diabetestalk.net

Starvation Ketoacidosis Pdf

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 >>

Severe Ketoacidosis Secondary To Starvation In A Frutarian Patient

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 >>

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

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

Abstract 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. Discover the world's research 14+ million members 100+ million publications 700k+ research projects Join for free Starvation Ketoacidosis: A Cause of Severe Anion Gap Metabolic Nupur Sinha, Sindhaghatta Venkatram, and Gilda Diaz-Fuentes Division of Pulmonary and Critical Care Medicine, Bronx Lebanon Hospital Center and Albert Einstein College of Medicine, Correspondence should be addressed to Nupur Sinha; [email protected] Received  February ; Revised  May ; Accepted  May ; Published Continue reading >>

Ketoacidosis Versus Ketosis

Ketoacidosis Versus Ketosis

Some medical professionals confuse ketoacidosis, an extremely abnormal form of ketosis, with the normal benign ketosis associated with ketogenic diets and fasting states in the body. They will then tell you that ketosis is dangerous. Testing Laboratory Microbiology - Air Quality - Mold Asbestos - Environmental - Lead emsl.com Ketosis is NOT Ketoacidosis The difference between the two conditions is a matter of volume and flow rate*: Benign nutritional ketosis is a controlled, insulin regulated process which results in a mild release of fatty acids and ketone body production in response to either a fast from food, or a reduction in carbohydrate intake. Ketoacidosis is driven by a lack of insulin in the body. Without insulin, blood sugar rises to high levels and stored fat streams from fat cells. This excess amount of fat metabolism results in the production of abnormal quantities of ketones. The combination of high blood sugar and high ketone levels can upset the normal acid/base balance in the blood and become dangerous. In order to reach a state of ketoacidosis, insulin levels must be so low that the regulation of blood sugar and fatty acid flow is impaired. *See this reference paper. Here's a table of the actual numbers to show the differences in magnitude: Body Condition Quantity of Ketones Being Produced After a meal: 0.1 mmol/L Overnight Fast: 0.3 mmol/L Ketogenic Diet (Nutritional ketosis): 1-8 mmol/L >20 Days Fasting: 10 mmol/L Uncontrolled Diabetes (Ketoacidosis): >20 mmol/L Here's a more detailed explanation: Fact 1: Every human body maintains the blood and cellular fluids within a very narrow range between being too acidic (low pH) and too basic (high pH). If the blood pH gets out of the normal range, either too low or too high, big problems happen. Fact 2: The Continue reading >>

Hyperuricemia In Diabetic Ketoacidosis

Hyperuricemia In Diabetic Ketoacidosis

This article has no abstract; the first 100 words appear below. THERE is considerable clinical1 2 3 4 5 6 7 and biochemical8 , 9 evidence suggesting but not firmly establishing a relation of uric acid with carbohydrate and lipid metabolism. Uric acid resembles alloxan in its chemical configuration, and there have been preliminary observations provoking the concept of "uric acid diabetes."8 , 9 Although the diabetogenic effects of uric acid have not been proved to exist in man there is at least some statistical evidence of a high incidence of diabetes with hyperuricemia or gout or both.3 , 7 Other observations include the influence of insulin on precipitating acute gout,10 the coincidence of hypercholesterolemia,3 hyperuricemia and hyperglycemia11 and the effects of starvation, . . . †Assistant professor of medicine, Hahnemann Medical College and Hospital. Continue reading >>

Post-bariatric Surgery Starvation Ketoacidosis And Lipase Elevation In The Absence Of Dka Or Pancreatitis

Post-bariatric Surgery Starvation Ketoacidosis And Lipase Elevation In The Absence Of Dka Or Pancreatitis

