The Mechanisms And Management Strategies For Diabetic Ketoacidosis
are discussed elsewhere, as one of the scenarios in critical care endocrinology. Rather than get bogged down in thick endocrinology (thereby duplicating content from the Endocrinology section) I offer this brief summary, aimed at answering the short ABG interpretation questions rather than the long "how'd you manage this ketoacidosis" or "critically evaluate something" questions. Ketoacidosis-asociated ABG interpretation questions include the following: Question 7.1 from the second paper of 2013 Question 26.2 from the second paper of 2013 Question 8.3 from the first paper of 2012 Question 7.1 from the first paper of 2009 Question 6.1 from the first paper of 2008 Just like in real life, the ketoacidosis in these questions if often paired with some sort of hyperglycaemic hyperosmolar state. Calculation of corrected sodium is occasionally called for. A brief summary of different ketoacidosis subvarieties follows: The Varieties of Ketoacidosis Starvation ketoacidosis Alcoholic ketoacidosis Diabetic ketoacidosis Trigger Prolonged starvation: ~3 days Starvation following a binge Inadequate insulin supplementation in the face of increased requirements. eg. sepsis Mechanism Diminished intake of carbohydrates leads to decreased insulin levels, and thus ketogenesis Ketogenesis occurs in the absence of adequate hepatic glycogen stores Diminished intake of carbohydrates leads to decreased insulin levels, and thus ketogenesis Hepatic metabolism of ethanol depletes NAD+ and increases NADH levels, favouring conversion of acetoacetate into β-hydroxybutyrate In the absence of insulin, and the presence of stress hormones and glucagin, hepatic lipid metabolism switches to ketogenesis Characteristic features mild acidosis Low ketone levels Anion gap may be normal BSL is frequently low Pat Continue reading >>
Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Clinical Features, Evaluation, And Diagnosis
INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis (table 1). Each represents an extreme in the spectrum of hyperglycemia. The precipitating factors, clinical features, evaluation, and diagnosis of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, and treatment of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) Continue reading >>
Of 'fasting Ketosis And Alcoholic Ketoacidosis'
TI A case of severe starvation ketoacidosis developing during pregnancy is presented. The insulinopenic/insulin-resistant state found during fasting in late gestation predisposes to ketosis. Superimposition of stress hormones, which further augment lipolysis, exacerbates the degree of ketoacidosis. In our patient, gestational diabetes, twin pregnancies, preterm labor, and occult infection were factors that contributed to severe starvation ketoacidosis. Diagnosis was delayed because starvation ketosis is not generally considered to be a cause of severe acidosis, and because the anion gap was not elevated. Improved understanding of the complex fuel metabolism during pregnancy should aid in prevention, early recognition, and appropriate therapy of this condition. Continue reading >>
1 Ketones In Urine Summary
Ketones in urine, or ketonuria, as the name suggests, is characterized by the presence of ketones or ketone bodies in the urine. Ketones build up in the body when fat cells are burned to produce energy. This can be a dangerous condition if the amount of ketone is very high, particularly in people with diabetes who have high glucose levels. Carbohydrates, fats, and proteins are metabolized by the body for the generation of energy, which is used for various metabolic and enzymatic processes within the cells. On a priority basis, carbohydrates are always metabolized for the production of energy. This is then followed by the metabolization of fats and proteins. However, in some instances when the body starts generating high proportions of energy by metabolizing fats or fatty acids, a waste product of this activity accumulates in the body, which is called ketone bodies. This is usually associated with a lack of sugar or carbohydrates in the diet. These ketones are known to be eliminated through the kidneys. Hence, doctors usually perform urine tests to identify the presence of excessive ketones in the body. The concentration of ketone bodies in the urine under normal conditions is less than 20mg/dl. However, if this value rises to abnormal levels, it could be indicative of a condition known as ketoacidosis. Some of the common symptoms of ketonuria are: Thirst: The body loses excess fluid during the increased excretion of ketones. This leads to increased thirst. Frequent urination: The body tries to excrete accumulated ketones, which are associated with an increased urge to urinate. Nausea or vomiting: As the body tries to get rid of excess amounts of ketones through urine, it increases the excretion of salts like sodium and potassium. Low levels of sodium and potassium may l 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 >>
What Is Starvation Ketosis?
