also producing high levels of glucose elevating hormones such as glucagon and have depleted glycogen stores. These hormones cause the lipolysis which helps generate ketones for fuel. The addition of exogenous insulin in this state risks hypoglycaemia. Once provided with adequate carbohydrate the insulin levels will rise and counter-regulatory hormone levels will fall, resolving the ketosis. Alcoholics are another group prone to ketosis (alcoholic ketoacidosis (AKA)) and are particularly prone to hypoglycaemia; administration of insulin to those patients would have to be with caution and literature3 on AKA reports resolution without insulin administration, although there is little evidence outside of case reports. Starved patients and alcoholics are also both at risk of thiamine deficiency. Depletion of body thiamine stores can occur within four weeks. It is important to consider this, as administration of IV glucose in thiamine deficiency can Continue reading >>
Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma
Prashanth Rawla1, Anantha R Vellipuram2, Sathyajit S Bandaru3 and Jeffrey Pradeep Raj4[1] Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA [2] Texas Tech University Health Sciences Center, El Paso, Texas, USA [3] Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA [4] Department of Pharmacology, St John’s Medical College, Bangalore, India Summary Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine ketones should be checked in ill patients with diabetes regardless of blood glucose levels. Background Diabetic ket Continue reading >>
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