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Dka Management Uptodate

Spilleautomater Dka Management Uptodate

Spilleautomater Dka Management Uptodate

dka management - uptodatecom Related Video "Spilleautomater Dka Management Uptodate" (647 movies): You Want Something Special About dka management uptodate? It solves the. @ Diabetes Management Uptodate Diabetic Foot Care Handout The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. SIGN UP FOR THE DIABETES SELFMANAGEMENT. Diabetes Management Uptodate Diabetic Diary The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. DIABETES MANAGEMENT UPTODATE The. Diabetes Management Uptodate: : The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. DIABETES MANAGEMENT UPTODATE. Diabetic Ketoacidosis Diabetic Ketoacidosis 2 American Family Physician Volume 87, Number 5 March 1, 2013 Management of DKA in Adults SIGN UP FOR treatment of dka uptodate THE treatment of dka uptodate DIABETES SELFMANAGEMENT NEWSLETTER! The REAL cause of dka management uptodate! Why Do Not Click To Get it. dka management uptodate, The Secret of Nature. Stop wasting your time with unanswered searches. Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Authors Gosmanov AR, Gosmanova E, Dillard-Cannon E Accepted for publication 13 May 2014 Checked for plagiarism Yes Peer reviewer comments 2 Aidar R Gosmanov,1 Elvira O Gosmanova,2 Erika Dillard-Cannon3 1Division of Endocrinology, Diabetes and Metabolism, 2Division of Nephrology, Department of Medicine, 3Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA Abstract: Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Letter about this article has been published This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>

Hyperglycemic Crises: Diabetic Ketoacidosis (dka), And Hyperglycemic Hyperosmolar State (hhs)

Hyperglycemic Crises: Diabetic Ketoacidosis (dka), And Hyperglycemic Hyperosmolar State (hhs)

Go to: Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute metabolic complications of diabetes mellitus that can occur in patients with both type 1 and 2 diabetes mellitus. Timely diagnosis, comprehensive clinical and biochemical evaluation, and effective management is key to the successful resolution of DKA and HHS. Critical components of the hyperglycemic crises management include coordinating fluid resuscitation, insulin therapy, and electrolyte replacement along with the continuous patient monitoring using available laboratory tools to predict the resolution of the hyperglycemic crisis. Understanding and prompt awareness of potential of special situations such as DKA or HHS presentation in comatose state, possibility of mixed acid-base disorders obscuring the diagnosis of DKA, and risk of brain edema during the therapy are important to reduce the risks of complications without affecting recovery from hyperglycemic crisis. Identification of factors that precipitated DKA or HHS during the index hospitalization should help prevent subsequent episode of hyperglycemic crisis. For extensive review of all related areas of Endocrinology, visit WWW.ENDOTEXT.ORG. Go to: INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) represent two extremes in the spectrum of decompensated diabetes. DKA and HHS remain important causes of morbidity and mortality among diabetic patients despite well developed diagnostic criteria and treatment protocols (1). The annual incidence of DKA from population-based studies is estimated to range from 4 to 8 episodes per 1,000 patient admissions with diabetes (2). The incidence of DKA continues to increase and it accounts for about 140,000 hospitalizations in the US in 2009 (Figure 1 a) (3). Continue reading >>

Treatment And Complications Of Diabetic Ketoacidosis In Children And Adolescents

Treatment And Complications Of Diabetic Ketoacidosis In Children And Adolescents

INTRODUCTION Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus (T1DM), with a case fatality rate ranging from 0.15 percent to 0.31 percent [1-3]. DKA also can occur in children with type 2 DM (T2DM); this presentation is most common among youth of African-American descent [4-8]. (See "Classification of diabetes mellitus and genetic diabetic syndromes".) The management of DKA in children will be reviewed here (table 1). There is limited experience in the management and outcomes of DKA in children with T2DM, although the same principles should apply. The clinical manifestations and diagnosis of DKA in children and the pathogenesis of DKA are discussed elsewhere. (See "Clinical features and diagnosis of diabetic ketoacidosis in children and adolescents" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) DEFINITION Diabetic ketoacidosis – A consensus statement from the International Society for Pediatric and Adolescent Diabetes (ISPAD) in 2014 defined the following biochemical criteria for the diagnosis of diabetic ketoacidosis (DKA) [9]: Hyperglycemia – Blood glucose of >200 mg/dL (11 mmol/L) AND Metabolic acidosis – Venous pH <7.3 or a plasma bicarbonate <15 mEq/L (15 mmol/L) AND Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Clinical Features, Evaluation, And Diagnosis

