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Dka Anion Gap Range

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 >>

Serum Anion Gap | Usmle Pearls

Serum Anion Gap | Usmle Pearls

Formula: SAG = (Na+ + K+) (Cl + HCO3) When Used? To differentiate between the causes of Metabolic Acidosis. Interpretation: If SAG is >12 then the metabolic acidosis is Increased Anion Gap Metabolic Acidosis. Remember the mnemonic MUDPILES for Increased Anion Gap Metabolic Acidosis: Methanol, Uremia, DKA, Propylene Glycol, Iron Poisoning/Isoniazid, Lactic Acidosis, Ethylene Glycol, Salicylates. Formula: OG = Measured Serum Osmolality Calculated Serum Osmolality When Used? To diagnose poisoning by certain alcohols. Interpretation: If >10, consider Ethanol, Methanol, Ethylene Glycol, Isopropyl Alcohol and Propylene Glycol Intoxication. (Remember Isopropyl Alcohol has Increased OG but not Increased SAG! (i.e. doesnt cause AG Metabolic Acidosis)) When Used? To differentiate between causes of Normal AG Metabolic Acidosis i.e. to differentiate between RTA vs Diarrhea as cause of the Normal AG Metabolic Acidosis Interpretation: Remember by (Na+ + K+ Cl) we are actually measuring (Urine Cations Urine Anions), the major Cation in Urine that is not usually measured is NH4+, so if UAG is negative that means Increased NH4+ (i.e. acid) excretion in the Urine which should be the case in any acidosis INCLUDING Diarrhea! But, if renal function is not normal as in RTA, NH4+ is not excreted in Urine and so UAG will be 0 or Positive. So, in Normal Anion Gap Metabolic Acidosis, if: UAG = Negative value > Diarrhea (Remember NeGUTive) Formula: Stool Osmolality (usually not measured and replaced by 290 for ease of calculation) 2 (stool Na+ + stool K+) When Used? To differentiate Secretory vs Osmotic Diarrhea SOG >100 = Osmotic Diarrhea (e.g. Lactose Intolerance) Continue reading >>

Electrolytes

Electrolytes

On This Site 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 >>

How To Calculate Anion Gap

How To Calculate Anion Gap

Edit Article The body naturally strives for balance and equilibrium. When extra H ions or acids are released, the body suffers from a condition referred to as metabolic acidosis. This increases the respiratory rate and decreases your plasma levels. Anion gap is used to determine the exact reason of this condition. It determines unmeasured anions which are the phosphates, sulfates, and proteins in the plasma. Calculating anion gap is very simple given the standard formula. To get started, see Step 1 below. Continue reading >>

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) should be suspected in ill patients with diabetes. If either DKA or HHS is diagnosed, precipitating factors must be sought and treated. DKA and HHS are medical emergencies that require treatment and monitoring for multiple metabolic abnormalities and vigilance for complications. A normal blood glucose does not rule out DKA in pregnancy. Ketoacidosis requires insulin administration (0.1 U/kg/h) for resolution; bicarbonate therapy should be considered only for extreme acidosis (pH7.0). Note to readers: Although the diagnosis and treatment of diabetic ketoacidosis (DKA) in adults and in children share general principles, there are significant differences in their application, largely related to the increased risk of life-threatening cerebral edema with DKA in children and adolescents. The specific issues related to treatment of DKA in children and adolescents are addressed in the Type 1 Diabetes in Children and Adolescents chapter, p. S153. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are diabetes emergencies with overlapping features. With insulin deficiency, hyperglycemia causes urinary losses of water and electrolytes (sodium, potassium, chloride) and the resultant extracellular fluid volume (ECFV) depletion. Potassium is shifted out of cells, and ketoacidosis occurs as a result of elevated glucagon levels and absolute insulin deficiency (in the case of type 1 diabetes) or high catecholamine levels suppressing insulin release (in the case of type 2 diabetes). In DKA, ketoacidosis is prominent, while in HHS, the main features are ECFV depletion and hyperosmolarity. Risk factors for DKA include new diagnosis of diabetes mellitus, insulin omission, infection, myocardial infarc 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 >>

