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The article compares 2 perspectives on acid-base considerations. The formal view, of Stewart, is suitable for exact calculations, but less intuitively understandable, since it does not deal with the question of the internal mechanisms of acid-base processes, but suffices to satisfy formal physical-chemical laws. And the intuitive view, which provides a comprehensible qualitative idea of the direction, toward acidosis or alkalosis, in which acid-base will evolve. The article further explains the nature of dilutional and hyperchloremic acidosis and shows that not NaCl but water in solution is its cause. [ABSTRACT FROM AUTHOR]

BackgroundThe exact mechanism of hyperammonemia is thought to be multifactorial, but is not yet fully understood. No studies have yet reported hyperammonemia combined with Fanconi syndrome caused by deferasirox.Case presentationA 10-year-old girl was admitted for vomiting and altered consciousness. Blood testing revealed hyperammonemia and normal liver and coagulation functions. During hospitalization, the patient also exhibited hyperchloremic metabolic acidosis, hypokalemia, hyponatremia, and hypophosphatemia. Additionally, urinalysis revealed glucose and protein levels clinically consistent with Fanconi syndrome. The patient had a history of severe beta-thalassemia and had received intermittent blood transfusions for approximately ten years. The patient had been administered oral deferasirox at a 400 mg/day dose at the age of four, which had been gradually increased to the current 750 mg/day dosage. Upon admission, deferasirox was discontinued and treatment including mechanical ventilation, continuous blood purification therapy for ammonia reduction and acidosis, and electrolyte imbalance corrections was administered. Subsequently, serological markers returned to normal, urine test findings improved. To the best of our knowledge, this is the first report of a case of hyperammonemia with Fanconi syndrome owing to deferasirox.ConclusionsFor effective management and long-term follow-up of chronic diseases in children, pediatricians must master standardized treatments and the adverse reactions of various drugs. When symptoms are difficult to explain clinically, we must trace the source and adjust the treatment plan to maximize improving the patient's prognosis.

Euglycemic ketoacidosis associated with SGLT2 inhibitors, also referred to as gliflozins, is a rare but potentially fatal clinical entity characterized by metabolic acidosis with normal or only mildly elevated glycemia, predominantly in patients with type 2 diabetes mellitus. In addition to ketoacidosis, hyperchloremic acidosis may also contribute significantly to metabolic acidosis. Relative hypoglycemia induced by gliflozins and concomitant stress condition lead to decreased insulin level and increased glucagon, cortisol, and catecholamines, which stimulates ketogenesis. At the same time, gliflozins induce com‑ plex renal metabolic dysfunction, in particular impaired renal elimination of acids and renal ammoniogenesis, resulting in hyperchloremic acidosis. In patients treated with gliflozins, acid-base balance and ketonemia should be checked in a timely manner when their condition worsens. Treatment of acidosis consists of discontinuation of gliflozin and administration of insulin at a dose sufficient to suppress ketogenesis. Because of the risk of acidosis, gliflozins should be discontinued at least 3 days before elective surgery and resumed only after stabilization and reliable restoration of oral intake. Similarly, gliflozins should be discontinued in most hospitalized nonsurgical patients with risk factors for the development of acidosis, such as in patients with acute infection, acute heart disease, stroke, fasting before examination, or alcohol abuse. [ABSTRACT FROM AUTHOR]

Euglycemic ketoacidosis is a rare but potentially fatal complication of treatment with SGLT2 inhibitors (gliflozins). However, similar euglycemic ketoacidosis may rarely occur with other antidiabetic drugs or conditions such as pregnancy or alcohol abuse. We describe 3 cases of our patients with euglycemic ketoacidosis associated with gliflozins and 1 case associated with the DPP4 inhibitor sitagliptin and discuss in detail the acid-base disturbances present and the distinction of euglycemic ketoacidosis from classical ketoacidosis in type 1 diabetes. [ABSTRACT FROM AUTHOR]

