Hyperchloremia (high Chloride Levels)
Hyperchloremia is an electrolyte imbalance that occurs when theres too much chloride in the blood. Chloride is an important electrolyte that is responsible for maintaining the acid-base (pH) balance in your body, regulating fluids, and transmitting nerve impulses. The normal range for chloride in adults is roughly between 98 and 107 milliequivalents of chloride per liter of blood (mEq/L). Your kidneys play an important role in the regulation of chloride in your body, so an imbalance in this electrolyte may be related to a problem with these organs. It may also be caused by other conditions, like diabetes or severe dehydration , which can affect the ability of your kidneys to maintain chloride balance. The symptoms that may indicate hyperchloremia are usually those linked to the underlying cause of the high chloride level. Often this is acidosis , in which the blood is overly acidic. These symptoms may include: Like sodium, potassium, and other electrolytes, the concentration of chloride in your body is carefully regulated by your kidneys. The kidneys are two bean-shaped organs located just below your rib cage on both sides of your spine. They are responsible for filtering your blood and keeping its composition stable, which allows your body to function properly. Hyperchloremia occurs when the levels of chloride in the blood become too high. There are several ways that hyperchloremia can occur. These include: intake of too much saline solution while in the hospital, such as during a surgery Hyperchloremic acidosis, or hyperchloremic metabolic acidosis, occurs when a loss of bicarbonate (alkali) tips the pH balance in your blood toward becoming too acidic (metabolic acidosis). In response, your body holds onto chloride, causing hyperchloremia. In hyperchloremic acidosis, 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 >>
Hyperchloremic Metabolic Acidosis: Nonrenal Causes
Hyperchloremic Metabolic Acidosis: Nonrenal Causes In the previous chapter, we discussed both hypo- and hyperkalemic hyperchloremic metabolic acidoses due to renal causes. In this chapter, we will discuss hypokalemic hyperchloremic metabolic acidosis due to nonrenal causes, mostly gastrointestinal (GI) disorders. Table 30.1 shows nonrenal causes of hyperchloremic metabolic acidosis. This is a preview of subscription content, log in to check access Atia AN, Buchman AL. Oral rehydration solutions in non-cholera diarrhea: a review. Am J Gastroenterol. 2009;104:2596604. CrossRef PubMed Google Scholar Batlle DC. Hyperchloremic metabolic acidosis. In: Seldin DW, Giebisch G, editors. The regulation of acid-base balance. New York: Raven Press; 1989. p. 31951. Google Scholar Charney AN, Danowitz M. Gastrointestinal influences on hydrogen ion balance. In: Gennari FJ, Adrogu HJ, Galla JH, Madias NE, editors. Acid-base disorders and their treatment. Boca Raton: Taylor & Francis; 2005. p. 20940. CrossRef Google Scholar Field M. Intestinal ion transport and the pathophysiology of diarrhea. J Clin Invest. 2003;111:93143. CrossRef PubMed PubMedCentral Google Scholar Gennari FJ, Weise WJ. Acid-base disturbances in gastrointestinal disease. Clin J Am Soc Nephrol. 2008;3:18618. CrossRef PubMed Google Scholar Kent AJ, Banks MR. Pharmacological management of diarrhea. Gastroenterol Clin N Am. 2010;39:495507. CrossRef Google Scholar Kunzelmann K, Mall M. Electrolyte transport in the mammalian colon: mechanisms and implications for disease. Physiol Rev. 2002;82:24589. CrossRef PubMed Google Scholar Wesson DE, Laski M. Hyperchloremic metabolic acidosis due to intestinal losses and other nonrenal causes. In: Gennari FJ, Adrogu HJ, Galla JH, Madias NE, editors. Acid-base disorders and their tre 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 >>
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 >>
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 >>
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 Acidosis
Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more... 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 Continue reading >>
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 >>
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
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 >>
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 >>
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 >>
Mechanism Of Hyperchloremic Metabolic Acidosis | Anesthesiology | Asa Publications
Mechanism of Hyperchloremic Metabolic Acidosis Lawrence R. Miller, MD ; Jonathan H. Waters, MD ; Charlton Provost Department of Anesthesiology FHP, Inc., Fountain Valley, California, Department of Anesthesiology, University of California, Irvine Medical Center, 101 City Drive South, Route 81A, Orange, California 92668. Mechanism of Hyperchloremic Metabolic Acidosis Anesthesiology 2 1996, Vol.84, 482-483.. doi: Anesthesiology 2 1996, Vol.84, 482-483.. doi: Lawrence R. Miller, Jonathan H. Waters, Charlton Provost; Mechanism of Hyperchloremic Metabolic Acidosis. Anesthesiology 1996;84(2):482-483.. 2018 American Society of Anesthesiologists Mechanism of Hyperchloremic Metabolic Acidosis You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account To the Editor:--Several points in the case report "Transient Perioperative Metabolic Acidosis in a Patient with Ileal Bladder Augmentation" [1] merit further discussion. We do not believe that the transient perioperative hyperchloremic metabolic acidosis in this patient required the presence of the ileal bladder augmentation. We accept that prolonged contact of urine with bowel mucosa will allow for water reabsorption, passive chloride reabsorption, and active HCO3sup - secretion, leading to a net HCO sub 3 sup - loss and metabolic acidosis. In this patient, an indwelling urinary catheter was placed preoperatively, and although the catheter was transiently obstructed at the initiation of surgery, the decreased time of contact between the urine and bowel mucosa inherent with bladder drainage mitigates the importance of the ileal augmented bladder. In our opinion, the principal reason for the acidosis was the large chloride load infused into Continue reading >>
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 >>