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 >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

Sodium-glucose Co-transporter 2 Inhibitors For The Treatment Of Type 2 Diabetes Mellitus

Sodium-glucose Co-transporter 2 Inhibitors For The Treatment Of Type 2 Diabetes Mellitus

INTRODUCTION Current treatments for type 2 diabetes have centered on increasing insulin availability (either through direct insulin administration or through agents that promote insulin secretion), improving sensitivity to insulin, delaying the delivery and absorption of carbohydrate from the gastrointestinal tract, or increasing urinary glucose excretion. Sodium-glucose co-transporter 2 (SGLT2) inhibitors reduce blood glucose by increasing urinary glucose excretion. This topic will review the mechanism of action and therapeutic utility of SGLT2 inhibitors for the treatment of type 2 diabetes mellitus. A general discussion of the initial management of blood glucose and the management of persistent hyperglycemia in adults with type 2 diabetes is presented separately. (See "Initial management of blood glucose in adults with type 2 diabetes mellitus" and "Management of persistent hyperglycemia in type 2 diabetes mellitus".) MECHANISM OF ACTION The SGLT2 is expressed in the proximal tubule and mediates reabsorption of approximately 90 percent of the filtered glucose load. SGLT2 inhibitors promote the renal excretion of glucose and thereby modestly lower elevated blood glucose levels in patients with type 2 diabetes. The ability to lower blood glucose and glycated hemoglobin (A1C) levels is limited by the filtered load of glucose and the osmotic diuresis that is caused by this therapy. Moreover, although the currently developed SGLT2 inhibitors almost completely block proximal tubular glucose reabsorption, the measured inhibition is less than 50 percent based on urine glucose excretion. The glucose-lowering effect is independent of insulin (beta cell function and insulin sensitivity). Thus, they do not usually cause hypoglycemia in the absence of therapies that otherwise cau Continue reading >>

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Best Case Ever 58 Euglycemic Dka

Best Case Ever 58 Euglycemic Dka

This is EM Cases Best Case Ever 58 – Euglycemic DKA with Walter Himmel, the walking encyclopedia of emergency medicine. It’s not only run of the mill DKA, starvation and alcoholic ketoacidosis that can cause a metabolic acidosis with elevated ketones. Euglycemic DKA can be caused by the newer diabetes medications sodium-glucose co-transporter 2 inhibitors like Canagliflozin; and it’s important to recognize this tricky diagnosis early and initiate treatment for DKA despite a normal serum glucose level, because DKA can lead to serious complications like renal failure, cerebral edema, ARDS, shock, and death. Podcast production, sound design and editing by Anton Helman; Written by Anton Helman, June 2017 Euglycemic DKA can occur in any diabetic and has been reported in the literature since the 1970’s, but there has recently been a rise in incidence of euglycemic DKA associated with sodium-glucose co-transporter 2 inhibitors (SGLT-2 inhibitors, or the “zins”) such as Canagliflozin, Dapagliflozin and Empagliflozin. When to suspect euglycemic DKA Any patient with Type 1 or 2 diabetes taking SGLT-2 inhibitors who presents with nausea, vomiting, SOB or malaise or is found to have a metabolic acidosis should have blood drawn for serum ketones. Triggers of euglycemic DKA are similar to the triggers for any DKA: Alcohol use, infection and reduced oral intake. Distinguishing euglycemic DKA from alcoholic DKA Alcoholic ketoacidosis may also present with nausea, vomiting, malaise, ketones and anion gap metabolic acidosis. The key differentiating factor besides the obvious history of heavy alcohol use vs a diabetic taking an SGLT-2 inhibitor, is that patients with alcoholic ketoacidosis tend to have frankly low glucose. How is treatment of euglycemic DKA different? In addit Continue reading >>