Abstract Background Euglycemic diabetic ketoacidosis associated with SGLT2 inhibitors is a rare, relatively new and potentially fatal clinical entity, characterized by metabolic acidosis with normal or only moderately elevated glycemia. The mechanisms are not fully understood but involve increased ketogenesis and complex renal metabolic dysfunction, resulting in both ketoacidosis and hyperchloremic acidosis. We report a rare case of fatal empagliflozin-associated acidosis with profound hyperchloremia and review its pathogenesis. Case presentation A patient with type 2 diabetes mellitus treated with empagliflozin underwent an elective hip replacement surgery. Since day 4 after surgery, he felt generally unwell, leading to cardiac arrest on the day 5. Empagliflozin-associated euglycemic diabetic ketoacidosis with severe hyperchloremic acidosis was identified as the cause of the cardiac arrest. Conclusions This unique case documents the possibility of severe SGLT2 inhibitor-associated mixed metabolic acidosis with a predominant hyperchloremic component. Awareness of this possibility and a high index of suspicion are crucial for correct and early diagnosis.

Background: Euglycemic diabetic ketoacidosis associated with SGLT2 inhibitors is a rare, relatively new and potentially fatal clinical entity, characterized by metabolic acidosis with normal or only moderately elevated glycemia. The mechanisms are not fully understood but involve increased ketogenesis and complex renal metabolic dysfunction, resulting in both ketoacidosis and hyperchloremic acidosis. We report a rare case of fatal empagliflozin-associated acidosis with profound hyperchloremia and review its pathogenesis. Case presentation: A patient with type 2 diabetes mellitus treated with empagliflozin underwent an elective hip replacement surgery. Since day 4 after surgery, he felt generally unwell, leading to cardiac arrest on the day 5. Empagliflozin-associated euglycemic diabetic ketoacidosis with severe hyperchloremic acidosis was identified as the cause of the cardiac arrest. Conclusions: This unique case documents the possibility of severe SGLT2 inhibitor-associated mixed metabolic acidosis with a predominant hyperchloremic component. Awareness of this possibility and a high index of suspicion are crucial for correct and early diagnosis. [ABSTRACT FROM AUTHOR]

Copyright of Die Nephrologie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: The exact mechanism of hyperammonemia is thought to be multifactorial, but is not yet fully understood. No studies have yet reported hyperammonemia combined with Fanconi syndrome caused by deferasirox., Case Presentation: A 10-year-old girl was admitted for vomiting and altered consciousness. Blood testing revealed hyperammonemia and normal liver and coagulation functions. During hospitalization, the patient also exhibited hyperchloremic metabolic acidosis, hypokalemia, hyponatremia, and hypophosphatemia. Additionally, urinalysis revealed glucose and protein levels clinically consistent with Fanconi syndrome. The patient had a history of severe beta-thalassemia and had received intermittent blood transfusions for approximately ten years. The patient had been administered oral deferasirox at a 400 mg/day dose at the age of four, which had been gradually increased to the current 750 mg/day dosage. Upon admission, deferasirox was discontinued and treatment including mechanical ventilation, continuous blood purification therapy for ammonia reduction and acidosis, and electrolyte imbalance corrections was administered. Subsequently, serological markers returned to normal, urine test findings improved. To the best of our knowledge, this is the first report of a case of hyperammonemia with Fanconi syndrome owing to deferasirox., Conclusions: For effective management and long-term follow-up of chronic diseases in children, pediatricians must master standardized treatments and the adverse reactions of various drugs. When symptoms are difficult to explain clinically, we must trace the source and adjust the treatment plan to maximize improving the patient's prognosis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2024 Zhou, Xiong, Feng and Jiang.)

Abstract Background Isotonic saline (IS) is widely used to secure perioperative cardiovascular stability. However, the high amount of chloride in IS can induce hyperchloremic acidosis. Therefore, IS is suspected to increase the risk of acute kidney injury (AKI). Biomarkers may have potential as indicators. Methods In a double-blinded, placebo-controlled study, 38 patients undergoing primary uncemented hip replacement were randomized to IS or PlasmaLyte (PL). Infusion was given during surgery as 15 ml/kg the first hour and 5 ml/kg the following two hours. Urinary samples were collected upon admission and the day after surgery. As surgery was initiated, urine was collected over the course of 4 h. Hereafter, another urine collection proceeded until the morning. Urine was analyzed for markers of AKI neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1). Arterious and venous blood samples for measurements of pH and plasma electrolytes including chloride (p-Cl) were collected as surgery was initiated, at the end of surgery and the following morning. Results IS induced an increase in p-Cl (111 ± 2 mmol/L after IS and 108 ± 3 after PL, p = 0.004) and a decrease in pH (7.39 ± 0.02 after IS and 7.43 ± 0.03 after PL, p = 0.001). Urinary NGAL excretion increased in both groups (ΔNGAL: 5.5 [4.1; 11.7] μg/mmol creatinine p = 0.004 after IS vs. 5.5 [2.1;9.4] μg/mmol creatinine after PL, p

