diabetestalk.net

How To Induce Ketoacidosis

How Does Diabetic Ketoacidosis Cause Vomiting?

How Does Diabetic Ketoacidosis Cause Vomiting?

DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body’s cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can’t get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn’t available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body’s metabolic processes aren’t able to function as well. A higher level of ketones also affects levels of sugar and electrolytes in the body. As ketones accumulate in the blood, more ketones will be passed in the urine, taking sodium and potassium salts out with them. Over time, levels of sodium and potassium salts in the body become depleted, which can cause nausea and vomiting. The result is a vicious cycle. The most important prevention strategies are to monitor blood glucose levels routinely, keep blood glucose levels controlled (e.g., Continue reading >>

Do Sglt2 Inhibitors Like Invokana Cause Ketoacidosis?

Do Sglt2 Inhibitors Like Invokana Cause Ketoacidosis?

In an announcement released May 15, the FDA called attention to 20 case reports it had received between March 2013 and June 6, 2014 of 20 persons, most with type 2 diabetes, who had been treated with Sodium-glucose Cotransporter-2 (SGLT2) Inhibitors such as canagliflozin (Invokana), dapagliflozin (Farxiga, Forxiga), and empagliflozin (Jardiance), for an average of 2 weeks, but in some for as much as six months and who had diabetic ketoacidosis. Diabetic ketoacidosis is typically a condition of uncontrolled diabetes seen in type 1 diabetes, or in adolescents with severe type 2 diabetes, with elevated blood glucose and evidence of ketoacidosis with elevated blood or urine ketones and acidosis with a high blood “anion gap,” reflecting the presence of substances called organic anions in the bloodstream. Another unusual feature noted in the FDA release was that blood glucose levels were typically only mildly elevated, below 200 mg/dl. What is ketoacidosis? The body uses insulin not only to move glucose into cells, but also as a signal to increase fat and protein synthesis in fat cells and other body tissues. When a persons who does not have diabetes goes a long period without eating, ketones act as an important source of energy. Their insulin concentrations in blood fall, acting as a negative signal to cause the body to break down fat into fatty acids and protein into amino acids. A subsequent step, also signaled by low levels of insulin, is the further breakdown of fatty acids and the removal of amino groups from certain amino acids to form ketone bodies, particularly an organic acid called beta-hydroxy butyrate, as well as acetoacetic acid, which is less important in ketoacidosis but which is measured in urine ketone test strips. For a diabetic person who has true insu Continue reading >>

Complete Resolution Of Olanzapine-induced Diabetic Ketoacidosis

Complete Resolution Of Olanzapine-induced Diabetic Ketoacidosis

We report the case of a nondiabetic man who developed diabetic ketoacidosis associated with high-dose olanzapine. Olanzapine has been associated with diabetic ketoacidosis and also with weight gain, lipid abnormalities, and the development of type 2 diabetes. This case is of interest both because of the sudden onset and because the patient's blood glucose stabilized 1 month after discontinuation of olanzapine, thus allowing insulin therapy to be discontinued. The patient has now been stabilized on ziprasidone with no further abnormalities in blood glucose. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci Continue reading >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

Diabetic ketoacidosis is a serious metabolic complication of diabetes with high mortality if undetected. Its occurrence in pregnancy compromises both the fetus and the mother profoundly. Although predictably more common in patients with type 1 diabetes, it has been recognised in those with type 2 diabetes as well as gestational diabetes, especially with the use of corticosteroids for fetal lung maturity and β2-agonists for tocolysis.1–3 Diabetic ketoacidosis usually occurs in the second and third trimesters because of increased insulin resistance, and is also seen in newly presenting type 1 diabetes patients. With increasing practice of antepartum diabetes screening and the availability of early and frequent prenatal care/surveillance, the incidence and outcomes of diabetic ketoacidosis in pregnancy have vastly improved. However, it still remains a major clinical problem in pregnancy since it tends to occur at lower blood glucose levels and more rapidly than in non-pregnant patients often causing delay in the diagnosis. The purpose of this article is to illustrate a typical patient who may present with diabetic ketoacidosis in pregnancy and review the literature on this relatively uncommon condition and provide an insight into the pathophysiology and management. MAGNITUDE OF THE PROBLEM In non-pregnant patients with type 1 diabetes, the incidence of diabetic ketoacidosis is about 1–5 episodes per 100 per year with mortality averaging 5%–10%.4 The incidence rates of diabetic ketoacidosis in pregnancy and the corresponding fetal mortality rates from different retrospective studies5–8 are summarised in the table 1. As is evident from the table, both the incidence and rates of fetal loss in pregnancies have fallen in recent times compared with those before. In 1963 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 >>

