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Paradoxical Acidosis

Renal Fellow Network: The Urine's The Thing...

Renal Fellow Network: The Urine's The Thing...

Vomiting or nasogastric tube (NG) decompression can lead to metabolic alkalosis, often associated with hypokalemia. When asked what the source of the K loss is, most people assume it is lost in the gastric fluid. However, gastric fluid only contains about 9 mEq/L of potassium, hardly enough to lead to profound hypokalemia. While it is true that cellular shift due to alkalosis could explain some of the hypokalemia, the primary source of potassium loss is via the urine. Metabolic alkalosis induced by GI loss leads to volume depletion. In this setting, secondary hyperaldosteronism ensues, leading to sodium retention and potassium wasting, hence the hypokalemia. Further, such GI losses are also associated with chloride depletion. Maintenance of electroneutrality usually obligates chloride reabsorption along with sodium retention. But in chloride depleted states, this is not possible. Instead the lumen-negative gradient (due to sodium reabsorption without chloride following) obligates cation excretion, usually potassium or hydrogen ions. Additionally, the hyperaldosteronism increases H+ excretion via effects on the H-ATPase. Together these explain the paradoxical aciduria associated with GI loss-induced metabolic alkalosis as hydrogen is excreted despite alkalemia. The chloride depleted state, as well as the sodium retention induced by volume depletion, also lead to maintenance of the alkalosis by limiting bicarbonate excretion by a variety of mechanisms. It is for this reason that such alkaloses are termed saline responsive, indicated by a low urine chloride - administration of saline leads to correction of hypovolemia and therefore removes the stimulus to aldosterone, while at the same time chloride replenishment allows for the excretion of bicarbonate while minimizing H+ Continue reading >>

Internal Medicine: What Is Paradoxic Aciduria Causes And Treatments?... - Prognosis Questions

Internal Medicine: What Is Paradoxic Aciduria Causes And Treatments?... - Prognosis Questions

thanks but how does the low potassium occur. due to the Na/k pump in the kidney? Anonymous healthcare provider - 4 years ago due to high circulating aldosterone which is induced by hypovolemia. after vomiting or nasogastric drainage ( i mean huge amounts) patients become hypovolemic, this causes activation of renin angiotensin aldosterone system in order to retain water. since aldosterone causes renal K loss, hypokalemia is caused by compensation by aldosterone. also, the massive vomiting and large gastric effluent cause massive potassium loss. in fact it is this loss that actually cause urinary proton loss which result to aciduria as there is little potassium to excrete in exchange for sodium reabsorption. so H ions are lost what you mean is that there is little K in exchange for H not Na.during hypokalemia in order to keep plasma K at reasonable levels K-H pump at distal nephron excretes H in exchange with K causing aciduria what you say is something differen related with ENaC channels understand that d main etiology is persistent loss of gastric effluent which causes hypokalaemia and hypovolaemia and metabolic alkalosis.the angiotensin aldosterone system which should normally cause sodium retension ,potassium loss and fluid retension. but because potassium already is deficient, the kidney resort to losing H instead of K. this results to aciduria instead of the expected. alkaluria in such condition Get Prognosis: Questions to answer this question Continue reading >>

Pyloric Stenosis: Fluid Therapy

Pyloric Stenosis: Fluid Therapy

Home / ABA Keyword Categories / P / Pyloric stenosis: Fluid therapy Pyloric stenosis is a medical emergency, not a surgical emergency. The patient should not be operated on until there has been adequate fluid and electrolyte resuscitation. According to Barash, the infant should have normal skin turgor, and the correction of the electrolyte imbalance should produce a sodium level that is >130 mEq/L, a potassium level that is at least 3 mEq/L, a chloride level that is >85 mEq/L and increasing, and a urine output of at least 1 to 2 mL/kg/hr. These patients need a resuscitation fluid of full-strength, balanced salt solution and, after the infant begins to urinate, the addition of potassium. The cardinal findings in pyloric stenosis are dehydration, metabolic alkalosis, hypochloremia, and hypokalaemia. Loss of gastric fluid leads to volume depletion and loss of sodium, chloride, acid (H+) and potassium. This results in a hypokalemic, hypochloremic metabolic alkalosis. The kidneys attempt to maintain normal pH by excreting excess HCO3.The kidneys attempt to conserve sodium at the expense of hydrogen ions, which can lead to paradoxical aciduria. In more severe dehydration, renal potassium losses are also accelerated owing to an attempt to retain fluid and sodium. According to Smith, The initial therapeutic approach is aimed at repletion of intravascular volume and correction of electrolyte and acid-base abnormalities (e.g., 5% dextrose in 0.45% NaCl with 40 mmol/L of potassium infused at 3 L/m2 per 24 hours). Most children respond to therapy within 12 to 48 hours, after which surgical correction can proceed in a nonemergent manner. The use of cimetidine has also been shown to rapidly normalize the metabolic alkalosis in patients with hypertrophic pyloric stenosis." In particu Continue reading >>