ABSTRACT: In this study we evaluated the effects of the prepartum anionic diet on the electrolyte balance and calcemia of high producing dairy cows in the first days of lactation, and investigated the impact on the frequency of subclinical hypocalcemia (SCH). Sixty healthy Holstein cows, producing 30 kg of milk/day, handled in intensive system (compost barn), were distributed in groups (n=15) according to lactation order: first, second, third, and fourth to sixth. In the last three weeks before calving they received a diet with negative DCAD (-6mEq/100g DM) and high chloride content. After calving, they received a diet with positive DCAD (18mEq/100g DM). Urine pH was measured before calving. Serum Na+, Cl-, K+, and total Ca concentrations, and the strong ion difference (SID3) were determined in samples taken soon after calving (0h), 24, 48, 72 and 96h after. The frequencies of SCH were determined considering the critical value of 2.125mmol/L (8.5mg/dL). Two-way repeated measures ANOVA and chi-square test were used for comparisons. The cows eliminated acidic urine before calving. Na+, K+, Cl-, and SID3 values did not differ between groups. Na+ and K+ did not vary between days; Cl- was elevated at calving and decreased until 72h; and SID3 was reduced at calving and increased up to 48h. The Ca levels were reduced until 24h and increased up to 72h. Cows of third and fourth to sixth lactations presented lower values up to 24h. SCH was observed in almost half of the cows (43.3% to 55%) until 48h. The maintenance of hypocalcemia for three or more consecutive days occurred in 53.3% of third and fourth to sixth lactations cows. Ingestion of a high chloride prepartum anionic diet led to hyperchloremic acidosis and this imbalance was reversed on the second postpartum day. The induced effects on electrolyte and acid-base balances were not able to prevent the occurrence of SCH in the first days of lactation.

Extremely preterm neonates (< 28 wk) are at risk of metabolic complications like hypocalcemia, hypophosphatemia, hyponatremia, and metabolic acidosis. Many of these complications are often the result of prematurity per se, while some of them may be the result of prolonged parenteral nutrition. Most of the complications occur in the initial few weeks of hospital stay, but hyponatremia, hypocalcemia, and hypophosphatemia may persist for longer periods of time. Optimizing enteral nutrition along with fortification helps in promoting optimal growth and overcoming the aforementioned problems. The authors report one such extremely preterm neonate with hyperchloremic metabolic acidosis, the cause of which is uncommon and not reported previously in the literature. [ABSTRACT FROM AUTHOR]

Copyright of Der Urologe A is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract Background Chloride is speculated to have nephrotoxic properties. In healthy subjects we tested the hypothesis that acute chloride loading with 3% saline would induce kidney injury, which could be prevented with the loop-diuretic furosemide. Methods The study was designed as a randomized, placebo-controlled, crossover study. Subjects were given 3% saline accompanied by either placebo or furosemide. Before, during and after infusion of 3% saline we measured glomerular filtration rate (GFR), fractional excretion of sodium (FENa), urinary chloride excretion (u-Cl), urinary excretions of aquaporin-2 (u-AQP2) and epithelial sodium channels (u-ENaCγ), neutrophil gelatinase-associated lipocalin (u-NGAL) and kidney injury molecule-1 (u-KIM-1) as marker of kidney injury and vasoactive hormones: renin (PRC), angiotensin II (p-AngII), aldosterone (p-Aldo) and arginine vasopressin (p-AVP). Four days prior to each of the two examinations subjects were given a standardized fluid and diet intake. Results After 3% saline infusion u-NGAL and KIM-1 excretion increased slightly (u-NGAL: 17 ± 24 during placebo vs. -7 ± 23 ng/min during furosemide, p = 0.039, u-KIM-1: 0.21 ± 0.23 vs − 0.06 ± 0.14 ng/ml, p

