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Why Is Dka Metabolic Acidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis

© 1996–2017 themedicalbiochemistrypage.org, LLC | info @ themedicalbiochemistrypage.org Definition of Diabetic Ketoacidosis The most severe and life threatening complication of poorly controlled type 1 diabetes is diabetic ketoacidosis (DKA). DKA is characterized by metabolic acidosis, hyperglycemia and hyperketonemia. Diagnosis of DKA is accomplished by detection of hyperketonemia and metabolic acidosis (as measured by the anion gap) in the presence of hyperglycemia. The anion gap refers to the difference between the concentration of cations other than sodium and the concentration of anions other than chloride and bicarbonate. The anion gap therefore, represents an artificial assessment of the unmeasured ions in plasma. Calculation of the anion gap involves sodium (Na+), chloride (Cl–) and bicarbonate (HCO3–) measurements and it is defined as [Na+ – (Cl– + HCO3–)] where the sodium and chloride concentrations are measured as mEq/L and the bicarbonate concentration is mmol/L. The anion gap will increase when the concentration of plasma K+, Ca2+, or Mg2+ is decreased, when organic ions such as lactate are increased (or foreign anions accumulate), or when the concentration or charge of plasma proteins increases. Normal anion gap is between 8mEq/L and 12mEq/L and a higher number is diagnostic of metabolic acidosis. Rapid and aggressive treatment is necessary as the metabolic acidosis will result in cerebral edema and coma eventually leading to death. The hyperketonemia in DKA is the result of insulin deficiency and unregulated glucagon secretion from α-cells of the pancreas. Circulating glucagon stimulates the adipose tissue to release fatty acids stored in triglycerides. The free fatty acids enter the circulation and are taken up primarily by the liver where Continue reading >>

D-lactate: A Novel Contributor To Metabolic Acidosis And High Anion Gap In Diabetic Ketoacidosis

D-lactate: A Novel Contributor To Metabolic Acidosis And High Anion Gap In Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA),the most common and serious acute complication of diabetes, is characterized by hyperglycemia and severe high–anion-gap metabolic acidosis with ketonemia (1). In DKA, the high anion gap is attributed largely to excessive production of blood ketone bodies, and serum β-hydroxybutyrate quantification is recommended for the diagnosis and monitoring of DKA (2). However, even counting of all the ketone bodies, including β-hydroxybutyrate, does not account for the entire anion gap, suggesting that there are additional sources of anion production in DKA. We recently demonstrated that plasma d-lactate concentrations were greatly increased in DKA compared with the concentrations in diabetic patients or a healthy control group (3). Nevertheless, the clinical value of d-lactate measurement in metabolic acidosis, especially the contribution of d-lactate to the metabolic acidosis and high anion gap in DKA, is not well appreciated. We report here that decreasing d-lactate concentrations are associated with improved clinical situations, whereas increased lactate concentrations are associated with the severity of metabolic acidosis and high anion gap in patients with DKA. The study included 38 diabetic patients with DKA, 42 diabetic patients without DKA, and 40 healthy controls. The institutional ethics review board of the First Affiliated Hospital of Wenzhou Medical College approved the study, and written informed consent was obtained from all study participants. For patients with DKA, blood samples were collected at the time of admission to the emergency room and following medical treatment after admission, when the patient's condition became stabilized. Plasma methylglyoxal was assayed by LC-MS (3). Plasma d-lactate concentration was determined by an e Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>

For Patients And Visitors

For Patients And Visitors

Definition Metabolic acidosis is a condition in which there is too much acid in the body fluids. Alternative Names Acidosis - metabolic Causes Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Prolonged lack of oxygen from shock, heart failure, or severe anemia Seizures Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Severe dehydration Symptoms Most symptoms are caused by the underlying disease or condition that is causing the metabolic acidosis. Metabolic acidosis itself most often causes rapid breathing. Acting confused or very tired may also occur. Severe metabolic acidosis can lead to shock or death. In some situations, metabolic acidosis can be a mild, ongoing (chronic) condition. Exams and Tests These tests can help diagnose acidosis. They can also determine whether the cause is a breathing problem or a metabolic problem. Tests may include: Arterial blood gas Basic metabolic panel, (a group of blood tests that measure your sodium and potassium levels, kidney function, and other chemicals and function Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

<< Guidelines For The Ed Management Of Pediatric Diabetic Ketoacidosis (dka)

