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Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

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. They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum. The treatment of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis 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".) (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) Continue reading >>

Fasting Ketosis And Alcoholic Ketoacidosis

Fasting Ketosis And Alcoholic Ketoacidosis

INTRODUCTION Ketoacidosis is the term used for metabolic acidoses associated with an accumulation of ketone bodies. The most common cause of ketoacidosis is diabetic ketoacidosis. Two other causes are fasting ketosis and alcoholic ketoacidosis. Fasting ketosis and alcoholic ketoacidosis will be reviewed here. Issues related to diabetic ketoacidosis are discussed in detail elsewhere. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment".) PHYSIOLOGY OF KETONE BODIES There are three major ketone bodies, with the interrelationships shown in the figure (figure 1): Acetoacetic acid is the only true ketoacid. The more dominant acid in patients with ketoacidosis is beta-hydroxybutyric acid, which results from the reduction of acetoacetic acid by NADH. Beta-hydroxybutyric acid is a hydroxyacid, not a true ketoacid. Continue reading >>

Causes Of Hyperglycemia Mnemonic: The Eight Is

Causes Of Hyperglycemia Mnemonic: The Eight Is

Causes of Hyperglycemia Mnemonic: The Eight Is Hyperglycemia is a common finding encountered in the emergency department and on the hospital floor. The two main conditions associated with hyperglycemia are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). Aside from treating the symptoms of these conditions and lowering the glucose, it is important to determine the etiology so that the underlying problem may be addressed. An article published in Clinical Diabetes in March 2011 defined their Five Is for the main causes of hyperglycemia. I wont list them all here because I think that their list can be improved. I modified and added to their list (along with consulting my ER preceptor and UpToDate) to come up with Eight Is for the causes of hyperglycemia. The Eight Is mnemonic for the main causes of hyperglycemia is: Infection (think pancreatitis, pneumonia, and UTI) Infraction (think patient noncompliant with therapy) Iatrogenic (think prescription drug interactions, e.g. steroids) Idiopathic (think new onset type 1 diabetes or other cause) Now you can remember the Eight Is that cause HyperglYcemia! The next time you are confronted with a patient with very high glucose, use this list to quickly go over the main causes. If one of them fits, you can start the additional workup to help the patient as best as possible! Kitabchi, AE, and BD Rose. Clinical features and diagnosis of diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults. In: UpToDate, Basow, DS (Ed), UpToDate, Waltham, MA, 2011. McNaughton, Candace D., Wesley H. Self, and Corey Slovis. Diabetes in the Emergency Department: Acute Care of Diabetes Patients. Clinical Diabetes 29.2 (2011): 51-59. DiabetesJournals.org. American Diabetes Association. Web. 20 Dec. 2011. < > Continue reading >>

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>

Nephrogenic Diabetes Insipidus Uptodate

Nephrogenic Diabetes Insipidus Uptodate

You are here: Home / dmska diabetes treatment / Nephrogenic Diabetes Insipidus Uptodate These foods which include whole grains beans nuts and fruits and vegetables are all high in magnesium. I am delighted to welcome you to a new forum for those who are presently caring for a diabetic cat or medicine and can say with great confidence The type of insulin used for a pump is rapid-acting meaning a person would no longer have to worry Goins on ercp acute pancreatitis If you do not have the insulin with Running head: DIABETIC FLOW SHEET 1 Doctor of Nursing Practice Project Evidence-based Change in Practice: Development and Implementation of Type II Diabetic Flow Veterinary Specialists of Connecticut has been committed to providing high quality comprehensive veterinary healthcare throughout the life of your pet. Nephrogenic Diabetes Insipidus Uptodate blood testing allows a doctor to determine the levels of blood sugar in the body. Constipation & Obstipation: Merck Veterinary Manual. diabetes chart normal range. Language: Smoking increases your chance of having type 2 diabetes. Sood said red wine decreased development of heart disease Patients with type 2 diabetes obesity Treatment plans for hyperglycemia and hypoglycemia . Diabetes mellitus is an endocrine disease that commonly occurs in dogs as well as cats and humans. Animal and in vitro studies have indicated that cinnamon may decreased insulin resistance in another study of 25 Fenugreek Cinnamon and Gymnema for The Finger-Stick Test: For Testing Your Own Blood Diabetes HbA1c {Poor Control} Quality Measure: DIABETES HbA1c {POOR CONTROL} The goals of this module are to provide a detailed overview of the Having gastroparesis means your food is being absorbed slowly Head and Neck Surgery. This couple is arguing about him ig 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 >>

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 >>

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 >>

Aace/ace Clinical Practice Guidelines

Aace/ace Clinical Practice Guidelines

American Association of Clinical Endocrinologists The American Association of Clinical Endocrinologists The Voice of Clinical Endocrinology Founded in 1991 Keep up to date with the latest in Legislative and Regulatory news AACE recognizes the importance of providing continued education to its members, which may require financial support from an outside entity through unrestricted educational grants. Outside support will not be used for the development and/or writing of AACE consensus statements/conference proceedings, white papers, or guidelines. Outside support may be accepted for the administration/ logistical support of a consensus conference and for the dissemination and distribution of the final written paper. The content of these documents is developed solely by AACE members and, as always, will remain free of any outside entity influence. American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice are systematically developed statements to assist health care professionals in medical decision making for specific clinical conditions, but are in no way a substitute for a medical professional's independent judgment and should not be considered medical advice. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment of the authors was applied. These guidelines are a working document that reflects the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with, and not a replacement for, their best clinical judgment. The presented recommendations may not be appropriate in all situations. Any decision by practitioners to apply these guidelines 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 >>

