Case Study

Caudal vena cava thrombus with dissolution, also protein losing nephropathy (PLN) in a 8 year old MN Jack Russell Terrier dog

This 8 year old MN Jack Russull Terrier dog initially presented with abdominal distension and ascites. Chemistry revealed low total protein at 4.2, low albumin at 1.9, phosphorus low at 1.0, calcium low at 8.1, cholesterol was high at 332. Urine protein to creatinine ratio was high at 5.4, microalbuminuria was high at >30. Urinalysis reveled protein of 3+, blood 1+ and transitional epithelia elevated at 2-3.

Sonographic Differential Diagnosis

Initial exam revealed slight small intestines due to inflammatory bowel disease, lymphangectasia, lymphoma or edema.
Differential diagnosis for ascites include right sided heart failure, portal hypertension, hypoalbuminemia, pancreatitis, peritonitis, uroabdomen, hemoabdomen, and neoplasia.
The appearance of the pancreas can be due to nodular hyperplasia, aging changes, pancreatitis, edema and neoplasia cannot be completely excluded.

Image Interpretation

On initial ultrasound the patient had a large amount of ascites. The left kidney measured 4.38 cm and the right kidney measured 4.29 cm, both normal in size. Renal cortical echogenicity was normal as is the corticomedullary distinction. The small intestinal walls were slightly thickened and measured between 0.42-0.47 cm with normal wall differentiation. Slight mucosal stippling was noted as well. The area of the left pancreatic limb was normal in appearance but the right pancreatic limb was slightly mottled with a subtle nodular appearance, but no evidence of larges masses were seen. This area measured 4.08 x 1.51 cm.
Repeat exam 3 weeks later revealed complete resolution of the ascites with normal portal vein velocity at 22 cm/sec. The vena cava revealed reduction of the tissue structure now confirmed to be thrombus and measured 2.69 x 0.46 cm with bloodflow that appears to tap around the thrombus in the vena cava at the diaphragmatic inlet.
Repeat ultrasound examination 5 weeks later revealed persistent, minor, degenerative renal changes with hypervascular cortices. This is consistent with protein losing nephropathy. Minor mineralization was noted in both kidneys, yet non obstructive. The remainder of the abdomen was unremarkable without progression. Thrombus noted on the prior sonogram in the vena cava appears to have completely resolved on the Plavix/aspirin combination.

Outcome

The patient initially did well at home after the 5 week follow-up exam, but 2 months later the patient was humanely euthanized due to kidney failure.

Comments

At the time of the initial exam it was recommended to await lab work to evaluate the albumin level as hypoalbuminemia is a common cause for a transudate acidic fluid with no protein.

Further workup ultimately would include a cause of hypoalbuminemia if this is diagnosed by evaluating the urine protein to creatinine ratio and possibly a bile acids test to assess liver function. If this is a panhypoproteinemia this may be due to protein losing enteropathy and would merit additional diagnostic tests with a PLI folate, B12 and possibly gastrointestinal biopsies. It should be noted that a quick peek at the heart was done to ensure that there is no evidence of right sided heart failure to cause ascites and there was not.

Follow-up exam 3 weeks later: Thrombus was still present. However, it iwas significantly reduced in width allowing now hepatic vein and vena caval flow into the thorax. The kidneys presented chronic glomerulonephritis pattern with increased vasculature. Tick borne disease panel and empirical treatment with Doxycycline would be recommended.

Follow-up exam 5 weeks later: Age related renal changes. Suggestive of protein losing enteropathy. Recommendation was continuation of low dose aspirin therapy given the protein losing nephropathy. However, Plavix can be stopped at this time. Congratulations on thorough management of this case. Dietary assessment, ace inhibitor therapy such as Benazepril, aspirin therapy and nutraceuticals would be recommended for the protein losing nephropathy.