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Hyperchloremic Metabolic Acidosis

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Renal tubular acidosis (RTA) is a group of disorders affecting the renal tubular cells that result in hyperchloremic metabolic acidosis with a normal anion gap. Renal tubular acidosis (RTA) is a group of disorders affecting the renal tubular cells that result in hyperchloremic metabolic acidosis with a normal anion gap. Hyperchloremic metabolic acidosis with a normal anion gap Type I: Distal or classic RTA (H+ retention) Etiology: Underlying cause is usually undetermined, but is generally acquired Renal tubular toxins: Heavy metals, ethylene glycol, drugs (gentamicin, cephalosporins, tetracyclines, salicylate) Type I (distal or classic RTA) is caused by an inability of the distal tubule cells to secrete H+ or to produce acidic urine. There is excessive K+ secretion and severe hypokalemia. Type II (proximal RTA) is caused by a failure of HCO3 resorption in the proximal tubule with subsequent loss of HCO3 into urine. The proximal tubule is the site where the majority of filtered HCO3- is reabsorbed via Na+ and H+ exchange and the breakdown of carbonic acid to carbon dioxide and water under the influence of carbonic anhydrase. Hydrogen ions are usually secreted when HCO3 ion is reabsorbed. Failure to reabsorb HCO3 results in excessive urinary losses, basic urine pH, and systemic acidosis. Hyperchloremia develops because of renal conservation of chloride to maintain electroneutrality consequent to HCO3 loss. Christine E. Kurschat, Seth L. Alper, in Molecular and Genetic Basis of Renal Disease , 2008 Renal tubular acidosis (RTA) is a failure of renal regulatory mechanisms to maintain systemic pH homeostasis. Patients present with hyperchloremic metabolic acidosis in the setting of an inappropriate inability to acidify urine pH below 5.5. The associated clinical syndrome can Continue reading >>

Is Correcting Hyperchloremic Acidosis Beneficial?

Is Correcting Hyperchloremic Acidosis Beneficial?

You are here: Home / PULMCrit / Is correcting hyperchloremic acidosis beneficial? Is correcting hyperchloremic acidosis beneficial? An elderly woman presents with renal failure due to severe dehydration from diarrhea. She has a hyperchloremic acidosis from diarrhea with a chloride of 115 mEq/L, bicarbonate of 15 mEq/L, and a normal anion gap. During her volume resuscitation, should isotonic bicarbonate be used to correct her hyperchloremic acidosis? Does correcting her hyperchloremic acidosis actually help her, or does this just make her numbers better? The use of bicarbonate for treatment of metabolic acidosis is controversial. However, this controversy centers primarily around use of bicarbonate for management of lactic acidosis or ketoacidosis.Treatment of these disorders requires reversing the underlying disease process, with bicarbonate offering little if any benefit.Hyperchloremic metabolic acidosis is different.Whether due to bicarbonate loss or volume repletion with normal saline, the primary problems is a bicarbonate deficiency.Treating this with bicarbonate is a logical and accepted approach: Giving bicarbonate to a patient with a true bicarbonate deficit is not controversial. Controversy arises when the decrease in bicarbonate concentration is the result of its conversion to another base, which, given time, can be converted back to bicarbonate However, clinicians are often reluctant to treat hyperchloremic metabolic acidosis with bicarbonate, since the benefits of treatment are unclear.This post will attempt to clarify the rationale for treatment. Resuscitation with balanced crystalloids improves renal function There is growing evidence that resuscitation with normal saline impairs renal blood flow and function ( Young 2014 ).For example, Chowdhury 2012 inve Continue reading >>

