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What Lab Values Indicate Dka?

Can Serum Β-hydroxybutyrate Be Used To Diagnose Diabetic Ketoacidosis?

Can Serum Β-hydroxybutyrate Be Used To Diagnose Diabetic Ketoacidosis?

Abstract OBJECTIVE—Current criteria for the diagnosis of diabetic ketoacidosis (DKA) are limited by their nonspecificity (serum bicarbonate [HCO3] and pH) and qualitative nature (the presence of ketonemia/ketonuria). The present study was undertaken to determine whether quantitative measurement of a ketone body anion could be used to diagnose DKA. RESEARCH DESIGN AND METHODS—A retrospective review of records from hospitalized diabetic patients was undertaken to determine the concentration of serum β-hydroxybutyrate (βOHB) that corresponds to a HCO3 level of 18 mEq/l, the threshold value for diagnosis in recently published consensus criteria. Simultaneous admission βOHB and HCO3 values were recorded from 466 encounters, 129 in children and 337 in adults. RESULTS—A HCO3 level of 18 mEq/l corresponded with βOHB levels of 3.0 and 3.8 mmol/l in children and adults, respectively. With the use of these threshold βOHB values to define DKA, there was substantial discordance (∼≥20%) between βOHB and conventional diagnostic criteria using HCO3, pH, and glucose. In patients with DKA, there was no correlation between HCO3 and glucose levels on admission and a significant but weak correlation between βOHB and glucose levels (P < 0.001). CONCLUSIONS—Where available, serum βOHB levels ≥3.0 and ≥3.8 mmol/l in children and adults, respectively, in the presence of uncontrolled diabetes can be used to diagnose DKA and may be superior to the serum HCO3 level for that purpose. The marked variability in the relationship between βOHB and HCO3 is probably due to the presence of other acid-base disturbances, especially hyperchloremic, nonanion gap acidosis. Recently published consensus criteria for diagnosing diabetic ketoacidosis (DKA) include a serum bicarbonate (HCO3) Continue reading >>

Lab Test

Lab Test

Measurement of beta-hydroxybutyrate in whole blood, serum, or plasma to evaluate ketone-producing metabolic energy deficits that usually occur when there is insufficient carbohydrate metabolism, thereby increasing the catabolism of fatty acids. Clinical Application Common tests for ketone bodies, such as Acetest, Chemstrip, and Ketostix, do not detect beta-hydroxybutyrate. A handheld meter sensor system is available to monitor beta-hydroxybutyrate and glucose levels. Elevated levels beta-hydroxybutyrate is diagnostic of ketoacidosis, whereas the absence of concomitant hyperglycemia supports the diagnosis of alcoholic ketoacidosis (AKA). Levels ³ 3 mmol/L are indicative of ketoacidosis. In very severe diabetic ketoacidosis (DKA), the beta-hydroxybutyrate serum concentration may exceed 25 mmol/L. Patients presenting with isopropanol intoxication can present with high acetone levels without any acidosis, anion gap or abnormal glucoses levels. Plasma (lithium-heparin or fluoride-oxalate), serum, or perchloric acid (PCA) extracts can be analyzed. EDTA-plasma samples will produce values that are 60% lower than specimens preserved with fluoride-oxalate or PCA. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci Continue reading >>

Diagnosis

Diagnosis

Print If your doctor suspects diabetic ketoacidosis, he or she will do a physical exam and various blood tests. In some cases, additional tests may be needed to help determine what triggered the diabetic ketoacidosis. Blood tests Blood tests used in the diagnosis of diabetic ketoacidosis will measure: Blood sugar level. If there isn't enough insulin in your body to allow sugar to enter your cells, your blood sugar level will rise (hyperglycemia). As your body breaks down fat and protein for energy, your blood sugar level will continue to rise. Ketone level. When your body breaks down fat and protein for energy, acids known as ketones enter your bloodstream. Blood acidity. If you have excess ketones in your blood, your blood will become acidic (acidosis). This can alter the normal function of organs throughout your body. Additional tests Your doctor may order tests to identify underlying health problems that might have contributed to diabetic ketoacidosis and to check for complications. Tests might include: Blood electrolyte tests Urinalysis Chest X-ray A recording of the electrical activity of the heart (electrocardiogram) Treatment If you're diagnosed with diabetic ketoacidosis, you might be treated in the emergency room or admitted to the hospital. Treatment usually involves: Fluid replacement. You'll receive fluids — either by mouth or through a vein (intravenously) — until you're rehydrated. The fluids will replace those you've lost through excessive urination, as well as help dilute the excess sugar in your blood. Electrolyte replacement. Electrolytes are minerals in your blood that carry an electric charge, such as sodium, potassium and chloride. The absence of insulin can lower the level of several electrolytes in your blood. You'll receive electrolytes throu 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 >>

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 >>

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 >>

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic Ketoacidosis (dka) - Topic Overview

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your blood (electrolyt 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 >>