8.7 Use Of Bicarbonate In Metabolic Acidosis

8.7 Use Of Bicarbonate In Metabolic Acidosis

8.7 Use of Bicarbonate in Metabolic Acidosis Metabolic acidosis causes adverse metabolic effects (see Section 5.4 ). In particular the adverse effects on the cardiovascular system may cause serious clinical problems. Bicarbonate is an anion and cannot be given alone. Its therapeutic use is as a solution of sodium bicarbonate. An 8.4% solution is a molar solution (ie it contains 1mmol of HCO3- per ml) and is the concentration clinically available in Australia. This solution is very hypertonic (osmolality is 2,000 mOsm/kg). The main goal of alkali therapy is to counteract the extracellular acidaemia with the aim of reversing or avoiding the adverse clinical effects of the acidosis (esp the adverse cardiovascular effects). Other reasons for use of bicarbonate in some cases of acidosis are: to promote alkaline diuresis (eg to hasten salicylate excretion) 8.7.2 Undesirable effects of bicarbonate administration In general, the severity of these effects are related to the amount of bicarbonate used. These undesirable effects include: 8.7.3 Important points about bicarbonate 1. Ventilation must be adequate to eliminate the CO2 produced from bicarbonate Bicarbonate decreases H+ by reacting with it to to produce CO2 and water. For this reaction to continue the product (CO2) must be removed. So bicarbonate therapy can increase extracellular pH only if ventilation is adequate to remove the CO2. Indeed if hypercapnia occurs then as CO2 crosses cell membranes easily, intracellular pH may decrease even further with further deterioration of cellular function. 2. Bicarbonate may cause clinical deterioration if tissue hypoxia is present If tissue hypoxia is present, then the use of bicarbonate may be particularly disadvantageous due to increased lactate production (removal of acidotic i Continue reading >>

Hypochloremic Hypokalemic Metabolic Alkalosis

Hypochloremic Hypokalemic Metabolic Alkalosis

SDN members see fewer ads and full resolution images. Join our non-profit community! Hypochloremic Hypokalemic Metabolic Alkalosis Example: gastric outlet obstruction or pyloric stenosis Can somebody explain this electrolyte abnormality in terms that make sense and are also correct? I understand it, at least I think I do. However, I keep hearing slightly conflicting explanations about the renal compensations going on. P.S. -- this is a super highly pimped topic in my experience Example: gastric outlet obstruction or pyloric stenosis Can somebody explain this electrolyte abnormality in terms that make sense and are also correct? I understand it, at least I think I do. However, I keep hearing slightly conflicting explanations about the renal compensations going on. P.S. -- this is a super highly pimped topic in my experience Example: gastric outlet obstruction or pyloric stenosis Can somebody explain this electrolyte abnormality in terms that make sense and are also correct? I understand it, at least I think I do. However, I keep hearing slightly conflicting explanations about the renal compensations going on. P.S. -- this is a super highly pimped topic in my experience Pyloric stenosis is results from hypertrophy of the circular muscle of the pylorus. This in turn results in gastric outlet obstruction from the constricted circular muscle. The gastric outlet obstruction then causes non-bilious, projectile vomiting (hallmark of the diagnosis of pyloric stenosis) which depletes hydrochloric acid from the stomach. This depletion of hydrochloric acid causes a hypocholemic metabolic alkalosis and dehydration because of the loss of H+ and Cl- ions in addition to fluid. Renal compensation for this loss of H+ ions is by preserving protons at the expense of potassium and thus hyp Continue reading >>

