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John A Kellum - One of the best experts on this subject based on the ideXlab platform.

  • normal saline resuscitation worsens lactic Acidosis in experimental sepsis
    Critical Care, 2012
    Co-Authors: Feihu Zhou, Matthew E Cove, Z Peng, Jeffrey Bishop, Kia Singbartl, John A Kellum
    Abstract:

    Infusing large volumes of 0.9% sodium chloride (saline) causes Hyperchloremic Acidosis. The clinical relevance of this effect remains contentious and saline is still the most commonly used resuscitation fluid in the US. However, a recent trial showed that saline or albumin in saline increased mortality in children with malarial sepsis, compared to no fluid [1]. Infusion of these fluids may have perpetuated the underlying metabolic Acidosis sepsis, causing cardiovascular collapse and death. In this study, we investigated the effect of saline versus a balanced crystalloid (plasmalyte) in a cecal ligation and puncture (CLP) model of sepsis. We hypothesized that saline resuscitation would increase Acidosis and worsen hemodynamics, compared to resuscitation using a balanced crystalloid.

  • Hyperchloremic Acidosis increases circulating inflammatory molecules in experimental sepsis
    Chest, 2006
    Co-Authors: John A Kellum, Mingchen Song, Eyad Almasri
    Abstract:

    Rationale Hyperchloremic Acidosis is common in the critically ill and is often iatrogenic. We have previously shown that Hyperchloremic Acidosis increases nuclear factor-κB DNA binding in lipopolysaccharide-stimulated RAW 264.7 cells. However, evidence that Hyperchloremic Acidosis leads to increased inflammation in vivo has been limited to nitric oxide. Objectives To determine if Acidosis, induced by dilute hydrochloric acid (HCl) infusion, will increase circulating inflammatory mediator levels in an experimental model of severe sepsis in rats. Methods Eighteen hours after inducing lethal sepsis by cecal ligation and puncture in 20 adult, male, Sprague-Dawley rats, we randomized animals into three groups. In groups 2 and 3, we began an IV infusion of 0.1 N HCl to reduce the standard base excess (SBE) by 5 to 10 mEq/L and 10 to 15 mEq/L, respectively. In group 1, we infused a similar volume of lactated Ringer solution. In all groups infusion continued 8 h or until the animal died. Measurements and main results We measured arterial blood gases, whole-blood lactate, and chloride, tumor necrosis factor (TNF), interleukin (IL)-6, and IL-10 levels at 0 h, 4 h, and 8 h. All measured cytokines increased over time. Compared to group 1, animals in groups 2 and 3 exhibited greater increase in all three cytokines, with the greatest increases seen with severe Acidosis. Conclusion Moderate (SBE, – 5 to – 10) and severe (SBE, – 10 to – 15) Acidosis, induced by HCl infusion, increases circulating levels of IL-6, IL-10, and TNF in normotensive septic rats.

  • lactate versus non lactate metabolic Acidosis a retrospective outcome evaluation of critically ill patients
    Critical Care, 2006
    Co-Authors: Kyle J Gunnerson, Melissa Saul, John A Kellum
    Abstract:

