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Background The plasma ionized calcium concentration (cCa2+ ) represents the biologically active form of calcium and is the preferred method for evaluating calcium status in animals. Different pH-corrective equations have been developed for human plasma, but the validity of the equations for bovine plasma is unknown. Hypothesis We hypothesized that pH-corrective equations for bovine plasma would be similar to those used for human plasma; cCa2+ was dependent on the plasma concentrations of total calcium (cTCa), chloride (cCl), L-lactate (cLactate), and albumin (cAlbumin); and the in vitro and in vivo cCa2+ -pH relationships would differ. Animals Ten healthy calves (in vitro study), 1426 critically ill calves. Methods The in vitro plasma log10 (cCa2+ )-pH relationship was determined by CO2 tonometry of 465 plasma samples. Plasma cCl was altered by equivolume dilution of plasma with 3 electrolyte solutions of different cCl. The in vivo plasma cCa2+ -pH relationship was investigated and validated using clinicopathologic data extracted from the medical records of 950 (model development) and 476 (model validation) critically ill calves. Results pH-corrective equations for bovine plasma were similar to those used for human plasma. Plasma cCa2+ increased in vitro with increases in plasma cCl. Plasma cCa2+ in critically ill calves was associated with plasma cTCa, blood pH, plasma cCl, serum cMg, and cL-lactate (R2 = 0.69) but not plasma cAlbumin. Conclusions and clinical importance Calculation of cCa2+ from cTCa in calf plasma or serum requires adjustment for at least pH and cCl when 1 or both are outside the reference range.

OBJECTIVE Concomitant presence of renal tubular acidosis (RTA) and autoimmune diseases is indicative of the potential role of immune factors in the pathogenesis of RTA. Our study aimed to detect the serum antibodies to renal tubular epithelial cells in RTA patients. METHODS We enrolled 11 RTA patients, eight primary Sjogren's syndrome (pSS) patients and eight healthy controls (HC). Serum biochemical test, urinary regular test, and 24 hours urinary protein quantification were measured using a fully automated analyzer. Immunofluorescence assay was performed to detect the antibodies to subunit B1 and subunit B2 of v-H+-ATPases (adenosine triphosphatases) in the serum of the participants. RESULTS Clinically, RTA patients showed hyperchloremia, acidosis and paradoxical alkaline urine. We detected the serum antibodies to renal tubular epithelial cells and there were 6/11 positive in RTA patients, much higher than that in the pSS group (0/8) and the HC group (0/8). Subsequently, we demonstrated that in normal renal tissue, the B1 subunit of v-H+-ATPase specifically expressed in intercalated cells, while the B2 subunit continuously expressed along the lumen of renal tubular epithelial cells. Moreover, the antibody to subunit B1/B2 of v-H+-ATPase was positive in the sera of 6 RTA patients (54%), while it was negative in both the pSS and HC group. CONCLUSIONS We detected the presence of serum autoantibodies to subunit B1 and subunit B2 of v-H+ -ATPase in RTA patients. Our findings may provide novel mechanism insights into the pathogenesis of RTA and the potential diagnostic utility of antibodies to v-H+ -ATPase in the classification of RTA.

Background The American Society for Parenteral and Enteral Nutrition Adult Nutrition Support Core Curriculum describes clinical conditions that warrant cautious use of parenteral nutrition (CCWCPN). The Core Curriculum authors acknowledge there is no evidence for specific criteria suggested for the clinical conditions. Consequently, the purpose of this study was to determine the impact of a baseline CCWCPN on the development of subsequent metabolic complications in patients receiving parenteral nutrition (PN). Methods Adult patients initiated on PN from May 2014 to July 2015 at Cooper University Hospital were included in this retrospective study. The impact of a CCWCPN on the development of the following was determined: acid-base disturbances, hepatobiliary complications, hypercapnia, hyperchloremia, hyperglycemia, hypernatremia, hypertriglyceridemia, hypochloremia, hypoglycemia, hypokalemia, hypophosphatemia, and refeeding syndrome. Results Three hundred forty-one patients were included (mean age, 61.7 years; mean duration of PN, 8.5 days; central PN, 97%). Metabolic complications occurred more frequently in patients with a baseline CCWCPN than without these conditions (77% vs 53%, P = .001). Subgroup analyses for the development of metabolic complications in patients with or without each individual baseline CCWCPN yielded the following statistically significant results: hypernatremia (93% vs 57%, P = .007) and hyperchloremia (86% vs 57%, P = .033). Conclusions Hospitalized adult patients with a baseline CCWCPN were more likely to develop a metabolic complication when receiving PN. Baseline hypernatremia and hyperchloremia were associated with the development of metabolic complications. Baseline CCWCPN should be recognized upon initiation of PN; practitioners should closely monitor patients to minimize subsequent metabolic complications.