Anion Gap (blood) - Health Encyclopedia - University Of Rochester Medical Center

Anion Gap (blood) - Health Encyclopedia - University Of Rochester Medical Center

If you may have swallowed a poison, such as wood alcohol, salicylate (in aspirin), and ethylene glycol (in antifreeze), your provider may test your blood for it. If your provider thinks you have ketoacidosis, you might need a urine dipstick test for ketone compounds. Ketoacidosis is a health emergency. Many things may affect your lab test results. These include the method each lab uses to do the test. Even if your test results are different from the normal value, you may not have a problem. To learn what the results mean for you, talk with your healthcare provider. Results are given in milliequivalents per liter (mEq/L). Normal results are 3 to 10mEq/L, although the normal level may vary from lab to lab. If your results are higher, it may mean that you have metabolic acidosis. Hypoalbuminemia means you haveless albumin protein than normal. If you have this condition, your expected normal result must be lower. The test requires a blood sample, which is drawn through a needle from a vein in your arm. Taking a blood sample with a needle carries risks that include bleeding, infection, bruising, or feeling dizzy. When the needle pricks your arm, you may feel a slight stinging sensation or pain. Afterward, the site may be slightly sore. Being dehydrated or retaining water in your body can affect your results. Antibiotics such as penicillin can also affect your results. You don't need to prepare for this test. But be sure your healthcare provider knows about all medicines, herbs, vitamins, and supplements you are taking. This includes medicines that don't need a prescription and any illicit drugs you may use. Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is a condition that results from when the body is deprived of the ability to use glucose as an energy source. Usually this is due to a lack of insulin. Insulin is used to uptake glucose into the cells to be used for energy. If there is no insulin or the cells are resistant to insulin, the blood sugar levels increase to dangerous levels for the patient. It seems counter intuitive that the patient wouldn't have energy with such high levels of glucose, but this glucose is essentially unusable without insulin. Because your body needs energy to survive, it starts turning to alternative fuel sources (fat). Fat cells start breaking down and, as a result, release ketones (which are acidic) into the bloodstream. Hence the name: diabetic ketoacidosis. “High levels of ketones can poison the body. When levels get too high, you can develop DKA. DKA may happen to anyone with diabetes, though it is rare in people with type 2. Treatment for DKA usually takes place in the hospital. But you can help prevent it by learning the warning signs and checking your urine and blood regularly.” Causes The most common causes of DKA are not getting enough insulin, having a severe infection, becoming dehydrated, or a combination of these issues. It seems like it occurs mainly in patients with type one diabetes. Symptoms Some of the symptoms that people experience with DKA include the following: Excessive thirst and urination (more water is pulled into the urine as a result of high ketone loss in the urine) Lethargy Breathing very quickly (patients have a very high level of acids in their bloodstream and they try to "blow" off carbon dioxide by breathing quickly) A fruity odor on their breath (ketones have a fruity smell) Nausea and vomiting (the body tries to get rid of acid Continue reading >>

Metabolic Acidosis Nursing Management And Interventions - Nurseslabs

Metabolic Acidosis Nursing Management And Interventions - Nurseslabs

Metabolic Acidosisis an acid-base imbalance resulting from excessive absorption or retention of acid or excessive excretion of bicarbonate produced by an underlying pathologic disorder. Symptoms result from the bodys attempts to correct the acidotic condition through compensatory mechanisms in the lungs , kidneys and cells. Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is within normal limits. If the primary problem is the accumulation of organic anions (such as ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct this imbalance include an increase in respirations to blow off excess CO2, an increase in ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and sodium . High anion gap acidosis occurs in diabetic ketoacidosis ; severe malnutrition or starvation, alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g., salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH4Cl. Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in renal tubular acidosis, hyperalimentation, vomiting/ diarrhea , small-bowel/pancreatic fistulas, and ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying drugs (e.g., ammonium chloride). This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit. Use of carbonic anhydrase inhibitors or anion-exchan Continue reading >>