    Acid–base abnormalities are common in the intensive care unit (ICU). Differences in outcome exist between respiratory and metabolic Acidosis in similar pH ranges. Some forms of metabolic Acidosis (for example, lactate) seem to have worse outcomes than others (for example, chloride). The relative incidence of each type of disorder is unknown. We therefore designed this study to determine the nature and clinical significance of metabolic Acidosis in critically ill patients. An observational, cohort study of critically ill patients was performed in a tertiary care hospital. Critically ill patients were selected on the clinical suspicion of the presence of lactic Acidosis. The inpatient mortality of the entire group was 14%, with a length of stay in hospital of 12 days and a length of stay in the ICU of 5.8 days. We reviewed records of 9,799 patients admitted to the ICUs at our institution between 1 January 2001 and 30 June 2002. We selected a cohort in which clinicians caring for patients ordered a measurement of arterial lactate level. We excluded patients in which any necessary variable required to characterize an acid–base disorder was absent. A total of 851 patients (9% of ICU admissions) met our criteria. Of these, 548 patients (64%) had a metabolic Acidosis (standard base excess < -2 mEq/l) and these patients had a 45% mortality, compared with 25% for those with no metabolic Acidosis (p < 0.001). We then subclassified metabolic Acidosis cases on the basis of the predominant anion present (lactate, chloride, or all other anions). The mortality rate was highest for lactic Acidosis (56%); for strong ion gap (SIG) Acidosis it was 39% and for Hyperchloremic Acidosis 29% (p < 0.001). A stepwise logistic regression model identified serum lactate, SIG, phosphate, and age as independent predictors of mortality. In critically ill patients in which a measurement of lactate level was ordered, lactate and SIG were strong independent predictors of mortality when they were the major source of metabolic Acidosis. Overall, patients with metabolic Acidosis were nearly twice as likely to die as patients without metabolic Acidosis.

  • effects of Hyperchloremic Acidosis on arterial pressure and circulating inflammatory molecules in experimental sepsis
    Chest, 2004
    Co-Authors: John A Kellum, Mingchen Song, Ramesh Venkataraman
    Abstract:

    Study objective: To determine the effects of Hyperchloremic Acidosis, induced by dilute HCl infusion, on BP and circulating inflammatory mediators in an experimental model of severe sepsis in the rat. Design: Randomized, open-label, controlled experiment. Setting: University research laboratory. Participants: Twenty-four adult, male, Sprague-Dawley rats. Intervention: Eighteen hours after inducing lethal sepsis by cecal ligation and puncture, animals were randomized and classified into three groups. In groups 2 and 3, we began an IV infusion of 0.1 N HCl to reduce the standard base excess (SBE) by 5 to 10 mEq/L and 10 to 15 mEq/L, respectively. In group 1, we infused a similar volume of lactated Ringer solution. In all groups, infusions were continued fo r8ho runtil the animals died. Measurements: We measured mean arterial pressure (MAP), arterial blood gases, electrolytes, plasma nitrate/nitrite, tumor necrosis factor (TNF)-, interleukin (IL)-6, and IL-10 levels at 0 h, 3h , 6h , and 8h . Results: MAP remained stable in group 1 but decreased in groups 2 and 3 (p < 0.001), such that at 8 h MAP was much higher in group 1 (94 9.2 mm Hg) [ SD] compared to either group 2 (71.6 20.1 mm Hg) or group 3 (49.4 33.2 mm Hg) [p 0.01]. This change in MAP correlated with the increase in plasma Cl (R 2 0.50, p < 0.0001) and less well with the decrease in pH (R 2 0.24, p < 0.001). Afte r6ho fAcidosis, plasma nitrite levels were significantly higher in group 2 animals compared to either group 1 or group 3 animals (p < 0.05). Plasma TNF-, IL-6, or IL-10 levels were not significantly different from control animals. Conclusion: Moderate Acidosis (SBE of 5 to 10 mEq/L), induced by HCl infusion, worsened BP and increased plasma nitrate/nitrite levels but had no effect on circulating cytokines in septic rats. However, severe Acidosis (SBE of 10 to 15 mEq/L), while still causing hypotension, did not affect plasma nitrate/nitrite levels. (CHEST 2004; 125:243–248)

  • fluid resuscitation and Hyperchloremic Acidosis in experimental sepsis improved short term survival and acid base balance with hextend compared with saline
    Critical Care Medicine, 2002
    Co-Authors: John A Kellum
    Abstract:

    Objective To compare resuscitation with 0.9% saline with Hextend, a synthetic colloid in a balanced electrolyte solution, in terms of acid-base status and survival time in an experimental model of septic shock in the rat.Design Randomized, open-label, controlled experiment.Setting University researc

Mutsuhito Kikura - One of the best experts on this subject based on the ideXlab platform.

