We describe two cases of massive intraoperative haemorrhage due to rupture of oesophageal or gastrointestinal varices after clamping of collateral hepatic portal veins. One case was treated by supported therapy and direct ligation while the other was treated by compression with an SB tube.
Both cases occurred during the anhepatic phase when the hepatic portal vein was clamped. There have been a few similar previous case reports of massive bleeding from varices due to portal hypertension during liver transplant.4,5
In a case of massive upper gastrointestinal haemorrhage immediately after cross-clamping of the inferior vena cava and hepatic portal vein, arterial pressure was maintained by inotropes and repeated transfusion, and the varices were overseen successfully without relapse.4
Bladder tamponade due to vesical varices has been reported during the anhepatic phase of liver transplantation and was treated by direct ligation.5
In our report, haemorrhage also occurred due to a temporary increase in portal vein pressure. In this scenario, veno-venous bypass, which reduces systemic venous congestion and may protect the recipient from the effects of reduced cardiac output and altered systemic vascular resistance, is an option. However, it is controversial.6
At our centre, veno-venous bypass is instituted only as a last resort in the presence of marked haemodynamic instability. Both the piggyback technique and the establishment of a portocaval shunt require temporary restriction of flow through the portal system, which in turn creates an increase in portal pressure. This pressure alteration could induce variceal rupture at the time of flow restriction, and this may have been the mechanism in our cases.
In both cases, an NG tube had already been placed blindly by the surgeon in ward just before they came to the operating theatre. In Case 1, although a gastrointestinal varix ruptured, the tube was obstructed and the stomach provided a temporary blood reservoir resulting in delayed diagnosis. However, in Case 2, rupture of the oesophageal varix was diagnosed immediately because of the nasogastric tube. Careful attention to the nasal tube is recommended in patients with a previously treated varix.
Most patients with cirrhosis and varices have haemorrhage within a year of diagnosis, and about two-thirds of these patients will have recurrent variceal bleeding, most within 6 months of the index episode.7
In both of our patients, at least 1 yr had passed since the last bleeding episode, and endoscopy before operation showed no signs of bleeding. Intraoperative drugs for portal hypertension, such as β-adrenergic blockers or vasopressin, may prevent bleeding by reducing the pressure.8
The SB tube is used less commonly as endoscopic intervention is now available, but has been used successfully for gastrointestinal haemorrhage related to liver transplantation,9
and should be considered as a potential intervention in an emergency situation.
In conclusion, acute variceal haemorrhage should always be considered during LDLT in patients with a history of upper gastrointestinal bleeding. When clamping the hepatic portal vein, the nasogastric tube should be carefully observed.