Evaluation of transurethral cystoscopy and excretory urography for diagnosis of ectopic ureters in female dogs: 25 cases (1992-2000)

OBJECTIVE: To evaluate transurethral cystoscopy and excretory urography for diagnosis of ectopic ureter in female dogs and identify concurrent urogenital abnormalities. DESIGN: Retrospective study. ANIMALS: 25 female dogs. PROCEDURE: Medical records of female dogs that underwent transurethral cystoscopy, excretory urography, and ventral cystotomy were reviewed for signalment, history, physical examination findings, results of bacteriologic culture of urine, and surgical findings. Videotapes of transurethral cystoscopy and radiographic studies were reviewed systematically without knowledge of surgical findings. RESULTS: Ectopic ureters were diagnosed in 24 of 25 (96%) of the dogs, bilaterally in 22 of 24 (91.6%) dogs. Cystoscopic evaluation yielded a correct diagnosis in all dogs when results of ventral cystotomy were used as the diagnostic standard. Cystoscopic evaluation identified a terminal ureteral opening for all ureters. Urethral fenestrations, troughs, striping, and tenting were identified. Abnormalities of the vestibule were identified in all examinations available for review (24/25). The paramesonephric septal remnant and its association with ectopic ureters were identified and characterized by cystoscopy. Radiographic findings were discordant with surgical findings and correctly identified 36 of 46 (78.2%) ectopic ureters and 2 of 4 normal ureters. Hydroureter and renal abnormalities were associated with distal urethral ectopic ureters on radiographic evaluations. CONCLUSIONS AND CLINICAL RELEVANCE: Transurethral cystoscopy was accurate and minimally invasive for identification and classification of ectopic ureters in dogs. Contrast radiography had limitations in diagnosis of ectopic ureters. Cystoscopic findings and associated vaginal and vestibular abnormalities support abnormal embryologic development in the pathogenesis of ectopic ureters.     

Acid-base and hormonal abnormalities in dogs with naturally occurring diabetes mellitus

OBJECTIVE: To examine acid-base and hormonal abnormalities in dogs with diabetes mellitus. DESIGN: Cross-sectional study. ANIMALS: 48 dogs with diabetes mellitus and 17 healthy dogs. PROCEDURES: Blood was collected and serum ketone, glucose, lactate, electrolytes, insulin, glucagon, cortisol, epinephrine, norepinephrine, nonesterified fatty acid, and triglyceride concentrations were measured. Indicators of acid-base status were calculated and compared between groups. RESULTS: Serum ketone and glucose concentrations were significantly higher in diabetic than in healthy dogs, but there was no difference in venous blood pH or base excess between groups. Anion gap and strong ion difference were significantly higher and strong ion gap and serum bicarbonate concentration were significantly lower in the diabetic dogs. There were significant linear relationships between measures of acid-base status and serum ketone concentration, but not between measures of acid-base status and serum lactate concentration. Serum insulin concentration did not differ significantly between groups, but diabetic dogs had a wider range of values. All diabetic dogs with a serum ketone concentration > 1,000 micromol/L had a serum insulin concentration < 5 microU/mL. There were strong relationships between serum ketone concentration and serum glucagon-insulin ratio, serum cortisol concentration, and plasma norepinephrine concentration. Serum beta-hydroxybutyrate concentration, expressed as a percentage of serum ketone concentration, decreased as serum ketone concentration increased. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that ketosis in diabetic dogs was related to the glucagon-insulin ratio with only low concentrations of insulin required to prevent ketosis. Acidosis in ketotic dogs was attributable largely to high serum ketone concentrations.     

Hyponatremia: a quick reference.

This article serves as a quick reference for hyponatremia. Guidelines for analysis and causes, signs, and a stepwise approach are presented.     

Treatment of Ionized Hypercalcemia in 12 Cats (2006–2008) Using PO‐Administered Alendronate

Background

Long‐term treatment of cats with ionized hypercalcemia using alendronate has not been evaluated.

Hypothesis/Objectives

Alendronate is well tolerated in treatment of ionized hypercalcemia in cats.

Animals

A total of 12 cats with ionized hypercalcemia.

Methods

Prospective study of 12 cats with ionized hypercalcemia of idiopathic origin was identified by telephone and email communication with a convenience sample of consulting veterinarians. Cats were treated with alendronate at a dose of 5–20 mg per feline PO q7d. Serum ionized calcium concentration (iCa) was measured before beginning treatment with alendronate, and after 1, 3, and 6 months of treatment. Alendronate dosage was adjusted according to iCa. Evaluation included physical examination, CBC, biochemistry profile, and diagnostic imaging. The owners and referring veterinarians were questioned about any observed adverse effects. The Wilcoxon matched‐pairs signed rank test was used to compare baseline iCa to iCa at different time periods.