Background Chloride-rich fluids have been found to associate with an increased risk for acute kidney injury (AKI) among intensive care unit (ICU) patients. Studies evaluating the association of plasma chloride (Cl) with the development of AKI are few. We hypothesized that higher plasma Cl is associated with an increased risk for the development of AKI. Methods In this sub-study of the prospective FINNAKI study, we analyzed Cl values measured during ICU stay in two ICUs at a tertiary center including 445 patients. We calculated time-weighted mean values within the first 24 h in ICU for plasma Cl (ClTWM 24). We analyzed the association of ClTWM 24 primarily with the development of AKI, and secondarily with 90-day mortality. Results Based on the first measured Cl value, 350 of 445 patients [78.7 (95 CI, 74.8–82.5)] had hyperchloremia (P-Cl > 106 mmol/l) and 48 [10.8 (95 CI, 7.9–13.7)] severe hyperchloremia (P-Cl > 114 mmol/l). Altogether 217 of 445 [48.8% (95% CI 44.2–53.4%)] patients developed AKI. Of these 217, AKI was diagnosed in 62 (28.6%) after 24 h from ICU admission and were included in the analysis regarding development of AKI. ClTWM 24 was associated with an increased risk for the development of AKI (OR1.099; 1.003–1.205) after multivariable adjustments. According to ClTWM 24, no difference in 90-day mortality between severely hyperchloremic patients and others existed. Conclusions More than three of four critically ill patients had hyperchloremia and 1 of 10 had its severe form. Higher time-weighted mean chloride was independently associated with an increased risk for AKI.

Objective To describe the use of ProcalAmine as a source of parenteral nutrition in hospitalized dogs and to report complications possibly referable to its use. Design Retrospective study. Settings Private veterinary teaching hospital. Animals Thirty-six dogs hospitalized in ICU receiving ProcalAmine between October 2010 and March 2013. Interventions None. Measurements and Main Results The most common underlying disease process in this population of dogs was trauma (n = 8). Median duration of administration was 4 days and median resting energy requirement provided via ProcalAmine was 33%. ProcalAmine was administered via central catheters in 86% of cases and via peripheral catheters in 14% of cases. The overall mechanical complication rate was 19%. Metabolic complications possibly associated with ProcalAmine administration were documented in 12/36 dogs. Hyponatremia was most commonly identified (n = 6) followed by hyperglycemia (n = 4), hypochloremia (n = 2), azotemia (n = 2), metabolic alkalosis (n = 2), hyperchloremia (n = 1), and metabolic acidosis (n = 1). Conclusion ProcalAmine appears to be relatively safe and a viable option for parenteral nutrition in ill and injured dogs. Due to the potential for electrolyte derangements and other metabolic complications, daily monitoring of these parameters is advisable.

Summary Background The use of isotonic electrolytic solutions for the intraoperative fluid management in children is largely recognized, but the exact composition still needs to be defined. Objectives The primary objective of this randomized controlled open trial was to compare the changes in chloride plasma concentration using two intraoperative isotonic fluid regimens (Sterofundin vs normal saline, both added with 1% of glucose) in children undergoing major surgery. Secondary objectives were to compare changes in other electrolytes, renal function, and the occurrence of hypoglycemia. Methods Children aged between 1 and 36 months, scheduled for major surgery, were randomized to receive Sterofundin or saline during the intraoperative time. Children with preoperative electrolyte abnormalities, hemodynamic instability, and severe renal or hepatic dysfunction were excluded. The primary outcome was the Δ of Cl− (Δ = change in plasma concentration between post- and pre-infusion), and secondary outcomes included Δ of other electrolytes and intraoperative hypoglycemia. Results A total of 240 patients were included in the two study sites and randomized to receive Sterofundin plus 1% glucose or normal saline plus 1% glucose, in a open fashion (229 were finally analyzed). Δ of Cl− and Mg++ was statistically less relevant in patients who received intraoperative Sterofundin, and Δ of the other electrolytes was comparable between the two study groups. Relative risk of hyperchloremia was significantly higher when large volumes were infused (over than 46.7 ml·kg−1), regardless of type of crystalloid infused. Hypoglycemia occurred in two of 229 patients. Conclusions Sterofundin is safer than normal saline in protecting young children undergoing major surgery against the risk of increasing plasma chlorides and the subsequent metabolic acidosis.