Background: Isotonic saline (IS) is widely used to secure perioperative cardiovascular stability. However, the high amount of chloride in IS can induce hyperchloremic acidosis. Therefore, IS is suspected to increase the risk of acute kidney injury (AKI). Biomarkers may have potential as indicators.Methods: In a double-blinded, placebo-controlled study, 38 patients undergoing primary uncemented hip replacement were randomized to IS or PlasmaLyte (PL). Infusion was given during surgery as 15 ml/kg the first hour and 5 ml/kg the following two hours. Urinary samples were collected upon admission and the day after surgery. As surgery was initiated, urine was collected over the course of 4 h. Hereafter, another urine collection proceeded until the morning. Urine was analyzed for markers of AKI neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1). Arterious and venous blood samples for measurements of pH and plasma electrolytes including chloride (p-Cl) were collected as surgery was initiated, at the end of surgery and the following morning.Results: IS induced an increase in p-Cl (111 ± 2 mmol/L after IS and 108 ± 3 after PL, p = 0.004) and a decrease in pH (7.39 ± 0.02 after IS and 7.43 ± 0.03 after PL, p = 0.001). Urinary NGAL excretion increased in both groups (ΔNGAL: 5.5 [4.1; 11.7] μg/mmol creatinine p = 0.004 after IS vs. 5.5 [2.1;9.4] μg/mmol creatinine after PL, p < 0.001). No difference was found between the groups (p = 0.839). Similarly, urinary KIM-1 excretion increased in both groups (ΔKIM-1: IS 115.8 [74.1; 156.2] ng/mmol creatinine, p < 0.001 vs. PL 152.4 [120.1; 307.9] ng/mmol creatinine, p < 0.001). No difference between the groups (p = 0.064). FENa increased (1.08 ± 0.52% after IS and 1.66 ± 1.15% after PL, p = 0.032). ENaC excretion was different within groups (p = 0.019).Conclusion: A significantly higher plasma chloride and a lower pH was present in the group receiving isotonic saline. However, u-NGAL and u-KIM-1 increased significantly in both groups after surgery despite absence of changes in creatinine. These results indicate that surgery induced subclinical kidney injury. Also, the IS group had a delayed sodium excretion as compared to the PL group which may indicate that IS affects renal sodium excretion differently from PL.Trial Registration: ClinicalTrials.gov Identifier:  NCT02528448 , 19/08/2015. [ABSTRACT FROM AUTHOR]

Context and Aims: Off-pump coronary artery bypass graft (OPCABG) is a form of CABG surgery. It is performed without the use of cardiopulmonary bypass machine as a surgical treatment for coronary heart disease. Acute kidney injury (AKI) is one of the common postoperative complications of OPCABG. Previous studies suggest important differences related to intravenous fluid (IVF) chloride content and renal function. We hypothesize that perioperative use of chloride restricted IVFs may decrease incidence and severity of postoperative AKI in patients undergoing OPCABG. Methods: Six hundred patients were randomly divided into two groups of 300 each. In Group A (n = 300), chloride liberal IVFs, namely, hydroxyethyl starch (130/0.4) in 0.9% normal saline (Voluven), 0.9% normal saline, and Ringer's lactate were used for perioperative fluid management. In Group B (n = 300), chloride-restricted IVFs, namely, hydroxyethyl starch (130/0.4) in balanced colloid solution (Volulyte) and balanced salt crystalloid solution (PlasmaLyte A), were used for perioperative fluid management. Serum creatinine values were taken preoperatively, postoperatively at 24 h and at 48 h. Postoperative AKI was determined by AKI network (AKIN) criteria. Results: In Group A, 9.2% patients and in Group B 4.6% patients developed Stage-I AKI determined by AKIN criteria which was statistically significant (P < 0.05). Conclusion: Perioperative use of chloride restricted IVF was found to decrease incidence of postoperative AKI. The use of chloride liberal IVF was associated with hyperchloremic metabolic acidosis.