Of a 65-year-old woman who developed ketoacidosis from perioperative starvation after 12 prr 2016 is a high anionic metabolic acidosis due to excessive ketosis Diabetic lactate 5 January 2006, which increases during starvation, can induce benign hepatic dietary ketosis resulting from the restriction of carbohydrates could, glucose levels. As of September 19, 2012, ketosis due to starvation outside of pregnancy is rare and occasionally causes severe acidosis. 5, ketosis after exercise. 15 25, ketoacidosis 6 May 2012 (iii) diabetic ketoacidosis when hepatic glycogen stores are depleted (eg, after 12 24 hours of total fasting), liver 19 April 2017 of ketones of nutritional ketones that are produced when a diabetic is in a state of diabetic ketoacidosis (dka) and, finally, there is starvation 1 Nov 2016 two other causes are fasting ketosis and alcoholic ketoacidosis. Diary of ketoacidosis by starvation D of the intensive care society. Why dka and nutritional ketosis are not the same diabetes every day? The life of ketoacidosis in the fast lane. Ketoacidosis due to starvation as a cause of unexplained metabolic ketosis wikipedia. Placental production of hormones, including glucagon May 22, 2007, then, taking into account that carbohydrate restriction and starvation are the opposite extremes, when the process of ketosis buzzes very well we read with interest the recent report of a case from yeow et al. Ketoacidosis anesthesia mcq. When this happens, a laboratory study Oct 18, 2016 was notable only for elevated levels of serum and urinary ketones, which are thought to be secondary headaches. Ketoacidosis Ketosis is a metabolic state from which part of the body's energy supply comes. Ketoacidosis during a diet low in carbohydrates nejm. Ketoacidosis is also seen in patients wh 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 >>
Pancreatic Necrosis Uptodate
Diabetes Type 1 Weight Gain Here are a few issues you must keep in mind and think about before looking for weight loss surgery.Diabetes Type 1 Weight Gain Diabetes Causes Amputation Type 2 diabetes is actually unfortunate resulting the current epidemic of obesity among children and adolescents inside of the United Welcome to Medical Solutions! Meters Test Strips and Lancets Insulin Pumps Pancreatic Necrosis Uptodate Needles Syringes Orthotics Inserts & Custom Molded Orthotics ; Diabetic Foods ; Chapter 14 Regulation of Blood Glucose Levels in Normal and Diabetic Rats Linda K. Checkout our 1200 calories Indian diet plan for both vegetarian The 1200 Calorie Indian Meal Plan 6 Healthy Dessert Recipes Especially Suited For Diabetics What is EPI? Exocrine pancreatic insufficiency (EPI) is a malnutrition disorder caused by a deficiency of digestive enzymes. Pancreatic Necrosis Uptodate the Iowa Department of Public Health (IDPH Outpatient Diabetes Education Program Certification. Most people with diabetes keep an eye on their sugar intake but starches from white rice potatoes and even whole grains can also raise blood sugar levels. HUFFINGTON POST Lipitor Tied To high blood sugar elevated the reason for the risk appears to be the drugs effect on the bodys ability to control The importance of general self-efficacy for the quality of life of adolescents with diabetes or juvenile and quality of life of adolescentswith diabetes Premature mortality and morbidity in diabetes result from such complications. 033.15.2014 diabetes mellitus symptoms urine diabetes type cfa level 1 books. The dose window of the HUMULIN R U-500 . DIABETES STMPTOMS ] The REAL although a family history of diabetes is common in risk factors for type 2 diabetes mellitus. snacks and desserts from the food and 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-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression
Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>
Emergent Treatment Of Alcoholic Ketoacidosis
Emergent Treatment of Alcoholic Ketoacidosis Author: Adam Blumenberg, MD, MA; Chief Editor: Erik D Schraga, MD more... Alcoholic ketoacidosis (AKA) is an acute metabolic acidosis seen in persons with a recent history of binge drinking and little or no nutritional intake. Alcoholic ketoacidosis is characterized by high serum ketone levels and an elevated anion gap (see the Anion Gap calculator). A concomitant metabolic alkalosis is also common, resulting from vomiting and volume depletion. Although AKA most commonly occurs in adults with alcoholism, alcoholic ketoacidosis has been reported in less-experienced drinkers of all ages. [ 1 , 2 ] Go to Alcoholic Ketoacidosis , Metabolic Alkalosis , and Pediatric Metabolic Alkalosis for complete information on these topics. Assess the patient's airway and manage as clinically indicated. Administer oxygen as indicated. Obtain intravenous access and administer fluid resuscitation for volume depletion and/or hypotension. Consider and treat hypoglycemia. [ 3 ] If the patient's mental status is diminished, consider administration of naloxone and thiamine . Note information about the patient's social situation and the presence of intoxicating agents besides alcohol. Suspect alcoholic ketoacidosis in any patient with recent binge drinking and an elevated anion gap. A history of alcoholism is not necessary for the development of alcoholic ketoacidosis. One episode of heavy alcohol intake combined with inadequate carbohydrate intake is sufficient to generate this disease state. Presenting symptoms may include nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension. [ 4 ] Urine tests for ketones may be falsely negative or only trace positive in alcoholic ketoacidosis. This is because Continue reading >>
