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Dka Anion Gap

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

Diabetic Ketoacidosis

© 1996–2017 themedicalbiochemistrypage.org, LLC | info @ themedicalbiochemistrypage.org Definition of Diabetic Ketoacidosis The most severe and life threatening complication of poorly controlled type 1 diabetes is diabetic ketoacidosis (DKA). DKA is characterized by metabolic acidosis, hyperglycemia and hyperketonemia. Diagnosis of DKA is accomplished by detection of hyperketonemia and metabolic acidosis (as measured by the anion gap) in the presence of hyperglycemia. The anion gap refers to the difference between the concentration of cations other than sodium and the concentration of anions other than chloride and bicarbonate. The anion gap therefore, represents an artificial assessment of the unmeasured ions in plasma. Calculation of the anion gap involves sodium (Na+), chloride (Cl–) and bicarbonate (HCO3–) measurements and it is defined as [Na+ – (Cl– + HCO3–)] where the sodium and chloride concentrations are measured as mEq/L and the bicarbonate concentration is mmol/L. The anion gap will increase when the concentration of plasma K+, Ca2+, or Mg2+ is decreased, when organic ions such as lactate are increased (or foreign anions accumulate), or when the concentration or charge of plasma proteins increases. Normal anion gap is between 8mEq/L and 12mEq/L and a higher number is diagnostic of metabolic acidosis. Rapid and aggressive treatment is necessary as the metabolic acidosis will result in cerebral edema and coma eventually leading to death. The hyperketonemia in DKA is the result of insulin deficiency and unregulated glucagon secretion from α-cells of the pancreas. Circulating glucagon stimulates the adipose tissue to release fatty acids stored in triglycerides. The free fatty acids enter the circulation and are taken up primarily by the liver where Continue reading >>

D-lactate: A Novel Contributor To Metabolic Acidosis And High Anion Gap In Diabetic Ketoacidosis

D-lactate: A Novel Contributor To Metabolic Acidosis And High Anion Gap In Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA),the most common and serious acute complication of diabetes, is characterized by hyperglycemia and severe high–anion-gap metabolic acidosis with ketonemia (1). In DKA, the high anion gap is attributed largely to excessive production of blood ketone bodies, and serum β-hydroxybutyrate quantification is recommended for the diagnosis and monitoring of DKA (2). However, even counting of all the ketone bodies, including β-hydroxybutyrate, does not account for the entire anion gap, suggesting that there are additional sources of anion production in DKA. We recently demonstrated that plasma d-lactate concentrations were greatly increased in DKA compared with the concentrations in diabetic patients or a healthy control group (3). Nevertheless, the clinical value of d-lactate measurement in metabolic acidosis, especially the contribution of d-lactate to the metabolic acidosis and high anion gap in DKA, is not well appreciated. We report here that decreasing d-lactate concentrations are associated with improved clinical situations, whereas increased lactate concentrations are associated with the severity of metabolic acidosis and high anion gap in patients with DKA. The study included 38 diabetic patients with DKA, 42 diabetic patients without DKA, and 40 healthy controls. The institutional ethics review board of the First Affiliated Hospital of Wenzhou Medical College approved the study, and written informed consent was obtained from all study participants. For patients with DKA, blood samples were collected at the time of admission to the emergency room and following medical treatment after admission, when the patient's condition became stabilized. Plasma methylglyoxal was assayed by LC-MS (3). Plasma d-lactate concentration was determined by an e Continue reading >>

Clinical Aspects Of The Anion Gap

Clinical Aspects Of The Anion Gap

The anion gap (AG) is a calculated parameter derived from measured serum/plasma electrolyte concentrations. The clinical value of this calculated parameter is the main focus of this article. Both increased and reduced anion gap have clinical significance, but the deviation from normal that has most clinical significance is increased anion gap associated with metabolic acidosis. This reflects the main clinical utility of the anion gap, which is to help in elucidating disturbances of acid-base balance. The article begins with a discussion of the concept of the anion gap, how it is calculated and issues surrounding the anion gap reference interval. CONCEPT OF THE ANION GAP - ITS DEFINITION AND CALCULATION Blood plasma is an aqueous (water) solution containing a plethora of chemical species including some that have a net electrical charge, the result of dissociation of salts and acids in the aqueous medium. Those that have a net positive charge are called cations and those with a net negative charge are called anions; collectively these electrically charged species are called ions. The law of electrochemical neutrality demands that, in common with all solutions, blood serum/plasma is electrochemically neutral so that the sum of the concentration of cations always equals the sum of the concentration of anions [1]. This immutable law is reflected in FIGURE 1, a graphic display of the concentration of the major ions normally present in plasma/serum. It is clear from this that quantitatively the most significant cation in plasma is sodium (Na+), and the most significant anions are chloride (Cl-) and bicarbonate HCO3-. The concentration of these three plasma constituents (sodium, chloride and bicarbonate) along with the cation potassium (K+) are routinely measured in the clinica Continue reading >>

