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 >>

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 >>

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Differential Diagnosis Disease/Condition Differentiating Signs/Symptoms Differentiating Tests Hyperosmolar hyperglycemic state (HHS) Patients are typically older than patients with DKA and are usually patients with type 2 diabetes. Older nursing home residents with poor fluid intake are at high risk. Symptoms evolve insidiously over days to weeks. Mental obtundation and coma are more frequent. Focal neurologic signs (hemianopia and hemiparesis) and seizures are also seen. Seizures may be the dominant clinical features. [1] Serum glucose is >600 mg/dL. Serum osmolality is usually >320 mOsm/kg. Urine ketones are normal or only mildly positive. Serum ketones are negative. Anion gap is variable but typically <12 mEq/L. Total chloride deficit is 5 to 15 mEq/kg. ABG: arterial pH is typically >7.30, whereas in DKA it ranges from 7.00 to 7.30. Arterial bicarbonate is >15 mEq/L. Lactic acidosis The presentation is identical to that of DKA. In pure lactic acidosis, the serum glucose and ketones should be normal and the serum lactate concentration should be elevated. Serum lactate >5 mmol/L. [1] Starvation ketosis Starvation ketosis results from inadequate carbohydrate availability resulting in physiologically appropriate lipolysis and ketone production to provide fuel substrates for muscle. The blood glucose is usually normal. Although the urine can have large amounts of ketones, the blood rarely does. Arterial pH is normal and the anion gap is at most mildly elevated. [1] Alcoholic ketoacidosis Classically, these patients are long-standing alcoholic people for whom ethanol has been the main caloric source for days to weeks. The ketoacidosis occurs when for some reason alcohol and caloric intake decreases. In isolated alcoholic ketoacidosis, the metabolic acidosis is usually mild 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 >>

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 >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. 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. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath 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 >>

Diabetic Ketoacidosis And Cerebral Edema

Diabetic Ketoacidosis And Cerebral Edema

Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center Introduction In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (1), accounting for 31% of deaths associated with DKA and 20% of all diabetic deaths, having surpassed aspiration, electrolyte imbalance, myocardial infarction, etc. Furthermore, diabetes mellitus remains an important cause of hospitalization of young children. The prevalence rate of diabetes continues to grow in all Western developed nations, nearly doubling every decade, resulting in 22,000 hospital admissions in children under 15 years of age for diabetes in the United States in 1994, the majority of which were due to ketoacidosis. With approximately 4 hospital admissions of children for DKA per 100,000 population per year (2), every PICU located in a major metropolitan center will conti Continue reading >>

Measure Electrolyte And Ketone Levels And Determine Anion Gap In Patients With Diabetes And Normal Sugar Levels

Measure Electrolyte And Ketone Levels And Determine Anion Gap In Patients With Diabetes And Normal Sugar Levels

DIABETIC KETOACIDOSIS DX: Diabetic Ketoacidosis (DKA) when the blood glucose is >=250 mg/dL, arterial pH <=7.30, serum bicarbonate <=15 mEq/L, and positive serum ketones. (Hyperglycemia, ketonemia, ketonuria, metabolic acidosis) Screening for Diabetic Ketoacidosis - Consider DKA if hyperglycemia, acidosis, or ketonemia are present. Screen all patients with moderate to severely elevated blood sugars (glucose >350 mg/dL). Measure electrolytes, glucose, ketones, and blood gases to determine whether anion gap metabolic acidosis is present in patients with positive ketones, constitutional symptoms, or suspicion of DKA. in patients with an anion gap metabolic acidosis. Measure serum glucose in patients with metabolic acidosis. in diabetes patients with infection, CVA, MI, or other illness. Measure serum glucose and if glucose >250 mg/dL, check the patient's electrolyte and ketone levels and anion gap. in diabetic patients with symptoms of nausea and vomiting (with polyuria, polydipsia), even if blood glucose is <250 mg/dL. if symptoms suggest DKA despite normal blood sugar levels. in patients on atypical antipsychotics who present with hyperglycemia. Measure anion gap and ketones in patients on atypical antipsychotics who present with moderate to severe hyperglycemia. SX: Dehydration with hypotension, hyperventilation with fruity "acetone" odor, polyphagia, polydipsia, polyuria, altered mental status, N&V. History and Physical Examination Elements for Diabetic Ketoacidosis History Type 1 diabetes - DKA is a frequent complication of type 1 diabetes Constitutional symptoms - DKA may show vague symptoms of lethargy, diminished appetite, and headache Polyuria, polydipsia - May precede the development of DKA by 1 or 2 days, especially if intercurrent illness (infection) is present 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 >>

Diabetes With Ketone Bodies In Dogs

Diabetes With Ketone Bodies In Dogs

Diabetes Mellitus with Ketoacidosis in Dogs Diabetes is a medical condition in which the body cannot absorb sufficient glucose, thus causing a rise the blood sugar levels. The term “ketoacidosis,” meanwhile, refers to a condition in which levels of acid abnormally increased in the blood due to presence of “ketone bodies”. In diabetes with ketoacidosis, ketoacidosis immediately follows diabetes. It should be considered a dire emergency, one in which immediate treatment is required to save the life of the animal. This condition typically affects older dogs as well as females. In addition, miniature poodles and dachshunds are predisposed to diabetes with ketoacidosis. Symptoms and Types Weakness Lethargy Depression Lack of appetite (anorexia) Muscle wasting Rough hair coat Dehydration Dandruff Sweet breath odor Causes Although the ketoacidosis is ultimately brought on by the dog's insulin dependency due to diabetes mellitus, underlying factors include stress, surgery, and infections of the skin, respiratory, and urinary tract systems. Concurrent diseases such as heart failure, kidney failure, asthma, cancer may also lead to this type of condition. Diagnosis You will need to give a thorough history of your dog’s health, including the onset and nature of the symptoms, to your veterinarian. He or she will then perform a complete physical examination, as well as a biochemistry profile and complete blood count (CBC). The most consistent finding in patients with diabetes is higher than normal levels of glucose in the blood. If infection is present, white blood cell count will also high. Other findings may include: high liver enzymes, high blood cholesterol levels, accumulation in the blood of nitrogenous waste products (urea) that are usually excreted in the urine (azo Continue reading >>

Diabetic Ketoacidosis Workup

Diabetic Ketoacidosis Workup

Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [17] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. 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 >>

More in ketosis