Delta Gap And Delta Ratio - Deranged Physiology

Delta Gap And Delta Ratio - Deranged Physiology

The delta gap and delta ratio, advantages and disadvantages . Once one has calculated the anion gap and finds it raised, one is almost obliged to figure out whether those anions have been solely responsible for the acidosis, or whether another (non-anion-gap) cause is lurking in the background. A brief review of this can be found in the "Required Reading" section hidden among the CICM Fellowship Exam preparation material.For actual education, the exam candidates are directed to the LITFL delta ratio page , and to the excellent online works of Kerry Brandis. The delta gap is a straight-out difference between the change in anion gap and the change in bicarbonate. Delta gap = (change in anion gap) - (change in bicarbonate) (The normal anion gap is assumed to be 12, and the normal HCO3is assumed to be 24.) A simplified equation which does not require a bicarbonate value is also available: -6 = Mixed high and normal anion gap acidosis -6 to 6 = Only ahigh anion gap acidosis exists over 6 = Mixed high anion gap acidosis and metabolic alkalosis Delta gap is essentially a tool to determine whether or not there is also a normal anion gap metabolic acidosis present.The normal value for delta gap is zero, and it should remain zero as anion gap and bicarbonate changetogether (mole for mole, in opposite directions). If the bicarbonate is changing significantlyless than the anion gap, the delta gap will become more and more positive, reflecting the fact that an alkalosis is present. If the change in bicarbonateis significantly greater than the change in anion gap, there is clearly some acidosis present which is unrelated to the anion gap rise, and thedelta gap will be very negative. Why -6 and +6?Keith Wrenn established these parameters in 1990 , using the normal values supplied to 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 >>

Anion Gap

Anion Gap

OVERVIEW Anion Gap = Na+ – (Cl- + HCO3-) The Anion Gap (AG) is a derived variable primarily used for the evaluation of metabolic acidosis to determine the presence of unmeasured anions The normal anion gap depends on serum phosphate and serum albumin concentrations An elevated anion gap strongly suggests the presence of a metabolic acidosis The normal anion gap varies with different assays, but is typically 4 to 12mmol/L (if measured by ion selective electrode; 8 to 16 if measured by older technique of flame photometry) If AG > 30 mmol/L then metabolic acidosis invariably present If AG 20-29mmol/L then 1/3 will not have a metabolic acidosis K can be added to Na+, but in practice offers little advantage ALBUMIN AND PHOSPHATE the normal anion gap depends on serum phosphate and serum albumin the normal AG = 0.2 x [albumin] (g/L) + 1.5 x [phosphate] (mmol/L) albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. every 1g/L decrease in albumin will decrease anion gap by 0.25 mmoles a normally high anion gap acidosis in a patient with hypoalbuminaemia may appear as a normal anion gap acidosis. this is particularly relevant in ICU patients where lower albumin levels are common HIGH ANION GAP METABOLIC ACIDOSIS (HAGMA) HAGMA results from accumulation of organic acids or impaired H+ excretion Causes (LTKR) Lactate Toxins Ketones Renal Causes (CATMUDPILES) CO, CN Alcoholic ketoacidosis and starvation ketoacidosis Toluene Metformin, Methanol Uremia DKA Pyroglutamic acidosis, paracetamol, phenformin, propylene glycol, paraladehyde Iron, Isoniazid Lactic acidosis Ethylene glycol Salicylates Effects of albumin Anion gap may be underesitmated in hypoalbuminaemia, because if albumin decreased by 1g/L then the anion gap decreases by 0.25 Continue reading >>

