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 | Washington Manual Of Medical Therapeutics
Washington Manual of Medical Therapeutics Type your tag names separated by a space and hit enter To view the entire topic, please sign in or purchase a subscription . The Washington Manual of Medical Therapeutics helps you diagnose and treat hundreds of medical conditions. Consult clinical recommendations from a resource that has been trusted on the wards for 50+ years. Explore these free sample topics: -- The first section of this topic is shown below -- The causes of a metabolic acidosis can be divided into those that cause an elevated AG and those with a normal AG. Many of the causes seen in clinical practice can be found in Table 12-3 . AG acidosis results from exposure to acids, which contribute an UA to the ECF. Common causes are DKA, lactic acidosis, and toxic alcohol ingestions. NonAG acidosis can result from the loss of from the GI tract. Renal causes due to renal excretion of or disorders of renal acid handling are referred to collectively as RTAs. loss occurs most commonly in the setting of severe diarrhea. The three forms of RTA correlate with the three mechanisms that facilitate renal acid handling: proximal bicarbonate reabsorption, distal H+ secretion, and generation of NH3, the principle urinary buffer. Urinary buffers reduce the concentration of free H+ in the filtrate, thus attenuating the back leak of H+, which occurs at low urinary pH. Proximal (type 2) RTA is caused by impaired proximal tubular reabsorption. Causes include inherited mutations (cystinosis), heavy metals, drugs (tenofovir, ifosfamide, carbonic anhydrase inhibitors), and multiple myeloma and other monoclonal gammopathies. Distal (type 1) RTA results from impaired distal H+ secretion. This may occur because of impairment in H+ secretion, as seen with a variety of autoimmune (Sjgren syn Continue reading >>
Metabolic Acidosis Treatment & Management
Approach Considerations Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred while the serum HCO3- level remained at 15 mEq/L. In lactic acidosis and diabetic ketoacidosis, the organic anion can r Continue reading >>
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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
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 >>
Mechanism Of Normochloremic And Hyperchloremic Acidosis In Diabetic Ketoacidosis
Oh M.S. · Carroll H.J. · Uribarri J. Man S. Oh, MD, Department of Medicine, State University of New York, Health Science Center at Brooklyn, Brooklyn, NY 11203 (USA) 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 >>
Treatment Of Acute Non-anion Gap Metabolic Acidosis
Go to: 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 of the serum anion gap: non-anion gap and high anion gap metabolic acidosis [1]. As implied, with the former acid–base disorder, the anion gap is within normal limits, whereas with the latter disorder it is increased. This categorization is primarily used to facilitate the differential diagnosis of metabolic acidosis. However, it also has relevance for predicting the clinical outcome and determining indications for treatment. Although many clinicians presume that acute metabolic acidosis in seriously ill patients will be due to a high anion gap acidosis, recent studies indicate that a non-anion gap metabolic acidosis or combination of non-anion gap and high anion gap metabolic acidosis might be more frequent [2, 3]. Based on these observations, it appears important to more clearly define the potential effects of non-anion gap metabolic acidoses on organ function as a basis for generating evidence-based guidelines for therapy. In the present review, we summarize our current understanding of the pathophysiology of acute non-anion gap acidosis, its clinical characteristics, its adverse effects on cellular function, and also the benefits and complications of therapy. Go to: Definition In non-anion gap or hyperchloremic metabolic acidosis, a reduction in serum [HCO3−] is matched by an approximately equivalent increase in the serum chloride concentration resulting in hypobicarbonatemia and hyperchloremia in the absence of an increase in the serum anion gap [4, 5]. In fact, since a decrease in blood pH alters the protonation of albumin (which normally makes up the majority of the anion gap), a slight Continue reading >>
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 >>
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 >>
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 >>
Therapy 3 Acid Base Disorders
O2 sat and PO2 does NOT affect acid-base balance Anion gap: measure that expresses the balance between circulating anions and cations [AG = Na - (HCO3 + Cl)] Recognize common causes, including medications, of primary acid-base disturbances 1. Anion gap (non volatile organic aicds) : albumin, Na, lipids, lithium 2. non-anion gap (only HCO3 and Cl involved) a. Drug - induced hyperkalemia: K-sparring diuretics, TMP, Heparin, ACE, ARB Recognize the presence and degree of physiologic compensation of acid base disorders Acute buffering of respiratory acidosis is accomplished by tissue buffers (protein, hemoglobin) Lungs adjust minute ventilation (rate and tidal volume) to change [CO2] to compensate for metabolic disorders Kidneys retain or excrete bicarbonate to compensate for changes in [CO2] Identify appropriate patient cases where treatment of acid-base disorders is indicated a. Treatment of reversible cause (ex. opioid discontinuation) b. Mechanical ventilation to aid in CO2 exchange c. NOT give sodium bicarbonate- Shift in equilibrium will result in more CO2 production d. Last line: May give THAM if unresponsive to ventilation 2. Chronic, compensated respiratory acidosis does not require treatment 1. Acute non-anion gap metabolic acidosis may require treatment to replace bicarbonate deficit a. Bicarbonate deficit can be corrected orally over hours to days 2. Chronic metabolic acidosis does not usually require emergent therapy 1. Treatment centers on correcting the underlying disorder 2. NON-effective: Giving bicarbonate only shifts the carbonic acid/bicarbonate buffer system to generating CO2 3. Often will correct numbers but NOT the underlying cause 2. Type 2 & 3: NO benefit from bicarb therapy Calculate a bicarbonate or other alkali replacement dose for an appropriate Continue reading >>
Metabolic Acidosis: Pathophysiology, Diagnosis And Management: Causes Of Metabolic Acidosis
Recommendations for the treatment of acute metabolic acidosis Gunnerson, K. J., Saul, M., He, S. & Kellum, J. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit. Care Med. 10, R22-R32 (2006). Eustace, J. A., Astor, B., Muntner, P M., Ikizler, T. A. & Coresh, J. Prevalence of acidosis and inflammation and their association with low serum albumin in chronic kidney disease. Kidney Int. 65, 1031-1040 (2004). Kraut, J. A. & Kurtz, I. Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment. Am. J. Kidney Dis. 45, 978-993 (2005). Kalantar-Zadeh, K., Mehrotra, R., Fouque, D. & Kopple, J. D. Metabolic acidosis and malnutrition-inflammation complex syndrome in chronic renal failure. Semin. Dial. 17, 455-465 (2004). Kraut, J. A. & Kurtz, I. Controversies in the treatment of acute metabolic acidosis. NephSAP 5, 1-9 (2006). Cohen, R. M., Feldman, G. M. & Fernandez, P C. The balance of acid base and charge in health and disease. Kidney Int. 52, 287-293 (1997). Rodriguez-Soriano, J. & Vallo, A. Renal tubular acidosis. Pediatr. Nephrol. 4, 268-275 (1990). Wagner, C. A., Devuyst, O., Bourgeois, S. & Mohebbi, N. Regulated acid-base transport in the collecting duct. Pflugers Arch. 458, 137-156 (2009). Boron, W. F. Acid base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368-2382 (2006). Igarashi, T., Sekine, T. & Watanabe, H. Molecular basis of proximal renal tubular acidosis. J. Nephrol. 15, S135-S141 (2002). Sly, W. S., Sato, S. & Zhu, X. L. Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis. Clin. Biochem. 24, 311-318 (1991). Dinour, D. et al. A novel missense mutation in the sodium bicarbonate cotransporter (NBCe1/ SLC4A4) Continue reading >>
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 >>
What Is Metabolic Acidosis?
Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>
