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Dka Vs Hyperosmolar Hyperglycemic State (hhs)

Dka Vs Hyperosmolar Hyperglycemic State (hhs)

Don't miss your chance to win free admissions prep materials! Click here to see a list of raffles . DKA vs Hyperosmolar hyperglycemic state (HHS) why is plasma osmolarity (Posm) always high in HHS, whereas DKA Posm is variable? Pathogenesis of DKA and HHS are discussed in the same article in uptodate but the Posm difference between the 2 is not clearly explained (at least to my feeble mind). The increase in plasma osmolality created by hyperglycemia pulls water out of the cells, expands the ECF, and thereby reduces the plasma sodium (Na) concentration. If a patient with normal serum electrolytes (Na = 140 mEq/L) rapidly developed a glucose concentration of 1000 mg/100 mL, and no urine was made, then that patients serum Na would fall to value between 119 and 126 mEq/L and the osmolality would increase to a level between 294 and 308 mosm/L. However, the osmolality usually increases to a greater degree because a large volume of relatively electrolyte-deficient urine is excreted during the evolution of the hyperglycemic state. The loss of this electrolyte-free water further raises the osmolality . In patients with ketoacidosis, high plasma acetone levels also contribute to the elevated osmolality." according to the pathogenesis flowchart (see figure 1) in this article ( Hyperglycemic Crises in Adult Patients With Diabetes ), there is no real difference in the pathogenesis to HHS first aid does mention than HHS is classically seen in elderly T2DM w/ limited ability to drink. is that the sole reason than HHS has hyperosmolarity? is the sugar way higher in HHS b/c T2DM patients have so much insulin resistance? whereas T1DM patients don't have insulin resistance T1DM is insulin dependent because they dont produce insulin at all, whereras T2DM has insulin resistance but produce 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 >>

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 >>

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As you were browsing something about your browser made us think you were a bot. There are a few reasons this might happen: You're a power user moving through this website with super-human speed. You've disabled JavaScript in your web browser. A third-party browser plugin, such as Ghostery or NoScript, is preventing JavaScript from running. Additional information is available in this support article. After completing the CAPTCHA below, you will immediately regain access to Continue reading >>

Management Of Diabetic Ketoacidosis In Adults

Management Of Diabetic Ketoacidosis In Adults

Management of diabetic ketoacidosis in adults Management of diabetic ketoacidosis in adults Insulin (blue dots) promotes glucose uptake in the liver and muscles, controlling blood sugar. Feeding/transition to subcutaneous insulin The first mealtime after the acidosis has resolved and the patient feels that he or she can tolerate food is the time to begin feeding the patient. Subcutaneous insulin should be started simultaneously. Dosing of subcutaneous insulin is given in basal/bolus fashion calculated first as total daily dose (TDD), which is based on insulin therapy the patient received at home prior to losing control. Alternatively, TDD may be estimated at 0.5 to 0.8 units/kg/day in an individual who has not previously been treated with insulin.3 Total daily insulin requirements may be significantly elevated for a few days following the resolution of DKA due to persistently elevated counter-regulatory hormone concentrations. These elevations predispose the patient to going back into acidosis if insulin levels are inadequate or stress levels increase further. Basal/bolus insulin therapy is generally broken down into long- and short-acting insulin as 50% basal and 50% bolus spread over three meals. Half of the TDD is given once daily as long-acting basal insulin (usually glargine [Lantus] or detemir [Levemir]). The other half is given as such short-acting insulin analogues as aspart (NovoLog), divided into thirds given at mealtime. For example, consider an individual weighing 90 kg with new onset type 1 diabetes who presents with DKA and is now controlled. Based on a TDD of 0.6 units/kg/day, a subcutaneous insulin strategy for this patient would include 54 units of insulin daily given as: 27 units basal (long-acting) insulin once daily; and 27 units short-acting insuli Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes mellitus or a complication during the course of a known disease. Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand (e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. There are two distinct forms: diabetic ketoacidosis (DKA), typically seen in type 1 diabetes, and hyperosmolar hyperglycemic state (HHS), occurring primarily in type 2 diabetes. In type 1 diabetes, no insulin is available to suppress fat breakdown, and the ketones resulting from subsequent ketogenesis manifest as DKA. This is in contrast to type 2 diabetes, in which patients can still secrete small amounts of insulin to suppress DKA, instead resulting in a hyperglycemic state predominated simply by glucose. The clinical presentation of both DKA and HHS is one of polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry oral mucosa, decreased skin turgor), and eventually mental status changes and coma. In patients with altered mental status, fingerstick glucose should always be checked in order to exclude serum glucose abnormalities. Several clinical findings pertaining only to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. HHS patients, in contrast to those with DKA, will present with more extreme volume depletion. The treatment of both DKA and HHS is primarily IV electrolyte and fluid replacement. Insulin for hyperglycemia may be given with caution and under vigilant monitoring of serum glucose. Other treatment options depend on the severity of symptoms and include bicarbonate and potassium replacement. Osmotic diuresis and hypovolemia Hypovolemia resulting from DKA can lead to acute 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: 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 >>

