diabetestalk.net

Dka Anion Gap Range

Arterial Blood Gases (blood Gases), Acidosis And Alkalosis

Arterial Blood Gases (blood Gases), Acidosis And Alkalosis

Sample The better choice is the Radial artery. The sample may be taken from the femoral artery or brachial. The tests are done immediately because oxygen and carbon dioxide are unstable. Arterial blood is better than the venous blood. For arterial blood don't use the tourniquet and no pull on the syringe plunger. For venous blood syringe or tubes are completely filled and apply a tourniquet for few seconds. Arterial VS Venous blood Arterial blood gives good mixture of blood from various areas of the body. Venous blood gives information of the local area from where the blood sample is taken. Metabolism of the extremity varies from area to area. Arterial blood measurement gives the better status of the lung oxygenating the blood. Arterial blood gives information about the ability of the lung to regulate the acid-base balance through retention or release of CO2. Precautions for the collection of blood Avoid pain and anxiety to the patient which will lead to hyperventilation. Hyperventilation due to any cause leads to decreased CO2 and increased pH. Keep blood cool during transit. Don't clench finger or fist. This will leads to lower CO2 and increased acid metabolites. pCO2 values are lower in the sitting or standing position in comparison with the supine position. Don't delay the performance of the test. Avoid air bubbles in the syringe. Excess of heparin decreases the pCO2 may be 40% less. Not proper mixing of the blood before running the test. Purpose of the test This test is done on the mostly hospitalized patient. Mostly the patients are on ventilator or unconscious. For patients in pulmonary distress. To assess the metabolic (renal) acid-base and electrolytes imbalance. Its primary use is to monitor arterial blood gases and pH of blood. Also used to monitor oxygenatio Continue reading >>

Osmolality Gap - Calculation And Interpretation

Osmolality Gap - Calculation And Interpretation

Osmolality Gap - Calculation and Interpretation Plasma osmolality is determined mainly by Sodium (NA), its counter ions, and uncharged species such as Glucose (GLU) and Urea (UN). Knowledge of the plasma concentration of these species allows calculation of the plasma osmolality quite accurately. The difference between measured osmolality (MO) and calculated osmolality (CO) is known as the osmolar gap (OG). A large positive (>15) osmolar gap can help identify the presence in plasma of substances such as ethanol, methanol, isopropanol, ethylene glycol, propylene glycol (found as a diluent for some intravenous medications such as lorazepam), and acetone. The formula given below was instituted at the University of Iowa Hospitals and Clinics for use on plasma samples starting November 2009 and is based on a published study comparing different calculated osmolality formulas (see ref. 3): (1). CO = 2 x NA + 1.15 * GLU/18 + BUN/2.8 : calculated osmolality To calculate the osmolar gap, plasma determination of MO, NA, GLU, and BUN are necessary. Proper interpretation of the OG also requires knowledge of the anion gap (AG = NA - HCO3 - CL), the blood pH, and qualitative testing of the plasma ketone bodies (KETO). Determinations of MO and for CO should be performed on the same plasma sample. An OG value greater than 15 has traditionally been considered a critical value or cutoff. Approximately 97% of osmolar gaps in patients are between -10 and +10. When the OG is combined with blood pH and AG, poisonings with toxic alcohols can be quickly recognized. The presence of low blood pH, elevated AG, and greatly elevated OG (>15) is a medical emergency that requires prompt treatment. The specific agent(s) responsible can be identified by the gas chromatographic assays for ethanol, methan 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 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 >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

Diagnosis of DKA: � Initial STAT labs include • CBC with diff • Serum electrolytes • BUN • Creatinine • Glucose • Arterial blood gases • Bicarbonate • Urinalysis • Lactate • Serum ketones • Calculation of the Anion Gap � serum anion gap = serum sodium – (serum chloride + bicarbonate) • Electrocardiogram Treatment Protocol for Diabetic Ketoacidosis Reviewed 5/2/2017 2 Updated 05/02/17 DKA Diagnostic Criteria: � Blood glucose >250 mg/dl � Arterial pH <7.3 � Bicarbonate ≤18 mEq/l � Anion Gap Acidosis � Moderate ketonuria or ketonemia 1. Start IV fluids (1 L of 0.9% NaCl per hr initially) 2. If serum K+ is <3.3 mEq/L hold insulin � Give 40 mEq/h until K ≥ 3.3 mEq/L 3. Initiate DKA Order Set Phase I (*In PREGNANCY utilize OB DKA order set) 4. Start insulin 0.14 units/kg/hr IV infusion (calculate dose) RN will titrate per DKA protocol Insulin Potassium Bicarbonate IVF Look for the Cause - Infection/Inflammation (PNA, UTI, pancreatitis, cholecystitis) - Ischemia/Infarction (myocardial, cerebral, gut) - Intoxication (EtOH, drugs) - Iatrogenic (drugs, lack of insulin) - Insulin deficiency - Pregnancy DKA/HHS Pathway Phase 1 (Adult) Approved by Diabetes Steering Committee, MMC, 2015, Revised DKA Workgroup 1_2016 Initiate and continue insulin gtt until serum glucose reaches 250 mg/dl. RN will titrate per protocol to achieve target. When sugar < 250 mg/dl proceed to DKA Phase II *In PREGNANCY when sugar <200 proceed to OB DKA Phase II *PREGNANCY � Utilize OB DKA order set Phase 1 � When glucose reaches 200mg/dL, Initiate OB DKA Phase 2 � Glucose goals 100-150mg/dL OB DKA Phase 2 Determine hydration status Hypovolemic shock Mild hypotensio 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 >>

