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What Lab Values Indicate Dka?

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

Blood Gas Measurements In Dka: Are We Searching For A Unicorn?

Introduction Recently there have been numerous publications and discussions about whether VBGs can replace ABGs in DKA. The growing consensus is that VBGs are indeed adequate. Eliminating painful, time-consuming arterial blood draws is a huge step in the right direction. However, the ABG vs. VBG debate overlooks a larger point: neither ABG nor VBG measurements are usually helpful. It is widely recommended to routinely obtain an ABG or VBG, for example by both American and British guidelines. Why? Is it helping our patients, or is it something that we do out of a sense of habit or obligation? Diagnosis of DKA: Blood gas doesn’t help These are the diagnostic criteria for DKA from the America Diabetes Association. They utilize either pH or bicarbonate in a redundant fashion to quantify the severity of acidosis. It is unclear what independent information the pH adds beyond what is provided by the bicarbonate. Practically speaking, the blood gas doesn’t help diagnose DKA. This diagnosis should be based on analysis of the metabolic derangements in the acid-base status (e.g. anion gap, beta-hydroxybutyrate level). The addition of a blood gas to serum chemistries only adds information about the respiratory status, which does not help determine if the patient has ketoacidosis. Management: Does the pH help? It is debatable whether knowing or attempting to directly “treat” the pH is helpful. The pH will often be very low, usually lower than would be expected by looking at the patient. This may induce panic. However, it is actually a useful reminder that acidemia itself doesn't necessarily cause instability (e.g. healthy young rowers may experience lactic acidosis with a pH <7 during athletic exertion; Volianitis 2001). A question often arises regarding whether bicarbonate 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis Definition Diabetic ketoacidosis is a dangerous complication of diabetes mellitus in which the chemical balance of the body becomes far too acidic. Description Diabetic ketoacidosis (DKA) always results from a severe insulin deficiency. Insulin is the hormone secreted by the body to lower the blood sugar levels when they become too high. Diabetes mellitus is the disease resulting from the inability of the body to produce or respond properly to insulin, required by the body to convert glucose to energy. In childhood diabetes, DKA complications represent the leading cause of death, mostly due to the accumulation of abnormally large amounts of fluid in the brain (cerebral edema). DKA combines three major features: hyperglycemia, meaning excessively high blood sugar kevels; hyperketonemia, meaning an overproduction of ketones by the body; and acidosis, meaning that the blood has become too acidic. Insulin deficiency is responsible for all three conditions: the body glucose goes largely unused since most cells are unable to transport glucose into the cell without the presence of insulin; this condition makes the body use stored fat as an alternative source instead of the unavailable glucose for energy, a process that produces acidic ketones, which build up because they require insulin to be broken down. The presence of excess ketones in the bloodstream in turn causes the blood to become more acidic than the body tissues, which creates a toxic condition. Causes and symptoms DKA is most commonly seen in individuals with type I diabetes, under 19 years of age and is usually caused by the interruption of their insulin treatment or by acute infection or trauma. A small number of people with type II diabetes also experience ketoacidosis, but this is rare give Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be 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 >>

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

The Facts Diabetic ketoacidosis (DKA) is a condition that may occur in people who have diabetes, most often in those who have type 1 (insulin-dependent) diabetes. It involves the buildup of toxic substances called ketones that make the blood too acidic. High ketone levels can be readily managed, but if they aren't detected and treated in time, a person can eventually slip into a fatal coma. DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. Although much less common, DKA can occasionally occur in people with type 2 diabetes under extreme physiologic stress. Causes With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body's cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can't get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn't available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body's metabolic processes aren't able 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 >>

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

As fat is broken down, acids called ketones build up in the blood and urine. In high levels, ketones are poisonous. This condition is known as ketoacidosis. Diabetic ketoacidosis (DKA) is sometimes the first sign of type 1 diabetes in people who have not yet been diagnosed. It can also occur in someone who has already been diagnosed with type 1 diabetes. Infection, injury, a serious illness, missing doses of insulin shots, or surgery can lead to DKA in people with type 1 diabetes. People with type 2 diabetes can also develop DKA, but it is less common. It is usually triggered by uncontrolled blood sugar, missing doses of medicines, or a severe illness. 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 >>

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 >>

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 >>

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 >>

Prospective Studies May Decrease The Incidence Of Dka In Type 1 Diabetes In Children

Prospective Studies May Decrease The Incidence Of Dka In Type 1 Diabetes In Children

Placing newborns in prospective studies to conduct genetic screenings with follow up may reduce the risk of DKA at diagnosis of type 1. Children, particularly those under the age of 5, are at the highest risk of experiencing Diabetic Ketoacidosis (DKA) at diagnosis of type 1 diabetes. This may be due to a delay in diagnosis by lack of knowledge of initial symptoms from parents or a misdiagnosis by clinicians with concurrent health issues. Currently, there are mixed data indicating whether DKA is increasing or decreasing in frequency. However, prior studies have shown that providing education on the initial symptoms of type 1 diabetes has shown to reduce the incidence of DKA at diagnosis. This can be seen in children with first-degree relatives who are more knowledgeable in the disease and can recognize initial symptoms. It is also seen in children enrolled in prospective studies for genetic testing of the disease and participating in follow ups. Oulu University Hospital in Finland have ongoing prospective studies since 1995. They have been genetically testing all newborn infants for HLA-conferred susceptibility of type 1 diabetes. One study hypothesized a decreased risk of DKA in children at diagnosis with type 1 diabetes who participated in prospective studies. Therefore, researchers conducted two study cohorts focusing information gathered by the prospective studies in Oulu University Hospital in Finland. A total of 1,164 patients were evaluated with an overlap of 485 children. Study cohort 1 had a sample size of 517 children. It included all children born in 1995-2012 with a diagnosis of type 1 diabetes by the end of 2014. Study cohort 2 had a sample size of 579. It included all children diagnosed with type 1 diabetes in 2002-2014. Study cohort 1 was divided into 4 s Continue reading >>

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