diabetestalk.net

Why Is Bun Elevated In Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

Publications

Publications

diabetic ketoacidosis, type 1 diabetes mellitus, type2 diabetes mellitus Objectives: Aim of this study was to record the epidemiological, clinical and biochemical features of DKA and their prognostic significance in adult diabetics. Patients and methods: The medical records of patients admitted due to DKA, between 2001 and 2006, were retrospectively reviewed. The patients were classified as type 1, type 2, based mainly on treatment history and autoantibody status, with c-peptide measurement for newly diagnosed patients. Results: Of 56 patients (19 male, 37 females) with mean average of age 63.6 years, 30(53.5%) had type 2 diabetes, 16(28.5%) had type 1 diabetes and 10 (18%) were newly diagnosed diabetics. In 32.2% of patients the precipitating factor of DKA was an acute infection, with most frequent urinary tract infections (50%). Potassium concentrations found to be abnormal in 42.8% of patients and 10.7% had hypokalemia in admission. The duration of hospitalization was 10±7.6 days. Type 1 DM group was more acidotic than Type 2 DM group (arterial pH, 7.16±0.18 vs 7.22±0.13, p=0.01),. In hospital mortality (12.5%) was significantly correlated with increased age (p<0.01). Conclusion: DKA occurs in a relatively high proportion in individuals with type 2 diabetes. The most frequent cause of DKA is acute infection. Advanced age is associated with an increased risk of mortality. Introduction Diabetic ketoacidosis (DKA) is a serious complication of diabetes mellitus (DM), characterised by the biochemical triad of hyperglycemia, ketonemia and acidosis (1, 2). As traditional teaching describes, DKA is typical of Type 1 DM, lately called insulin depended diabetes mellitus (IDDM). More recently, there have been multiple reports of DKA in patients with type 2 diabetes mellitus, Continue reading >>

Blood Ketones

Blood Ketones

On This Site Tests: Urine Ketones (see Urinalysis - The Chemical Exam); Blood Gases; Glucose Tests Elsewhere On The Web Ask a Laboratory Scientist Your questions will be answered by a laboratory scientist as part of a voluntary service provided by one of our partners, the American Society for Clinical Laboratory Science (ASCLS). Click on the Contact a Scientist button below to be re-directed to the ASCLS site to complete a request form. If your question relates to this web site and not to a specific lab test, please submit it via our Contact Us page instead. Thank you. Continue reading >>

Hyperglycemic Emergencies

Hyperglycemic Emergencies

Lana Kravarusic Doctor of Pharmacy Candidate, University of Florida Introduction Diabetes mellitus, if uncontrolled, may lead to serious hyperglycemic emergencies. The two most serious hyperglycemic emergencies are diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). (Hyperglycemic hyperosmolar state is synonymous with hyperosmolar syndrome and hyperglycemic hyperosmolar nonketotic state which are both older names.) DKA most commonly occurs in patients with Type 1 diabetes mellitus or pancreatic disease, while HHS occurs more frequently with Type 2 diabetes. The presentation of the two syndromes can be distinguished by several factors. Both DKA and HHS patients present with hyperglycemia, but DKA is characterized by ketonemia, ketonuria, and metabolic acidosis while HHS involves dehydration without significant ketoacidosis. It is also possible that a patient presents with a mixture of DKA and HHS.1 The incidence of DKA is estimated to be 4-8 per 1000 diabetic patients, but is likely an underestimation. Up to 25% of cases in the United States are discovered at diagnosis, especially in younger children. The current mortality rate is 2-5% with treatment, and is usually a result of the underlying associated illnesses rather than DKA itself.2 For example elderly patients (>65 years) may have a mortality rate as high as 20% due to comorbid conditions. In some rare cases, however, mortality is a result of a DKA complication such as cerebral edema which is estimated to occur in 0.7-1% of DKA cases in young adults and children. Therefore, children less than 5 years of age and elderly over the age of 65 are considered high-risk DKA patients.1 Currently, the incidence of HHS in the United States is thought to be less than 1 per 1000-person years, making HHS much Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

DKA is an acute complication of diabetes mellitus (usually type 1 diabetes) characterized by hyperglycemia, ketonuria, acidosis, and dehydration. Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat for fuel. Free fatty acids, released from the metabolism of fat, are converted to ketone bodies in the liver. Increase in the secretion of glucagon, catecholamines, growth hormone, and cortisol, in response to the hyperglycemia caused by insulin deficiency, accelerates the development of DKA. Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium, sodium, phosphate, and water. Serum glucose level is usually elevated over 300 mg/dL; may be as high as 1,000 mg/dL. Serum bicarbonate and pH are decreased due to metabolic acidosis, and partial pressure of carbon dioxide is decreased as a respiratory compensation mechanism. Serum sodium and potassium levels may be low, normal, or high due to fluid shifts and dehydration, despite total body depletion. Urine glucose is present in high concentration and specific gravity is increased, reflecting osmotic diuresis and dehydration. Observe for cardiac changes reflecting dehydration, metabolic acidosis, and electrolyte imbalance- hypotension; tachycardia; weak pulse; electrocardiographic changes, including elevated P wave, flattened T wave or inverted, prolonged QT interval. Administer replacement electrolytes and insulin as ordered. Flush the entire I.V. infusion set with solution containing insulin and discard the first 50 mL because plastic bags and tubing may absorb some insulin and the initial solution may contain decreased concentration of insulin. Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Jaime Moo-young, Md

