Serum Anion Gap: Its Uses And Limitations In Clinical Medicine
Abstract The serum anion gap, calculated from the electrolytes measured in the chemical laboratory, is defined as the sum of serum chloride and bicarbonate concentrations subtracted from the serum sodium concentration. This entity is used in the detection and analysis of acid-base disorders, assessment of quality control in the chemical laboratory, and detection of such disorders as multiple myeloma, bromide intoxication, and lithium intoxication. The normal value can vary widely, reflecting both differences in the methods that are used to measure its constituents and substantial interindividual variability. Low values most commonly indicate laboratory error or hypoalbuminemia but can denote the presence of a paraproteinemia or intoxication with lithium, bromide, or iodide. Elevated values most commonly indicate metabolic acidosis but can reflect laboratory error, metabolic alkalosis, hyperphosphatemia, or paraproteinemia. Metabolic acidosis can be divided into high anion and normal anion gap varieties, which can be present alone or concurrently. A presumed 1:1 stoichiometry between change in the serum anion gap (ΔAG) and change in the serum bicarbonate concentration (ΔHCO3−) has been used to uncover the concurrence of mixed metabolic acid-base disorders in patients with high anion gap acidosis. However, recent studies indicate variability in the ΔAG/ΔHCO3− in this disorder. This observation undercuts the ability to use this ratio alone to detect complex acid-base disorders, thus emphasizing the need to consider additional information to obtain the appropriate diagnosis. Despite these caveats, calculation of the serum anion gap remains an inexpensive and effective tool that aids detection of various acid-base disorders, hematologic malignancies, and intoxication Continue reading >>
Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis ). Lactic acidosis (due to physiologic processes) Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subsequent excretion of metabolites normalizes gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute kidney injury) Normal anion gap (hyperchloremic acidosis) Renal tubular acidosis, types 1, 2, and 4 The most common causes of a high anion gap metabolic acidosis are Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis ), but it also occurs with chronic alcoholism (see alcoholic ketoacidos Continue reading >>
Serum Anion Gap In Conditions Other Than Metabolic Acidosis
INTRODUCTION Determination of the serum anion gap (AG) is primarily used in the differential diagnosis of metabolic acidosis [1-4]. (See "Approach to the adult with metabolic acidosis", section on 'Physiologic interpretation of the serum anion gap'.) However, the serum AG can also become abnormal in other conditions, a finding that may be of diagnostic importance [1-5]. CALCULATION OF THE ANION GAP AND NORMAL VALUES The serum anion gap (AG) is calculated from the following formula: Serum AG = Measured cations - measured anions Since Na is the primary measured cation and Cl and HCO3 are the primary measured anions (calculator 1): Continue reading >>
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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 >>
High Anion Gap Metabolic Acidosis - Today's Pearl - Statpearls
High anion gap metabolic acidosis (HAGMA) is a subcategory of acidosis ofmetabolic (i.e., non-respiratory) etiology. Differentiation of acidosis into a particular subtype, whether high anion gap metabolic acidosisor non-aniongap metabolic acidosis(NAGMA), aids in the determinationof the etiology and hence appropriate treatment. Although there have been many broadly inclusive mnemonic devices for high anion gap metabolic acidosis, the use of "GOLD MARK" has gained popularity for its focus on causes common to the 21st century. Glycols (ethylene glycol, propylene glycol) Oxoproline (pyroglutamic acid, the toxic metabolite of excessive acetaminophen or paracetamol) L-Lactate (standard lactic acid seen in lactic acidosis) D-Lactate (exogenous lactic acid produced by gut bacteria) Methanol (this is inclusive of alcohols in general) Ketones (diabetic, alcoholic and starvation ketosis) Of note, metformin has been omitted from this list due to a lack of evidence for metformin-induced lactic acidosis. In fact, aCochrane review found substantial evidence that metformin was not a cause of lactic acidosis. The same could not be said ofthe older biguanide, phenformin, which does increase the incidence of lactic acidosis by approximately tenfold. Furthermore, the addition of massive rhabdomyolysis would be appropriate given the potentially large amounts of hydrogen ions released by muscle breakdown. High anion gap metabolic acidosis is one of the most common metabolic derangements seen in critical care patients. Exact numbers are not readily available. The most common method of evaluation of metabolic acidosis involves the Henderson-Hasselbalch equation and the Lewis model interpretation of biological acidosis which evaluates the plasma concentration of hydrogen ions. An alternative Continue reading >>
Metabolic Acidosis
Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis Paraldehyde, Phenformin (neither used in U.S. now) Propofol Infusion Syndrome has been proposed as a replacement in mnemonic Salicylate s (do not miss Chronic Salicylate Poisoning ) IV. Causes: Metabolic Acidosis and Normal Anion Gap (Hyperchloremia) Renal Tubular Acidosis (proximal or distal) V. Causes: Metabolic Acidosis and Elevated Osmolal Gap PaCO2 drops 1.2 mmHg per 1 meq/L bicarbonate fall Calculated PaCO2 = 1.5 x HCO3 + 8 (+/- 2) Useful in High Anion Gap Metabolic Acidosis Measured PaCO2 discrepancy: respiratory disorder Investigate normal Anion Gap Metabolic Acidosis Elevated in normal Anion Gap Metabolic Acidosis VII. Labs: Consider in Metabolic Acidosis with Increased Anion Gap Basic chemistry panel as above ( Serum Glucose , Blood Urea Nitrogen ) Rutecki (Dec 1997) Consultant, p. 3067-74 Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Metabolic Acidosis." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images Related Studies (from Trip Database) Open in New Window A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). Increased acidity in the blood secondary to acid base imbalance. Causes include diabetes, kidney failure and shock. ACIDOSIS METABOLIC, metabolic acidosis, metabolic acidosis (diagnosis), Acidosis metabolic, Metabolic acidosis NOS, Metabolic Acidoses, Acidosis, Metabolic, Acidoses, Metabolic, Metabolic Acidosis, acidosis metabolic, metabolic acidosis disorder, Acidosis, Metabolic acidosis (disorder), acidosis; metabolic, metabolic; acidosis, Metabolic acidosis, NOS, M Continue reading >>
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 >>
Normal Anion Gap Acidosis
Terry W. Hensle, Erica H. Lambert, in Pediatric Urology , 2010 Nonanion gap acidosis occurs in situations in which HCO3 is lost from the kidney or the gastrointestinal tract or both. When this occurs, Cl (along with Na+) is reabsorbed to replace the HCO3; this leads to the hyperchloremia, which leaves the anion gap in normal range.10 Diarrhea causes a hyperchloremic, hypokalemic metabolic acidosis. Treatment depends on the severity of the acidosis incurred. In mild to moderate acidosis (pH >7.2), fluid and electrolyte replacement is often all that is required. Once adequate renal perfusion is restored, excess H+ can be excreted efficiently, restoring the pH to normal. In severe acidosis (pH <7.2), the addition of intravenous bicarbonate may be needed to correct the metabolic deficit. Before bicarbonate is administered, a serum potassium level should be obtained. The addition of bicarbonate can worsen hypokalemia, leading to neuromuscular complications. Hyperchloremic acidosis also occurs with renal insufficiency and renal tubular acidosis.9,20 Katherine Ahn Jin, in Comprehensive Pediatric Hospital Medicine , 2007 As in any condition, the first priority in management is stabilizing the ABCs, as necessary. Management of metabolic acidosis is directed toward treating the underlying cause. In general, treating the causes of anion gap acidosis can regenerate bicarbonate within hours; however, nonanion gap acidosis can take days to resolve and may require exogenous bicarbonate therapy. Insulin, hydration, and electrolyte repletion will correct the acidosis in diabetic ketoacidosis. In addition to treating the underlying condition, lactic acidosis can be resolved by increasing tissue oxygenation using crystalloid, blood products, afterload reduction, inotropic agents (e.g., d Continue reading >>
The Anion Gap
The anion gap is a tool used to: Confirm that an acidosis is indeed metabolic Narrow down the cause of a metabolic acidosis Monitor the progress of treatment In a metabolic acidosis the anion gap is usually either ‘Normal’ or ‘High’. In rare cases it can be ‘low’, usually due to hypoalbuminaemia. An ABG machine will often give a print out of the anion gap, but it can also be useful to know how it is calculated. In blood, there are many cations and anions. However, the vast majority of the total number are potassium, sodium, chloride, or bicarbonate. The ‘anion’ gap is an artificial measure, which is calculated by subtracting the total number of anions (negatively charged ions – bicarbonate and chloride) from the total number of cations (sodium and potassium). Thus, the formula is: ([Na+]+ [K+]) –([Cl–]+ [HCO3–]) In reality, the concentration of potassium anions is negligible, and this often omitted. There are usually more measurable cations than anions, and thus a normal anion gap is value is positive. A normal value is usually 3-16, but may vary slightly depending on the technique used by the local laboratory. If the anion gap is <30, then there may not be ‘true’ high anion gap metabolic acidosis. In a healthy normal individual, the main unmeasured anions are albumin and phosphate. Almost all of the gap can be attributed to albumin. This means that in patients with hypoalbuminaemia and metabolic acidosis, there may be a normal anion gap. Be wary in severely unwell patients because they often have a low albumin. You can adjust for this in your calculation. Corrected anion gap: [AG] + (0.25 x (40-albumin)) In an unwell patient with a high anion gap metabolic acidosis (HAGMA) the anion gap is increased due: Accumulation of organic acids Inabili Continue reading >>
Differential Diagnosis Of Nongap Metabolic Acidosis: Value Of A Systematic Approach
