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Dka Vs Hhs Ppt

Dka/hhs. - Ppt Video Online Download

Dka/hhs. - Ppt Video Online Download

To view this video please enable JavaScript, and consider upgrading to a web browser that supports HTML5 video Published by Audrey Price Modified over 2 years ago 115,000 hospitalizations in U.S 10-30% of admissions with primary diagnosis of Diabetes Mortality fallen 22% over the past 20 years Lower incidence compared to DKA 1% of DM related admissions Much high mortality rate ~40% compared to <5% for DKA No significant improvement in recent past 5 Diagnosis Table with diagnostic parameters 11 Ketosis Prone T2DM Mostly minorities Presents with DKA African Americans and Hispanics Presents with DKA Require insulin treatment initially Can usually be transitioned quickly to Oral hypoglycemics as outpatient Due to Glucose toxicity or lipotoxicity to the Beta-Cells 12 Presentation Dehydration Weight loss Weakness Abdominal Pain polyuria, polydipsia Weight loss Weakness Abdominal Pain Correlates with severity of acidosis May be confused with Acute Abdomen Related to osmolality more than hyperglycemia or acidosis More common in HHS Signs & Symptoms related to underlying cause Infection, CV disease etc Diabetic patients may have silent cardiac ischemia precipitating DKA even without chest pain. Infection is the most common precipitating factor for DKA. Cocaine and other illicit drugs are a common factor in DKA. Prescription drugs only rarely are a precipitating cause of DKA. 15 Predisposing Factors Acute Illness Infection CVA/MI Acute Pancreatitis Venous Thromboembolism Acute Abdomen Renal Failure Heat Stroke Burns Subdural Hematoma Thyrotoxicosis Cushings Syndrome Find good table of factors 16 Predisposing Factors Drugs Previously undiagnosed diabetes Pregnancy Glucocorticoids Beta-Blockers Anti-Psychotics Thiazide Diuretics Niacin TPN Previously undiagnosed diabetes Pregnancy Continue reading >>

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic crises are discussed together followed by a separate section on lactic acidosis. DIABETIC KETOACIDOSIS (DKA) AND HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS) Definitions DKA has no universally agreed definition. Alberti proposed the working definition of “severe uncontrolled diabetes requiring emergency treatment with insulin and intravenous fluids and with a blood ketone body concentration of >5 mmol/l”.1 Given the limited availability of blood ketone body assays, a more pragmatic definition comprising a metabolic acidosis (pH <7.3), plasma bicarbonate <15 mmol/l, plasma glucose >13.9 mmol/l, and urine ketostix reaction ++ or plasma ketostix ⩾ + may be more workable in clinical practice.2 Classifying the severity of diabetic ketoacidosis is desirable, since it may assist in determining the management and monitoring of the patient. Such a classification is based on the severity of acidosis (table 1). A caveat to this approach is that the presence of an intercurrent illness, that may not necessarily affect the level of acidosis, may markedly affect outcome: a recent study showed that the two most important factors predicting mortality in DKA were severe intercurrent illness and pH <7.0.3 HHS replaces the older terms, “hyperglycaemic hyperosmolar non-ketotic coma” and “hyperglycaemic hyperosmolar non-ketotic state”, because alterations of sensoria may be present without coma, and mild to moderate ketosis is commonly present in this state.4,5 Definitions vary according to the degree of hyperglycaemia and elevation of osmolality required. Table 1 summarises the definition of Kitabchi et al.5 Epidemiology The annual incidence of DKA among subjects with type 1 diabetes is between 1% and 5% in European and American series6–10 and this incidence appear 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 >>

25-40% Of Newly Diagnosed Cases Present In Dka

25-40% Of Newly Diagnosed Cases Present In Dka

Case Scenario #1 What is your assessment? DKA exists when: Venous pH < 7.3 Serum bicarbonate < 15 mEq/dL Blood glucose > 300 mg/dL Presence of ketonemia/ketonuria How much fluid would you administer as a bolus? Would you administer bicarbonate? How much insulin would you administer? What IVF would you start? At what rate? * 10 - 20 cc/kg bolus of NS would be adequate. Though the patient is dehydrated (dry lips), his hemodynamics are good, with acceptable vitals and good perfusion. There would be no reason to administer more than 20 cc/kg fluids. While this patient is clearly acidemic, he is NOT in impending cardiovascular collapse and therefore there is no justification for the administration of bicarbonate. In fact, administration of bicarbonate has been associated with the development of cerebral edema. The “true†serum sodium is 143 133 + 0.016[700-100] Insulin is generally started at 0.1 u/kg/hr. Therefore, in this 30 kg patient, an insulin infusion of 3 u/hr of regular insulin should be initiated. IVF of NS should be started at ~ 2400 cc/m2/day, which is approximately 1.5 x maintenance Continue reading >>

Preventing Complications Of Dm Ppt.

