Background: Incidence of PVT is close to 4% in adult LDLT due to technical difficulties in PV
reconstructions, mainly related to a shorter vessel pedicle and limited vessel graft.
Most cases of PVT occur early (1 month from transplant) and the clinical presentation
is severe acute liver insufficiency or graft failure. When it occurs late (more than
4 weeks) recurrence of portal hypertension is a dominant feature. Without treatment
PVT is associated with poor survival. Therapeutic options for PVT range from systemic
anticoagulation to interventional radiological (IR) treatment, to surgical revision
to retransplantation. The IR options presented in the literature include thrombolysis,
portal vein angioplasty, stent placement and shunt occlusion if present. The IR approach
may be via percutaneous transhepatic (PT), via transjugular intrahepatic portosystemic
shunt (TIPS) creation or transplenic approach. Method(s): A total of 430 liver transplants were done at our institution between February 2017
and December 2018. Five cases of early PVT were referred to us for IR treatment. The
diagnosis was initially made on colour Doppler ultrasound and findings confirmed on
contrast CT. Portal vein access was taken by ultrasound guided direct percutaneous
trans-hepatic approach in all but 1 case where percutaneous trans-splenic approach
was taken. Urokinase (1 to 5 lac units) were used for thrombolysis, in 2 cases overnight
urokinase infusion was used at 50,000 units/h. Balloon dilatation was done with a
6 mm diameter balloon. Portal flow steal by a large shunt was present in 2 cases which
were closed by coils and covered stent respectively. Result(s): With IR treatment spontaneous portal vein flow was re-established in all but 1 patient
[Table 2]. Long term follow up is available in 2 patients (7 and 9 months respectively)
and they are doing well and shows excellent portal flow. The patient in whom spontaneous
portal flow could not be established (s. no 3) was taken for surgical re-exploration
after his liver enzymes increased remarkably next day. The surgical re-exploration
revealed HAT in addition to PVT. There were areas of liver necrosis on gross inspection.
Hepatic artery flow was re-establised after thrombectomy. However only sluggish portal
flow could be re-established. This patient expired 2 days later due to multi-organ
failure. One patient (s. no. 1) had undergone surgical re-exploration for concomitant
HAT and PVT one day before IR treatment. Another patient (s. no. 5) had surgical re-exploration
for HAT on POD 1 and had HAT recurrence on POD 6. Hepatic artery thrombolysis was
done successfully. However this patient had intracranial bleed on POD 8 likely due
to thrombolysis and died of liver insufficiency and progressive neurological deterioration
on POD 38. Conclusion(s): Evidence-based evaluation outcomes of surgical and IR techniques to manage PVT is
made difficult by its low incidence, which has heretofore prevented the publication
of prospective comparative trials and limited the publication of large, retrospective
series. However, IR therapies promise to avoid the risks of re-do operations in select
post-surgical patients, besides providing a fair idea of anatomic causes such as venous
redundancy, kinking, stenosis, anastomotic size mismatch and presence of shunts. IR
management may be safe in early PVT and can often identify the anatomical cause of
the PVT and corrective measures can be taken which might lead to long term improved
results. However more studies with larger sample size are required to establish the
safety and outcome of this approach. Our experience suggests that IR treatment is
feasible and safe in early PVT in LDLT patients with good outcomes in cases where
concomitant HAT is not present.