Jaime Moo-young, Md

Diabetic Ketoacidosis (DKA) Pathogenesis · Insufficient insulin for a given carbohydrate load decreased cellular metabolism of glucose · Increased gluconeogenesis, glycogenolysisHyperglycemia · Increased breakdown of free fatty acids as alternative energy source ketone and ketoacid accumulation · Hyperglycemiaserum hyperosmolality osmotic diuresis dehydration and electrolyte derangements (dehydration is most lethal!) · Seen almost exclusively in Type I diabetes; rarely in Type II Definition: Triad of 1. Hyperglycemia (usually between 500 – 800 mg/dL or 27.8-44.4 mmol/L) 2. Anion Gap Metabolic Acidosis (pH usually <7.30) 3. Ketonemia: -hydroxybutyrate, acetoacetate most significant ** Urine ketones do not make the diagnosis, but they can support it** Triggers (the “I’sâ€): Don’t forget to ask about these! · Insulin deficiency: insulin non-compliance, insufficient insulin dosing, new-onset Type I diabetes · Iatrognic: glucocorticoids, atypical antipsychotics, high-dose thiazide diuretics · Infection: UTI, pneumonia, TB · Inflammation: pancreatitis, cholecystitis · Ischemia/infarction: MI, stroke, gut ischemia · Intoxication: Alcohol, cocaine, other drugs Presentation · Symptoms · Polyuria, polydipsia, weight loss · Nausea, vomiting, abdominal pain · Fatigue, malaise · Associated trigger sx (fever/chills, chest pain, etc) · Signs · Volume depletion: skin turgor, dry axillae, dry mucus membranes, HR, BP · Altered mental status: stupor, coma · Kussmaul respirations: rapid, shallow breathing = hyperventilation to counteract metabolic acidosis · Fruity, acetone odor on breath Lab workup and findings · Hyperglycemia: > 250 mg/dL in serum, + glucose on urinalysis · Acidemia (pH <7. Continue reading >>

Lab Test

Lab Test

Measurement of serum or plasma blood urea nitrogen (BUN) for the evaluation and management of volume status and renal disorders. It is performed on patients undergoing routine laboratory testing and is usually performed as part of a multiphasic automated testing process. Adults: 10-20 mg/dL (3.6-7.1 mmol/L) Elderly: may be slightly higher than adult Children: 5-18 mg/dL (1.8-6.4 mmol/L) Infant: 5-18 mg/dL Newborn: 3-12 mg/dL Cord: 21-40 mg/dL Critical Values: >100 mg/dL (indicates serious impairment of renal function) Adrenal insufficiency - moderate elevations in BUN levels are consistent with both acute and chronic adrenal insufficiency. The increased Bun is largely due to dehydration secondary to aldosterone deficiency, which leads to excretion of sodium in excess of intake and results in azotemia. Patients with secondary adrenal insufficiency are less affected because of intact aldosterone secretion. Elevation is usually reversible with restoration of normal renal hemodynamics and circulating blood volume. Community-acquired pneumonia - In one study, an elevated BUN, along with increased respiratory rate and decreased diastolic blood pressure, was predictive of mortality in patients with community-acquired pneumonia. Hemolytic uremic syndrome (HUS) - BUN level is consistently increased with the elevation usually occurring very rapidly. The combination of renal insufficiency, a catabolic state, and reabsorption of blood from the GI tract can cause BUN levels to increase as much as 50 mg/dL/day. In children with uncomplicated dehydration and diarrhea, the BUN level should fall to one half the admission level within 24 hours; if this does not occur, renal disease should be suspected. Hemorrhagic shock - Acute tubular necrosis (ATN) from prolonged hypotension results in Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia — A Brief Review