The incidence and causes of metabolic alkalosis in dogs and cats have not been fully investigated.To describe the incidence, nature, and etiology of metabolic alkalosis in dogs and cats undergoing blood gas analysis at a veterinary teaching hospital.Dogs and cats at a veterinary medical teaching hospital.Acid-base and electrolyte results for dogs and cats measured during a 13-month period were retrospectively collected from a computer database. Only the first measured (venous or arterial) blood gas analyzed in a single hospitalization period was included. Animals with a base excess above the reference range for the species were included.A total of 1,805 dogs and cats were included. Of these, 349 (19%) were identified as having an increased standardized base excess, 319 dogs and 30 cats. The mixed acid-base disorder of metabolic alkalosis with respiratory acidosis was the most common abnormality identified in both dogs and cats. Hypokalemia and hypochloremia were more common in animals with metabolic alkalosis compared to animals without metabolic alkalosis. The 4 most commonly identified underlying diseases were respiratory disease, gastrointestinal tract obstruction, furosemide administration, and renal disease.Metabolic alkalosis was less common than metabolic acidosis in the same population of animals. Evidence of contraction alkalosis was present in many patients in this study. Hypokalemia and hypochloremia were more frequent in patients with metabolic alkalosis and suggest the importance of evaluation of acid-base status in conjunction with serum electrolyte concentrations.

Acute kidney injury (AKI) is a common complication in hospitalized patients and is associated with mortality, prolonged hospital length of stay, and increased healthcare costs. This paper reviews several areas of controversy in the identification and management of AKI. Serum creatinine and urine output are used to identify and stage AKI by severity. Although standardized definitions of AKI are used in research settings, these definitions do not account for individual patient factors or clinical context which are necessary components in the assessment of AKI. After treatment of reversible causes of AKI, patients with AKI should receive adequate volume resuscitation with crystalloid solutions. Balanced crystalloid solutions generally prevent severe hyperchloremia and could potentially reduce the risk of AKI, but additional studies are needed to demonstrate a clinical benefit. Intravenous albumin may be beneficial in patients with chronic liver disease either to prevent or attenuate the severity of AKI; otherwise, the use of albumin or other colloids (eg, hydroxyethyl starch) is not recommended. Diuretics should be used to treat volume overload, but they do not facilitate AKI recovery or reduce mortality. Nutrition consultation may be helpful to ensure that patients receive adequate, but not excessive, dietary protein intake, as the latter can lead to azotemia and electrolyte disturbances disproportionate to the patient's kidney failure. The optimal timing of dialysis initiation in AKI remains controversial, with conflicting results from two randomized controlled trials.

SUMMARY Many crystalloid and colloid plasma expanders can induce ‘hyperchloremic’ metabolic acidosis. This finding, first reported over 50 years ago, has received renewed interest following the recent availability of ‘balanced’ solutions. Several questions must be addressed and answered before making recommendations with regard to the use of these solutions. Do acidosis and hyperchloremia always go hand in hand? What is the clinical impact of hyperchloremic acidosis? Are all ‘balanced’ plasma expanders equivalent? Should isotonic saline-based plasma expanders be abandoned? Several elements of reflection are summarized in this brief review. On the basis on the currently available literature, it is not objectively possible to propose clear-cut guidelines.