Background: Amelioration of hyperchloremic acidosis (Cl-Ac), a common complication in chronic kidney disease (CKD), could preserve renal function in chronic kidney disease (CKD). However, the development of Cl-Ac in CKD has not been clarified yet. Methods: The degree of Cl-Ac, which is indicated as the bicarbonate concentration decrease with serum chloride concentration increase (∆[HCO3–]Cl), was compared with the estimated glomerular filtration rate (eGFR) by using CKD patient records. Results: In 307 records with metabolic acidosis, a spline curve obtained from the plot comparing ∆[HCO3–]Cl with eGFR showed that ∆[HCO3–]Cl did not change, increased, and decreased during eGFR decrease until 27, from 27 to 17.5, and from 17.5 mL/min/1.73 m2, respectively. Conclusion: By CKD progression, Cl-Ac progressed and regressed at the CKD stages G4 and G5, respectively. The regression would have reflected the shift of Cl-Ac to high anion gap acidosis. [ABSTRACT FROM AUTHOR]

Introduction: Familial hyperkalemic hypertension (FHHt) is an inherited disease characterized by hyperkalemia, hypertension, and hyperchloremic acidosis (HCA). The primary defect is a hyperactive sodium chloride co-transporter, expressed in the renal distal tubule. FHHt is caused by mutation in either WNK1, WNK4, KLHL3, or Cul3. The mechanism of HCA is not completely understood., Methods: Clinical and genetic data were collected from the largest family with FHHt described in the literature. Urine ammonia was measured in 26 family members. Epilepsy was diagnosed clinically., Results: Of the 85 family members, 44 are affected by the Q565E WNK4 mutation, and 28 are newly described. In genetically engineered mice, urinary ammonium was decreased. In our study, urine ammonium did not change. In 11 unaffected subjects, urine ammonia per creatinine was 8.013 ± 3.620 mm/mm, and in 15 subjects affected by FHHt, it was 8.990 ± 4.300 mm/mm (p = 0.546, not significant). Due to the large family size and prolonged follow-up, rare conditions can be identified. Indeed, two children have genetic generalized epilepsy and one child has migraine. The prevalence of epilepsy is 4.545% (2/44) much higher than in the general population (0.681%). This difference is statistically significant (χ2 with Yates correction = 5.127, p = 0.023)., Conclusions: We provide further evidence that the origin of HCA in FHHt lies in the proximal renal tubule. The association of FHHt with epilepsy leads us to speculate that the raised serum K in susceptible subjects may cause a rise in CSF K, and extracellular cerebral K, leading to epilepsy., (© 2023 The Author(s). Published by S. Karger AG, Basel.)

Intravenous fluid administration has been occurring for well over one hundred years for a variety of pediatric disease processes. Surprisingly, clinicians have yet to agree upon a standardized intravenous solution. There is ongoing debate regarding the administration of isotonic versus hypotonic fluids as maintenance solutions. In this article, we will review what is known about different maintenance solutions, discuss the potential complications with their use, and summarize the available evidence to help guide clinicians in their choice of maintenance fluids for their patients. [ABSTRACT FROM AUTHOR]

Context and Aims: Off-pump coronary artery bypass graft (OPCABG) is a form of CABG surgery. It is performed without the use of cardiopulmonary bypass machine as a surgical treatment for coronary heart disease. Acute kidney injury (AKI) is one of the common postoperative complications of OPCABG. Previous studies suggest important differences related to intravenous fluid (IVF) chloride content and renal function. We hypothesize that perioperative use of chloride restricted IVFs may decrease incidence and severity of postoperative AKI in patients undergoing OPCABG.Methods: Six hundred patients were randomly divided into two groups of 300 each. In Group A (n = 300), chloride liberal IVFs, namely, hydroxyethyl starch (130/0.4) in 0.9% normal saline (Voluven), 0.9% normal saline, and Ringer's lactate were used for perioperative fluid management. In Group B (n = 300), chloride-restricted IVFs, namely, hydroxyethyl starch (130/0.4) in balanced colloid solution (Volulyte) and balanced salt crystalloid solution (PlasmaLyte A), were used for perioperative fluid management. Serum creatinine values were taken preoperatively, postoperatively at 24 h and at 48 h. Postoperative AKI was determined by AKI network (AKIN) criteria.Results: In Group A, 9.2% patients and in Group B 4.6% patients developed Stage-I AKI determined by AKIN criteria which was statistically significant (P < 0.05).Conclusion: Perioperative use of chloride restricted IVF was found to decrease incidence of postoperative AKI. The use of chloride liberal IVF was associated with hyperchloremic metabolic acidosis. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The anion gap, in conjunction with other laboratory results, can be a useful clue in the differential diagnosis of metabolic acidosis. There are three primary causes of metabolic acidosis: loss of base, decreased renal excretion of acid, and increased acid production. Depending on the cause of metabolic acidosis, the anion gap may be elevated or normal. [ABSTRACT FROM AUTHOR]