Dka: Critical Care Lecture Series

Dka: Critical Care Lecture Series

Results from an absolute or relative deficiency of circulating insulin Absolute deficiency occurs in previously undiagnosed type 1 or when patients on treatment do not take their insulin, purposefully or inadvertently Relative deficiency happens when counter-regulatory hormones increase due to stress:sepsis, trauma, GI illness Increases-- catecholamines, glucagon, cortisol and growth hormone Low insulin with high counter-regulatory hormones causes an accelerated catabolic state Increase glucose production by the liver and the kidney Via glycogenolysis and gluconeogenesis Impaired peripheral glucose utilization resulting in hyperosmolarity and hyperglycemia Increased lipolysis and ketogenesis resulting in metabolic acidosis and ketonemia Hyperglycemia exceeding the renal threshold and hyperketonemia cause the osmotic diuresis, dehydration and obligatory loss of electrolytes Aggravated by vomiting These mechanisms continues to increase the counter-regulatory hormones which worsen the process Without intervention, life threatening metabolic acidosis and dehydration will occur 4 Continue reading >>

Diabetes Ketoacidosis

Diabetes Ketoacidosis

1. DIABETIC KETO-ACIDOSIS MANAGEMENT 2. INTRODUCTION  HHS and DKA are not mutually exclusive but rather two conditions that both result from some degree of insulin deficiency.  They can and often do occur simultaneously. In fact, one third of patients admitted for hyperglycemia exhibit characteristics of both HHS and DKA. 14th edition of Joslin's Diabetes Mellitus 3. DEFINITION DKA is defined as the presence of all three of the following: (i) Hyperglycemia (glucose >250 mg/dL) (ii) Ketosis, (iii) Acidemia (pH <7.3). 14th edition of Joslin's Diabetes Mellitus 4. PATHOPHYSIOLOGY Insulin Deficiency Glucose uptake Lipolysis Proteolysis Glycerol Free Fatty Acids Amino Acids Hyperglycemia Osmotic diuresis Ketogenesis Gluconeogenesis Glycogenolysis Dehydration Acidosis 14th edition of Joslin's Diabetes Mellitus 5. ROLE OF INSULIN  Required    for transport of glucose into: Muscle Adipose Liver  Inhibits lipolysis  Absence of insulin Glucose accumulates in the blood.  Uses amino acids for gluconeogenesis  Converts fatty acids into ketone bodies : Acetone, Acetoacetate, β-hydroxybutyrate.  6. DIABETIC KETOACIDOSIS PRECIPITATING EVENTS  Infection(Pneumonia / UTI / Gastroenteritis / Sepsis)  Inadequate insulin administration  Infarction(cerebral,  Drugs coronary, mesenteric, peripheral) (cocaine)  Pregnancy. Harrison’s Principle of internal medicine 18th edition p2977 7. SYMPTOMS DKA PHYSICAL FINDINGS can be the first Dehydration/hypotension presentation. Tachypnea/kussmaul Nausea/vomiting Thirst/polyuria Abdominal pain Shortnessof Tachycardia breath respirations/respiratory distress Fruity odour in breath. Abdominal tenderness(may resemble acute pancreatitis or surgical abdomen) Lethargy/obtundati Continue reading >>

Diagnosis And Management Of Hyperglycemic Emergencies

Diagnosis And Management Of Hyperglycemic Emergencies

1Division of Endocrinology, Department of Medicine, University of Mississippi School of Medicine; 2Medical Service, G.V. (Sonny) Montgomery VA Medical Center Jackson, MS; 3Department of Medicine, University of Mississippi School of Medicine, Jackson, MS, U.S.A. This article is aimed at providing a practical up-to-date review of the precipitating factors, diagnosis, management and secondary prevention of hyperglycemic emergencies (diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) to assist critical care physicians and hospitalists caring for these patients. Limitations of various guidelines include implementation in settings with an infrastructure different from that specified in the guidelines of a respective country, state, region or community. Appropriate individualized acute management of these conditions typically results in satisfactory clinical outcomes and may decrease the mortality rate from up to 20% in type 2 diabetics with hyperglycemic hyperosmolar state vs less than 2% in patients with DKA. DKA may be the first manifestation of type 1 diabetes and can also occur in type 2 diabetics depending on the state of insulin sufficiency/secretion. For type 1 diabetics, the transition period from adolescence to adulthood is particularly critical to prevent repetitive hospital admissions. Hyperglycemic emergencies are usually preventable but do depend on patient compliance and adherence as well as medical infrastructure. Patients of all ages should be both appropriately educated and assured continuous access to health care to prevent recurrences of these conditions. Diabetes mellitus, Hyperglycemia, Hyperosmolar state, Ketoacidosis, Treatment INTRODUCTION Diabetic ketoacidosis (DKA) and the hyperglycemic hyperosmolar state (HHS) are life-threatenin Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Epidemiology And Pathogenesis