Diluting Your Sugar | Sinaiem

Diluting Your Sugar | Sinaiem

By Jeff Nusbaum | Pearl of the Day | Comments are Closed | 15 August, 2016 | 0 Last week, we closed out the week by discussing the dischargable, benign sugars, but what about when you have the legit sugars. Were talking about DKA. While the algorithm for DKA is fairly straight forward fluids, insulin, replete lytes prn, admit / ICU consult, there are some often under appreciated subtleties we neglect in the ED. Lets start with fluid choice. Most clinicians empirically start volume resuscitation with 0.9% saline or normal saline. As weve all heard, there is very little truly normal about normal saline. Specifically in the context of DKA, one should worry about giving an acidic solution (with a pH of ~5.5) to an already acidotic patient. Other, perhaps more savvy clinicians reach for isolyte / plasmalyte. With a more physiologic pH, logically this makes sense, however one must be weary of giving potassium to a patient population that is typically hyperkalemic (often due to normal fluid shifts of acid base balance). So lets review some of the most commonly used ED fluids: This is clearly a complicated question, so what do the experts do. Uptodate recommends resuscitation with 0.9% saline at a rate of 15-20 mL/kg/hour. The American Diabetes Association similarly recommends initial resuscitation with 0.9% NS. So what should you do? There is no clear right answer, so check a gas and choose wisely. Kitabchi AB, Hirsch IB, Emmett M. Diabetic ketoacidosis and hyperosmolar hyperglycemia state in adults: treatment. Uptodate. Nathan DM, Mulder JE (EDs). Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic Crises in Adult Patients With Diabetes. Diabetes Care 2009 Jul; 32(7): 1335-1343. MUSC Health Pharmacy Services. Intravenous Fluid Comparison Table for large volume, Int 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 >>

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 >>

Euglycaemic Diabetic Ketoacidosis In A Patient With Type 2 Diabetes Started On Empagliflozin

Euglycaemic Diabetic Ketoacidosis In A Patient With Type 2 Diabetes Started On Empagliflozin

Euglycaemic diabetic ketoacidosis in a patient with type 2 diabetes started on empagliflozin 1Aga Khan University, Karachi, Sindh, Pakistan 2Department of Endocrinology, The Aga Khan University Hospital, Karachi, Sindh, Pakistan Correspondence to Dr Owais Rashid, owais.rashid{at}aku.edu Diabetes ketoacidosis (DKA) is largely associated with type 1 diabetes and has hyperglycaemia as a cardinal feature. We discuss the case of a 42-year-old man, a patient with type 2 diabetes, who presented to the emergency room, with nausea, vomiting and abdominal pain. He had recently changed his diabetes medications and started on an SGLT2 inhibitor (empagliflozin) along with metformin, pioglitazone, liraglutide and self-adjusted exogenous insulin. DKA was suspected in the wake of clinical examination and lab findings but glucose levels were below the cut-off for DKA; therefore, he was diagnosed with euglycaemic DKA. He was successfully managed with intravenous hydration and insulin infusion. We discuss the link of SGLT2 inhibitors with DKA and the pathophysiology behind euglycaemic DKA. The full text of all Editor's Choice articles and summaries of every article are free without registration The full text of Images in ... articles are free to registered users Only fellows can access the full text of case reports (apart from Editor's Choice) - become a fellow today, or encourage your institution to, so that together we can grow and develop this resource Don't forget to sign up for content alerts so you keep up to date with all the case reports as they are published, and let us know what you think by commenting on the Editor's blog 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 >>

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 >>

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