<< Guidelines For The Ed Management Of Pediatric Diabetic Ketoacidosis (dka)

Epidemiology, Etiology, And Pathophysiology Epidemiology and Etiology "Type 1" and "Type 2" Diabetes in Children Type 1 diabetes is the most common type of diabetes seen in children today. The primary metabolic derangement in type 1 diabetes is an absolute insulin deficiency. These patients will have a life-long dependence on insulin injections. The overall incidence of insulin-dependent diabetes is about 15 cases per 100,000 people per year (about 50,000 are diagnosed with type 1 diabetes each year). An estimated 3 children of every 1000 will develop insulin-dependent diabetes by the age of 20. Type 1 diabetes is primarily a disease of Caucasians. The worldwide incidence is highest in Finland and Sardinia and lowest in the Asian and black populations. Type 1 diabetes is more frequently diagnosed in the winter months (the reason for this is not known.) Interestingly, twins affected by type 1 diabetes are often discordant in the development of the disease.13 About 95% of cases of type 1 diabetes are the result of a genetic defect of the immune system, exacerbated by environmental factors.13 The autoimmune destruction of the beta cells of the pancreas results in the inability to produce insulin. Inheritance of type 1 diabetes is carried in genes of the major histocompatibility complex, the human leukocyte antigen (HLA) system. Eventually, this research may lead to a vaccine using the insulin B chain 8-24 peptides to actually prevent type 1 diabetes.13 It is currently thought that islet cells damaged by a virus produce a membrane antigen that may stimulate a response by T killer cells of the immune system in the genetically susceptible patient. The T killer cells misidentify the beta cell as foreign and destroy it. As the beta cells in the pancreas are destroyed, the remai Continue reading >>

Metabolic Acidosis - Dka (exam 4)

Metabolic Acidosis - Dka (exam 4)

Transcript of Metabolic Acidosis - DKA (Exam 4) ATI Metabolic Acidosis ATI Client Education - ATI The following are the five classic types of ABG results demonstrating balance and imbalance. ATI Metabolic Acidosis Laboratory Tests and Diagnostic Procedures • To determine the type of imbalance, follow these steps: Metabolic Acidosis - DKA Patient-Centered Care • For all acid-base imbalances, it is imperative to treat the underlying cause. Exam 4 Results from - ›› Excess production of hydrogen ions »»Diabetic ketoacidosis (DKA) »»Lactic acidosis »»Starvation »»Heavy exercise »»Seizure activity »»Fever »»Hypoxia »»Intoxication with ethanol or salicylates ›› Inadequate elimination of hydrogen ions »»Kidney failure ›› Inadequate production of bicarbonate »»Kidney failure »»Pancreatitis »»Liver failure »»Dehydration ›› Excess elimination of bicarbonate »»Diarrhea, ileostomy ›› Vital signs: bradycardia, weak peripheral pulses, hypotension, tachypnea ›› Dysrhythmias ›› Neurological: muscle weakness, hyporeflexia, flaccid paralysis, fatigue, confusion ›› Respiratory: rapid, deep respirations (Kussmaul respirations) ›› Skin: warm, dry, flushed • Step 1: Look at pH. - If less than 7.35, diagnose as acidosis . • Step 2: Look at PaCO2 and HCO3 - simultaneously. Determine which is in the expected reference range. Conclude that the other is the indicator of imbalance. Diagnose less than 22 or greater than 26 HCO3 - as metabolic in origin. Step 3: Combine diagnoses of Steps 1 and 2 to name the type of imbalance. - If greater than 7.45, diagnose as alkalosis. Diagnose less than 35 or greater than 45 PaCO2 as respiratory in origin. Step 4: Evaluate the PaO2 and the SaO2. • If the results are below the expected refe Continue reading >>