Pyloric Stenosis

Pyloric Stenosis

Pyloric Stenosis is a medial emergency that requires urgent fluid resuscitation and resolution of biochemical abnormalities. Definitive surgical treatment can then be undertaken to restore enteral nutrition. projectile vomiting in neonate (not billous) visible peristalsis and olive sized mass in epigastrium 5. initially, alkaline urine -> later, acidic urine decreased secretion of pancreatic HCO3- increased HCO3- presented to distal tubule and eliminated producing an alkaline urine loss of Na+ in urine until kidney adjusts to increased HCO3- load activation of renin-AG-ALD system to off set this and restore Na+ and H2O activation of rennin-AG-ALD system with produces loss of K+ in urine with extreme K+ loss in urine -> it gets reabsorbed in distal tubule with loss of H+ worsening metabolic alkalosis and producing and acidic urine initially, alkaline urine -> later, paradoxical aciduria inability to absorb enteral fluid and vomiting activation of rennin-AG-ALD system + ADH Fluid resuscitation determined by weight and degree of dehydration assessed clinically (tissue turgor, pulse, fontanelle, CR centrally, peripheral perfusion, respiratory rate) IV boluses of normal saline or colloid (4% albumin) 10-20mL/kg to restore circulating volume maintenance @ 4mL/kg/hr with 5% dextrose with 0.45% normal saline and 20mmoL KCl fluid therapy should be titrated to clinical variable including urine output (2mL/kg/hr) Laboratory criteria by which patient is sufficiently resuscitated for surgery ideally biochemical abnormalities would be normal before surgery however, variable associated with adequate resuscitation and resolution of metabolic alkalosis include: operation = splitting of the pylorus muscle longitudinally down to the mucosa (myomectomy) risk of pulmonary aspiration from g Continue reading >>

Bicarbonate Therapy And Intracellular Acidosis.

Bicarbonate Therapy And Intracellular Acidosis.

1. Clin Sci (Lond). 1997 Dec;93(6):593-8. Bicarbonate therapy and intracellular acidosis. (1)Renal Laboratory, St Thomas' Hospital, London, U.K. 1. The correction of metabolic acidosis with sodium bicarbonate remainscontroversial. Experiments in vitro have suggested possible deleterious effectsafter alkalinization of the extracellular fluid. Disequilibrium of carbon dioxideand bicarbonate across cell membranes after alkali administration, leading to thephenomenon of 'paradoxical' intracellular acidosis, has been held responsible forsome of these adverse effects. 2. Changes in intracellular pH in suspensions ofleucocytes from healthy volunteers were monitored using a fluorescentintracellular dye. The effect in vitro of increasing extracellular pH with sodiumbicarbonate was studied at different sodium bicarbonate concentrations. Lacticacid and propionic acid were added to the extracellular buffer to mimicconditions of metabolic acidosis. 3. The addition of a large bolus of sodiumbicarbonate caused intracellular acidification as has been observed previously.The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate wasadded as a series of small boluses the reduction in intracellular pH was small.Under conditions of initial acidosis this was rapidly followed by intracellularalkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect isminimal when the conditions approximate those seen in clinical practice. Wesuggest that the observed small and transient lowering of intracellular pH isinsufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis. Continue reading >>

Is Bicarbonate Ever Indicated In Dka? – Dr. E. Sosa

Is Bicarbonate Ever Indicated In Dka? – Dr. E. Sosa

Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, elevated serum ketones, and metabolic acidosis. To explain briefly, this disorder results from dysfunctional glucose metabolism in the context of insulin underproduction and/or insensitivity. Unable to utilize glucose, cells begin to consume fatty acids via anaerobic metabolism, leading to the buildup of acidic ketone bodies and other electrolyte abnormalities. Some common precipitants of this acutely life-threatening condition include infection and noncompliance with insulin therapy in known diabetics. DKA is often how new-onset diabetics initially present, but it can also be found in patients with acute pancreatitis, MI, and CVA. Nevertheless, the complexity of metabolic derangements that come with DKA can be formidable to manage, regardless of the precipitating insult.1 Resuscitation of a DKA patient involves aggressive fluid replacement and insulin administration, all while continuously managing sodium, potassium, chloride, phosphate, and bicarbonate shifts. For this review, we will focus on the management of low bicarbonate levels in metabolic acidosis. Since bicarbonate will be very low in severe cases, many physicians treat this metabolic acidosis with intravenous sodium bicarbonate, hoping to reverse the acidosis more quickly. However, this practice is controversial.2 There are three major adverse effects to consider when using bicarbonate: 1) When given continuously, the acidemic drive to blow off CO2 via hyperventilation is blunted. In the hypercapnic state that results, CO2 crosses the blood-brain barrier preferentially, leading to a paradoxical drop in cerebral pH and neurologic deterioration.3 2) It can actually slow ketone clearance by about 6 hours, causing a more refractory acidosis. Animal s Continue reading >>

A Case Of Renal Tubular Acidosis With Sjogrens Syndrome Showing Paradoxical Block Of Pth Due To Severe Hypomagnesemia

