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Euglycemic Dka Uptodate

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Summarized from Nyenwe E, Kitabchi A. The evolution of diabetic ketoacidosis: An update of its etiology, pathogenesis and management. Metabolism 2016; 65: 507-21 Diabetic ketoacidosis (DKA), which is an acute, potentially life-threatening complication of poorly controlled diabetes, is the subject of a recent comprehensive review article. The authors discuss epidemiological issues, revealing increasing incidence of DKA and decreasing mortality. Once inevitably fatal, DKA now has a reported mortality rate of <1 % in adults and 5 % in the elderly who also have one or more chronic illnesses, in addition to diabetes. They reveal that although DKA more commonly affects those with type 1 diabetes, around a third of cases occur in those with type 2 diabetes. This introductory section also reminds that DKA is characterized by the presence of three cardinal biochemical features: raised blood glucose (hyperglycemia); presence of ketones in blood and urine (ketonemia, ketonuria); and metabolic acidosis. Insulin deficiency is central to the development of these three biochemical abnormalities. The very rare occurrence of euglycemic DKA (DKA with normal blood glucose) is highlighted by reference to recent reports of this condition in patients treated with a relatively new class of antidiabetic drug (the SGLT 2 inhibitors) that reduces blood glucose by inhibiting renal reabsorption of glucose. There follows discussion of factors that precipitate DKA (omission or inadequate dosing of insulin, and infection are the most common triggers), and the possible mechanisms responsible for ketosis-prone type 2 diabetes. This latter condition, which was recognized as an entity only relatively recently, is distinguished by the development of severe but transient failure of pancreatic β-cells to m Continue reading >>

Diabetic Ketoacidosis With Sglt2 Inhibitors Is Manageable

Diabetic Ketoacidosis With Sglt2 Inhibitors Is Manageable

Diabetic Ketoacidosis With SGLT2 Inhibitors Is Manageable The euglycemic diabetic ketoacidosis (DKA) that has recently been associated with the use of sodiumglucose cotransporter 2 (SGLT2) inhibitors will probably turn out to be very infrequent in patients with type 2 diabetes and "predictable, detectable, and preventable" in those with type 1 diabetes, two leading clinical trialists assert in a new editorial published in the September issue of Diabetes Care. The piece by Julio Rosenstock, MD, of the Dallas Diabetes and Endocrine Center at Medical City, Texas, and Ele Ferrannini, MD, of the Institute of Clinical Physiology, Consiglio Nazionale delle Ricerche, Pisa, Italy accompanies the published versions of two related articles that had previously appeared online: a Janssen article demonstrating a low (but not zero) risk for DKA in a clinical-trial program of canagliflozin (Invokana, Janssen Pharmaceuticals, Inc), and a case series report of 13 episodes of euglycemic DKA in nine patients, seven with type 1 diabetes and two with type 2 diabetes, who developed the condition postoperatively. The issue initially came to light in May 2015, when the US Food and Drug Administration issued a notice on the basis of 20 cases of DKA associated with SGLT2 inhibitors reported to the agency's adverse-event reporting system database. A month later, the European Medicines Agency initiated a review and identified 101 cases worldwide associated with type 2 diabetes. Dr Rosenstock and Dr Ferrannini provide unpublished data from the other manufacturers of SGLT2 inhibitors on the US market, suggesting rates of DKA symptoms of 0.1% or less in randomized trials in more than 18,000 patients receiving dapagliflozin (multiple brands) and 7000 patients receiving empagliflozin (Jardiance, Boehri Continue reading >>

Diabetes Uptodate Flashcards | Quizlet

Diabetes Uptodate Flashcards | Quizlet

What HLA allele confers protection against the development of type 1 diabetes? A more generalized concept is that type 1A diabetes is prevented by a balance between what? Anti-insulinoma associated protein 2 (IA-2) Anti-ZnT8 (zinc transporter of islet beta cells) What are important autoantigens in type 1 diabetes? - once insulin is administered subQ, essentially all individuals develop insulin antibodies What are often the first autoantibodies to appear in children progressing to diabetes? Anti-GAD (glutamic acid decarboxylase) is found in approximately 70% of patients with type 1 diabetes at the time of diagnosis. Besides islets of Langerhans, where else in the body is this enzyme (GAD) found? As autoimmunity in type 1 diabetes progresses from initial activation to a chronic state, there is often an increase in the number of islet autoantigens targeted by T cells and autoantibodies. This condition is termed....? B cells are not required for the development of type 1 diabetes (although the diabetes did develop later than normal) - destruction of pancreatic beta cells is mediated principally by T cells The occurrence of type 1 diabetes in a 14 year old boy with X-linked agammaglobulinemia suggests what about the pathogenesis of type 1 diabetes? - coxsackie B virus specific IgM responses have been found in 39 percent of children with newly diagnosed type 1 diabetes Initiating factors of the immune response leading to type 1 DM are not well understood. One possibility is molecular mimicry due to homology between GAD and what? Patients with type 1 diabetes are at increased risk for developing other autoimmune diseases. What 2 specific ones are mentioned? Although cow's milk may be associated with an increase of risk for type 1 DM, what component of milk may be protective? Continue reading >>