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 >>

Severe Ketoacidosis Associated With Canagliflozin (invokana): A Safety Concern

Severe Ketoacidosis Associated With Canagliflozin (invokana): A Safety Concern

Case Reports in Critical Care Volume 2016 (2016), Article ID 1656182, 3 pages 1Section of Pulmonary and Critical Care Medicine, Providence Hospital and Medical Center, 16001 W 9 Mile Road, Southfield, MI 48075, USA 2Department of Internal Medicine, Providence Hospital and Medical Center, 16001 W 9 Mile Road, Southfield, MI 48075, USA Academic Editor: Kurt Lenz Copyright © 2016 Alehegn Gelaye et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Canagliflozin (Invokana) is a selective sodium glucose cotransporter-2 (SGLT-2) inhibitor that was first introduced in 2013 for the treatment of type 2 diabetes mellitus (DM). Though not FDA approved yet, its use in type 1 DM has been justified by the fact that its mechanism of action is independent of insulin secretion or action. However, some serious side effects, including severe anion gap metabolic acidosis and euglycemic diabetic ketoacidosis (DKA), have been reported. Prompt identification of the causal association and initiation of appropriate therapy should be instituted for this life threatening condition. 1. Introduction More than 5 million patients are admitted annually to intensive care units (ICUs) in the United States. A number of life threatening medical conditions, including diabetic ketoacidosis, can be associated with metabolic acidosis. Metabolic acidosis may also arise from several drugs and toxins through a variety of mechanisms. Since approval of the first-in-class drug in 2013, data have emerged suggesting that Sodium Glucose Transporter-2 (SGLT-2) inhibitors, including canagliflozin, may lead to diabetic ketoacidosis [1]. We pre 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 >>

References

References

Arterial samples: pH 7.36-7.44, HCO3 21-27, PCO2 36-44 Venous: pH 0.03 units lower, HCO3 similar, PCO2 3-8 higher Capillary: similar to arterial (assuming no prolonged tourniquet use, ischemia, etc) 1. Look at the pH. What is the primary process occurring? low pH and high PCO2: respiratory acidosis high pH and low PCO2: respiratory alkalosis high pH and high HCO3: metabolic alkalosis if the pH is near normal but PCO2 and HCO3 are significantly abnormal, there is likely a mixed disorder 2. Assess the degree/chronicity of compensation present. Acute respiratory acidosis: HCO3 increases by 1 me/L and pH decreased by 0.08 for every 10 mmHg increase in PCO2 Chronic respiratory acidosis (3-5 days for renal compensation): HCO3 increases by 4me/Lfor and pH decreased by 0.03 for every 10 mmHg increase in PCO2 Metabolic acidosis: Expected PCO2= 1.5 X HCO3 + 8 +/-2 (Winter's Formula) or the decimal digits of pH should be similar to the PCO2 (ie pH 7.25 should have a PCO2 of 25 in a metabolic acidosis). If the patient's PCO2 is higher than expected, there is a concurrent respiratory acidosis. If the patient's PCO2 is lower than expected, there is a concurrent respiratory alkalosis. If it similar to expected, the compensation is appropriate Metabolic alkalosis: PCO2 increases by 0.7 mmHg for every 1 meq/L increase in HCO3 3. If there is a metabolic acidosis, assess the anion gap. Elevated anion gap --> MUDPILES (Methanol, uremia, diabetic ketoacidosis, propylene glycol, INH, lactic acidosis, ethylene glycol, salicylates) If there is an elevated anion gap, consider calculating the / = Anion gap/ [HCO3-]. <0.4 is consistent with hyperchloremic nongap acidosis, <1 with high AG and normal AG acidosis, 1-2 pure AG acidosis, >2 concurrent metabolic alkalosis or preexisting compensated re Continue reading >>