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia — A Brief Review

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemia — A Brief Review SPECIAL FEATURE By Richard J. Wall, MD, MPH, Pulmonary Critical Care & Sleep Disorders Medicine, Southlake Clinic, Valley Medical Center, Renton, WA. Dr. Wall reports no financial relationships relevant to this field of study. Financial Disclosure: Critical Care Alert's editor, David J. Pierson, MD, nurse planner Leslie A. Hoffman, PhD, RN, peer reviewer William Thompson, MD, executive editor Leslie Coplin, and managing editor Neill Kimball report no financial relationships relevant to this field of study. INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most common and serious acute complications of diabetes mellitus. DKA is responsible for more than 500,000 hospital days annually in the United States, at an estimated annual cost of $2.4 billion. Both conditions are part of the spectrum of uncontrolled hyperglycemia, and there is sometimes overlap between them. This article will discuss and compare the two conditions, with a focus on key clinical features, diagnosis, and treatment. DIAGNOSTIC FEATURES In DKA, there is an accumulation of ketoacids along with a high anion gap metabolic acidosis (see Table below).1 The acidosis usually evolves quickly over a 24-hour period. The pH is often < 7.20 and initial bicarbonate levels are often < 20 mEq/L. DKA patients (especially children) often present with nausea, vomiting, hyperventilation, and abdominal pain. Blood sugar levels in DKA tend to be 300-800 mg/dL, but they are sometimes much higher when patients present in a comatose state. In HHS, there is no (or little) ketonemia but the plasma osmolality may reach 380 mOsm/kg, and as a result, patients often have neurologic complications such as coma. Bica Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Lab Values And Dka

Lab Values And Dka

Changes in laboratory values often give us clues to what is happening with our patients. I came across the following resource this morning and thought it was worth sharing. Here’s a handy table to help you identify diabetic ketoacidosis (DKA). The following equation can be used to calculate an anion gap: Anion gap = Na+(mEq/L) – [Cl-(mEq/L) + HCO3-(mEq/L)] You have an important role when caring for a patient with DKA. Thorough physical assessments, careful monitoring of laboratory values, and critical thinking are essential to avoid complications of this complex disorder. Have you cared for a patient with DKA? What are the common presenting signs and symptoms? Reference Donahey, E., Folse, S., Weant, K. (2012). Management of Diabetic Ketoacidosis. Advanced Emergency Nursing Journal, 34(3). Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is the most common acid–base disorder and can be life threatening. It results from excessive cellular acid production, reduced acid secretion, or loss of body alkali. The body has two buffering mechanisms to counteract an increase in acid. The initial response is to increase carbon dioxide excretion by increasing ventilation. The second response is increased renal excretion of acids and renal regeneration of bicarbonate. The adequacy of compensation can be assessed by the quick check method or the Winter formula (Table 2). Metabolic acidosis can be classified into two categories using the anion gap. Each category has a distinct differential diagnosis. Anion gap = [Sodium] – ([Chloride] + [Bicarbonate]) Normally, the anion gap is approximately 12 ± 2 meq/L (12 ± 2 mmol/L). Most unmeasured anions consist of albumin. Therefore, the presence of either a low albumin level or an unmeasured cationic light chain, which occurs in multiple myeloma, results in a low anion gap. Increased hydrogen ion concentration or decreased bicarbonate concentration will increase the gap. When the primary disturbance is a metabolic acidosis, the anion gap helps to narrow the diagnostic possibilities to an increased anion gap acidosis or a normal anion gap acidosis. Increased Anion Gap Metabolic Acidosis Common causes include ketoacidosis (diabetes mellitus, alcohol abuse, starvation), lactic acidosis, chronic kidney disease, salicylate toxicity, and ethylene glycol and methanol poisoning. Diabetic ketoacidosis is the most common cause of an increased anion gap acidosis, but a normal anion gap acidosis may be present early in the disease course when the extracellular fluid (ECF) volume is nearly normal. Ketoacidosis also may develop in patients with a histor Continue reading >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. PATHOGENESIS Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are in Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>

Evaluation Of Delirium

Evaluation Of Delirium

Diagnostic Tests Common Differential 1st Tests Other Tests Dementia the diagnosis of dementia is based predominantly on historical factors: diagnosis is clinical Pain diagnosis is clinical: causes of underlying pain should be sought (e.g., hip fracture) Stroke/cerebrovascular accident and transient ischemic attack neuroimaging (CT and/or MRI): ischemic CVA: hyperdense vessels at the site of blood clot in middle cerebral artery (MCA), posterior cerebral artery (PCA), or anterior cerebral artery (ACA); loss of insular stripe located between Sylvian fissure and basal ganglia is frequently associated with early MCA stroke; subtle mass effect; [78] hemorrhagic CVA: hyperdense to grey matter lesion at the site of hemorrhage; mass effect may also be evident but frequently subtle in early stroke more Findings frequently absent for transient ischemic attacks and ischemic strokes. Findings frequently absent for transient ischemic attacks and ischemic strokes. Myocardial infarction ECG: ST segment elevation or depression, or T wave changes serum troponin: elevated CXR: evidence of pulmonary congestion/ pleural effusion if secondary heart failure, may show enlarged cardiac shadow coronary angiogram: presence of thrombus with occlusion of the artery Acute systemic infection basic test panel (CBC, serum electrolytes, blood glucose, serum liver function tests, coagulation profile): elevated WBC count or leukopenia with sepsis; may be elevated urea and creatinine with sepsis; may be low platelets with sepsis; blood glucose may be elevated or, more rarely, low with sepsis; serum transaminases and serum bilirubin may be elevated with sepsis; may be prolonged or elevated INR, PT, aPTT more If shock is present, urgent simultaneous treatment required. WBC count may be normal in early stages Continue reading >>

More in ketosis