Hyperchloremia Why And How - Sciencedirect

Hyperchloremia Why And How - Sciencedirect

Volume 36, Issue 4 , JulyAugust 2016, Pages 347-353 Hyperchloremia Why and howHipercloremia: por qu y cmo Author links open overlay panel Glenn T.Nagami Open Access funded by Sociedad Espaola de Nefrologa Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance. La hipercloremia es una alteracin electroltica frecuente que se asocia a una serie de distintos trastornos clnicos. El rin desempea una funcin importante en la regulacin de la concentracin de cloruro a travs de diversos transportadores que se encuentran a lo largo de la nefrona. Sin embargo, puede aparecer hipercloremia cuando la prdida hdrica sea mayor que la de sodio y cloruro; cuando se sobrepase la capacidad de excretar el cloruro en exceso; o cuando la concentracin srica de bicarbonato sea baja y al mismo tiempo haya un aumento de cloruro, como sucede en la acidosis metablica con brecha aninica normal o en la alcalosis respiratoria. La heterognea naturaleza de las causas subyacentes de la hipercloremia determinar, en gran medida, el modo de tratar esta alteracin electroltica. Continue reading >>

Causes And Effects Of Hyperchloremic Acidosis

Causes And Effects Of Hyperchloremic Acidosis

Causes and effects of hyperchloremic acidosis 1Institute of Child Health, University of Liverpool, Eaton Road, Liverpool L12 2AP, UK This article has been cited by other articles in PMC. Gunnerson and colleagues [ 1 ] found in their retrospective study that critically ill patients with lactate acidosis had a higher mortality compared to patients with hyperchloremic acidosis, whose mortality was not significantly different from patients with no acidosis. Because of its iatrogenic etiology the authors commented that it is reassuring that hyperchloremic acidosis is not associated with an increased mortality. Previous randomized controlled trials have, however, generated concerns regarding the adverse effects of hyperchloremic acidosis associated with rapid isotonic saline administration. Rapid isotonic saline infusion predictably results in hyperchloremic acidosis [ 2 ]. The acidosis is due to a reduction in the strong anion gap by an excessive rise in plasma chloride as well as excessive renal bicarbonate elimination. In a randomized controlled trial with a mixed group of patients undergoing major surgery, isotonic saline infusion was compared to Hartmann's solution with 6% hetastarch with a balanced electrolyte and glucose solution. Two-thirds of patients in the isotonic saline group but none in the balanced fluid group developed hyperchloremic metabolic acidosis [ 3 ]. The hyperchloremic acidosis was associated with reduced gastric mucosal perfusion on gastric tonometry. Another randomized double blind trial of isotonic saline versus lactated Ringer's in patients undergoing aortic reconstructive surgery confirmed this result and the acidosis required interventions like bicarbonate infusion and was associated with the application of more blood products [ 4 ]. Hyperchlor 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 >>

Hyperchloremic Metabolic Acidosis: Is It Clinically Relevant?

Hyperchloremic Metabolic Acidosis: Is It Clinically Relevant?