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Epidemiology And Pathogenesis

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also called hyperosmotic hyperglycemic nonketotic state) are two of the most serious acute complications of diabetes. They each represent an extreme in the hyperglycemic spectrum. The epidemiology and the factors responsible for the metabolic abnormalities of DKA and HHS in adults will be discussed here. The clinical features, evaluation, diagnosis, and treatment of these disorders are discussed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment".) EPIDEMIOLOGY Diabetic ketoacidosis (DKA) is characteristically associated with type 1 diabetes. It also occurs in type 2 diabetes under conditions of extreme stress such as serious infection, trauma, cardiovascular or other emergencies, and, less often, as a presenting manifestation of type 2 diabetes, a disorder called ketosis-prone diabetes mellitus. (See "Syndromes of ketosis-prone diabetes mellitus".) DKA is more common in young (<65 years) patients, whereas hyperosmolar hyperglycemic state (HHS) most commonly develops in individuals older than 65 years [1,2]. The National Diabetes Surveillance Program of the Centers for Disease Control (CDC) estimated that there were 140,000 hospital discharges for DKA in 2009 in the United States, compared to 80,000 in 1988 (figure 1) [2]. Population-based data are not available for HHS. The rate of hospital admissions for HHS is lower than the rate for DKA, and accounts for less than 1 percent of all primary diabetic admissions [1,3-5]. The mortality rate for hyperglycemic crisis declined between 1980 and 2009 (figure 2) [6]. Mortality in Continue reading >>

Diabetic Ketoacidosis (dka) &

Diabetic Ketoacidosis (dka) &

DKA/HHS Presenting Signs Tachycardia Hypotension Dehydration Hypothermia Warm dry Skin Kussmaul Respiration Lethargy or Coma Fruity Odor DKA/HHS Precipitating Factors Infection Pneumonia Gastroenteritis UTI Sepsis Meningitis Influenza Mucormycosis Emotional Problems Trauma Acute Pancreatitis Myocardial Infarction Stroke Endocrine Acromegaly Thyrotoxicosis Cushing’s S. Omission of Antidiabetic Mx’s Drugs Any major Stress/Acute Illness DKA/HHS Drugs that can Precipitate Psychotropic Drugs Chlorpromazine Clozapine Risperidone Loxapine Steroids Immunosuppressants Beta Blockers Calcium Channel Blockers Diuretics Anticonvulsants Diazoxide DKA/HHS Pathogenesis Precipitating Factors Glucagon Catecholamines Cortisol Growth Hormone Absolute Insulin Deficiency Relative Insulin Deficiency Lipolysis FFAs Proteolysis Gluconeogenesis Ketogenesis Glycogenolysis Minimal Lipolysis Gluconeogenic Substrates Ketoacidosis Hyperglycemia Hyperosmolality Glucosuria (Osmotic Diuresis) Loss of Water & Electrolytes Triglycerides Hyperlipidemia Dehydration Decreased GFR DKA/HHS Enhanced Glucose Production G-6-P cAMP Glycogen F-6-P F-1,6-P2 PYR PFK-2 Fat CO2 Glucose Alanine F-2,6P2 Glycerol DKA/HHS Ketone Body Formation in Liver Fatty Acids Fatty Acyl-CoA Triglycerides Glucose Fatty Acyl-CoA Acetyl-CoA Acetoacetyl-CoA b-Hydroxy-b-methylglutaryl CoA Acetoacetate b -Hydroxybutyrate Acetone NADH NAD DKA/HHS Glucagon-induced Catabolic Cascade in Liver Glycogenolysis Glycogen Formation Gluconeogenesis Glycolysis Fatty acyl CoA Ketones Fatty Acids Malonyl-CoA Acetyl-CoA Glucose Glucose ACC DKA/HHS Ketone Body Utilization in Muscle b -Hydroxybutyrate Acetoacetate Acetoacetyl-CoA Acetyl-CoA Citric Acid Cycle Succinyl-CoA Succinate CoA EXTACELLULAR MITOCHONDRION b -Hydroxybutyrate Acetoacetate Continue reading >>

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