A Case Of Renal Tubular Acidosis With Sjogrens Syndrome Showing Paradoxical Block Of Pth Due To Severe Hypomagnesemia

, Volume 32, Issue4 , pp 496499 | Cite as A Case of Renal Tubular Acidosis with Sjogrens Syndrome Showing Paradoxical Block of PTH Due to Severe Hypomagnesemia Distal renal tubular acidosis (RTA) manifests either as Complete/Classical form or Incomplete/Latent Form. Distal RTA causes normal anion gap metabolic acidosis and hypokalemia. Interstitial Nephritis is the most frequent renal manifestation of Sjogrens, which presents as Distal RTA in 2540% of patients with Sjogrens syndrome. Magnesium deficiency is frequently associated with hypokalemia. Although serum calcium is the main physiological control for the secretion of parathyroid hormone (PTH) by the parathyroid, serum magnesium can also exert similar effects. While low levels of magnesium stimulate the secretion of PTH, very low serum concentrations tend to induce a paradoxical block of PTH release by activation of the alpha-subunits of heterotrimeric G-proteins. This mimicks the activation of calcium sensing receptor leading to inhibition of PTH secretion. Here we describe the case history of a 35-year-old lady who presented to our hospital with severe hypokalemia due to distal RTA and perhaps had a paradoxical block of PTH secretion in the setting of severe hypomagnesemia. Renal tubular acidosisSjogrens syndromeHypokalemiaHypomagnesemiaParadoxical block of PTH secretion This is a preview of subscription content, log in to check access Informed consent was obtained from the participant included in the study. Penney MD, Oleesky DA. Renal tubular acidosis. Ann Clin Biochem. 1999;36(408e):422. Google Scholar Unwin RJ, Shirley DG, Capasso G. Urinary acidification and distal renaltubular acidosis. J Nephrol. 2002;15(suppl 5):S142eS150. Google Scholar Siamopoulos KC, Elisaf M, Drosos AA, Mavridis AA, Moutsopoulos HM. Continue reading >>

Acquired Pyloric Stenosis Resulting In Hypokalaemic, Hyperchloraemic Normal Anion Gap Metabolic Acidosis. Persistent Vomiting In An Adult: Cause And Effect

Acquired Pyloric Stenosis Resulting In Hypokalaemic, Hyperchloraemic Normal Anion Gap Metabolic Acidosis. Persistent Vomiting In An Adult: Cause And Effect

A 24-year-old woman presented with a history of persistent vomiting for at least 3 months. This resulted in severe dehydration with risk of acute kidney injury. In addition to volume depletion, loss of gastric fluid resulted in a specific metabolic derangementhypokalaemic, hypochloraemic normal anion gap metabolic alkalosis with a reduced ionised calcium concentration and paradoxical aciduria. These metabolic changes were reflected in her ECG. Investigation demonstrated acquired gastric outflow tract obstruction secondary to a pyloric peptic ulcer. The patient was resuscitated with intravenous crystalloid and electrolyte supplements. The acquired pyloric stenosis was treated medically with a proton pump inhibitor and Helicobacter pylori eradication therapy with excellent recovery. Contributors PK is the sole author of this manuscript. The full text of all Editor's Choice articles and summaries of every article are free without registration The full text of Images in ... articles are free to registered users Only fellows can access the full text of case reports (apart from Editor's Choice) - become a fellow today, or encourage your institution to, so that together we can grow and develop this resource Don't forget to sign up for content alerts so you keep up to date with all the case reports as they are published, and let us know what you think by commenting on the Editor's blog Continue reading >>

Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications

Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications

Efficient Extra- and Intracellular Alkalinization Improves Cardiovascular Functions in Severe Lactic Acidosis Induced by Hemorrhagic Shock From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Bra Continue reading >>