Striped bass hybrids (Morone chrysops female x Morone saxatilis male) confined in a net for 10 minutes had significantly elevated corticosteroid levels (24.2 † 5.4 μg/100 ml) and significant hyperchloremia (150.02 † 2.7 meq/liter), in comparison with baseline levels of 0.8 † 0.1 μg/100 ml and 132.6 † 1.5 meq/liter, respectively. Hauling hybrids for 2 hours in freshwater significantly elevated corticosteroid levels (12.2 † 1.2 μg/100 ml) and reduced chloride levels (119.8 † 1.4 meq/liter). Corticosteroid levels remained high and hypochloremia developed within 24 hours after both netting and hauling. Although netting and hauling in 25 mg/liter MS-2223 or 10 g/liter NaC1 prevented chloride depletion during the stress, hypochloremia developed within 72 hours after the fish were transferred to freshwater. The development of hypochloremia several hours after handling indicates that hybrid bass that survive the initial stress do not necessarily recover, but may die in the days following handling. Fish anesthetized in 50 mg/liter MS-222 for 15 minutes prior to handling followed by hauling in water containing a combination of 25 mg/liter MS-222 and 10 g/liter NaCl did not develop hypochloremia within 72 hours after hauling; plasma corticosteroids were elevated during transport, but returned to nearly normal levels within 24 hours. This combination of 25 mg/liter MS-222 and 10 g/liter salt was the most successful handling medium tested.

A6 1/2-month-old Morgan filly was examined because of a history of abnormal behavior, teeth grinding, hypothermia, and electrolyte disturbances when weaned. She was from a breeding farm with several other Morgan horses. The 11-year-old dam had been purchased the year before as a proven broodmare, which had several previous foals. Breeding, gestation, and birth of this foal were normal. She was raised with 4 other mares and their offspring on pasture with free access to shelter in an open barn. Supplementary feeding consisted of oats and timothy hay. The owners reported that the foal showed unusual behavior, such as lack of apprehension of people, lack of distress from maternal separation, and a higher activity level than other foals of the same age. The foal extensively chewed the dam's tail and mane, masticated oats slowly with rapid jaw movements without actually swallowing them, and ground her teeth. She frequently nibbled the handler's clothes without biting, ate pebbles, and played with the salt block in the paddock. At 4 1/2 months of age, she was treated for suspected gastroduodenal ulcers and weaned. The referring veterinarian examined her 5 days after weaning because of dull demeanor and excessive teeth grinding. The foal was in thin body condition, hypothermic (37°C, 98.6°F), and tachycardic (60 beats per minute [bpm]) and had decreased borborygmi. Major abnormalities on serum biochemistry were severe hypernatremia (166 mmol/L; reference range 136–144 mmol/L) and hyperchloremia (128 mmol/L; reference range 94–104 mmol/L), azotemia (urea, 11.3 mmol/L; reference range 4.2–8.9 mmol/L), and hyperfibrinogenemia (5.2 g/L, reference range 1.6–2.9 g/L). The only abnormality on the CBC was hemoconcentration (PCV, 0.57 L/L; reference range 0.28–0.44 L/L). The foal was treated with penicillin procaine Ga (20,000 IU/kg [9072 IU/1b] IM q12h) and rifampinb (5 mg/kg [2.7 mg/1b] PO q8h). The next day the tachycardia worsened (120 bpm) and the foal was estimated to be 5–8% dehydrated. IV fluid therapy with lactated Ringer solutionc (LRS) was initiated, and the antibiotic was changed to ceftiofurd (2 mg/kg [0.91 mg/1b] IV q12h). The foal and dam were rejoined, and the foal's clinical status improved with resumption of nursing. Serial laboratory testing showed persistent hypernatremia 160 mmol/L) and hyperchloremia (123 mmol/L), azotemia urea 11.3 mmol/L and creatinine 168 umol/L; reference range 80–130 μmol/L), hyperglycemia (8.7 mmol/L; reference range 3.7–6.7 mmol/L), high aspartate aminotranferase activity (662 U/L; reference range 259–595 U/L), and high creatine kinase (CK) activity (1,196 U/L; reference range 108–430 U/L). The foal's condition improved and IV fluids were discontinued. Ceftiofur administration was discontinued and trimethoprim-sulfamethoxazolee (25 mg/kg [11.3 mg/1b] PO q12h) was administered for 3 days. During the next month the foal was stable but the abnormal behavior persisted. She was weaned again, and within days marked behavior changes such as circling, throwing the head around compulsively, and severe hind-end shivering recurred. At examination, the foal was dull, tachycardic (60 bpm), was hypothermic (33.6°C, 92.5°F), had dark red mucous membranes, and was estimated to be 5% dehydrated. Laboratory findings were similar to those of the previous tests except for high fibrinogen (7.1 g/L). The foal was again rejoined with the dam, treated with intramuscular penicillin, and referred

A 3-month-old Hereford heifer calf was presented for lethargy. Blood gas analysis and plasma biochemical testing revealed severe metabolic acidosis, azotemia, hyponatremia, hyperchloremia, and normal anion gap. Results of a urinalysis were consistent with acute tubular necrosis with inadequate acidification of urine based on the degree of acidemia. Salmonella enterica serovar agona was cultured from both urine and feces. The calf was treated with intravenous polyionic fluids, bicarbonate, and antimicrobials. Acidosis and azotemia resolved, and 4 months following initial presentation the heifer was clinically normal.