Go to: Recognition and Pathogenesis of the Hyperchloremia and Hypobicarbonatemia of Nongap Acidosis A nongap metabolic acidosis is characterized by a serum anion gap that is unchanged from baseline, or a decrease in serum [HCO3−] that exceeds the rise in the anion gap (5,6). Whenever possible, the baseline anion gap of the patient should be used rather than the average normal value specific to a particular clinical laboratory (6) and the anion gap should be corrected for the effect of a change in serum albumin concentration (7). These steps will reduce the chance that a co-existing high anion gap acidosis will be missed if the increase in the serum anion gap does not cause the value to exceed the upper limit of the normal range (8,9). Nongap metabolic acidosis (hyperchloremic) refers a metabolic acidosis in which the fall in serum [HCO3−] is matched by an equivalent increment in serum Cl− (6,10). The serum anion gap might actually decrease slightly, because the negative charges on albumin are titrated by accumulating protons (6,11). Hyperchloremic acidosis is a descriptive term, and does not imply any primary role of chloride in the pathogenesis of the metabolic acidosis. As shown in Figure 1, a nongap metabolic acidosis can result from the direct loss of sodium bicarbonate from the gastrointestinal tract or the kidney, addition of hydrochloric acid (HCl) or substances that are metabolized to HCl, impairment of net acid excretion, marked urinary excretion of organic acid anions with replacement with endogenous or administered Cl− (12,13), or administration of Cl−-rich solutions during resuscitation (14). The development of hyperchloremic acidosis from administration of HCl is easy to visualize, with titrated HCO3− being replaced by Cl−. Similarly, gastroin Continue reading >>
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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 >>
Metabolic Acidosis; Non-gap
Non-gap metabolic acidosis, or hyperchloremic metabolic acidosis, are a group of disorders characterized by a low bicarbonate, hyperchloremia and a normal anion gap (10-12). A non-gapped metabolic acidosis fall into three categories: 1) loss of base (bicarbonate) from the gastrointestinal (GI) tract or 2) loss of base (bicarbonate) from the kidneys, 3) intravenous administration of sodium chloride solution. Bicarbonate can be lost from the GI tract (diarrhea) or from the kidneys (renal tubular acidosis) or displaced by chloride. A. What is the differential diagnosis for this problem? Proximal renal tubular acidosis: (low K+) Distal renal tubular acidosis: (low or high K+) Prostaglandin Inhibitors, (aspirin, nonsteroidal anti-inflammatory drugs, cyclooxygenase 2 inhibitors) Adrenal insufficiency (primary or secondary) (high K+) Pseudoaldosteronism, type 2 (Gordon's 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. 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 Continue reading >>
Intro To Arterial Blood Gases, Part 2
Arterial Blood Gas Analysis, Part 2 Introduction Acute vs. Chronic Respiratory Disturbances Primary Metabolic Disturbances Anion Gap Mixed Disorders Compensatory Mechanisms Steps in ABG Analysis, Part II Summary Metabolic Madness -- Mixed Disorders Sometimes patients have a combination of metabolic disorders. For example, a diabetic with ketoacidosis (anion gap metabolic acidosis) could also be vomiting and losing gastric acid (metabolic alkalosis). In the setting of an anion gap metabolic acidosis, calculation of the "corrected serum bicarbonate" (sometimes called the "gap-gap") can help you find an additional non-gap metabolic acidosis or metabolic alkalosis. Where AG = anion gap and the normal anion gap = 12. Remember, metabolic disturbances alter the serum HCO3. With an anion gap acidosis each "extra added acid" is reflected as one less bicarbonate. Therefore if you ingest 5 mEq/L of acid, the serum bicarbonate will be decreased by 5 mEq/L (24 - 5 = 19 mEq/L). In other words, 5 mEq/L of bicarbonate is consumed to neutralize the extra acid and the measured HCO3 would be decreased to 19 mEq/L. For example, if the calculated anion gap is 20 and the normal anion gap is 12, then there are 8 "extra acids" that are being consumed by bicarbonate. The measured serum bicarbonate would then be approximately 16 mEq/L (24 - 8). In other words, for a pure anion gap acidosis, when you add the amount of unmeasured acid/lost bicarbonate (Measured AG - Normal AG) to the Measured HCO3, the "Corrected HCO3" should equal a normal serum HCO3 (22-26 mEq/L). If the "corrected HCO3" is above normal (> 26 mEq/L), then you also have a metabolic alkalosis because there are extra bicarbonates. If the "corrected HCO3" is below normal (< 22 mEq/L), then you also have an non-anion gap acidosis bec Continue reading >>
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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 >>
Treatment Of Acute Non-anion Gap Metabolic Acidosis
Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acid–base disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide might be less frequent than in high anion gap metabolic acidosis because of better tissue perfusion and the ability to eliminate carbon dioxide. Further basic and clinical research is needed to facilitate development of evidence-based guidelines for therapy of this important and increasingly common acid–base disorder. Introduction Acute metabolic acidosis (defined temporally as lasting minutes to a few days) has traditionally been divided into two major categories based on the level Continue reading >>