Potd: Euglycemic Dka

Potd: Euglycemic Dka

Todays POTD comes from Dr. Buckingham. Her clinical question: Can a patient present as a first time diabetic with euglycemic DKA? Hmmm Lets break question down. How do you diagnose diabetes in a patient? Symptomatic hyperglycemia with classic symptoms of thirst, polyuria, weight loss with a random BGM200mg/dL Oral glucose tolerance test with two hour plasma glucose 200 mg/dL Just as the name states, euglycemic DKA is diabetic ketoacidosis without the hyperglycemia. Patients will have the serum/urine ketones and anion gap metabolic acidosis of DKA while glucose levels are normal/mildly elevated (<200mg/dL). Patients that present with euglycemic DKA are usually those with poor carbohydrate intake, adequate hydration, use of insulin, alcohol intake, or use of sodium-glucose co-transporter 2 (SGLT2) inhibitors [Canagliflozin (Invokana), Dapagliflozin (Farxiga), Empagliflozin (Jardiance)]. Euglycemic DKA occurs more often in type 1 but can also occur in type 2 diabetes, and the most common symptom is vomiting. **Check labs for patients with concerning story of DM, poor carbohydrate intake and/or taking SGLT2 inhibitor, c/o nausea/vomiting/fatigue/SOB** So can someone present with no prior hx of diabetes and have euglycemic DKA? Maybe, if they have been having poor carbohydrate intake but tolerating fluids. However, also consider a broader differential diagnosis such as starvation ketoacidosis, alcoholic ketoacidosis, lactic acidosis, and drug toxicity. 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 >>

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 >>

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 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 Continue reading >>

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 >>

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 >>

Emergency Medicine Pharmd

Emergency Medicine Pharmd

Emergency medicine from the perspective of a pharmacist Trick of the Trade: Simplify Treatment of the SSTI In 2010, skin and soft tissue infections (SSTIs) accounted for approximately 4.2 million emergency department visits (1). With such a bread-and-butter emergency medicine encounter, one might not give a second thought as to whether the standard dosing is less than ideal. However, the nuance of appropriate pharmacokinetic dosing that drug references omit may be the more ideal approach. The most appropriate dosing regimen, based on pharmacokinetic parameters, may not be highlighted by tertiary drug resources (2).With a condition seen every day, we should be nailing the treatment. If we see it every day, we should be excellent at treating it, right? Lets start with the organisms likely to cause these infections. Generally, gram (+) streptococcal and staphylococcal species are our biggest offenders. For streptococcus, we can utilize first-generation cephalosporins or penicillins. Between 20-50% of SSTIs are secondary to community-acquired methicillin-resistant staphylococcus aureus (MRSA) (3). The Infectious Diseases Society of America guidelines offer insight for purulent and nonpurulent SSTIs, but does not specifically address the scenario of a purulent infection with cellulitis (4). For these patients we often prescribe two antibiotics, adding MRSA coverage with trimethoprim-sulfamethoxazole (Bactrim, TMP/SMX) or doxycycline based on local susceptibilities. In addition, recent literature comparing TMP/SMX to placebo for uncomplicated skin abscesses after drainage found significantly higher cure rates for those who received TMP/SMX (5). If there is concern for streptococcus, TMP/SMX has poor streptococcal coverage and an additional antimicrobial agent should be added Continue reading >>