Abstract We report a case of post bariatric surgery by laparoscopic sleeve gastrectomy who presented with post-surgical poor oral tolerance and high anion gap metabolic ketoacidosis, who was initially misdiagnosed with diabetic ketoacidosis and treated with volume supplementation without improvement. The metabolic derangements were found to be caused by starvation ketoacidosis, which was then treated with glucose supplementation, and the anion gap quickly closed. Moreover, this patient also presented with non-pancreatitis lipase elevation. This case highlights the recognition and management of post-bariatric surgery starvation ketoacidosis; additionally, clinicians should be vigilant about the interpretation and management of elevated lipase without clinical pancreatitis. To access this article, please choose from the options below Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Chapter 220. Diabetic Ketoacidosis

Chapter 220. Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. The incidence and prevalence of diabetes are rising; as of 2005, an estimated 7% of the U.S. population had diabetes. In patients age 60 or older, the prevalence is estimated to be 20.9%.1 DKA occurs predominately in patients with type 1 (insulin-dependent) diabetes mellitus, but unprovoked DKA can occur in newly diagnosed type 2 (non–insulin-dependent) diabetes mellitus, especially in blacks and Hispanics.2 Between 1993 and 2003, the yearly rate of ED visits for DKA per 10,000 U.S. population with diabetes was 64, with a trend toward an increased rate of visits among the black population compared with the white population.3 Europe has a comparable incidence. A better understanding of pathophysiology and an aggressive, uniform approach to diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers.4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (Figure 220-1). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion gap metabolic acidosis.4 Insulin deficiency. Patho Continue reading >>

Serum Ketones Test: What Does It Mean?

Serum Ketones Test: What Does It Mean?

What is a serum ketones test? A serum ketones test determines the levels of ketones in your blood. Ketones are a byproduct produced when your body uses only fat, instead of glucose, for energy. Ketones aren’t harmful in small amounts. When ketones accumulate in the blood, the body enters ketosis. For some people, ketosis is normal. Low-carbohydrate diets can induce this state. This is sometimes called nutritional ketosis. If you have type 1 diabetes, you may be at risk for diabetic ketoacidosis (DKA), which is a life-threatening complication in which your blood becomes too acidic. It can lead to a diabetic coma or death. Contact your doctor immediately if you have diabetes and have a moderate or high reading for ketones. Some newer blood glucose meters will test blood ketone levels. Otherwise, you can use urine ketone strips to measure your urine ketone level. DKA can develop within 24 hours and can lead to life-threatening conditions if left untreated. Although it’s rare, people with type 2 diabetes do develop DKA, according to Diabetes Forecast. Some people may also have alcoholic ketoacidosis from long-term alcohol abuse or starvation ketoacidosis from fasting too long. Call your doctor immediately if your blood sugar levels are high, your ketone levels are moderate or high, or if you’re feeling: pain in the abdomen nauseated or you’re vomiting for over 4 hours sick with a cold or the flu excessive thirst and symptoms of dehydration flushed, especially on your skin shortness of breath, or breathing rapidly You may also have a fruity or metallic scent on your breath, and a blood sugar level more than 240 milligrams per deciliter (mg/dL). All of these symptoms can be warning symptoms of DKA, especially if you have type 1 diabetes. The only complications that co Continue reading >>

Starvation Ketoacidosis In Pregnancy

Starvation Ketoacidosis In Pregnancy

Abstract Starvation ketosis outside pregnancy is rare and infrequently causes a severe acidosis. Placental production of hormones, including glucagon and human placental lactogen, leads to the insulin resistance that is seen in pregnancy, which in turn increases 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 is likely to have important implications for fetal survival as ketoacidosis in women with type 1 diabetes mellitus is associated with intrauterine death. This article features four cases of women with vomiting in the third trimester of pregnancy associated with a severe metabolic acidosis. The mechanism underlying ketogenesis, the evidence for accelerated ketogenesis in pregnancy and other similar published cases are reviewed. A proposed strategy for management of these women is presented. Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