Anion Gap

Anion Gap

Pathophysiology sample values BMP/ELECTROLYTES: Na+ = 140 Cl− = 100 BUN = 20 / Glu = 150 K+ = 4 CO2 = 22 PCr = 1.0 \ ARTERIAL BLOOD GAS: HCO3− = 24 paCO2 = 40 paO2 = 95 pH = 7.40 ALVEOLAR GAS: pACO2 = 36 pAO2 = 105 A-a g = 10 OTHER: Ca = 9.5 Mg2+ = 2.0 PO4 = 1 CK = 55 BE = −0.36 AG = 16 SERUM OSMOLARITY/RENAL: PMO = 300 PCO = 295 POG = 5 BUN:Cr = 20 URINALYSIS: UNa+ = 80 UCl− = 100 UAG = 5 FENa = 0.95 UK+ = 25 USG = 1.01 UCr = 60 UO = 800 PROTEIN/GI/LIVER FUNCTION TESTS: LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7 ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5 AST/ALT = 0.6 BU = 0.2 AF alb = 3.0 SAAG = 1.0 SOG = 60 CSF: CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.4 The anion gap[1][2] (AG or AGAP) is a value calculated from the results of multiple individual medical lab tests. It may be reported with the results of an Electrolyte Panel, which is often performed as part of a Comprehensive Metabolic Panel.[3] The anion gap is the difference between the measured cations (positively charged ions) and the measured anions (negatively charged ions) in serum, plasma, or urine. The magnitude of this difference (i.e., "gap") in the serum is often calculated in medicine when attempting to identify the cause of metabolic acidosis, a lower than normal pH in the blood. If the gap is greater than normal, then high anion gap metabolic acidosis is diagnosed. The term "anion gap" usually implies "serum anion gap", but the urine anion gap is also a clinically useful measure.[4][5][6][7] Calculation[edit] The anion gap is a calculated measure. This means that it is not directly measured by a specific lab test; rather, it is computed with a formula that uses the results of several individual lab tests, each of which measures the concentration of a specific anion or cation. The concentr Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

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

Metabolic Acidosis; Non-gap

Metabolic Acidosis; Non-gap

Pseudoaldosteronism, type 2 (Gordons syndrome) B. Describe a diagnostic approach/method to the patient with this problem. Metabolic acidosis can be divided into two groups based on anion gap. If an anion gap is elevated (usually greater than 12), see gapped metabolic acidosis. Diagnosis of the cause of non-gapped metabolic acidosis is usually clinically evident as it can be attributed to diarrhea, intravenous saline or by default, renal tubular acidosis. Occasionally, it may not be clear whether loss of base occurs due to the kidney or bowel. In such a case, one should calculate the urinary anion gap. The urinary anion gap (UAG) = sodium (Na+)+K+ chloride (Cl). Caution if ketonuria or drug anions are in the urine as it would invalidate the calculation. Renal tubular acidosis: UAG is positive value. As an aid, UAG is neGUTive when associated with bowel causes. Non-gapped metabolic acidosis can further be divided into two categories: 1. Historical information important in the diagnosis of this problem. The urinary anion gap is key to determining if the non-gapped metabolic acidosis is GI or renal. The urinary anion gap provides an estimate of the urinary ammonium (NH4+) excretion. The urinary anion gap is defined as UAG = Unmeasured Anion (UA) Unmeasured Cation (UC). As seen in diarrhea, bicarbonate is excreted via the gut triggering urinary ammonium excretion to maintain electroneutrality. This causes an increased UC (urinary NH4+) and results in a negative UAG. On the other hand, renal tubular acidosis involve the inability of the kidney to resorb bicarbonate. This causes an increased UA (urinary HCO3) and results in a positive UAG. It is worthy to understand how the urinary anion gap was derived. The cations present in urine include: Na+, K+, Ca2+, Mg. The anions in u Continue reading >>

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