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Normal Anion Gap Metabolic Acidosis

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 >>

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 >>

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 >>

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 >>

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 >>

Metabolic Acidosis (normal Anion Gap) - General Practice Notebook

Metabolic Acidosis (normal Anion Gap) - General Practice Notebook

Normal anion gap / hyperchloraemic acidosis: bicarbonate loss in the gut, e.g. pancreatic fistula, diarrhoea, utero-enterostomy distal - failure of acidification - proton pump failure treatment with excessive carbonic anhydrase inhibitors Home| About us| Facebook| Contact us| Authors| Help| FAQ This site is intended for the use of healthcare professionals only. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions. Copyright 2016 Oxbridge Solutions Ltd. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions Ltd receives funding from advertising but maintains editorial independence more... GPnotebook stores small data files on your computer called cookies so that we can recognise you and provide you with the best service. If you do not want to receive cookies please do not use GPnotebook. Continue reading >>

Prime Pubmed | Metabolic Acidosis Decreased Or Normal Anion Gap Journal Articles From Pubmed

Prime Pubmed | Metabolic Acidosis Decreased Or Normal Anion Gap Journal Articles From Pubmed

New Test, Old Disease: A Case Series of Diabetic Ketoalkalosis. [Journal Article] J Emerg Med 2019Jaramillo J, Joseph M, Sinert R JE CONCLUSIONS: We found that DKAlk is more common than previously reported. We recommend screening with BMP electrolytes and BHB levels for hyperglycemic ED patients who are vomiting or suspected of hypovolemia. Extracellular acidosis differentiates pancreatitis and pancreatic cancer in mouse models using acidoCEST MRI. [Journal Article] Neoplasia 2019; 21(11):1085-1090High RA, Randtke EA, Pagel MD N Differentiating pancreatitis from pancreatic cancer would improve diagnostic specificity, and prognosticating pancreatitis that progresses to pancreatic cancer would also improve diagnoses of pancreas pathology. The high glycolytic metabolism of pancreatic cancer can cause tumor acidosis, and different levels of pancreatitis may also have different levels of acidosis, so that extracellular acidos Differentiating pancreatitis from pancreatic cancer would improve diagnostic specificity, and prognosticating pancreatitis that progresses to pancreatic cancer would also improve diagnoses of pancreas pathology. The high glycolytic metabolism of pancreatic cancer can cause tumor acidosis, and different levels of pancreatitis may also have different levels of acidosis, so that extracellular acidosis may be a diagnostic biomarker for these pathologies. AcidoCEST MRI can noninvasively measure extracellular pH (pHe) in the pancreas and pancreatic tissue. We used acidoCEST MRI to measure pHe in a KC model treated with caerulein, which causes pancreatitis followed by development of pancreatic cancer. We also evaluated the KC model treated with PBS, and wild-type mice treated with caerulein or PBS as controls. The caerulein-treated KC cohort had lower pHe of 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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

Treatment Of Acute Non-anion Gap Metabolic Acidosis

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 >>

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