Diabetic Ketoacidosis Inducing Myocardial Infarction Secondary To Treatment With Dapagliflozin: A Case Report

Diabetic Ketoacidosis Inducing Myocardial Infarction Secondary To Treatment With Dapagliflozin: A Case Report

Go to: Case Report A 58‐year‐old male with dyslipidemia, an eight‐year history of T2DM, a family history, his mother, of T2DM, with no known micro‐ or macrovascular complications, was admitted to the emergency department for malaise, epigastric pain, polyuria, and progressive dyspnea which had begun 10 h ago. He had experienced a 2‐kg weight loss over the last few days. His usual medications included aspirin 100 mg q24 h, atorvastatin 40 mg q24 h, and metformin 850 mg q8 h, which had been switched to dapagliflozin 20 days before, due to poor glycemic control, with HbA1c 12% (108 mmol/mol). His vital signs included a heart rate of 122 bpm, respiratory rate 33 rpm, blood pressure 142/70 mmHg, temperature 36.1°C, and body mass index 22.5 kg/m2. On physical examination, somnolence, dry skin and mucous membranes, a Kussmaul breathing pattern, and a capillary refill of 3 sec were observed. Blood tests revealed hemoglobin 17.1 g/dL (13.5–18), leukocytes 19.5 × 103 (4–10 × 103), platelets 296 × 103 (150–450 × 103), glucose 248 mg/dL (60–100), creatinine 0.97 mg/dL (0.67–1.17), sodium 136 mmol/L (135–145), potassium 4.7 mmol/L (3.5–5.5), chloride 101 mmol/L (95–112), phosphate 4.9 mg/dL (2.5–4.5), amylase 70 U/L (10–115), lipase 28 U/L (1–67), pH 6.95 (7.35–7.45), pCO2 23 mmHg (35–45), HCO3 5 mmol/L (22–26), lactate 1.8 mmol/L (0–1.5), urine ketone bodies >150 mg/dL (0–0), CK 112 U/L (1–190), CK‐MB 7.3 ng/mL (0.1–5), and troponin I 0.07 ng/mL (0.001–0.05). The electrocardiogram (EKG) showed sinus rhythm with right bundle branch block, and nonspecific repolarization abnormalities. Because of the right bundle branch block was not previously known, a new troponin test was performed six hours later with a peak value of 4.28 ng/m Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

Pancreatic Ketoacidosis (kabadi Syndrome): Ketoacidosis Induced By High Circulating Lipase In Acute Pancreatitis

Pancreatic Ketoacidosis (kabadi Syndrome): Ketoacidosis Induced By High Circulating Lipase In Acute Pancreatitis

Broadlawns Medical Center, Des Moines University, Des Moines, Iowa and University of Iowa, Iowa City, Iowa, USA. *Corresponding Author: 17185, Berkshire Parkway Clive, Iowa, 50325, USA Phone +5152823041 E-mail [email protected] Visit for more related articles at JOP. Journal of the Pancreas Abstract Introduction Ketoacidosis is well established as a metabolic complication of both type 1 and type 2 diabetes Mellitus (Diabetic Ketoacidosis). It is often an initial presentation of type 1 diabetes in children and adolescents and occasionally in adults. Alternatively, it is induced of an onset of an acute disorder, e. g, sepsis, myocardial infarction, stroke, pregnancy etc. in subjects with type 1 and 2 diabetes. Ketoacidosis is also known to occur following an ethanol binge (Alcoholic Ketoacidosis). Finally, ketonemia with a rare progression to Ketoacidosis is documented to ensue following prolonged starvation. Methods The review of English literature for over 35 years from 01/1980 till 12/2015 for terms, 'ketonemia, ketonuria and ketoacidosis' 'pancreatic lipase' and 'acute pancreatitis'. Results 1) Description of individual patients presented as case reports, 2) Documentation of a series of consecutive subjects hospitalized for management of acute pancreatitis with special attention to establishing the prevalence of the disorder as well as examining the relationship between the severity of the disorder and occurrence of Ketoacidosis, 3) Studies demonstrating the relationship between progressively rising circulating pancreatic lipase concentrations with ketonuria, ketonemia and Ketoacidosis in subjects presenting with acute pancreatitis irrespective of the etiology and documenting resolution of ketonuria, ketonemia and ketoacidosis following the declining serum lipase leve Continue reading >>