Bun, Glucose, Creatinine

Bun, Glucose, Creatinine

Normal Values pH = 7.38 - 7.42 [H+] = 40 nM/L for a pH of 7.4 PaCO2 = 40 mm Hg [HCO3] = 24 meq/L Acid base definitions Acid base disorder is considered present when there is abnormality in HCO3 or PaCO2 or pH. Acidosis and alkalosis refer to in-vivo derangement's and not to any change in pH. Acidemia (pH < 7.38) and Alkalemia (pH >7.42) refer to derangement's of blood pH. Kidney and Respiratory system play a key roles in maintaining the acid base status. Primary Acid base disorders Metabolic acidosis loss of [HCO3] 0r addition of [H+] Metabolic alkalosis loss of [H+] or addition of [HCO3] Respiratory acidosis increase in pCO2 Respiratory alkalosis decrease in pCO2 Recquired lab values/information Arterial blood gases: pH, PaCO2,PaO2,Sat,CO BUN, Glucose, Creatinine FIO2 and Clinical history Anion and Cations ANIONS CATIONS Chloride Sodium Bicarbonate(Total CO2) Potassium Proteins Calcium Organic acids Magnesium Phosphates Sulfates Electrochemical balance means that the total anions are the same as total Cations. For practical purposes anion gap is calculated using only Sodium, Chlorides and Total CO2.((140-(104+24)) = 12. Compensatory measures Buffering---occurs immediately Respiratory regulation of pCO2 is intermediate (12-24 hours) Renal regulation of [H] and [HCO3] occurs more slowly (several days) Extracellular almost entirely through bicarbonate whose concentration highest of all buffers small contribution from phosphate Intracellular Hemoglobin can directly buffer protons H+ entry into RBC matched by exit of Na and K+ Hemoglobin can directly buffer dissolved intracellular conversion of Buffer systems Hemoglobin can directly buffer protons H+ entry into RBC matched by exit of Na and K+ Hemoglobin can directly buffer dissolved intracellular conversion of Bicarbonate Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

Anion Gap

Anion Gap

Na(mmol/L )K(mmol/L ) ClCO2(mmol/L )(mmol/L ) ANION GAP Anion Gap = Na + K - Cl - C02 = ???. Often the potassium is not included in the anion gap calculation, like this: Angion Gap = Na - Cl - C02 = ???. DELTA ANION GAP The delta anion gap is the observed anion gap - 12, which is normal, and is ???. The delta bicarbonate is the observed total CO2 (from electrolytes) subtracted from 27 and is . The bicarbonate gap measures the delta anion gap minus the delta bicarbonate and is . It is abnormal for the bicarbonate gap to vary more than 6. CORRECTING FOR HYPOALBUMINEMIA Observed Albumin g/dL g/L* If the albumin is low, as in nephrotic syndrome, it will affect the anion gap Correct anion gap=Observed anion gap +.25(normal albumin-observed albumin) for alb measured in g/L and is ??? *The international units for albumin is g/L - If you are adding values in SI units, we divided by 10. REVIEWS © 2008-14, Stephen Z. Fadem, M.D., FASN. All rights reserved. No part of this application may be duplicated without written permission from the author. DISCLAIMER: The licensee or user understand and agree that the technology and content of this application are provided for educational purposes only. All calculations must be checked for accuracy and confirmed before use, clinical or otherwise. All medical decisions must be based upon the clinical judgment of a licensed physician. Licensee or user assumes the duty to have any and all laboratory values or calculations verified by a licensed physician. Neither licensor nor its associated authors or other entities warrant the accuracy of any information provided by or resulting from the technology or the content for clinical management, and licensee or user agree that no such persons or entities shall be liable for any adverse consequences r 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 >>

Clinical Usefulness Of The Serum Anion Gap

Clinical Usefulness Of The Serum Anion Gap

Clinical Usefulness of the Serum Anion Gap Division of Nephrology, Department of Internal Medicine, Chonbuk National University Medical School, Chonbuk, Korea. Correspondence author: Sung Kyew Kang, M.D., Department of Internal Medicine, Chonbuk National University Medical School, Chonbuk, Korea. Tel: 063)250-1677, Fax: 063)254-1609, [email protected] Copyright 2006 The Korean Society of Electrolyte and Blood Pressure Research This article has been cited by other articles in PMC. The anion gap in the serum is useful in the interpretation of acid-base disorders and in the diagnosis of other conditions. In the early 1980s, ion-selective electrodes for specific ionic species were introduced for the measurement of serum electrolytes. This new method has caused a shift of the anion gap from 124 mEq/L down 63 mEq/L. It is worthy for clinicians to understand the range of normal anion gap and the measuring methods for serum sodium and chloride in the laboratories that support their practice. While an increase in the anion gap is almost always caused by retained unmeasured anions, a decrease in the anion gap can be generated by multiple mechanisms. Keywords: Anion gap, Ion-selective electrode The serum anion gap is a helpful parameter in the clinical diagnosis of various conditions. The commonest application of the anion gap is to classify cases of metabolic acidosis into those that do and those that do not have unmeasured anions in the plasma ( Table 1 ). In this article, we briefly review the significance of the anion gap and the approach to the use of the serum anion gap. Anion Gap in Major Causes of Metabolic Acidosis As charge balance precluded the existence of any gaps, the more accurate term should really be 'difference between unmeasured anions and unmeasured cations' Continue reading >>

More in ketosis