Bicarbonate Treatment Of Acidosis Produces Paradoxical Acidosis In The Brain

Bicarbonate Treatment Of Acidosis Produces Paradoxical Acidosis In The Brain

BICARBONATE TREATMENT OF ACIDOSIS PRODUCES BICARBONATE TREATMENT OF ACIDOSIS PRODUCES Acidemia despite its origin is treated by quick correction of blood pH via intravenous (IV) infusion of sodium bicarbonate (NaHCO3) to alleviate potentially the dangerous effects of the acidotic state (Naylor et al. 2006). However, rapid NaHCO3 infusion increases CSF pCO2 and worsens the acidosis in the cerebrospinal This is known as paradoxical CSF acidosis. Changes in CSF during metabolic acidosis need to be investigated Both NaHCO3 regimens are clinically safe. Rapid NaHCO3 therapy is an acceptable method of treating acutely acidotic calves. However, the effect of NaHCO3 therapy on ND needs further investigation and appears dependent on the cause of acidosis. G.A. Zello1, A.W.A.S. Abeysekara1, K. Lohmann2 and J.M. Naylor2 College of Pharmacy and Nutrition1, Western College of Veterinary Medicine2, University of Saskatchewan 110 Science Place Saskatoon, Saskatchewan, CANADA. Blood and CSF samples were collected at pre, post acidotic and during NaHCO3 therapy. Samples were immediately analyzed for pH, bicarbonate (HCO3-) and gasses (pCO2). D- and L-lactate concentrations in CSF and serum were measured using an HPLC system fitted with a stereo-specific reverse-phase chiral column and a UV detector (236 nm). Neurological assessment was blinded and performed when physiological samples were taken. The scoring system was based on strength of reflexes (suck, menace, palpebral, tactile) and ability to stand. The total neurological disturbance (ND) score was the sum of the individual scores. Highly depressed or comatose calves had maximum score of 10 while Data were analysed as a repeated measures ANOVA (SPSS v13, 2003) to distinguish treatment and time effects. SNK (mean comparison) was per Continue reading >>

Sodium Bicarbonate - An Overview | Sciencedirect Topics

Sodium Bicarbonate - An Overview | Sciencedirect Topics

Jamie McElrath Schwartz, ... Donald H. Shaffner, in Smith's Anesthesia for Infants and Children (Eighth Edition) , 2011 Sodium bicarbonate causes an acid-base reaction in which bicarbonate combines with hydrogen ion to form water and carbon dioxide, resulting in an elevated blood pH: Because sodium bicarbonate generates CO2, adequate alveolar ventilation must be present before its administration. As respiratory failure is the leading cause of cardiac arrest in children, caution should be taken before sodium bicarbonate administration in the face of preexisting respiratory acidosis. Sodium bicarbonate use during CPR is one of the most controversial issues in the literature related to cardiac arrest. This stems from lack of evidence of benefit during CPR in animals and humans, as well as the potential adverse effects associated with sodium bicarbonate administration. Literature on sodium bicarbonate use in CPR dates back to the 1960s, but there are little data demonstrating a beneficial impact on human survival (Levy, 1998). In animal models of resuscitation from cardiac arrest, sodium bicarbonate has been associated with increased survival in few studies and with no difference in survival in many studies (Andersen et al., 1967; Redding and Pearson, 1968; Kirimli et al., 1969; Lathers et al., 1989; Bleske et al., 1992; Neumar et al., 1995; Vukmir et al., 1995). Administration of sodium bicarbonate to humans experiencing cardiopulmonary arrest has been associated with increased mortality in retrospective reviews and nonblinded prospective studies (Suljaga-Pechtel et al., 1984; Skovron et al., 1985; Delooz and Lewi, 1989). Several studies in both humans and animals document deleterious effects on physiologic endpoints such as myocardial performance, arterial blood pressure Continue reading >>

Bicarbonate Therapy And Intracellular Acidosis

Bicarbonate Therapy And Intracellular Acidosis

1. The correction of metabolic acidosis with sodium bicarbonate remains controversial. Experiments in vitro have suggested possible deleterious effects after alkalinization of the extracellular fluid. Disequilibrium of carbon dioxide and bicarbonate across cell membranes after alkali administration, leading to the phenomenon of 'paradoxical' intracellular acidosis, has been held responsible for some of these adverse effects. 2. Changes in intracellular pH in suspensions of leucocytes from healthy volunteers were monitored using a fluorescent intracellular dye. The effect in vitro of increasing extracellular pH with sodium bicarbonate was studied at different sodium bicarbonate concentrations. Lactic acid and propionic acid were added to the extracellular buffer to mimic conditions of metabolic acidosis. 3. The addition of a large bolus of sodium bicarbonate caused intracellular acidification as has been observed previously. The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate was added as a series of small boluses the reduction in intracellular pH was small. Under conditions of initial acidosis this was rapidly followed by intracellular alkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect is minimal when the conditions approximate those seen in clinical practice. We suggest that the observed small and transient lowering of intracellular pH is insufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis. Do you want to read the rest of this article? ... However, an experimental study by Benjamin et al. on dogs subjected to hemorrhagic shoc Continue reading >>

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany et al. 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. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>

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