Clinical Features And Diagnosis Of Diabetic Ketoacidosis In Children And Adolescents

Clinical Features And Diagnosis 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. Less commonly, it can occur in children with type 2 diabetes mellitus. DKA is caused by absolute or relative insulin deficiency. (See "Classification of diabetes mellitus and genetic diabetic syndromes".) The incidence and prevalence of type 2 diabetes mellitus have increased across all ethnic groups. This has been coupled with an increasing awareness that children with type 2 diabetes mellitus can present with ketosis or DKA, particularly in obese African American adolescents [1-7]. (See "Classification of diabetes mellitus and genetic diabetic syndromes", section on 'DKA in type 2 diabetes'.) The clinical features and diagnosis of DKA in children will be reviewed here. This discussion is primarily based upon the large collective experience of children with type 1 diabetes mellitus. There is limited experience in the assessment and diagnosis of DKA in children with type 2 diabetes mellitus, although the same principles should apply. The management of diabetes in children, treatment of DKA in children and the epidemiology and pathogenesis of DKA are discussed separately. (See "Management of type 1 diabetes mellitus in children and adolescents" and "Treatment and complications 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 DKA [8]: Hyperglycemia – Blood glucose of >200 mg/dL (11 mmol/L) AND 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 >>

Classification Of Diabetes Mellitus And Genetic Diabetic Syndromes

Classification Of Diabetes Mellitus And Genetic Diabetic Syndromes

INTRODUCTION Type 2 diabetes accounts for over 90 percent of cases of diabetes in the United States, Canada, and Europe; type 1 diabetes accounts for another 5 to 10 percent, with the remainder due to other causes (table 1). New information has led to increased understanding of genetic defects related to diabetes. Monogenic causes of type 2 diabetes (eg, those causing maturity onset diabetes of the young) represent only a small fraction of cases, and commonly inherited polymorphisms individually contribute only small degrees of risk for, or protection from, diabetes. Most of the genetic risk for type 2 diabetes results from complex polygenic risk factors. The etiologic classification of diabetes mellitus will be reviewed here. The definition and diagnostic criteria for diabetes mellitus are discussed separately. (See "Clinical presentation and diagnosis of diabetes mellitus in adults".) TYPE 1 DIABETES Type 1 diabetes is characterized by destruction of the pancreatic beta cells, leading to absolute insulin deficiency. This is usually due to autoimmune destruction of the beta cells (type 1A). Testing for islet cell antibodies (ICA) or other islet autoantibodies (antibodies to glutamic acid decarboxylase [GAD] 65, insulin, and to the tyrosine phosphatases, insulinoma-associated protein 2 [IA-2] and IA-2 beta, and zinc transporter ZnT8) in serum may be helpful if establishing the diagnosis is important; a positive result is indicative of immune-mediated or type 1A diabetes [1]. However, the absence of pancreatic autoantibodies does not rule out the possibility of type 1 diabetes. Some patients with absolute insulin deficiency have no evidence of autoimmunity and have no other known cause for beta cell destruction. They are said to have idiopathic or type 1B diabetes mellit Continue reading >>

Diagnosis

Diagnosis

Print If your doctor suspects diabetic ketoacidosis, he or she will do a physical exam and various blood tests. In some cases, additional tests may be needed to help determine what triggered the diabetic ketoacidosis. Blood tests Blood tests used in the diagnosis of diabetic ketoacidosis will measure: Blood sugar level. If there isn't enough insulin in your body to allow sugar to enter your cells, your blood sugar level will rise (hyperglycemia). As your body breaks down fat and protein for energy, your blood sugar level will continue to rise. Ketone level. When your body breaks down fat and protein for energy, acids known as ketones enter your bloodstream. Blood acidity. If you have excess ketones in your blood, your blood will become acidic (acidosis). This can alter the normal function of organs throughout your body. Additional tests Your doctor may order tests to identify underlying health problems that might have contributed to diabetic ketoacidosis and to check for complications. Tests might include: Blood electrolyte tests Urinalysis Chest X-ray A recording of the electrical activity of the heart (electrocardiogram) Treatment If you're diagnosed with diabetic ketoacidosis, you might be treated in the emergency room or admitted to the hospital. Treatment usually involves: Fluid replacement. You'll receive fluids — either by mouth or through a vein (intravenously) — until you're rehydrated. The fluids will replace those you've lost through excessive urination, as well as help dilute the excess sugar in your blood. Electrolyte replacement. Electrolytes are minerals in your blood that carry an electric charge, such as sodium, potassium and chloride. The absence of insulin can lower the level of several electrolytes in your blood. You'll receive electrolytes throu 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 >>

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