Case Study

Splenic and portal vein thrombosis and prehepatic portal hypertension in an 8 year old Chow dog with immune-mediated thrombocytopenia.

An 8-year-old MN Chow Chow mix was presented for anorexia and weight loss. On physical examination, multiple petechiae on gums and abdomen were evident. Abnormalities on CBC were anemia, neutrophilia, eosinopenia, thrombocytopenia, and mild leukocytosis. The patient was treated with IV fluids, Flagyl, famotidine, doxycycline, sucralfate, and prednisone. The patient was discharged 24-hours later, and owner was advised to follow-up with rDVM within two days. A month later, the patient was presented due to a distended abdomen and fluctuating CBC values. The patient had a recent history of starting azathioprine treatment. Physical examination found the patient bright, alert and responsive, with visible muscle wasting, slightly tacky pink mucous membranes, no petechia present, and a distended abdomen with a palpable fluid wave. PCV/TP was 36/5.3. A cursory ultrasound showed extensive free fluid in the abdomen with extensive fibrin deposits. Radiographs showed decreased detail/fluid in the abdomen and no visible thoracic masses.

DX

Splenic vein thrombosis, portal vein thrombosis, pre-hepatic portal hypertension and ascites.

Sonographic Differential Diagnosis

Complete splenic vein thrombosis with portal vein thrombosis causing secondary portal hypertension and ascites. Volume contracted vena cava in the post hepatic region.

Image Interpretation

The abdomen in this patient presented a mild to moderate amount of anechoic ascites primarily in the mid to caudal abdomen and around the liver lobes. The liver was uniform in contour and hypovolemic. The vena cava at the level of the diaphragmatic inlet was hypovolemic as well (Image 5, video 4). As a result the hepatic veins were hypovolemic. The portal vein presented a thrombus with reactive omentum in the area of the portal hilus (Image 6, Video 6-8). This continued into the splenic vein, which presented complete thrombosis that reached the spleen with areas of complete thrombosis of the splenic vein (Images 1 & 3, Videos 1 & 2). Arterial blood flow to the spleen appeared present at this time. Reactive omentum was noted in this region as well as the associated intestinal tract. The patient was visibly painful upon the region of the splenic vein that was thrombosed. Given this presentation, emerging bowel infarction could be an issue. Anechoic ascites is visible (Image 4, video 3). The vena cava and hepatic vasculature is subnormal in volume (Image 5/video 4) indicating systemic dehydration and ruling out causes of ascites deriving from the thorax (i.e right sided heart failure, obstructive masses and deep caval thrombosis). Note that the portal vein is near completely void of Doppler signals indicating thrombosis while, even though volume contracted, the vena cava shows solid color flow filling (Image 6/video 6-8). This is confirmed with the more sensitive power Doppler (image 4, video 8). This portal vein obstruction, likely enhanced by the splenic vein thrombosis cascading into the portal vein at the splenic portal junction, is the cause of portal hypertension and the resultant secondary ascites/transudate. Normally in portal hypertension, the spectral Doppler would reveal a portal vein velocity < 15 cm/sec. However, in this case, spectral Doppler could not be utilized due to complete thrombosis and lack of detectable flow.

Outcome

Abnormalities on CBC and blood chemistry were thrombocytopenia, severely elevated ALP activity, moderately elevated ALT activity, and low total protein. The patient was humanely euthanized.

Comments

Normally in portal hypertension the spectral Doppler would reveal a portal vein velocity < 15 cm/sec. However, in this case, spectral Doppler could not be utilized owing to complete thrombosis and lack of detectable flow.

Clinical Differential Diagnosis

Thrombocytopenia – destruction (IMT, neoplasia, infectious disease, systemic inflammatory disease), consumption (DIC, bleeding), sequestration (splenic disease), poor production (bone marrow disease.) Ascites – transudate (liver disease, cardiac disease), modified transudate (liver disease, cardiac disease, neoplasia), exudate (bacterial, urine, bile, blood.)

Sampling

It was recommended that the patient be transferred to a 24-hour care facility for intensive care, plasma transfusion, coagulation panel, abdominocentesis with cytology and potential culture and sensitivity, as well as a repeat sonogram. Plavix or aspirin therapy or heparin was also suggested. Abnormalities on CBC and blood chemistry were thrombocytopenia, severely elevated ALP activity, moderately elevated ALT activity, and low total protein.