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 >>

Euglycemic Diabetic Ketoacidosis: A Review

Euglycemic Diabetic Ketoacidosis: A Review

Euglycemic Diabetic Ketoacidosis: A Review Author(s): Anar Modi , Department of Endocrinology, Diabetes & Metabolism, Cooper University Hospital, Camden, New Jersey, United States Abhinav Agrawal* , Department of Medicine, Monmouth Medical Center, 300 Second Avenue, Long Branch, New Jersey, United States Farah Morgan . Department of Endocrinology, Diabetes & Metabolism, Cooper University Hospital, Camden, New Jersey, United States Introduction: Diabetic ketoacidosis (DKA) is one of the most serious complications of diabetes.It is characterised by the triad of hyperglycemia (blood sugar >250 mg/dl), metabolic acidosis(arterial pH <7.3 and serum bicarbonate <18 mEq/L) and ketosis. Rarely these patients can present withblood glucose (BG) levels of less than 200 mg/dl, which is defined as euglycemic DKA. The possibleetiology of euglycemic DKA includes the recent use of insulin, decreased caloric intake, heavy alcoholconsumption, chronic liver disease and glycogen storage disorders. DKA in pregnancy has also beenreported to present with euglycemia. The recent use of sodium glucose cotransporter 2 (SGLT2) inhibitorshas shed light on another possible mechanism of euglycemic DKA. Clinicians may also be misledby the presence of pseudonormoglycemia. Conclusion: Euglycemic DKA thus poses a challenge to physicians, as patients presenting with normalBG levels in ketoacidosis may be overlooked, leading to a delay in appropriate management strategies.In this article, we review all the possible etiologies and the associated pathophysiology of patients presentingwith euglycemic DKA. We also discuss the approach to diagnosis and management of suchpatients. Despite euglycemia, ketoacidosis in diabetic patients remains a medical emergency and mustbe treated in a quick and appropriate mann Continue reading >>

Jci -liver And Kidney Metabolism During Prolonged Starvation

Jci -liver And Kidney Metabolism During Prolonged Starvation

Liver and kidney metabolism during prolonged starvation Elliott P. Joslin Research Laboratory, Boston, Massachusetts 02215 Cardiovascular Unit, the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115 Cardiovascular Unit, Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115 Peter Bent Brigham Hospital, Boston, Massachusetts 02115 Joslin Diabetes Foundation, Inc., Boston, Massachusetts 02215 Find articles by Owen, O. in: JCI | PubMed | Google Scholar Elliott P. Joslin Research Laboratory, Boston, Massachusetts 02215 Cardiovascular Unit, the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115 Cardiovascular Unit, Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115 Peter Bent Brigham Hospital, Boston, Massachusetts 02115 Joslin Diabetes Foundation, Inc., Boston, Massachusetts 02215 Find articles by Felig, P. in: JCI | PubMed | Google Scholar Elliott P. Joslin Research Laboratory, Boston, Massachusetts 02215 Cardiovascular Unit, the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115 Cardiovascular Unit, Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115 Peter Bent Brigham Hospital, Boston, Massachusetts 02115 Joslin Diabetes Foundation, Inc., Boston, Massachusetts 02215 Find articles by Morgan, A. in: JCI | PubMed | Google Scholar Elliott P. Joslin Research Laboratory, Boston, Massachusetts 02215 Cardiovascular Unit, the Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115 Cardiovascular Unit, Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115 Peter Bent Brigham Hospital, Boston, Massachusetts 02115 Joslin Diabetes Foundation, Inc., Boston, Massachusetts 02215 Find articles by Wahren, J. Continue reading >>

Extreme Gestational Starvation Ketoacidosis: Case Report And Review Of Pathophysiology

Extreme Gestational Starvation Ketoacidosis: Case Report And Review Of Pathophysiology

A case of severe starvation ketoacidosis developing during pregnancy is presented. The insulinopenic/insulinresistant 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 >>

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 >>

More in ketosis