Preventing Complications Of Dm Ppt.

-give 20-30g CHO or Glucagon 1mg (retest in 15 min) -Give Iglucagon SQ (repeat in 10 min if pt is still unresponsive) --at hospital give 25-50% dextrose IV bolus --slower adrenergic response to falling glucose (shaky, nervous, tachycardia) Acute complications of Poor Glycemic control -Hyperglycemic crisis associated with fluid and electrolyte loss -manifestation of insulin deficiency (severe) Characteristics: Hyperglycemia, ketoacids, hemoconcentration, acidosis, coma -Kussmal respiration (rapid and deep) --trying to expel CO2 to increase the pH 3. Proliferative (overgrowth of abnormal blood vessels on the retina --very thin and prone to aneurysm) regular ophthalmologic exams (with dilated pupils) report any floaters, flashing lights, or changes in vision --decreased blood flow to Bowman's capsule avoid nephrotoxic drugs and dye (hydrate after tests with contrast medium) check serum creatinine, albumin, and creatinine clearance (already have decreased blood supply and wound healing) -Decreased/altered Sensation (bilateral, symmetrical, lower extremities) Preventing Injury with decreased sensation -wear leather, canvas shoes (dry between wearing) -do not cross legs, wear restrictive clothing at knee/thigh (avoid large seams that dig into skin) Continue reading >>

Confidential And Proprietary Any Use Of This Material Without Specific Permission Is Strictly Prohibited.

Confidential And Proprietary Any Use Of This Material Without Specific Permission Is Strictly Prohibited.

State of Ohio Overview of the diabetic ketoacidosis (DKA)/ hyperglycemic hyperosmolar state (HHS) episode of care CONFIDENTIAL AND PROPRIETARY Any use of this material without specific permission is strictly prohibited. CONFIDENTIAL AND PROPRIETARY Any use of this material without specific permission is strictly prohibited. December 23, 2016 | 1 Overview of the diabetic ketoacidosis (DKA)/hyperglycemic hyperosmolar state (HHS) episode of care 1. CLINICAL OVERVIEW AND RATIONALE FOR DEVELOPMENT OF THE DKA/HHS EPISODE 1.1 Rationale for development of the DKA/HHS episode of care DKA and HHS are among the most serious acute complications of diabetes. Clinically, DKA and HHS differ only by the degree of dehydration and the severity of metabolic acidosis. Both require prompt diagnosis and treatment. According to the American Diabetes Association, DKA accounts for more than $1 of every $4 spent on direct care for adult patients with Type I diabetes, and $1 of every $2 spent on patients experiencing multiple morbidities.1 In the United States, approximately 145,000 hospitalizations occur for DKA each year with an average cost of $17,500 per patient.2 The direct and indirect total annual cost of hospitalizations is estimated to be $2.4 billion.3 While the hospitalization rate for HHS is less than one percent of all diabetes-related admissions, death occurs in an estimated 5-16 percent of these patients, a rate 10 times higher than that of DKA.4 The complex pathophysiology of both DKA and HHS requires careful selection of approaches to restore glycemic control and deficiencies in intravascular volume and electrolytes. Appropriate treatment also includes the diagnosis and management of the underlying precipitating event. Death in patients with DKA/HHS is typically caused by the und 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 >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Background Hyperosmolar hyperglycemic state (HHS) is one of two serious metabolic derangements that occurs in patients with diabetes mellitus (DM). [1] It is a life-threatening emergency that, although less common than its counterpart, diabetic ketoacidosis (DKA), has a much higher mortality rate, reaching up to 5-10%. (See Epidemiology.) HHS was previously termed hyperosmolar hyperglycemic nonketotic coma (HHNC); however, the terminology was changed because coma is found in fewer than 20% of patients with HHS. [2] HHS is most commonly seen in patients with type 2 DM who have some concomitant illness that leads to reduced fluid intake, as seen, for example, in elderly institutionalized persons with decreased thirst perception and reduced ability to drink water. [3] Infection is the most common preceding illness, but many other conditions, such as stroke or myocardial infarction, can cause this state. [3] Once HHS has developed, it may be difficult to identify or differentiate it from the antecedent illness. (See Etiology.) HHS is characterized by hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis. Most patients present with severe dehydration and focal or global neurologic deficits. [2, 4, 5] The clinical features of HHS and DKA overlap and are observed simultaneously (overlap cases) in up to one third of cases. According to the consensus statement published by the American Diabetes Association, diagnostic features of HHS may include the following (see Workup) [4, 6] : Effective serum osmolality of 320 mOsm/kg or greater Profound dehydration, up to an average of 9L Detection and treatment of an underlying illness are critical. Standard care for dehydration and altered mental status is appropriate, including airway management, intravenous (I Continue reading >>

