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Objectives To investigate the acid‐base status of sick goats using the simplified strong ion difference (sSID) approach, to establish the quantitative contribution of sSID variables to changes in blood pH and HCO3 − and to determine whether clinical, acid‐base, and biochemical variables on admission are associated with the mortality of sick goats. Animals One hundred forty‐three sick goats. Methods Retrospective study. Calculated sSID variables included SID using 6 electrolytes unmeasured strong ions (USI) and the total nonvolatile buffer ion concentration in plasma (Atot). The relationship between measured blood pH and HCO3 −, and the sSID variables was examined using forward stepwise linear regression. Cox proportional hazard models were constructed to assess associations between potential predictor variables and mortality of goats during hospitalization. Results Hypocapnia, hypokalemia, hyperchloremia, hyperlactatemia, and hyperproteinemia were common abnormalities identified in sick goats. Respiratory alkalosis, strong ion acidosis, and Atot acidosis were acid‐base disorders frequently encountered in sick goats. In sick goats, the sSID variables explained 97% and 100% of the changes in blood pH and HCO3 −, respectively. The results indicated that changes in the respiratory rate (

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.

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.

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

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 2-year-old male Labrador Retriever was presented to the University of Missouri Veterinary Teaching Hospital with the primary complaints of polydipsia, polyuria, and joint or muscle pain. Low blood urea nitrogen concentration, hyperchloremia, and marked proteinuria were the only abnormalities in a serum biochemical profile and urinalysis. Decreased creatinine clearance and increased renal fractional excretion of sodium, potassium, calcium, and phosphorus were detected by renal clearance studies. Increased excretion of most amino acids was found by amino acid analysis of urine, but not all amino acids were lost with equal magnitude. Amino acids with secondary amino groups or basic side chains were lost at increased rates, whereas those with acidic side chains were not. These differences could be related to defects in specific renal amino acid transport mechanisms. Identification of these transport mechanisms may allow for pharmacologic intervention at the point of renal loss to alleviate clinical signs of disease.