Thrombosis of the portal venous system may be due to intra-abdominal disease or thrombophilic disorders. Portal venous thrombosis is not uncommon in patients with established chronic liver disease, occurring in 11% to 21% of those with cirrhosis1 2
Other local predisposing factors include malignant invasion of the portal vein, pancreatitis and intra-abdominal sepsis. In the absence of gastrointestinal pathology, 40% to 60% of patients with thrombosis of the portal venous system are found to have thrombophilic disorders3 4
and the proportion of patients classified as having idiopathic thrombosis has fallen with advances in genetic typing.5
While blunt abdominal trauma has been linked with thrombosis of the portal vein and its tributaries, this clinical entity is very rare. A literature review identified three cases where an exhaustive search for a cause had failed to reveal an alternative aetiology.6–8
Because thrombosis of the portal venous system is uncommon, especially in the absence of cirrhosis, the data on the benefits of treatment are restricted to case reports and retrospective studies. Intravenous or intra-arterial catheter-directed thrombolytic treatment has been shown to be effective in the resolution of acute portal vein thrombosis.9–14
However, the risks of haemorrhage from varices with thrombolytic treatment must be considered. Anticoagulation, however, appears to be safe in portal venous system thrombosis. A large study involving 136 patients without cirrhosis or malignancy showed no increased risk of bleeding or death from haemorrhage in the anticoagulated group.15
A retrospective study reported that in patients without cirrhosis or cancer, 45% had improved portal flow with anticoagulants compared with only 15% of those left without treatment.16
There are no guidelines with regards the duration of anticoagulants or the target INR range, but it seems appropriate to consider patients on an individual basis. A longer course of anticoagulants will be needed in patients with widespread thrombus extending into the splanchnic veins and with underlying thrombophilic disorders.17
The possible relevance of pre-existing liver disease is this case report must be addressed. There was no clinical evidence of chronic liver disease, nor were there any predisposing factors. The investigations showed a negative screen for the causes of liver disease and there was no evidence, on CT scan or at gastroscopy, of features suggestive of portal hypertension. Although the liver function tests were abnormal during admission, they returned towards normal. The cause of this disturbance remains uncertain but may be a consequence of the thrombosis itself. The intermittent rise in unconjugated bilirubin may be accounted for by underlying Gilbert's syndrome.
The close temporal relationship between the abdominal injury and the onset of pain strongly supports the aetiology of this patient's portal venous system thrombosis being blunt abdominal trauma. This may well have been aggravated by an underlying thrombophilic state although the screen for this was negative. However, the patient's history of thromboembolic disease would support a currently undiagnosed abnormality in coagulation. There is little evidence from the patient to support alternative causes for portal venous system thrombosis.
- To consider abdominal venous thrombosis in patients with blunt abdominal trauma
- To consider abdominal venous thrombosis as a cause of abdominal pain
- Treatment of abdominal venous thrombosis is with anticoagulantion.