SUMMARYFirst, do no harm. These words have been the doctrine of medicine since its inception. The era of evidence-based medicine now compels us to provide scientific evidence that we indeed do no harm and that the treatments we prescribe have a beneficial effect. The colloid/crystalloid debate continues to evolve and is as hotly contested now as it was a decade ago. There may be some international differences in the use of colloids or crystalloids, but most of us continue to use both. Whatever our preferred choice of intravenous fluid for the treatment of hypovolemia, clinical outcome studies suggest that when? and how much? are probably more important questions than what?. There are now a wide variety of fluids available to the clinician and most differ markedly in their composition. Aside from the gross classification of IV fluids into colloids and crystalloids, they may be subclassified into balanced or unbalanced categories, i.e., those that contain concentrations of electrolytes similar to those in the plasma and those that do not (see Table 1).The very fact that normal saline is unphysiological was recognized many years ago. This fact led Alexis Hartmann to develop Hartmann's solution in an attempt to produce an isotonic alkalizing solution. He recognized the need for proportionately more sodium than chloride1, which led to a solution very similar to Ringer's original2. The existence of hyperchloremic acidosis has been recognized in many areas for some time, e.g., diabetic ketoacidosis and ammonium chloride poisoning, and is generally termed a low-anion gap acidosis. There is now mounting evidence that the administration of intravenous saline and saline-based fluids is the commonest avoidable cause of clinically relevant hyperchloremic acidosis. Do you want to re Continue reading >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Hyperchloremic acidosis is a known complication of intestinal bypass, due to both intestinal bicarbonate loss and renal tubular acidosis (RTA). Julian L. Seifter, in Goldman's Cecil Medicine (Twenty Fourth Edition) , 2012 Hyperchloremic Metabolic Acidosis of Nonrenal Origin Associated with Hypokalemia Hypokalemic, hyperchloremic acidosis may result from loss of a body fluid that is low in Cl relative to Na+ and K+ when compared with the ratio of Cl to Na+ in extracellular fluid. For example, stool losses of Na+, K+, and HCO3 in small bowel diarrhea or organic acid anions of bacterial origin in colonic diarrhea lead to hyperchloremic acidosis (Chapter 142). Pancreatic secretions (Chapter 201) or heavy losses from ileostomy sites may lead to loss of bicarbonate-containing fluids. Secretagogues such as vasoactive intestinal peptide (VIP), which is associated with neoplasms of the pancreas or sympathetic chain (Chapter 201), cause large losses of HCO3 in stool, with a resulting hypokalemic, hyperchloremic metabolic acidosis. Concomitant gastric achlorhydria is part of the syndrome known as watery diarrhea, hypokalemic, hypochlorhydric acidosis. Urinary diversions, such as ureterosigmoidostomies and ileal loops, may increase chloride absorption in exchange for bicarbonate in the intestinal segment and lead to hyperchloremic acidosis. Thomas D. DuBose, in Therapy in Nephrology & Hypertension (Third Edition) , 2008 Both uremic acidosis and hyperchloremic acidosis of renal insufficiency require oral alkali replacement to maintain [HCO3] between 20 and 24 mEq/L. This can usually be accomplished with relatively modest amounts of alkali (1-1.5 mEq/kg/day). Sodium citrate (Shohl's Solution or Bicitra) has been shown to enhance the absorption of aluminum from the gastrointestinal t 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 >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Normal albumin-corrected anion gap acidosis Hyperchloremic acidosis is a common acid-base disturbance in critical illness, often mild (standard base excess >-10 mEq/L). Definitions of hyperchloremic acidosis vary. The best are not based on chloride concentrations, but on the presence of metabolic acidosis plus the absence of significant concentrations of lactate or other unmeasured anions. 2. standard base excess less than -3 mEq/L or bicarbonate less than 22 mmol/L, 3. Albumin corrected anion gap normal (5-15 mEq/L). A normal strong ion gap is an alternative indicator of the absence of unmeasured anions, although rarely used clinically and offering little advantage over the albumin corrected anion gap. The degree of respiratory compensation is relevant. It is appropriate if PaCO2 approximates the two numbers after arterial pH decimal point (e.g. pH=7.25, PaCO2=25 mm Hg; this rule applies to any primary metabolic acidosis down to a pH of 7.1). Acidosis is severe if standard base excess is less than -10 mEq/L, or pH is less than 7.3, or bicarbonate is less than 15 mmol/L. Common causes in critical illness are large volume saline administration, large volume colloid infusions (e.g. unbalanced gelatine or starch preparations) following resolution of diabetic keto-acidosis or of other raised anion gap acidosis, and post hypocarbia. Hyperchloremic acidosis often occurs on a background of renal impairment/tubular dysfunction. It is usually well tolerated, especially with appropriate respiratory compensation. The prognosis is largely that of the underlying condition. If associated with hyperkalemia, think of hypo-aldosteronism (Type 4 RTA), especially if diabetic. With persistent hypokalemia, think of RTA Types 1 and 2. Hyperchloremic acidosis is usually well tolerated in the Continue reading >>

Hyperchloremic Metabolic Acidosis With Cholestyramine Therapy For Biliary Cholestasis

Hyperchloremic Metabolic Acidosis With Cholestyramine Therapy For Biliary Cholestasis

