A 9-year-old spayed female miniature schnauzer presented for lower urinary tract signs.
History. The dog had a 2-month history of pollakiuria and stranguria. Free-catch urinalysis done by the referring veterinarian showed hematuria and pyuria. Aerobic bacterial urine culture showed bacterial growth, although the organism was not quantified or identified. Microbial susceptibility showed that the bacteria were susceptible to numerous antibiotics, including amoxicillin and cefadroxil. The dog was treated with oral amoxicillin for 2 weeks.
Clinical signs resolved during antibiotic therapy, but recurred 4 days after amoxicillin was discontinued. The dog was then treated with oral cefadroxil for 2 weeks but again clinical signs returned a few days after antibiotics were discontinued. A second voided urinalysis showed persistent hematuria and pyuria. The owner elected further workup of the problem. Antibiotics were discontinued 5 days before presentation. At the time of presentation, the patient was consuming a complete and balanced, dry commercial maintenance diet.
Physical Examination. The dog weighed 7.2 kg; body condition score was 4 of 5. The urinary bladder felt thickened and contracted. No abnormalities were found on rectal examination or during the remainder of the physical examination.
Initial Diagnostic Procedures. Clinical signs of pollakiuria, stranguria, hematuria, and pyuria localized the problem to the lower urinary tract (LUT). The 3 most likely causes for LUT disease in this dog were urinary tract infection (UTI), urolithiasis, and neoplasia. Results of a complete blood count, serum biochemical profile, urinalysis, and urine culture are shown in Table 1. Survey abdominal radiographs were performed (Figure 1, above. Survey lateral abdominal radiograph showing uroliths present in the bladder).
Diagnosis: Urinary tract infection, bladder calculi, and portal systemic shunt
Further Diagnostics. To confirm the mineral composition of the uroliths, the urinary bladder was catheterized and the "jiggle technique"1 was used to aspirate some small stones through the urinary catheter into a syringe for quantitative mineral analysis (cvm.umn.edu/depts/minnesotaurolithcenter/home.html). Stones as small as a pinhead can be submitted for analysis. Knowing the mineral composition of uroliths before initiating therapy can help determine whether further diagnostics are warranted and what therapeutic options are available.
Quantitative analysis of uroliths obtained through the catheter revealed that they were composed of 45% MAP and 55% AAU. It is not uncommon for infection-induced struvite uroliths in dogs to have a small amount (< 25%) of AAU with no obvious liver dysfunction. Protein (purine) metabolism in healthy dogs results in excretion of allantoin in urine, as well as small amounts of uric acid. If urine becomes supersaturated with ammonium ions, which is what occurs during formation of infection-induced struvite uroliths, some ions may react with uric acid already present in urine to form AAU. However, if AAU is more than 25% of the mineral composition of uroliths, the possibility of a PSS should be considered. On the other hand, if the mineral composition of the uroliths is 100% AAU, they may not have been visible on survey abdominal radiographs.
To further assess liver function, a serum bile acid test was done on day 2 of admission. The results were elevated (Table 2), and a tentative diagnosis of PSS was made. Based on the breed of this dog, the PSS was probably extrahepatic and amenable to surgical correction.2
Treatment. Treatment initiated on day 1 consisted of oral clavamox for the UTI. The urine culture indicated that the bacteria were susceptible to this antibiotic. A second urine culture done 7 days later was sterile. Antibiotics were continued until the time of surgery.
Cystotomy was performed, and mineral composition of these stones was similar to the stones retrieved via the "jiggle technique." Cranial mesenteric arteriography was done to confirm the diagnosis of PSS and to determine whether it was amenable to surgical correction (Figure 2). The portal postcaval shunt was attenuated 75% at the time of surgery, and postattenuation arteriography was performed (Figure 3).