#51: Diabetes Treatment In 2017: New Meds, Insulin, And Cardiac Risk Reduction

#51: Diabetes Treatment In 2017: New Meds, Insulin, And Cardiac Risk Reduction

Get cozy with these new drugs for diabetes treatment. Don’t be scared, they won’t bite. On this episode, we interview Endocrinologist and current president of AACE, Dr. Jonathan D. Leffert, MD, FACP, FACE, ECNU about how to utilize the myriad of new diabetes drugs on the marketplace including SGLT2 inhibitors, DPP4 inhibitors, GLP1 agonists, and new ultra long acting insulins. Plus, we’ll teach you how to choose between agents, common side effects, A1C goals, and the cardiovascular benefits of these newer agents. Help patients afford their meds with this resource from AACE Full show notes available at Join our newsletter mailing list. Rate us on iTunes, recommend a guest or topic and give feedback at [email protected] Case: Case from Kashlak Memorial Hospital: 49 yo M with HTN, BMI 29, hyperlipidemia, family history of premature CAD (dad age 45yo), and type 2 diabetes with A1C increase from 6.4% to 9% while on metformin monotherapy. Clinical Pearls: Latent autoimmune diabetes of aging (LADA): Autoimmune disease similar to type 1 diabetes (DM1). Suspect if older adult presents w/new insulin dependence. Check glutamic acid decarboxylase (GAD) antibodies, which are most sensitive and specific. Often positive in LADA/DM1. Can also check islet cell Ab or insulin autoantibodies. A1C and anemia: Based on red cell (RBC) survival. Falsely high a1c if RBC turnover is low → Older RBCs that accumulate more glucose e.g. Iron, vitamin B12, or folate deficiency anemia. Falsely low a1c if rapid RBC turnover e.g. hemolysis, or on treatment for iron, B12, or folate deficiency, or erythropoietin injections (Source: UptoDate) Fructosamine and A1C: Fructosamine is bound to albumin in blood. Turnover of albumin is about 28 days vs 120 days for hemoglobin. Thus, fructosamine pr Continue reading >>

Best Case Ever 58 Euglycemic Dka - Emergency Medicine Cases (podcast)

Best Case Ever 58 Euglycemic Dka - Emergency Medicine Cases (podcast)

MP3 • Episode home • Series home • Public Feed Discovered by Player FM and our community copyright is owned by the publisher, not Player FM, and audio streamed directly from their servers. 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... 203 episodes available.A new episode about every11 days. How do you distinguish cellulitis from the myriad of cellulitis mimics? At what point do we consider treatment failure for cellulitis? What is the best antibiotic choice for patients who are allergic to cephalosporins? Which patients with cellulitis or skin abscess require IV antibiotics? Coverage for MRSA? What is the best and most resource wi ... In anticipation of EM Cases Episode 109 Recognition and Management of Skin and Soft Tissue Infections with Melanie Baimel and Andrew Morris we have Dr. Morris telling us his Best Case Ever of a nurse that he worked with diagnosed with Necrotizing Fasciitis. We discuss some of the diagnostic pearls for this difficult diagnosis as well as issues ... This month's EM Cases Best Case Ever podcast features Dr. Catherine Varner, Emergency Physician at Sinai Health System and researcher at Schwartz-Reisman Emergency Medicine Institute (SREMI) discussing the key pitfalls in the diagnosis of ectopic pregnancy and ruptured ectopic pregnancy. It turns out that we're missing the diagnosis more than w ... Just one case of missed pediatric physical abuse I consider a travesty. The sad state of af 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 >>

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 >>

Prevalence Of Diabetes Ketoacidosis Rises And Still No Strict Treatment Adherence

Prevalence Of Diabetes Ketoacidosis Rises And Still No Strict Treatment Adherence

Prevalence of Diabetes Ketoacidosis Rises and Still No Strict Treatment Adherence Author(s): Alex Jervis , Susannah Champion , Gemma Figg , Jane Langley , Gary G. Adams . Insulin Diabetes Experimental Research Group, Faculty of Medicine and Health Sciences, The University of Nottingham, Nottingham, NG7 2UH, United Kingdom. Diabetes ketoacidosis (DKA) should be managed following clear written guidelines. However, evidence suggests thathealthcare professionals do not always adhere strictly to the agreed guidelines. Objective: This investigation aimed to review the management of DKA in a hospital setting, to assess what DKA treatmentwas implemented and its effectiveness on patient care. As a result of the study, it was also anticipated that the datawould highlight other matters of interest, such as whether certain categories of people are more prone to DKA. Method: A retrospective audit was carried out on patients case notes in hospitals within the East Midlands, UK. Thismethod prevents study outcomes being swayed because DKA management has already taken place. To reduce selectionbias the most recent available case notes were selected. All patients aged 39 and under who were admitted to the emergency department with DKA in the 3 year period between1st August 2009 and February 2012 had their case notes examined 142 cases of DKA came within this category. Results: It was found that the DKA protocol being implemented was not based on the most up-to-date evidence available.It was also established that despite the existence of a hospital protocol, some healthcare professionals failed to follow theguidelines. This particular finding was confirmed to be statistically significant with a p value of 0.0409. Additionally, Actrapidwas the only intravenous insulin used, despite inadeq Continue reading >>

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