Steroid Induced Diabetic Ketoacidosis (dka) In A 13 Year Old Female With Renal Disorder

Steroid Induced Diabetic Ketoacidosis (dka) In A 13 Year Old Female With Renal Disorder

1Department of Paediatrics and Child Health, Faculty of Clinical Sciences, College of Health Sciences, University of Port Harcourt, Nigeria 2University of Port Harcourt Teaching Hospital, Nigeria *Corresponding Author: Department of Paediatrics University of Port Harcourt Teaching Hospital Port Harcourt, Rivers State, Nigeria E-mail: [email protected] Citation: Jaja T, Anochie IC, Eke FU (2012) Steroid Induced Diabetic Ketoacidosis (DKA) in a 13 year Old Female with Renal Disorder. Pediatr Therapeut 2:109. doi:10.4172/2161-0665.1000109 Copyright: © 2012 Jaja T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Pediatrics & Therapeutics Abstract Background: Diabetic ketoacidosis (DKA) is a common complication of poorly controlled diabetes mellitus in children and a rare complication of steroid therapy. Patients on steroid therapy may develop hyperglycemia as a complication, but presentation with DKA is rather unusual. Aim: To highlight a rare clinical entity of DKA induced by prednisolone in a 13 year old female on treatment for nephrotic syndrome. Case report: NC was a 13 year old female who presented with first episode of generalized body swelling, oliguria, massive proteinuria and hypercholesterolenaemia with normal renal function. She was not a known diabetic and had no family history of diabetes mellitus. She was started on prednisolone at 20 mg three times daily for nephrotic syndrome. Two weeks after commencement of prednisolone, she developed DKA with blood glucose of 31.1 mmol/l, glycosuria and ketonuria. She received intravenous in Continue reading >>

Ketoacidosis In Diabetic Pregnancy

Ketoacidosis In Diabetic Pregnancy

Diabetic ketoacidosis (DKA) is a serious medical and obstetrical emergency previously considered typical of type 1 diabetes but now reported also in type 2 and GDM patients. Although it is a fairly rare condition, DKA in pregnancy can compromise both fetus and mother. Metabolic changes occurring during pregnancy predispose to DKA in fact it can develop even in setting of normoglycemia. This article will provide the reader with information regarding the pathophysiology underlying DKA, in particular euglycemic DKA, and will provide information regarding all possible effects of ketones on the fetus. Continue reading >>

What Is The Difference Between Ketogenic Diet And Starvation?

What Is The Difference Between Ketogenic Diet And Starvation?

I really must track down how the unscientific drivel that the ketogenic diet is some sort of a starvation response got started. The only link between starvation and the ketogenic diet is the production of ketones in the body. I know certain Quora gurus posit such crap repeatedly but it’s not true. Ketones as a natural process in the body The body produces ketones naturally. It’s likely a protective mechanism due to the evolutionary instability of the food supply. Most of the time ketone levels are quite low. However, anytime the food supply gets interrupted, even short times like at night during sleep, the body starts to produce ketones. Ketones and fat metabolism Ketones are made in the liver from fat. One of the reasons people measure ketone levels in the body is that they are a marker for increased fat utilization in the body. There are two fuel partitioning schemes in the human body. The body can utilize glucose and glycogen or the body can utilize fats (dietary and body) and ketones. There are some overlaps in the utilization of these schemes but when foods that are easily broken down into glucose are withdrawn the body will start to burn fats and ketones as sources of energy. Ketones and starvation The similarity between starvation and the ketogenic diet is that both involve higher levels of circulating ketones in the body. This makes sense since in both situations foods that are easily broken down into glucose have been withdrawn. In both situations, levels of blood glucose and glycogen stores are lower and the body must fuel with other substances. Some tissues in the body are perfectly happy (and in many ways) prefer utilizing fats as fuels. However, some tissues need levels of glucose. These tissues when faced with lower glucose intake in the diet must rely Continue reading >>