Hyperchloremic Metabolic Acidosis With Cholestyramine Therapy for Biliary Cholestasis Cholestyramine is a hydrophilic, insoluble anion-exchange resin that removes substantial amounts of bile acids from the enterohepatic circulation by binding them in a compound that cannot be reabsorbed through the intestine. It has been used without complication in children with biliary cholestasis associated with biliary atresia1 and in the treatment of intractable diarrhea in infants.2.3 The case reported here deals with hyperchloremic acidosis as a complication of cholestyramine therapy in a 6-month-old infant with intercurrent infection, and adds to other reports of this finding by Hartline,4 Primak and McGurk,5 and Kleinman.6 Report of a Case.The patient was first referred to the pediatric consultation service at Mt Zion Hospital in San Francisco at the age of 10 weeks, when a diagnosis of intrahepatic cholestasis secondary to intrahepatic biliary atresia was made and confirmed by open liver biopsy. Cholestyramine therapy was begun six weeks prior to this 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 >>

Hyperchloremic Metabolic Acidosis Due To Cholestyramine: A Case Report And Literature Review

Hyperchloremic Metabolic Acidosis Due To Cholestyramine: A Case Report And Literature Review

Hyperchloremic Metabolic Acidosis due to Cholestyramine: A Case Report and Literature Review Fareed B. Kamar 1and Rory F. McQuillan 2 1University of Calgary, Suite G15, 1403-29 Street NW, Calgary, AB, Canada T2N 2T9 2University of Toronto and University Health Network, Toronto General Hospital, Room 8N-842, 200 Elizabeth Street, Toronto, ON, Canada M5G 2C4 Received 13 July 2015; Accepted 30 August 2015 Copyright 2015 Fareed B. Kamar and Rory F. McQuillan. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Cholestyramine is a bile acid sequestrant that has been used in the treatment of hypercholesterolemia, pruritus due to elevated bile acid levels, and diarrhea due to bile acid malabsorption. This medication can rarely cause hyperchloremic nonanion gap metabolic acidosis, a complication featured in this report of an adult male with concomitant acute kidney injury. This case emphasizes the caution that must be taken in prescribing cholestyramine to patients who may also be volume depleted, in renal failure, or taking spironolactone. The orally administered medication cholestyramine is a nonabsorbable anion exchange resin that serves as a bile acid sequestrant. It has been used in the treatment of hypercholesterolemia, pruritus due to biliary obstruction and elevated bile acid levels, and diarrhea due to bile acid malabsorption in the setting of ileal disease or resection [ 1 ]. Adverse effects are uncommon, though typical gastrointestinal reactions include constipation, nausea, and flatulence [ 1 ]. A handful of reports have described the rare complication of metabolic acidosis [ 1 11 ]. The following case a Continue reading >>

Sid Hyperchloremic Acidosis

Sid Hyperchloremic Acidosis

Strong ions are cations and anions that exist as charged particles dissociated from their partner ions at physiologic pH. The SID (Strong Ion Difference) is the difference between the positively- and negatively-charged strong ions in plasma. This method of evaluating acid-base disorders was developed to help determine the mechanism of the disorder rather than simply categorizing them into metabolic vs. respiratory acidosis/alkalosis as with the Henderson-Hasselbalch equation. Strong cations predominate in the plasma at physiologic pH leading to a net positive plasma charge of approximately +40: SID = [strong cations] [strong anions] = [Na+ + K+ + Ca2+ + Mg2+] [Cl- + lactate- + SO42-] Disturbances that increase the SID increase the blood pH while disorders that decrease the SID lower the plasma pH. According to the law of electroneutrality the sum of positive charges is equal to the sum of negative charges. Therefore the SID must be equal to the sum of weak anions in the body (such as bicarbonate, albumin, and phosphate). Hyperchloremic acidosis may result from chloride replacing lost bicarbonate. Such bicarbonate-wasting conditions may be seen in the kidneys (renal tubular acidosis) or the GI tract (diarrhea). This may also occur with aggressive volume resuscitation with normal saline (>30cc/kg/hr) due to excessive chloride administration impairing bicarbonate resorption in the kidneys. The strong ion difference of normal saline is 0 (Na+ = 154mEq/L and Cl- = 154mEq/L SID = 154 154 = 0). Therefore, aggressive administration of NS will decrease the plasma SID causing an acidosis. Administering a solution with a high SID such as sodium bicarbonate should be expected to treat this strong ion acidosis. Continue reading >>

Mechanism Of Normochloremic And Hyperchloremic Acidosis In Diabetic Ketoacidosis

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 >>

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 >>

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