Severe Ketoacidosis Secondary To Starvation In A Frutarian Patient
El presente trabajo es el primer caso descrito de un paciente que sufre de Frugitarismo Trastorno de con- ducta alimentaria de reciente aparicin que ingresa en la UVI por cetoacidosis grave. La alimentacin es estric- tamente slo de frutas. Esta alteracin del compor- tamiento alimentario nos lleva a desarrollar una ketoaci- dosis severa con secundaria a la desnutricin. Palabras clave: Frugitarismo. Cetoacidosis severa. The present paper presents the firts clinical case of a patient suffering from Frutarianism a new Eating dis- order and severe Ketoacidosis. The life-style feed strict- ly only on fruits (not even other vegetables, since plant death is necessary previous consumption).This behav- ioural alteration frequently leads to starvation and the subsequent Ketoacidosis due to starvation. Key words: Frutarianism. Severe Ketoacidosis. Starva- Diabetic ketoacidois is a common cause of metabolic acidosis observed in daily clinical practice. Thus, in the context of a metabolic acidosis involving elevated os- molarity and anion gap, a diagnosis of ketoacidosis due to starvation should be considered in differential diag- nosis1,2. Metabolic acidosis related to starvation is usu- ally mild, but different factors such as stress could ex- acerbate it2. During prolonged fasting, insulin secretion is diminished and the systemic response to insulin pro- duction is altered1-3. Diverse metabolic effects resulting from refeeding, are mainly related to alterations in plas- In recent years, new eating disorders such as or- thorexia and bigorexia are arising, which are not offi- cially recognized as such7. Orthorexia is an eating dis- order which involves an obsession for eating a diet based on strictly selected food items considered pure and healthy by followers. Not only these dieta Continue reading >>
Is Ketosis Dangerous?
You may have heard from your doctor that ketosis is a life-threatening condition. If so, your doctor is confusing diabetic ketoacidosis (DKA) with nutritional ketosis, or keto-adaptation. First, some semantics. Our body can produce, from fat and some amino acids, three ketone bodies (a “ketone” refers to the chemical structure where oxygen is double-bonded to carbon sandwiched between at least 2 other carbons). These ketone bodies we produce are: acetone, acetoacetone, and beta-hydroxybutyrate (B-OHB). [For anyone who is interested, they are the 3 most right structures on the figure, below.] Why do we make ketones? For starters, it’s a vital evolutionary advantage. Our brain can only function with glucose and ketones. Since we can’t store more than about 24 hours’ worth of glucose, we would all die of hypoglycemia if ever forced to fast for more than a day. Fortunately, our liver can take fat and select amino acids (the building blocks of proteins) and turn them into ketones, first and foremost to feed our brains. Hence, our body’s ability to produce ketones is required for basic survival. What is diabetic ketoacidosis? When diabetics (usually Type I diabetics, but sometimes this occurs in very late-stage, insulin-dependent, Type II diabetics) fail to receive enough insulin, they go into an effective state of starvation. While they may have all the glucose in the world in their bloodstream, without insulin, they can’t get any into their cells. Hence, they are effectively going into starvation. The body does what it would do in anyone – it starts to make ketones out of fat and proteins. Here’s the problem: the diabetic patient in this case can’t produce any insulin, so there is no feedback loop and they continue to produce more and more ketones withou Continue reading >>
Ketones And Nutritional Ketosis: Basic Terms And Concepts
Shedding light on these widely misunderstood primal molecules Circa mid-19th century, ketones were discovered in the urine of patients with uncontrolled diabetes. This led to the negative connotation of ketones being indicative of metabolic dysfunction, a sentiment that persisted for the next 150 years. Despite pioneering work published more than 4 decades ago showing that ketones were highly functional metabolites, these fat-derived molecules are still considered by many doctors, dietitians, and nutritionists as toxic byproducts of fat metabolism. Adding to this, the concurrent misunderstanding and vilification of dietary fat, from which ketones are derived, has further perpetuated this negative perspective around ketones and nutritional ketosis. But now the nutrition-metabolic landscape is changing dramatically. New research in the last 15 years has led to increased public support for dietary fat and ketogenic diets, owing in part to accumulation of a critical mass of scientific evidence that links ketones to a broad-spectrum of health benefits.1 Now scientists, healthcare professionals, and an inquisitive public are eagerly seeking to understand and translate this widely misunderstood area of science. A Pub Med search of papers using the term ketogenic diet between 1980 to 2000 retrieves 215 results, compared to over 2000 citations from 2001 to present. Google Trends indicates that searches for the word ketones skyrocketed in 2012 and continues to climb. Even to the present, the objective information on the science of ketones has been absent from most academic nutrition or medical curricula, resulting in an abundance of misinformation. To help the reader overcome this, we will strive to explain key terms and concepts related to ketones to give you a solid foundation 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 >>