Canadian Diabetes Association Clinical Practice Guidelines Hyperglycemic Emergencies In Adults

Canadian Diabetes Association Clinical Practice Guidelines Hyperglycemic Emergencies In Adults

guidelines.diabetes.ca | 1-800-BANTING (226-8464) | diabetes.ca Copyright © 2013 Canadian Diabetes Association 1 Clinical Practice Guidelines CPG Tool Kit Professional Publications Diabetes Educator Study Resources & Educator Resources Food and Nutrition Tools CDA-CSEM Annual Conference Key Points Suspect DKA or HHS in an ill patient with hyperglycemia (usually) – medical emergency DKA = ketoacidosis is prominent HHS = ECFV contraction + hyperosmolarity Rx = FLUIDS, POTASSIUM, INSULIN (DKA) Treat precipitating cause Prevention is critical 2013 guidelines.diabetes.ca | 1-800-BANTING (226-8464) | diabetes.ca Copyright © 2013 Canadian Diabetes Association 2 Clinical Practice Guidelines CPG Tool Kit Professional Publications Diabetes Educator Study Resources & Educator Resources Food and Nutrition Tools CDA-CSEM Annual Conference Hyperglycemic Emergencies DKA = Diabetic Ketoacidosis HHS = Hyperosmolar Hyperglycemic State Common features: Insulin deficiency ïƒ hyperglycemia ïƒ urinary loss of water and electrolytes ïƒ Volume depletion + electrolyte deficiency + hyperosmolarity Insulin deficiency (absolute) + glucagon ïƒ Ketoacidosis (in DKA) guidelines.diabetes.ca | 1-800-BANTING (226-8464) | diabetes.ca Copyright © 2013 Canadian Diabetes Association 3 Clinical Practice Guidelines CPG Tool Kit Professional Publications Diabetes Educator Study Resources & Educator Resources Food and Nutrition Tools CDA-CSEM Annual Conference DKA Ketoacidosis ECFV contraction Milder hyperosmolarity Normal to high glucose May haveLOC Beware hypokalemia Must use insulin Absolute insulin deficiency + glucagon HHS Minimal acid-base problem ECFV contraction Hyperosmolarity Marked hyperglycemia Marked LOC Beware hypokalemia May need insulin Relative insulin 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 >>

Diabetic Emergencies

Diabetic Emergencies

AUTHORS Jeremy Rohrlich, MD, Emergency Medicine Resident, Department of Emergency Medicine, University of Texas Southwestern, Parkland Hospital, Dallas. Richard Williams, DO, Emergency Medicine Resident, Department of Emergency Medicine, University of Texas Southwestern, Parkland Hospital, Dallas. Fernando Benitez, MD, Professor, Department of Emergency Medicine, University of Texas Southwestern, Dallas. Larissa Velez, MD, Program Director and Vice-Chair for Education, Department of Emergency Medicine, University of Texas Southwestern, Dallas. PEER REVIEWER Catherine A. Marco, MD, FACEP, Professor, Emergency Medicine and Surgery, Wright State University, Dayton, OH. Statement of Financial Disclosure To reveal any potential bias in this publication, and in accordance with Accreditation Council for Continuing Medical Education guidelines, we disclose that Dr. Farel (CME question reviewer) owns stock in Johnson & Johnson. Dr. Schneider (editor), Dr. Stapczynski (editor), Ms. Fessler (nurse planner), Dr. Rohrlich (author), Dr. Williams (author), Dr. Benitez (author), Dr. Velez (author), Dr. Marco (peer reviewer), Ms. Mark (executive editor), and Ms. Coplin (executive editor) report no financial relationships with companies related to the field of study covered by this CME activity. EXECUTIVE SUMMARY Suspect diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar state (HHS) in an ill patient with hyperglycemia. In DKA, the acidosis is prominent. In HHS, volume contraction and hyperosmolality are prominent. DKA treatment sequence is fluids, potassium (if low), and insulin. Identify and treat precipitating causes. Point-of-care glucose testing devices may give false values, especially using capillary blood. In the treatment of an unresponsive hypoglycemic patient, consider Continue reading >>

