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Saline Induced Hyperchloremic Metabolic Acidosis Mechanism

Urinary Strong Ion Difference Is A Major Determinant Of Plasma Chloride Concentration Changes In Postoperative Patients

Urinary Strong Ion Difference Is A Major Determinant Of Plasma Chloride Concentration Changes In Postoperative Patients

To show that alterations in the plasma chloride concentration ([Cl-]plasma) during the postoperative period are largely dependent on the urinary strong ion difference ([SID]urine=[Na+]urine+[K+]urine-[Cl-]urine) and not on differences in fluid therapy. Measurements were performed at intensive care unit admission and 24 hours later in a total of 148 postoperative patients. Patients were assigned into one of three groups according to the change in [Cl-]plasma at the 24 hours time point: increased [Cl-]plasma (n=39), decreased [Cl-]plasma (n=56) or unchanged [Cl-]plasma (n=53). On admission, the increased [Cl-]plasma group had a lower [Cl-]plasma (1055 versus 1094 and 1063mmol/L, p<0.05), a higher plasma anion gap concentration ([AG]plasma) and a higher strong ion gap concentration ([SIG]). After 24 hours, the increased [Cl-]plasma group showed a higher [Cl-]plasma (1114 versus 1044 and 1073mmol/L, p<0.05) and lower [AG]plasma and [SIG]. The volume and [SID] of administered fluids were similar between groups except that the [SID]urine was higher (3837 versus 1822 and 2318mmol/L, p<0.05) in the increased [Cl-]plasma group at the 24 hours time point. A multiple linear regression analysis showed that the [Cl-]plasma on admission and [SID]urine were independent predictors of the variation in [Cl-]plasma 24 hours later. Changes in [Cl-]plasma during the first postoperative day were largely related to [SID]urine and [Cl-]plasma on admission and not to the characteristics of the infused fluids. Therefore, decreasing [SID]urine could be a major mechanism for preventing the development of salineinduced hyperchloremia. Key words: Postoperative care; Isotonic solutions/adverse effects; Urine/analysis; Chlorides/metabolism Chloride is the primary anion in the extracellular fluid. The Continue reading >>

Mechanism Of Hyperchloremic Metabolic Acidosis | Anesthesiology | Asa Publications

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 >>

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment of acute non-anion gap metabolic acidosis Medical and Research Services VHAGLA Healthcare System, Division of Nephrology, VHAGLA Healthcare System Correspondence to: Jeffrey A. Kraut; E-mail: [email protected] Search for other works by this author on: Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Jeffrey A. Kraut, Ira Kurtz; Treatment of acute non-anion gap metabolic acidosis, Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acidbase 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 migh Continue reading >>

Why Is Saline So Acidic (and Does It Really Matter?)

Why Is Saline So Acidic (and Does It Really Matter?)

Int J Med Sci 2013; 10(6):747-750. doi:10.7150/ijms.5868 Why Is Saline So Acidic (and Does It Really Matter?) Consultant, Intensive Care Unit, Royal Adelaide Hospital; Clinical Senior Lecturer, Discipline of Acute Care Medicine, University of Adelaide, Adelaide, Australia. This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) License . See for full terms and conditions. Reddi BA. Why Is Saline So Acidic (and Does It Really Matter?). Int J Med Sci 2013; 10(6):747-750. doi:10.7150/ijms.5868. Available from Commercial 0.9% saline solution for infusion has a pH around 5.5. There are many reasons for this acidity, some of them still obscure. It is also true that infusion of normal saline can lead to metabolic acidaemia, yet the link between the acidity of saline solution and the acidaemia it can engender is not straightforward. This commentary draws together the known and putative sources of acidity in saline solutions: it turns out that the acidity of saline solution is essentially unrelated to the acidaemia complicating saline infusion. Keywords: saline, acidaemia, titratable acidity, crystalloid, balanced solution, Grotthuss. One might well think that ordinary commercial 0.9% saline solution for infusion would be neutral, with a pH of 7. In fact it is quite acidic: pH being reported as low as 4.6. 1 Why does this simple solution have a pH so far removed from the physiology it is designed to support? And should junior doctors be concerned about what impact this in vitro acidity has on their patients? It is widely recognized that resuscitation with 0.9% saline can cause acidaemia, but oddly enough the natural assumption that this is because of the intrinsic acidity of the infusion fluid turns out to be wrong. As we shall Continue reading >>

Hyperchloremic Acidosis

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 >>

Saline-induced Hyperchloremic Metabolic Acidosis And Clinical Outcomes In Critically Ill Patients

Saline-induced Hyperchloremic Metabolic Acidosis And Clinical Outcomes In Critically Ill Patients

Saline-induced Hyperchloremic Metabolic Acidosis and Clinical Outcomes in Critically ill Patients Co-Investigators: Gilles Clermont, MD , Raghavan Murugan, MD , Lan Kong, PhD Hyperchloremic metabolic acidosis (HCA) is a common complication arising secondary to large-volume (saline) resuscitation (LVR) in patients. Several large clinical studies have documented the development of HCA during critical illness but none could adequately evaluate the impact of HCA on patient clinical outcomes. At present, 0.9% saline is the standard of care for volume resuscitation of critically ill patients throughout the world. However, data from animal experiments indicate that HCA is associated with hemodynamic instability, development of renal dysfunction, inflammatory response induction and decreased survival. Our preliminary clinical data also suggest that HCA is associated with prolonged hospitalization, greater number of days in the intensive care unit (ICU) and increased mortality compared to standardized intensive care unit mortality rates. Using a large dataset of critically ill patients from the intensive care units (ICUs) at the University of Pittsburgh Medical Center we will assess the incidence of HCA, the association between HCA and development of acute kidney injury (AKI), and the association between HCA and adverse clinical outcomes. This study will help investigators ascertain the relative effect of HCA on clinical endpoints so that future development of resuscitation fluids can be better informed. Continue reading >>

Nephron Power: Consult Rounds: Why Does Infusion Of Normal Saline Cause Metabolic Acidosis?