Results

Alendronate treatment resulted in a decrease in iCa in all 12 cats. The median percentage change in iCa was −13.2%, −15.9%, and −18.1% (range, −29.6 to +7.6; −30.5 to −1.9; −45.8 to +1.5%) at the 1, 3, and 6 month time points, respectively. Baseline iCa was significantly different from 1 month (P = .0042), 3 months (P = .0005), and 6 months (P = .0015). No adverse effects were reported for any of the cats.

Conclusions and Clinical Importance

Alendronate was well tolerated and decreased iCa in most cats for the 6‐month period of observation.     

Uses and effectiveness of pamidronate disodium for treatment of dogs and cats with hypercalcemia

Uncorrected hypercalcemia can cause clinical signs such as polyuria, polydipsia, vomiting, diarrhea, lethargy, and depression and contributes to the development of primary renal failure and soft tissue mineralization. Treatment of hypercalcemia includes diagnosis and treatment of the underlying disease process and some combination of excracellular fluid volume expansion by administration of fluids intravenously and administration of glococorticosteroids, salmon calcitonin, and furosemide. Bisphosphonates such as pamidronate disodium also may be safe and effective in the treatment of hypercalcemia. The purpose of our study was to characterize the efficacy and safety of pamidronate in the treatment of hypercalcemia attritutable to several different disease processes in the dog and cat. Seven dogs and 2 cats were administered pamidronate at a dose of 1.05-2.0 mg/kg IV for a variety of disease processes, including neoplasia (n = 4), calcipotriene toxicity (n = 3), nocardiosis (n = 1), and idiopathic hypercalcemia with chronic renal failure (n = 1). In all the animals, IV pamidronate administration rapidly decreased serum calcium concentrations without evident toxicosis. Two animals received pamidronate several times without obvious toxicosis. On the basis of the findings in our retrospective study, pamidronate may be a safe and effective drug with which to lower both serum total and ionized calcium concentrations in patients with hypercalcemia arising from a wide variety of underlying disease processes.     

Ventilatory and Metabolic Compensation in Dogs With Acid-Base Disturbances

Ventilatory and metabolic compensation to acid-base disturbances is reviewed. The mechanisms for compensation as well as the values obtained from several studies using normal dogs and dogs with experimentally induced diseases are provided. Compensation is not the same in dogs and human beings. Dogs have a better ability to adapt to most respiratory disorders, and human beings adapt better to metabolic acidosis. In metabolic alkalosis and chronic respiratory acidosis there is no difference in compensation between these species. Ventilatory compensation for metabolic disorders in dogs is the same whether they have metabolic acidosis or metabolic alkalosis, whereas metabolic compensation in respiratory disturbances is less effective in acidosis. Values for the expected changes in PCO₂ in dogs with metabolic acidosis and metabolic alkalosis, and for bicarbonate concentration (HCO₃-) in dogs with acute and chronic respiratory alkalosis and acidosis are presented.     

Peritoneal dialysis in dogs and cats: 27 cases (1976-1987)

The records of 25 dogs and 2 cats treated with peritoneal dialysis during an 11-year period were evaluated. The indications for peritoneal dialysis were acute renal failure in 21 animals, chronic renal failure in 5 animals, and azotemia of undetermined cause in 1 animal. Peritoneal dialysis resulted in a significant (P less than 0.05) decrease in serum urea nitrogen concentration in 19 of the dogs and a significant (P less than 0.05) decrease in serum creatinine in 20 dogs. The most common complication of peritoneal dialysis was hypoalbuminemia (11 animals affected). Other common complications were dialysate retention/catheter obstruction (8 animals), peritonitis (6 animals), hypochloremia (6 animals), and subcutaneous leakage of dialysate (6 animals). Twelve dogs and 2 cats died during treatment, 6 dogs were euthanatized, and 1 dog was lost to follow-up evaluation. The remaining 6 dogs survived and were discharged from the hospital after successful peritoneal dialysis. On the basis of the results of this study, the authors concluded that peritoneal dialysis, although associated with a high complication rate, was a successful technique for reducing azotemia in dogs with acute and chronic renal failure. Survival rates were poor because of the severity of the underlying renal diseases.