  • effect of furosemide under Hyperchloremic Acidosis on intraoperative oliguria and acute kidney injury in patients with normal renal function
    Nephron, 2019
    Co-Authors: Mutsuhito Kikura, Junko Nishino, Yuji Suzuki, Masahiro Uraoka
    Abstract:

    Background: Renal function tends to deteriorate in a Hyperchloremic acidifying environment, which is reflected by a decrease in the difference between sodium and chloride. Objectives: To examine the effect of furosemide administered under Hyperchloremic Acidosis on intraoperative oliguria and acute kidney injury in patients with preoperatively normal renal function. Methods: In patients undergoing abdominal or orthopedic surgeries (April 2010–November 2018), we retrospectively identified patients who preoperatively had a normal renal function but experienced intraoperative oliguria under Hyperchloremic Acidosis (a sodium-chloride difference < 30 mEq/L) without dehydration. We compared the perioperative urine output and the incidence of postoperative acute kidney injury between patients who intraoperatively received an initial dose of 5 mg of furosemide (the furosemide group) and patients who did not intraoperatively receive furosemide (the control group). Results: We identified 62 patients in the furosemide group and 48 patients in the control group. The furosemide group intraoperatively received 0.11 ± 0.06 mg/kg of furosemide (range 0.06–0.39 mg/kg). Compared to the control group, the furosemide group had greater urine output (mL/kg/h) in the operating room (1.1 ± 0.7 vs. 0.3 ± 0.1, p < 0.01) and on postoperative day 1 (1.2 ± 0.5 vs. 1.1 ± 0.4, p = 0.02). The incidence of postoperative acute kidney injury was lesser in the furosemide group than that in the control group (8.0 vs. 27.0%, p < 0.01; multivariate OR 0.18; 95% CI 0.05–0.61; p < 0.01). Conclusions: In surgery patients under Hyperchloremic Acidosis, furosemide (0.1 mg/kg) resolved intraoperative oliguria and reduced the incidence of postoperative acute kidney injury.

  • Hyperchloremic Acidosis is associated with acute kidney injury after abdominal surgery
    Nephrology, 2017
    Co-Authors: Yosuke Toyonaga, Mutsuhito Kikura
    Abstract:

    AIM Hyperchloremic Acidosis may have an important role as a precursor of acute kidney injury (AKI) in the Hyperchloremic environment induced by chloride-rich fluids, but this remains unclear. We tested the hypothesis that Hyperchloremic Acidosis assessed by the Stewart approach is associated with postoperative AKI. METHODS A historical cohort study was conducted in adult patients who had normal renal function preoperatively and required admission to the intensive care unit after elective abdominal surgery. The Risk, Injury, Failure, Loss of kidney function, End stage kidney disease (RIFLE) classification was used for definition of AKI. RESULTS Of 206 patients (144 male, 69.9%) included in the study, 42 (20.4%) had postoperative AKI (AKI group) and 164 (79.6%) did not (non-AKI group). Base excess-chloride (BE-Cl) and strong ion difference (SID, approximated as Na-Cl) decreased, and the chloride level on postoperative day 1 increased compared with preoperative values in both groups (P < 0.05). In the AKI group, BE-Cl and SID were lower, and chloride was higher than in the non-AKI group (P < 0.05). The intraoperative load of chloride ions in fluids increased the risk of postoperative AKI (P < 0.01). In multivariate logistic regression analysis, postoperative BE-Cl < -7 mEq/L (i.e. SID <31 mEq/L) was an independent risk factor for AKI (odds ratio; 2.8, 95% CI; 1.2-6.4, P = 0.01). In the AKI group, stays in the intensive care unit and in hospital were longer than those in the non-AKI group (P < 0.05). CONCLUSION Hyperchloremic Acidosis is associated with postoperative AKI, and this may be attenuated by reducing the intraoperative chloride load.