Endocrine Emergencies

Endocrine Emergencies

This activity is intended for clinicians in primary care, notably emergency medicine, internal medicine, family medicine, diabetes and endocrinology, nurses, and medical students. The goal of this activity is to provide background and essential, practical information for healthcare providers to aid in the recognition and management of endocrine emergencies. Upon completion of this activity, participants will be able to: List common precipitating and risk factors of thyroid storm Describe diagnosis, including presentation, symptoms, and laboratory findings of thyroid storm Discuss treatment and the mortality rate of both treated and untreated thyroid storm Describe clinical presentation and findings of myxedema coma Recognize symptoms and interpret laboratory data of someone in DKA Discuss how to treat electrolyte abnormalities seen with DKA Describe how to recognize and treat adrenal crisis As an organization accredited by the ACCME, Medscape, LLC requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest. Medscape, LLC encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content. Assistant Professor of Medicine, Uniformed Services University of Health Science, Bethesda, Maryland; Internal Medicine Resident, Walter Reed Army Medical Center, Washington, DC Disclosure: Anita A. Shah, DO, has disclosed no rel Continue reading >>

Ketoacidosis Litfl Medical Blog Ccc Acid-base

Ketoacidosis Litfl Medical Blog Ccc Acid-base

ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or even elevated the poor oral intake results in decreased glycogen stores, a decrease in insulin levels and an increase in glucagon levels hepatic metabolism of ethanol to acetaldehyde and then to acetate both involve Continue reading >>

Ketoacidosis

Ketoacidosis

GENERAL ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. CAUSES The three major types of ketosis are: (i) Starvation ketosis (ii) Alcoholic ketoacidosis (iii) Diabetic ketoacidosis STARVATION KETOSIS when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. patients are usually not diabetic. ALCOHOLIC KETOSIS Presentation a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or Continue reading >>

Anion Gap

Anion Gap

SEEBRI NEOHALER should not be initiated in patients with acutely deteriorating or potentially life-threatening episodes of COPD or used as rescue therapy for acute episodes of bronchospasm. Acute symptoms should be treated with an inhaled short-acting beta2-agonist. As with other inhaled medicines, SEEBRI NEOHALER can produce paradoxical bronchospasm that may be life threatening. If paradoxical bronchospasm occurs following dosing with SEEBRI NEOHALER, it should be treated immediately with an inhaled, short-acting bronchodilator; SEEBRI NEOHALER should be discontinued immediately and alternative therapy instituted. Immediate hypersensitivity reactions have been reported with SEEBRI NEOHALER. If signs occur, discontinue immediately and institute alternative therapy. SEEBRI NEOHALER should be used with caution in patients with severe hypersensitivity to milk proteins. SEEBRI NEOHALER should be used with caution in patients with narrow-angle glaucoma and in patients with urinary retention. Prescribers and patients should be alert for signs and symptoms of acute narrow-angle glaucoma (e.g., eye pain or discomfort, blurred vision, visual halos or colored images in association with red eyes from conjunctival congestion and corneal edema) and of urinary retention (e.g., difficulty passing urine, painful urination), especially in patients with prostatic hyperplasia or bladder-neck obstruction. Patients should be instructed to consult a physician immediately should any of these signs or symptoms develop. The most common adverse events reported in ≥1% of patients taking SEEBRI NEOHALER, and occurring more frequently than in patients taking placebo, were upper respiratory tract infection (3.4% vs 2.3%), nasopharyngitis (2.1% vs 1.9%), oropharyngeal pain (1.8% vs 1.2%), urinary t Continue reading >>

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. ​ The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the critically ill. Adjusted anion gap = observed anion gap + 0.25 * ([normal albumin]-[observed albumin]), where the given albumin concentrations are in g/L; if given in g/dL, the correction factor is 2.5.(3) HHS is defined by a plasma glucose level >600 mg/dL, with an effective serum osmolality >320 mOsm/kg. HHS was originally named hyperosmolar hyperglycemic nonketotic coma; however, this name was changed because relatively few patients exhibit coma-like symptoms. Effective serum osmolality = 2*([Na] + [K]) + glucose (mg/dL)/18.(2) Urea is freely diffusible across cell membranes, thus it will Continue reading >>