Background: In resuscitation, normal saline could cause hyperchloremic metabolic acidosis, while balanced electrolyte solution is a crystalloid fluid resembling blood plasma with lower chloride content. This study compared the effect of normal saline and balanced electrolyte solution Ringerfundin (BES) as the resuscitation fluid in diabetic ketoacidosis (DKA) patients. Parameters applied in this study were standard base excess (SBE) as resuscitation's result indicator and strong ion difference (SID) to measure chloride's influence in developing hyperchloremic acidosis. Methods: A prospective, randomized, single blind controlled trial was conducted at the Emergency Department of Cipto Mangunkusumo Hospital. Thirty subjects with blood sugar >250 mg/dl, arterial pH <7.35 mg/dl, and positive blood ketone were randomly allocated to receive either normal saline (NS) or RingerfundinO (BES) as the standardized resuscitation protocol. Data analysis was performed using the unpaired T-test and the Mann Whitney test to compare the SBE and the SID means between both groups. Additional parameters were the level of consciousness, blood sugar level, vital signs, blood gas analysis, lactate, electrolyte, and blood ketone. Results: The mean SID in the BES group was significantly greater than the NS group of all measurements (p<0.05). The BES group had significantly higher mean SBE compared to the NS group at 18 hours (-4.88±5.69 vs -9.68±5.64; p=0.009), 24 hours (-3.99±4.27 vs -8.7±5.35; p=0.023), and 48 hours (-4.06±4.11 vs -7.01±5.46; p=0.009). BES resulted in non¬significant higher delta SBE and sId than NS. Additional parameters were not different between both groups. Conclusion: This study showed that fluid resuscitation of DKA patients with BES resulted in slightly but not significantly higher mean actual SBE and SID than NS. suggesting that BES as an alternative fluid resuscitation to prevent hyperchloremic acidosis in diabetic ketoacidosis patients was not superior to NS. [ABSTRACT FROM AUTHOR]

Background and Objectives: Large-volume administration of 0.9% saline are known to causes hyperchloremic metabolic acidosis (HMA) due to its high chloride load. Balanced or physiological fluids with inorganic ions are not associated with the same disturbance. The purpose of this study was to see whether balanced crystalloid and colloid solutions cause less disturbances in postoperative acid base status than sodium chloride based solutions in patients undergoing elective open gastrointestinal surgery. Methodology: Study subjects were patients aged between 30-60 years, ASA grades I and II, undergoing elective open gastrointestinal surgery, were selected as per proposed sampling design and were allotted into two groups, by the help of simple randomization process. Patients in the Group B received Hartmann's solution and 6% hetastarch in balanced electrolyte and glucose solution and patients in the Group N received 0.9% sodium chloride solution and 6% hetastarch in 0.9% sodium chloride solution. Arterial blood samples were taken from both the groups of patients just prior to and 30 min after surgery. Baseline and final acid base status, heart rate, mean blood pressure, peripheral temperature, as well as urine output before, during and after surgery were recorded up to 48 hours. Prevalence of development of HMA was determined by appropriate statistical technique. Results: The mean chloride level of normal saline group postoperatively was 118.66 ± 5.75 mmol/L (Normal range: 98-106 mmol/L) whereas in balanced saline group it was 103.27 ± 2.29 mmol/L, arterial pH was 7.31 ± 0.29 and 7.4 ± 0.02 respectively. Hence the changes in chloride level as well as arterial pH were significant in normal saline group versus balanced fluid group. Conclusion: Normal saline based fluids cause significant alteration in arterial chloride and pH levels against the use of balanced fluids in gastrointestinal surgery. [ABSTRACT FROM AUTHOR]