Nephron Power: Consult Rounds: Why Does Infusion Of Normal Saline Cause Metabolic Acidosis?

Consult Rounds: Why does infusion of normal saline cause metabolic acidosis? Why does infusion of normal saline cause metabolic acidosis? This should be an easyanswer but when you review the literature, the literature is all over theplace( literally!!).Collection of responses I received when I asked few expertsin the field: 1. Thebicarbonate ions are diluted bythe isotonic fluid,and acidosis occursas a result. 2. The fall in serum bicarbonate is dueto the expansion of the extracellular fluid volume withlarge IV fluids 3. The "strong ion difference" (SID) helpsexplain this that in order to maintain electroneutrality. Since there is diluting fluid, water must dissociate, providing excess protons which leads to metabolic acidosis. - via the stewart method of acid base 4. Usually 60% of the filtered bicarbonate load isreabsorbed in euvolemia. When extracellular volume is low the proximaltubular absorption is increased, maybe to 80%,due to changes in oncoticpressure and hydrostatic pressure of peri tubular capillaries and glomerulus.This results in increased reabsorption in setting of volume depletion.When extracellular volume is increased then proximal tubular absorptionof bicarbonate is decreased, thus an acidosis. 5. The ph of normal saline is 5.5, won'tthat also lead to dissociation and use of Hco3 and cause an acidic environment 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 >>

How Exactly Does 0.9% Saline Cause Hyperchloremic Metabolic Acidosis? Something To Do With It's Strong Iron Difference But I Can't Quite Grasp It. : Medicalschool

How Exactly Does 0.9% Saline Cause Hyperchloremic Metabolic Acidosis? Something To Do With It's Strong Iron Difference But I Can't Quite Grasp It. : Medicalschool

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Chloride In Critical Illness

Chloride In Critical Illness

Home | Critical Care Compendium | Chloride in Critical Illness Chloride is the majoranion in the extracellular fluid (ECF) and is the second most importantcontributor to plasma tonicity The possibility of harm from hyperchloraemia, particularly in the context of fluid resuscitation with chloride-rich solutions such as normal saline, is an area of intense research interest If chloride excess is harmful it may be an important confounder in studies that suggest that positive fluid balance is harmful in ICU patients Some expert clinicians advocate the use of chloride-poor balanced salt solutions in preference to normal saline for fluid resuscitation, replacement and maintenance The major trial of buffered crystalloids versus normal saline in ICU patients, the SPLIT trial, found no difference in rates of acute kidney injury (AKI), rates of renal replacement therapy or in-hospital mortality. 133 to 202 mmol or 7.8 to 11.8 g/day for adult men (USA) 99 to 133 mmol or 5.8 to 7.8 g/day for adult women(USA) Renal excretion is the primary means of chloride elimination 180 mmol/d chloride excreted (99.1% of filtered is reabsorbed) renal proximal tubules are the major site of reabsorption distal intercalated cells also involved (type A cells: proton efflux, type B cells: HCO3 efflux, chloride reabsorption) chloride reabsorption involves members of the solute carrier (SLC) gene families SLC26 (primarily chloride-anion exchangers) and SLC4 (primarily chloride-bicarbonate and anion exchangers and sodium-bicarbonate co-transporters) The macula densa is a collection of densely packed epithelial cells at the junction of the thick ascending limb (TAL) and distal convoluted tubule (DCT) detection of high sodium chloride concentrations by the macula densa leads totubuloglomerular feedback: c 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 >>

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 >>

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 >>

Causes And Effects Of Hyperchloremic Acidosis

Causes And Effects Of Hyperchloremic Acidosis

Causes and effects of hyperchloremic acidosis Metabolic AcidosisIsotonic SalineHetastarchGastric TonometrySynthetic Colloid 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 ]. Hyperchloremia was found to have profound effects on eicosanoid release i Continue reading >>

Normal Saline Intoxication - Deranged Physiology

Normal Saline Intoxication - Deranged Physiology

Uncontrolled pancreatic secretions as a cause of acidosis The overzealous administration of sodium chloride causes a normal anion gap metabolic acidosis by decreasing the strong ion difference. This is the archetypal normal anion gap acidosis. Previously discussed calculations suggest that every bag of saline increases the serum chloride by 3mmol/L. In Stewarts terms, normal saline has a strong ion difference of 0mmol/L (given how equal the concentrations of sodium and chloride are), and thus adding it to a body fluid will decrease the strong ion difference. The strong ion difference of Hartmanns, on the other hand, is 28mmol/L, and so it has a much gentler acidifying effect. This has been demonstrated experimentally in a cohort of 5 septic patients; and the theory is discussed in detail here . Change in strong ion difference following the infusion of normal saline The above graph is adopted from Lobo et al, who in 2003 infused a series of healthy volunteers with 2000ml of normal saline to study the difference between sodium chloride and Hartmanns solution. Now, enough saline-bashing. If we remain faithful to the interpretation of acid base disorders in terms of the strong ion difference, we will find that any other fluid which has a low string ion difference will produce a similar picture; perhaps not by increasing the chloride (if it contains no chloride) but by forcing the body fluid to equilibrate with a fluid which has an SID of 0mmol/L Continue reading >>

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