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What Causes Normal Anion Gap Acidosis?

Normal Anion Gap Acidosis

Normal Anion Gap Acidosis

In renal physiology , normal anion gap acidosis, and less precisely non-anion gap acidosis, is an acidosis that is not accompanied by an abnormally increased anion gap . The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second. The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis): Diarrhea : due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl, results in a decrease in the plasma Na+ concentration relative to the Clconcentration. This scenario can be avoided if formulations such as lactated Ringers solution are used instead of normal saline to replace GI losses. [2] Continue reading >>

Diarrhoea As A Cause Of Normal Anion Gap Acidosis - Deranged Physiology

Diarrhoea As A Cause Of Normal Anion Gap Acidosis - Deranged Physiology

Diarrhoea As a Cause of Normal Anion Gap Acidosis Diarrhoea can result in a metabolic acidosis by causing a disproportionate loss of sodium, and thus decreasing the strong ion difference The change in strong ion difference due to intestinal electrolyte losses However, precisely what sort of acid-base disturbance will occur depends entirely on what is being lost, and how. Which is frequently difficult to establish. The content of the gastrointestinal fluid losses is likely to vary from patient to patient, depend strongly on the diet, and be dependent on whether there are any attempts at reclamation (i.e. if the colon is still making an effort to retain electrolytes). Pancreatic secretions, a major source of loss for fluid with a large strong ion difference (which the bowel doesnt get a chance to reclaim) are discussed elsewhere . Similarly, a small bowel fistula with a large output (eg. a high output ileostomy) deserves its own mention . Broad generalizations can be made: the stool transit time is important, as is the volume. If the stool does not spend very long in the colon, reabsorption cannot occur, and electrolyte loss is inevitable. In short, diarrhoea tends to cause a hyponatremic hypokalemic metabolic acidosis, most of the time. A general rule is that a metabolic acidosis due to loss of lower gastrointestinal contents will only occur if the volume of loss is massive, and the fluid being lost must have a larger than average strong ion difference. The loss of large amounts of fluid places the kidneys at an additional disadvantage, by decreasing the glomerular filtration rate. As a result, the rate at which the acid-base disorder can be corrected decreases. So what is the electrolyte content of diarrhoea? I guess one might say it varies. No two stools are alike. A Continue reading >>

Acid-base Disorders

Acid-base Disorders

Content currently under development Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause. Continue reading >>

Differential Diagnosis Of Nongap Metabolic Acidosis: Value Of A Systematic Approach

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 >>

Metabolic Acidosis; Non-gap

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 >>

Causes Of Non-anion Gap Metabolic Acidosis

Causes Of Non-anion Gap Metabolic Acidosis

Bicarbonate-rich fluid excreted into the intestines where it is lost (GI loss of HCO3). There is an additional mechanism by which NH4Cl causes a non-AG metabolic acidosis. It is similar to the mechanism by which TPN causes a non-AG metabolic acidosis. Either the NH4Cl or the amino acids in TPN are meatbolized to HCl which causes a transient non-AG metabolic acidosis. The decreased pH and decreased HCO3 stimulate renal tubular reabsorption and generation of HCO3 (secretion of H+). You only end up with a metabolic acidosis if the addition of acid overrides the ability of the renal tubules to secrete H+ and generate NH3+ for excretion in the urine, usually a short-lived process. In prolonged hypercapnia renal tubular cells compensate for a prolonged respiratory alkalosis by decreasing reclaimation and generation of HCO3 (which takes 12-24 hrs for full affect). If the respiratory alkalosis resolves rapidly, reclaimation and generation of HCO3 will return to normal over 1-2 days. During this period you can get a (resolving) non-AG metabolic acidosis. The two main causes you for non-anion gap metabolic acidosis are diarrhea and RTA . Most of the time you can distinguish between these two based on the history alone.Another way to think about the differential diagnosis of non-anion gap metabolic acidosisis to ask whether or not there is GI loss or Renal loss of bicarbonate. If the history does not provide an obvious explanation, you can distinguish between GI vsrenal bicarbonate losses by determining the urine anion gap(urine AG = urine Na + urine K - urine Cl), where a positive value indicates renalbicarbonate loss and a largely negative value indicates extra-renal bicarbonate loss. Why is that? Because if a large amount of HCO3 is lost, a large amount ofNH+ is excreted in th Continue reading >>

Normal Anion Gap Acidosis

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 >>

Renal Fellow Network: Mnemonic For Non-anion Gap Metabolic Acidosis

Renal Fellow Network: Mnemonic For Non-anion Gap Metabolic Acidosis

Mnemonic for NON-Anion Gap Metabolic Acidosis As I've mentioned previously on this blog, the "MUDPALES" mnemonic for anion gap metabolic acidosis is one of the most successful medical mnemonic's of all time. A less successful (and admittedly less useful) mnemonic exists for non-anion gap metabolic acidoses (NAGMA), which I learned as a resident. It's "HARDUP", which stands for the following: H = hyperalimentation (e.g., starting TPN). R = renal tubular acidosis (Type I = distal; Type II = proximal; Type IV = hyporeninemic hypoaldosteronism. U = uretosigmoid fistula (because the colon will waste bicarbonate). P = pancreatic fistula (because of alkali loss--the pancreas secretes a bicarbonate-rich fluid). Practically speaking however, the two main causes you really have to remember for NAGMA are DIARRHEA or RENAL TUBULAR ACIDOSIS, which 90% of the time you can distinguish between based on the history alone. Another way to think about the differential diagnosis of NAGMA is to ask whether or not there is GI LOSS or RENAL LOSS of bicarbonate. If the history does not provide an obvious explanation, one can distinguish between GI versus renal bicarbonate losses by determining the urine anion gap (urine AG = urine Na + urine K - urine Cl), where a positive value indicates renal bicarbonate loss whereas a largely negative value indicates extra-renal bicarbonate loss. Continue reading >>

Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

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 >>

Acid-base Physiology

Acid-base Physiology

8.4.1 Is this the same as normal anion gap acidosis? In hyperchloraemic acidosis, the anion-gap is normal (in most cases). The anion that replaces the titrated bicarbonate is chloride and because this is accounted for in the anion gap formula, the anion gap is normal. There are TWO problems in the definition of this type of metabolic acidosis which can cause confusion. Consider the following: What is the difference between a "hyperchloraemic acidosis" and a "normal anion gap acidosis"? These terms are used here as though they were synonymous. This is mostly true, but if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis. This could be considered a 'relative hyperchloraemia'. However, you should be aware that in some cases of normal anion-gap acidosis, there will not be a hyperchloraemia if there is a significant hyponatraemia. In a disorder that typically causes a high anion gap disorder there may sometimes be a normal anion gap! The anion gap may still be within the reference range in lactic acidosis. Now this can be misleading to you when you are trying to diagnose the disorder. Once you note the presence of an anion gap within the reference range in a patient with a metabolic acidosis you naturally tend to concentrate on looking for a renal or GIT cause. 1. One possibility is the increase in anions may be too low to push the anion gap out of the reference range. In lactic acidosis, the clinical disorder can be severe but the lactate may not be grossly high (eg lactate of 6mmol/l) and the change in the anion gap may still leave it in the reference range. So the causes of high anion gap acidosis should be considered in patients with hyperchloraemic acidosis if the cause of the acidosis is otherwise not apparent. Continue reading >>

Normal Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

Home | Critical Care Compendium | Normal Anion Gap Metabolic Acidosis Normal Anion Gap Metabolic Acidosis (NAGMA) HCO3 loss and replaced with Cl- -> anion gap normal if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis -> this could be considered a ‘relative hyperchloraemia’. Extras – RTA, ingestion of oral acidifying salts, recovery phase of DKA loss of bicarbonate with chloride replacement -> hyperchloraemic acidosis secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. some typical at risk clinical situations are: external drainage of pancreatic or biliary secretions (eg fistulas) this should be easily established by history normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule in patients receiving acetazolamide (or other carbonic anhydrase inhibitors), proximal reabsorption of bicarbonate is decreased resulting in increased distal delivery and HCO3- appears in urine this results in a hyperchloraemic metabolic acidosis and is essentially a form of proximal renal tubular acidosis but is usually not classified as such. hyperchloraemic metabolic acidosis commonly develops during therapy of diabetic ketoacidosis with normal saline oral administration of CaCl2 or NH4Cl is equivalent to giving an acid load both of these salts are used in acid loading tests for the diagnosis of renal tubular acidosis CaCl2 reacts with bicarbonate in the small bowel resulting in the production of insoluble CaCO3 and H+ the hepatic metabolism of NH4+ to urea results in an equivalent production of H+ REASONS WHY ANION GAP MAY BE NORMAL DESPITE A ‘HIGH ANION GAP METABOLIC ACIDOSIS’ 1. Continue reading >>

The Anion Gap

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 >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Practice Essentials This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses, in particular the renal tubular acidoses (RTAs). [1, 2] It also addresses approaches to the diagnosis and management of these disorders. A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na+) - [(HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured. An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture. A normal AG acidosis is characterized by a lowered bicarbonate concentration, which is counte Continue reading >>

Metabolic Acidosis And The Anion Gap

Metabolic Acidosis And The Anion Gap

Decrease in pH due to decrease in serum HCO3- Related to either loss of HCO3- or gain of H+ caused by: -Exogenous acid=e.g. ethylene glycol overdose -Kidneys=e.g. proximal renal tubular acidosis (Type 2 RTA) 3. Inability to excrete normal daily acid production by kidneys-e.g. advanced kidney disease, distal renal tubular acidosis (Type 1 RTA) Laboratory Findings in Metabolic Acidosis Decreased pCO2 (to compensate for low HCO3-) Clinically divide metabolic acidoses based on whether patient has elevated anion gap or normal anion gap Anion Gap=difference between measured cations and anions What are the common circulating cations and anions? Cations: Sodium, Potassium, Calcium, Magnesium, Proteins Anions: Chloride, Bicarbonate, Sulfates, Phosphates, Albumin, Other proteins Not practical to measure all of these, so the ones easiest to measure/in greatest abundance are measured=Sodium, Chloride, and Bicarbonate Normal Anion Gap Metabolic Acidosis (Hypercholermic metabolic acidosis) Normal anion gap metabolic acidosis characterized by decrease in bicarbonate and increase in chloride =HCl+NaHCO3-> NaCl +H2CO3-> CO2+ H2O+ NaCl H+ +Cl- +HCO3- -> Cl- + H2CO3-> H2O+CO2 +Cl- Net result=loss of bicarbonate and gain of chloride HCO3- replaced by measured anion (Cl-), so sum of Cl- + HCO3- remains unchanged=no change in anion gap What are the main causes of normal anion gap metabolic acidosis? Decreased ability to excrete H+ by kidney What are metabolic consequences of diarrhea or renal HCO3- wasting? 2. In response to volume loss and to maintain electroneutrality the kidney will hold on to Cl- 3. Sum result is loss of HCO3- and gain of Cl- What are metabolic consequences of the kidneys inability to excrete adequate H+? 2. Is buffered by HCO3- (H+ +HCO3- ->H2CO3-> H2O+CO2) Occurs when Continue reading >>

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