P219 Non-cirrhotic, non-malignant acute portal vein thrombosis – should we be doing more?

Introduction For cases of non-cirrhotic, non-malignant acute portal vein thrombosis (aPVT) guidance (European Association for the Study of the Liver Clinical Practice Guidelines: vascular diseases of the liver. J Hepatology, 2016) advises treatment with low molecular weight heparin (LMWH), screening for prothrombotic conditions, anticoagulation for at least 6 months and repeat CT imaging at 6–12 months to assess recanalisation. Thrombolysis and/or interventional radiology may also be considered in the acute management. We audited the management of these cases in our centre to inform the development of an aPVT treatment pathway. Methods A retrospective search of PACS was done for inpatient CT scans from 2013–2018 where the report contained any of: ‘portal vein thrombosis’, ‘mesenteric vein thrombosis’, ‘portomesenteric vein thrombosis’ or acronyms: ‘PVT’, ‘SMVT’, ‘PMVT’. Cases of chronic PVT, cirrhosis or malignancy were excluded. Electronic notes were examined to identify underlying aetiology at diagnosis and how the aPVT was managed. Results 98 cases of aPVT were identified over the 5-year period. 35 were excluded due to malignancy (22) and cirrhosis (13). The remaining 63 cases were true non-cirrhotic, non-malignant aPVT. Pancreatitis was the commonest aetiology (32%) followed by intra-abdominal infection (24%), post abdominal surgery (19%), unprovoked (16%) and other (9%). 9 patients died before discharge and a further 3 died within 6 months of diagnosis. None underwent thrombolysis or interventional radiology treatment. Only 21% (n=13) had evidence of a thrombophilia screen. 59% (n=37) of cases were anticoagulated of which 50% had LMWH with bridging to warfarin, 44% LWMH only and 6% rivaroxaban. Duration of anticoagulation could be ascertained in 28 patients: 43% had 6 months, 39% lifelong, 7% had 4 months and the other 3 cases separately had 6 weeks, 2 months and 12 months. Of the 51 patients who survived >6 months after diagnosis 59% had repeat CT imaging. The majority (n=23) were anticoagulated and there was recanalisation in 61%, partial recanalisation in 13% and cavernous transformation in 26%. 83% of those with cavernous transformation had portal hypertension. 6 of the non-anticoagulated cases had a repeat CT. 1 had partial recanalisation and had developed varices. The other 5 had recanalisation but notably these cases were non-occlusive aPVT. Conclusions This audit highlighted inconsistencies in the management of non-cirrhotic, non-malignant aPVT in our centre. On assessment of recanalisation several cases had cavernous transformation and resultant portal hypertension but many did not get this assessment and so their risk of portal hypertension is unknown. As a result of these findings we are developing an aPVT pathway to guide clinicians, minimise complications of aPVT and develop a consistent approach in our trust.