Introduction: Since the aim of fluid therapy in diabetic ketoacidosis (DKA) is to remove ß-hydroxybutyrate with Na from the kidneys, the first recommended fluid is 0.9% NaCl. BECl (Na-Cl-32) is the best chloride evaluation. Administering fluids with BECl <32 in DKA may cause hyperchloremic acidosis. This study investigates the effect of the administered fluids with BECl <32 and BECl ≥32 on metabolic acid-base status in the first 6 hours of DKA. Materials and Methods: Patients with DKA admitted to intensive care units (ICU) in the last 15 years were retrospectively evaluated. Demographic data, blood gas samples, and strong ion gap (SIG) were recorded at the ICU admission and the 6th hour. According to BECl values of administered fluids in the first 6 hours, patients were separated into two groups: Group I (Fluids with BECl<32) and group II (fluids with BECl ≥32). SPSS Version 28 was used for statistical analysis. Results: DKA was detected in forty-seven (0.2%) of 15,364 patients. Thirty-two (GI=26; GII=6) patients with DKA were included in the study. Demographics and blood gas parameters at the ICU admission and SIG, Na, K, lactate, and glucose levels at the 6th hour were similar in groups. At the 6th hour, pH, PaCO2, HCO3, SBE, and Na-Cl difference in GI were significantly lower (p<0.001, p=0.016, p=0.011, p=0.022 and p<0.001, respectively), whereas Cl was significantly higher than GII (p=0.023). Conclusion: Although SIG is decreased by administering fluids with BECl <32 in DKA, the reason for the lack of expected increase in HCO3 and SBE and continued hypocapnia at the 6th hour is the iatrogenic hyperchloremia. Hence, the usage of fluids with BECl <32 in DKA should be avoided, and the fluid therapy algorithm of DKA should be reconsidered. [ABSTRACT FROM AUTHOR]

Background: Citrate, the currently preferred anticoagulant for continuous veno-venous hemofiltration (CVVH), may influence acid-base equilibrium.Methods: The effect of 2 different citrate solutions on acid-base status was assessed according to the Stewart-Figge approach in two consecutive cohorts of critically ill adult patients. The first group received Prismocitrate 10/2 (PC10/2; 10 mmol citrate/L). The next group was treated with Prismocitrate 18/0 (PC18; 18 mmol citrate/L). Both groups received bicarbonate-buffered fluids in post-dilution.Results: At similar citrate flow, the metabolic acidosis present at baseline in both groups was significantly attenuated in PC18 patients but persisted in PC10/2 patients after 24 h of treatment (median pH 7,42 vs 7,28; p = 0.0001). Acidosis in the PC10/2 group was associated with a decreased strong ion difference and an increased strong ion gap (respectively 43 vs. 51 mmol/L and 17 vs. 12 mmol/L, PC10/2 vs. PC18; both p = 0.001). Chloride flow was higher in PC10/2 than in PC18 subjects (25.9 vs 14.3 mmol/L blood; p < 0.05).Conclusion: Correction of acidosis was blunted in patients who received 10 mmol citrate/L as regional anticoagulation during CVVH. This could be explained by differences in chloride flow between the applied citrate solutions inducing hyperchloremic acidosis. [ABSTRACT FROM AUTHOR]

Copyright of Reanimation is the property of Lavoisier and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Renal tubular acidosis (RTA) is essentially characterized by normal anion gap and hyperchloremic metabolic acidosis. It is important to understand that despite knowing the disease for 60-70 years, complexities in the laboratory tests and their interpretation still make clinicians cautious to diagnose and label types of tubular disorder. Hence, we are writing this mini-review to emphasize on the step wise approach to RTA with some understanding on its basic etiopathogenesis. This will definitely help to have an accurate interpretation of urine and blood reports in correlation with the clinical condition. RTA can be a primary or secondary defect and results either due to abnormality in bicarbonate ion absorption or hydrogen ion secretion. Primary defects are common in children due to gene mutation or idiopathic nature while secondary forms are more common in adults. We are focusing and explaining here in this review all the clinical and laboratory parameters which are essential for making the diagnosis of RTA and excluding the extrarenal causes of hyperchloremic, normal anion gap metabolic acidosis. [ABSTRACT FROM AUTHOR]

Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acid-base disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide might be less frequent than in high anion gap metabolic acidosis because of better tissue perfusion and the ability to eliminate carbon dioxide. Further basic and clinical research is needed to facilitate development of evidencebased guidelines for therapy of this important and increasingly common acid-base disorder. [ABSTRACT FROM AUTHOR]