Diabetes Urine Tests

Diabetes Urine Tests

Urine tests may be done in people with diabetes to evaluate severe hyperglycemia (severe high blood sugar) by looking for ketones in the urine. Ketones are a metabolic product produced when fat is metabolized. Ketones increase when there is insufficient insulin to use glucose for energy. Urine tests are also done to look for the presence of protein in the urine, which is a sign of kidney damage. Urine glucose measurements are less reliable than blood glucose measurements and are not used to diagnose diabetes or evaluate treatment for diabetes. They may be used for screening purposes. Testing for ketones is most common in people with type 1 diabetes. Type 1 Diabetes: What Are The Symptoms? This test detects the presence of ketones, which are byproducts of metabolism that form in the presence of severe hyperglycemia (elevated blood sugar). Ketones are formed from fat that is burned by the body when there is insufficient insulin to allow glucose to be used for fuel. When ketones build up to high levels, ketoacidosis (a serious and life-threatening condition) may occur. Ketone testing can be performed both at home and in the clinical laboratory. Ketones can be detected by dipping a test strip into a sample of urine. A color change on the test strip signals the presence of ketones in the urine. Ketones occur most commonly in people with type 1 diabetes, but uncommonly, people with type 2 diabetes may test positive for ketones. The microalbumin test detects microalbumin, a type of protein, in the urine. Protein is present in the urine when there is damage to the kidneys. Since the damage to blood vessels that occurs as a complication of diabetes can lead to kidney problems, the microalbumin test is done to check for damage to the kidneys over time. Can urine tests be used to Continue reading >>

Infection As A Trigger Of Diabetic Ketoacidosis In Intensive Care—unit Patients

Infection As A Trigger Of Diabetic Ketoacidosis In Intensive Care—unit Patients

Together with hyperglycemic coma, diabetic ketoacidosis (DKA) is the most severe acute metabolic complication of diabetes mellitus [ 1 ]. Defined by the triad hyperglycemia, acidosis, and ketonuria, DKA can be inaugural or complicate known diabetes [ 2 ]. Although DKA is evidence of poor metabolic control and usually indicates an absolute or relative imbalance between the patient's requirements and the treatment, DKA-related mortality is low among patients who receive standardized treatment, which includes administration of insulin, correction of hydroelectrolytic disorders, and management of the triggering factor (which is often cessation of insulin therapy, an infection, or a myocardial infarction) [ 3–8 ]. Although there is no proof that diabetics are more susceptible to infection, they seem to have more difficulty handling infection once it occurs [ 9 , 10 ]. Indeed, several aspects of immunity are altered in diabetic patients: polymorphonuclear leukocyte function is depressed, particularly when acidosis is present, and leukocyte adherence, chemotaxis, phagocytosis, and bactericidal activity may also be impaired [ 11–15 ]. Joshi et al. [ 10 ] reported recently on the lack of clinical evidence that diabetics are more susceptible to infection than nondiabetic patients. Nevertheless, infection is a well-recognized trigger of DKA. Earlier studies have investigated the prevalence of infection as a trigger of DKA and the impact of antimicrobial treatment [ 2 , 15–18 ]. However, none of these studies were of intensive care unit (ICU) patients only. Furthermore, most were descriptive, included small numbers of patients, used univariate analysis only, and did not designate infection as the sole outcome variable of interest. Efforts to identify correlates of infection h Continue reading >>

15l. Loriaux (ed.), Endocrine Emergencies: Recognition And Treatment, Contemporary Endocrinology 74, Doi 10.1007/978-1-62703-697-9_2, © Springer Science+business Media New York 2014

15l. Loriaux (ed.), Endocrine Emergencies: Recognition And Treatment, Contemporary Endocrinology 74, Doi 10.1007/978-1-62703-697-9_2, © Springer Science+business Media New York 2014

Précis 1. Clinical setting—Any altered state of well being in the context of signifi cant hyperglycemia in a patient with type 1 (DKA) or advanced type 2 diabetes mel- litus (DKA or HHS), particularly during acute illness, may signify one of these diabetic emergencies. 2. Diagnosis (a) History: Most patients with diabetic ketoacidosis (DKA) or with hyperos- molar hyperglycemic state (HHS) will have a history of diabetes, and a his- tory of altered insulin dose, infection, signifi cant medical “stressâ€. Antecedent symptoms of polyuria and polydipsia, lassitude, blurred vision, and mental status changes may predominate the clinical picture. With DKA, abdominal pain and tachypnea are often present. (b) Physical examination usually reveals an altered sensorium, signs of volume contraction/dehydration (tachycardia, hypotension, dry mucus membranes, “tenting†of the skin); in DKA, the odor of acetone in the breath. (c) Laboratory evaluation. The diagnostic criteria for DKA include blood glu- cose above 250 mg/dL, arterial pH < 7.30, serum bicarbonate < 15 mEq/l Chapter 2 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic Syndrome Beatrice C. Lupsa and Silvio E. Inzucchi B. C. Lupsa , M.D. (*) • S. E. Inzucchi , M.D. Section of Endocrinology , Yale University School of Medicine , Yale-New Haven Hospital, 333 Cedar Street, FMP 107 , P.O. Box 208020 , New Haven , CT 06520 , USA e-mail: [email protected] 16 and moderate degree of ketonemia and/or ketonuria. Patients with HHS present with extreme hyperglycemia (blood glucose > 600 mg/dL), increased osmolality (> 320 mOsm/kg) and profound dehydration/volume contrac- tion. The laboratory evaluation of a patient with hyperglycemic emergency should include measurement of blood glucose and he 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 >>

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 >>

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