Pulmcrit- Dominating The Acidosis In Dka

Pulmcrit- Dominating The Acidosis In Dka

Management of acidosis in DKA is an ongoing source of confusion. There isn’t much high-quality evidence, nor will there ever be (1). However, a clear understanding of the physiology of DKA may help us treat this rationally and effectively. Physiology of ketoacidosis in DKA Ketoacidosis occurs due to an imbalance between insulin dose and insulin requirement: Many factors affect the insulin requirement: Individuals differ in their baseline insulin resistance and insulin requirements. Physiologic stress (e.g. hypovolemia, inflammation) increases the level of catecholamines and cortisol, which increases insulin resistance. Hyperglycemia and metabolic acidosis themselves increase insulin resistance (Souto 2011, Gosmanov 2014). DKA treatment generally consists of two phases: first, we must manage the ketoacidosis. Later, we must prepare the patient to transition back to their home insulin regimen. During both phases, success depends on balancing insulin dose and insulin requirement. Phase I (Take-off): Initial management of the DKA patient with worrisome acidosis Let’s start by considering a patient who presents in severe DKA with worrisome acidosis. This is uncommon. Features that might provoke worry include the following: bicarbonate < 7 mEq/L pH < 7 (if measured; there is generally little benefit from measuring pH) clinically ill-appearing (e.g., dyspnea, marked Kussmaul respirations) These patients generally have severe metabolic acidosis with respiratory compensation. This creates two concerns: If the metabolic acidosis worsens, they may decompensate. The patient is depending on respiratory compensation to maintain their pH. If they should fatigue and lose the ability to hyperventilate, their pH would drop. It is important to reverse the acidosis before the patient m Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your blood (electrolyt Continue reading >>

Severe Ketoacidosis Associated With Canagliflozin (invokana): A Safety Concern

Severe Ketoacidosis Associated With Canagliflozin (invokana): A Safety Concern

Case Reports in Critical Care Volume 2016 (2016), Article ID 1656182, 3 pages 1Section of Pulmonary and Critical Care Medicine, Providence Hospital and Medical Center, 16001 W 9 Mile Road, Southfield, MI 48075, USA 2Department of Internal Medicine, Providence Hospital and Medical Center, 16001 W 9 Mile Road, Southfield, MI 48075, USA Academic Editor: Kurt Lenz Copyright © 2016 Alehegn Gelaye 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. Abstract Canagliflozin (Invokana) is a selective sodium glucose cotransporter-2 (SGLT-2) inhibitor that was first introduced in 2013 for the treatment of type 2 diabetes mellitus (DM). Though not FDA approved yet, its use in type 1 DM has been justified by the fact that its mechanism of action is independent of insulin secretion or action. However, some serious side effects, including severe anion gap metabolic acidosis and euglycemic diabetic ketoacidosis (DKA), have been reported. Prompt identification of the causal association and initiation of appropriate therapy should be instituted for this life threatening condition. 1. Introduction More than 5 million patients are admitted annually to intensive care units (ICUs) in the United States. A number of life threatening medical conditions, including diabetic ketoacidosis, can be associated with metabolic acidosis. Metabolic acidosis may also arise from several drugs and toxins through a variety of mechanisms. Since approval of the first-in-class drug in 2013, data have emerged suggesting that Sodium Glucose Transporter-2 (SGLT-2) inhibitors, including canagliflozin, may lead to diabetic ketoacidosis [1]. We pre Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. 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 >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Respiratory Failure In Diabetic Ketoacidosis

Respiratory Failure In Diabetic Ketoacidosis

Go to: INTRODUCTION Ketoacidosis in subjects with type 1, or less frequently, type 2 diabetes mellitus remains a potentially life-threatening diabetic manifestation. The subject has justifiably attracted attention in the literature. Sequential reviews[1-9] have documented important changes in the clinical concepts that are related to diabetic ketoacidosis (DKA) and its management. A large number of case series of DKA have addressed various aspects of its clinical presentation and management. For this review, we selected representative studies focused on management, outcome, age differences, gender differences, associated morbid conditions, ethnicity and prominent clinical and laboratory features[10-35]. In recognition of the complexity of treatment, the recommendation to provide this care in intensive care units was made more than 50 years ago[36]. Severe DKA is treated in intensive care units today[31]. Evidence-based guidelines for the diagnosis and management of DKA have been published and frequently revised in North America[37,38] and Europe[39]. Losses of fluids and electrolytes, which are important causes of morbidity and mortality in DKA, vary greatly between patients. Quantitative methods estimating individual losses and guiding their replacement have also been reported[40,41]. The outcomes of DKA have improved with new methods of insulin administration[42] and adherence to guidelines[43-46]. The aim of treatment is to minimize mortality and prevent sequelae. One study documented that the target of zero mortality is feasible[42]. However, mortality from DKA, although reduced progressively in the early decades after the employment of insulin treatment[1], remains high. Up to fifty plus years ago, mortality from DKA was between 3% and 10%[1,16]. A recent review re Continue reading >>

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