Michael Eisenhut - One of the best experts on this subject based on the ideXlab platform.

  • causes and effects of Hyperchloremic Acidosis
    Critical Care, 2006
    Co-Authors: Michael Eisenhut
    Abstract:

    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 in renal tissue, leading to vasoconstriction and a reduction of the glomerular filtration rate [5]. The increased eicosanoid release may also explain the findings of reduced gastric perfusion in the hyperchloremia mentioned above [3]. The main adverse effect of saline induced Hyperchloremic Acidosis, however, may be the action that is taken to correct the abnormality. Acidosis is often seen as a reflection of poor organ perfusion or poor myocardial function and a negative base excess may prompt the application of boluses of more saline containing fluids exacerbating the Acidosis, the use of blood products, escalation of inotrope support and initiation of ventilatory support [6,7]. The safety of Hyperchloremic Acidosis has not been established in prospective studies and in patients with different types of critical illness. Particularly in critically ill patients with other co-morbidities like renal disease, more physiological electrolyte solutions (e.g., Ringers lactate solution) may be preferable to isotonic saline and a slow fluid replacement protocol safer than rapid infusions.

  • letter causes and effects of Hyperchloremic Acidosis
    2006
    Co-Authors: Michael Eisenhut
    Abstract:

    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].

Niall T M Galloway - One of the best experts on this subject based on the ideXlab platform.

  • early experience with the use of gastric segment in lower urinary tract reconstruction in adult patient population
    Urology, 1997
    Co-Authors: Ajay Singla, Niall T M Galloway
    Abstract:

    Abstract Objectives To review our experience with the potential use of stomach as a substitute to bowel in lower urinary tract reconstruction in adults. Methods Twenty-two adult patients underwent lower urinary tract reconstruction using stomach. Fourteen patients had augmentation cystoplasty and in 8 patients a continent reservoir was constructed; mean followup was 9.8 months. In 6 patients, gastric tube was constructed and used as catheterizable stoma. Results Renal functions remained stable or improved in all patients. Two patients developed hypochloremic alkalosis. There was significant decrease in urinary pH. All patients were completely continent, with no problems in mucus production. There was no mortality or significant morbidity. Conclusions Stomach offers a good alternative to ileum or colon for bladder reconstruction. Stomach has various unique advantages, such as less mucus production, acidic milieu in the urine, and protection against Hyperchloremic Acidosis.

Herbert D Spapen - One of the best experts on this subject based on the ideXlab platform.

  • renal tubular Acidosis with Hyperchloremic Acidosis harmless with a sting
    Critical Care, 2015
    Co-Authors: Patrick M Honore, Rita Jacobs, Inne Hendrickx, Elisabeth De Waele, Viola Van Gorp, Herbert D Spapen
    Abstract:

    Brunner et al. [1] showed a higher than previously described prevalence of renal tubular Acidosis (RTA) in critically ill patients with Hyperchloremic metabolic Acidosis (HMA). They elegantly demonstrated that this condition often remains unrecognized owing to the simultaneous presence of metabolic alkalosis, mainly attributed to low plasma albumin levels, and was not associated with increased morbidity or mortality. HMA was thought to result from altered renal chloride handling as seen in RTA and was considered a nonharmful physiological response. In contrast with the study of Brunner et al., HMA is most often exogenously induced by too liberal infusion of chloride-containing intravenous fluids for hydration and resuscitation purposes [2]. HMA indeed has no proven impact on ICU and hospital mortality but may precipitate acute kidney injury. It could be assumed that a combination of HMA and RTA only guarantees a relatively stable but fragile acid–base equilibrium with preserved renal function provided the external chloride load remains limited. Excess or overzealous administration of chloride may well precipitate or exacerbate acute kidney injury in these patients. Conversely, early identification of the HMA/RTA combination strongly pleads against a liberal chloride infusion policy and may eventually offer kidney protection!