Thirty-four dogs suffering from severe babesiosis caused by Babesia canis rossi were included in this study to evaluate acid-base imbalances with the quantitative clinical approach proposed by Stewart. All but 3 dogs were severely anemic (hematocrit

A 25-year-old man with a history of toluene sniffing was admitted to the hospital because of tetraparesis. Laboratory examination revealed severe hypopotassemia, hyperchloremia, metabolic acidosis with a normal anion gap, elevation of serum GOT, GPT, CK, and alkaluria, and incresed urinary excretion of hippuric acid. Alkaluria despite metabolic acidosis and severely decreased serum bicarbonate were consistent with distal renal tubular acidosis. Increased urinary excretion of hippuric acid indicated exposure to toluene, and these findings were highly suggestive of toluene-induced renal tubular acidosis. He gradually recovered with abstinense from toluene sniffing and oral supplement with potassium and bicarbonate.

Richards CE, Drayton M, Jenkins H, Peters TJ. Effect of different chloride infusion rates on plasma base excess during neonatal parenteral nutrition. Acta Paediatr 1993;82:678–82. Stockholm. ISSN 0803–5253 Routine biochemical monitoring of parenterally fed newborn infants revealed plasma chloride levels which were higher than widely quoted reference ranges. The parenteral nutrition solutions were reformulated to reduce the chloride infusion rate. In a historically controlled study, 28 infants receiving the original formulation were compared with 31 infants receiving the new formulation. The mean plasma chloride level was 4.8 mmol/l lower in the new formulation group than in the original formulation group (95% confidence interval 2.5–7.2 mmol/l). The mean base excess level was 3.1 mmol/l higher in the new formulation group than in the original formulation group (95% confidence interval 1.9–4.8 mmol/l). A reduction in the chloride load by using acetate salts can be safely achieved and may decrease the plasma chloride levels and decrease acidosis during the first seven days of life.

A 16-year-old patient required intermittent positive pressure ventilation for hypokalaemic muscle weakness resulting from metabolic complications of combined colonic bladder augmentation and incomplete voiding via a prosthetic sphincter. Catheter re-establishment of urinary flow and electrolyte replacement produced dramatic metabolic and clinical improvement allowing the return of adequate spontaneous respiration.

An infant was cleansed with 2% clorhexidine gluconate (CHG) because of repeated sepsis episodes from skin colonization. Asymptomatic hyperchloremia ensued, most likely associated with CHG therapy. Fourty-eight hours after CHG therapy withdrawal, serum chloride levels returned to normal. Hyperchloremia may be a reversible adverse effect of extensive use of CHG.

Cholestyramine is a nonabsorbable anion exchange resin that is used predominantly for the treatment of hypercholesterolemia in adults and the management of acute diarrhea in children. The authors report two cases of severe hyperchloremic nonanion gap metabolic acidosis associated with the use of cholestyramine therapy. The authors recommend that patients taking cholestyramine who have concomitant renal insufficiency or who are volume depleted or who are taking spironolactone be monitored carefully for the emergence of a hyperchloremic metabolic acidosis.

This study evaluated the physiological response of rainbow trout to hooking stress after being played under standardized conditions (0–5 min) and estimated the time needed for recovery (to 72 h). Plasma osmolality and chloride measurements were used to evaluate osmoregulatory disturbances and gill ion-exchange function, and plasma glucose was used as an index of the generalized nonspecific physiological stress response. Hooking stress caused more severe blood chemistry differences in hatchery fish than in wild trout. Also, hooking stress imposed a greater stress on larger than on smaller hatchery rainbow trout. Higher water temperatures aggravated the delayed hyperglycemia and hyperchloremia in both hatchery and wild trout but only about 3 days were needed for recovery at 4, 10, or 20 C.