Calculating The Anion Gap In Diabetic Ketoacidosis

Calculating The Anion Gap In Diabetic Ketoacidosis

Practical Pointers Discover Shortcuts Devised by Colleagues Patients with diabetic ketoacidosis (DKA) frequently have hyperglycemia. Serum sodium in these patients should not be corrected for hyperglycemia to calculate the anion gap for acidosis because extracellular fluid shifts caused by hyperglycemia will dilute serum chloride and bicarbonate. If serum sodium is corrected for hyperglycemia, it will give an erroneously high anion gap and an erroneous severity of acidosis in DKA.1,2 This is an important yet not well-known fact. Continue reading >>

Closing The Anion Gap: Contribution Of D-lactate To Diabetic Ketoacidosis

Closing The Anion Gap: Contribution Of D-lactate To Diabetic Ketoacidosis

Abstract Results The plasma fasting glucose, β-hydroxybutyrate, and blood HbA1c levels were highly elevated in DKA. Plasma anion gap was significantly increased in DKA (20.59 ± 6.37) compared to either the diabetic (7.50 ± 1.88) or the control group (6.53 ± 1.75) (p < 0.001, respectively). Moreover, plasma d-lactate levels were markedly increased in DKA (3.82 ± 2.50 mmol/l) compared to the diabetic (0.47 ± 0.55 mmol/l) or the control group (0.25 ± 0.35 mmol/l) (p < 0.001, respectively). Regression analysis demonstrated that d-lactate was associated with acidosis and anion gap (r = 0.686, p < 0.001). Conclusions Plasma d-lactate levels are highly elevated and associated with metabolic acidosis and the high anion gap in DKA. Laboratory monitoring of d-lactate will provide valuable information for assessment of patients with DKA. 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 >>

Anion Gap

Anion Gap

The anion gap is the difference between primary measured cations (sodium Na+ and potassium K+) and the primary measured anions (chloride Cl- and bicarbonate HCO3-) in serum. This test is most commonly performed in patients who present with altered mental status, unknown exposures, acute renal failure, and acute illnesses. [1] See the Anion Gap calculator. The reference range of the anion gap is 3-11 mEq/L The normal value for the serum anion gap is 8-16 mEq/L. However, there are always unmeasurable anions, so an anion gap of less than 11 mEq/L using any of the equations listed in Description is considered normal. For the urine anion gap, the most prominently unmeasured anion is ammonia. Healthy subjects typically have a gap of 0 to slightly normal (< 10 mEq/L). A urine anion gap of more than 20 mEq/L is seen in metabolic acidosis when the kidneys are unable to excrete ammonia (such as in renal tubular acidosis). If the urine anion gap is zero or negative but the serum AG is positive, the source is most likely gastrointestinal (diarrhea or vomiting). [2] Continue reading >>

Mind The Gap: Anion Gap Acidosis

Mind The Gap: Anion Gap Acidosis

A step by step approach to uncovering the cause of an elevated anion gap metabolic acidosis. We learn about the MUD PILES, the causes of anion gap acidosis, as medical students. And it gets even further drilled into us in residency. But sorting out a gap acidosis can be real challenge, even with a nifty mnemonic. To help us get smarter in understanding some of the nuance of gap acidosis, Sean Nordt, MD, PharmD. Case: Alcoholic, diabetic with a blood glucose of 295, bicarbonate of 12, and an anion gap 28. Is this alcoholic ketoacidosis (AKA), diabetic ketoacidosis (DKA), toxic alcohol, something else? What is the cognitive process for sorting out this anion gap acidosis? Nordt: Without additional history, send… -Ethanol level -VBG -UA -Serum ketones (acetone and beta hydroxybutyrate) if possible -Serum calcium- a good surrogate marker for ethylene glycol. Most hospitals have a volatile alcohol screen looking for methanol and isopropanol, but not ethylene glycol. To detect ethylene glycol, you’ll need to look at surrogate markers. -Start IV fluids Case continues: The patient has a normal mental status. Heart rhythm is sinus tachycardia in the low 100s. To treat this sinus tachycardia, he gets the sinus tachycardia antidote – 3 liters of normal saline. Since AKA (a starvation and volume depletion ketosis) is high on the differential diagnosis, he also gets a hamburger and apple juice. His labs are rechecked and few hours later and his bicarbonate is unchanged at 12 and anion gap drops slightly from 28 to 24. How fast should the anion gap and serum bicarbonate to correct in AKA? Nordt: It should start to improve in 1-2 hours and takes about 5-7 hours to reverse. If the anion gap and bicarbonate aren’t improving (or getting worse) in an hour or two, think about an al Continue reading >>

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Get Unlimited Access On Medscape.

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