Current Concepts

Portal Vein Thrombosis, In Depth

Portal vein thrombosis is being recognized with increased frequency in small animals due to greater awareness of hypercoagulable states and greater use of abdominal ultrasound in animals with gastrointestinal signs.  The veins of the hepatic portal system drain the digestive organs, spleen and pancreas and deliver blood to the liver via the hepatic portal vein. The portal vein is responsible for delivering close to 75 percent of the hepatic blood supply, the remaining being provided by hepatic arteries.  Obstruction of the portal vein occurs most commonly secondary to thrombus formation, or due to neoplastic infiltration and secondary thrombus formation.

A predisposing cause for hypercoagulability is identified in most dogs with portal vein thrombosis (PVT). These concurrent conditions include chronic hepatitis, abdominal neoplasia, congenital hepatic vascular disease, pancreatitis, prior invasive abdominal procedures such as splenectomy or portosystemic shunt ligation, abdominal trauma, corticosteroid administration, sepsis and systemic inflammatory response syndrome. Interestingly, in a retrospective of 33 dogs with PVT performed at Tufts, nearly half of the dogs were receiving glucocorticoids at the time of diagnosis.

Portal vein thrombi are classified as either acute or chronic, although they likely represent a continuum of the same disorder. In some patients, the PVT develops slowly and silently. Signs can be subtle or non-specific, such as mild gastrointestinal upset or the development of ascites secondary to portal hypertension.  In these cases, an index of suspicion for potential thrombosis (such as a disease known to be associated with PVT) must prompt the clinician to seek an abdominal ultrasound, and to evaluate specifically the portal vein.  Abdominal ultrasound is a fairly sensitive (it picked up 81 percent of the PVT in our recent retrospective study) but it is a highly operator-dependent modality.  CT angiography, also available at Tufts, is the gold standard for diagnosis and has been used in some dogs.  Some dogs with PVT develop acute clinical signs.  These signs include abdominal pain, acute onset of vomiting and diarrhea, abdominal effusion, and cardiovascular collapse. These dogs are usually thrombocytopenic with mild-to-moderate increases in serum liver enzymes. The development of clinical signs may herald the presence of a larger PVT or propagation to involve the mesenteric vasculature.  In these cases, aggressive volume replacement in the form of intravenous fluids and blood products may be required for stabilization.

In a retrospective study of PVT in 6 cats conducted at Tufts by Rogers et al, clinical signs included lethargy, inappetance, vomiting, abdominal distension, and acute collapse. The most common physical examination finding was abdominal pain, and all cats had abnormalities documented on liver biopsy including hepatic neoplasia, cholangitis, hepatic necrosis, and portosystemic shunt.  Another study describing necropsy findings in dogs with PVT showed that 6 out of 11 dogs had thrombi documented elsewhere including the pulmonary artery and the aorta. In this study, 10 of 11 dogs had received corticosteroids. In a retrospective study of dogs with PVT, the most common physical examination finding was shock in 30% of cases, followed by abdominal pain, abdominal distension, hyper- or hypothermia, icterus, and petechia. Multiple thrombi were documented concurrently in many of these dogs both on abdominal ultrasound and at the time of necropsy.

Treatment for PVT consists of supportive care, treatment of any underlying disease process, and anticoagulation. Surgical removal of  the thrombus may be indicated in cases of refractory cardiovascular collapse secondary to severe portal hypertension. The optimal method of anticoagulation has not been determined, however, the combination of a heparin and a platelet inhibitor (such as aspirin or clopidogrel) is used most commonly at Tufts.  Anti Xa monitoring performed in our coagulation laboratory allows our clinicians to identify the optimal heparin dose, and serial abdominal ultrasounds can help monitor response to therapy. Over time, collateral vessel formation allows for alleviation of clinical signs. In people prognosis for PVT is good if recognized and treated early. In small animals the prognosis seems largely based on the underlying disease, and can be good if stabilization is achieved early. Unless a clear contraindication exists, our general recommendation is to begin anticoagulation as soon as the PVT is identified.