Ketosis: Fear, Uncertainty And Doubt

Ketosis: Fear, Uncertainty And Doubt

Perhaps nothing is more damaging to the new low-carber than the intentional spread of fear, uncertainty and doubt regarding the state of ketosis compared to the dangerous state of ketoacidosis. The former is a natural and healthy state of existence, the latter is a condition that threatens the life of type 1 diabetics and type 2 diabetics whose disease has progressed to the point where their pancreatic beta cells can no longer produce insulin (ketoacidosis is also a risk for alcoholics). So if you’re not an alcoholic, a type 1 diabetic or a late-stage type 2 diabetic, fear of ketosis is misdirected. You should regard with suspicion anyone who confuses the two and warns you against a low-carb diet because they cannot tell the difference. The confusion between ketosis and ketoacidosis is a sign of a grave misunderstanding of basic biology (if not a complete lack of critical faculty). So too is the assumption that ketosis is the “early stage” of ketoacidosis or that “ketosis leads to ketoacidosis” in a person whose pancreas is still able to produce insulin. If you don’t trust me (and why should you), you should consider listening to some people who know a lot more about this than either you or I ever will: Nutritional ketosis is by definition a benign metabolic state… by contrast, ‘diabetic ketoacidosis’ is an unstable and dangerous condition that occurs when there is inadequate pancreatic insulin response to regulate serum B-OHB. This occurs only in type-1 diabetics or in late stage type-2 diabetics with advanced pancreatic burnout. (Dr. Phinney & Dr. Volek, The Art and Science of Low Carbohydrate Living, p.4) Later in the book (p.80), Phinney and Volek explain further: [Type-1 diabetics] need insulin injections not just to control blood glucose levels, Continue reading >>

Ketoacidosis

Ketoacidosis

Ketoacidosis is a metabolic state associated with high concentrations of ketone bodies, formed by the breakdown of fatty acids and the deamination of amino acids. The two common ketones produced in humans are acetoacetic acid and β-hydroxybutyrate. Ketoacidosis is a pathological metabolic state marked by extreme and uncontrolled ketosis. In ketoacidosis, the body fails to adequately regulate ketone production causing such a severe accumulation of keto acids that the pH of the blood is substantially decreased. In extreme cases ketoacidosis can be fatal.[1] Ketoacidosis is most common in untreated type 1 diabetes mellitus, when the liver breaks down fat and proteins in response to a perceived need for respiratory substrate. Prolonged alcoholism may lead to alcoholic ketoacidosis. Ketoacidosis can be smelled on a person's breath. This is due to acetone, a direct by-product of the spontaneous decomposition of acetoacetic acid. It is often described as smelling like fruit or nail polish remover.[2] Ketosis may also give off an odor, but the odor is usually more subtle due to lower concentrations of acetone. Treatment consists most simply of correcting blood sugar and insulin levels, which will halt ketone production. If the severity of the case warrants more aggressive measures, intravenous sodium bicarbonate infusion can be given to raise blood pH back to an acceptable range. However, serious caution must be exercised with IV sodium bicarbonate to avoid the risk of equally life-threatening hypernatremia. Cause[edit] Three common causes of ketoacidosis are alcohol, starvation, and diabetes, resulting in alcoholic ketoacidosis, starvation ketoacidosis, and diabetic ketoacidosis respectively.[3] In diabetic ketoacidosis, a high concentration of ketone bodies is usually accomp 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 >>

More in ketosis