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>

Slides Current Until 2008

Slides Current Until 2008

Slides current until 2008 Diabetic ketoacidosis and hyperosmolar hyperglycaemic state Abdulrahman Al shaikh.Asso professor, consultant endo. Al shaikh Slides current until 2008 * Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS) are two acute complications of diabetes. HHS used to be called hyperosmolar hyperglycaemic non-ketotic syndrome (HHNS or HONK). There is a comprehensive review of the subject by Kitabchi et al in Diabetes Care 2001. DKA and HHS Curriculum Module III-6 Slide * of 55 Slides current until 2008 What is DKA? Absolute or relative insulin deficiency Increase in counter-regulatory hormones Breakdown of fat and muscle Biochemical triad hyperglycaemia ketoacids metabolic acidosis High blood glucose, ketones, acidosis and dehydration Al shaikh Slides current until 2008 * DKA occurs when a deficiency in insulin – either absolute or relative – prevents glucose from entering cells, which leads to increasing hyperglycaemia. The secretion of counter-regulatory hormones (glucagon, epinephrine, growth hormone and cortisol) resulting in a massive release of glucose from the liver, contributes to this hyperglycaemia. This is followed by the uncontrolled breakdown of adipose and muscle tissues (catabolism). Fatty acids are released and are rapidly metabolized into ketones, which have strong acidity, to act as an alternative fuel in the absence of glucose and insulin. The excessive production of ketones lowers the blood’s pH and leads to metabolic acidosis. DKA is characterized as the biochemical triad involving: Hyperglycaemia – normally blood glucose higher than 11mmol/L (191mg/dL) Excessive ketoacids in blood and urine Metabolic acidosis – pH below 7.3 DKA and HHS Curriculum Module III-6 Slide * of 55 Slides Continue reading >>

Management Of The Hyperosmolar Hyperglycaemic State (hhs) In Adults With Diabetes (aug 2012)

Management Of The Hyperosmolar Hyperglycaemic State (hhs) In Adults With Diabetes (aug 2012)

Management of the hyperosmolar hyperglycaemic state (HHS) in adults with diabetes (Aug 2012) Management of the hyperosmolar hyperglycaemic state (HHS) in adults with diabetes (Aug 2012) Unlike the other common diabetes emergency, diabetic ketoacidosis (DKA), guidelines on the management of the hyperglycaemic hyperosmolar state (HHS) in adults are uncommon and often there is little to differentiate them from the management of DKA. However, HHS is different and treatment requires a different approach. The person with HHS is often elderly, frequently with multiple co-morbidities but always very sick. Even when specific hospital guidelines are available, adherence to and use of these is variable amongst the admitting teams. In many hospitals these patients are managed by non-specialist teams, and it is not uncommon for the most junior member, who is least likely to be aware of the hospital guidance, to be given responsibility for the initial management of this complex and challenging condition. Diabetes specialist teams are rarely involved at an early stage and sometimes never at all. To address these issues the Joint British Diabetes Societies (JBDS) for inpatient care, supported by NHS Diabetes, has produced up-to-date guidance for healthcare professionals to diagnose and manage HHS. JBDS-IP is supported by Diabetes UK, the Association of British Clinical Diabetologists (ABCD) and the Diabetes Inpatient Specialist Nurse UK Group. The aim of JBDS-IP is to improve inpatient diabetes care throughout the UK. This is mainly through the development and use of high quality evidence based guidelines, and through better inpatient care pathways. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis (DKA) A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone. Can occur in both Type I Diabetes and Type II Diabetes In type II diabetics with insulin deficiency/dependence The presenting symptom for ~ 25% of Type I Diabetics. Hyperosmolar Hyperglycemic State (HHS) An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia. Occurs predominately in Type II Diabetics A few reports of cases in type I diabetics. The presenting symptom for 30-40% of Type II diabetics. Diagnostic Criteria for DKA and HHS Mild DKA Moderate DKA Severe DKA HHS Plasma glucose (mg/dL) > 250 > 250 > 250 > 600 Arterial pH 7.25-7.30 7.00-7.24 < 7.00 > 7.30 Sodium Bicarbonate (mEq/L) 15 – 18 10 - <15 < 10 > 15 Urine Ketones Positive Positive Positive Small Serum Ketones Positive Positive Positive Small Serum Osmolality (mOsm/kg) Variable Variable Variable > 320 Anion Gap > 10 > 12 > 12 variable Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma Causes of DKA/HHS Stressful precipitating event that results in increased catecholamines, cortisol, glucagon. Infection (pneumonia, UTI) Alcohol, drugs Stroke Myocardial Infarction Pancreatitis Trauma Medications (steroids, thiazide diuretics) Non-compliance with insulin Diagnostic Studies in DKA/HHS Chemistry ï‚ Glucose  Bicarbonate Anion gap = (Na+) – (Cl- + HCO3-) Frequently seen: ï‚ BUN/creatinine (dehydration) ï‚ potassium  sodium Pseudohyponatremia: to correct, add 1.6 mEq of sodium to every 100mg/dL of glucose above normal Serum acetones Positive in Continue reading >>

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