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Hepatic arterial buffer response after pediatric living donor liver transplantation: report of a case
Y Sanada1, K Mizuta, T Urahashi
1Department of Transplant Surgery, Jichi Medical University, and Department of Pharmacy, Jichi Medical University Hospital, Shimotsuke City, Tochigi, Japan. yuki371@jichi.ac.jp
Insights
Excessive portal vein flow after living-donor liver transplantation (LDLT) can decrease hepatic artery flow. This pressure imbalance resolved spontaneously, improving blood flow and suggesting potential for early intervention in high-risk pediatric liver transplant patients.
Area of Science:
- Hepatology
- Transplant Surgery
- Pediatric Gastroenterology
Background:
- High portal pressure post-living-donor liver transplantation (LDLT) risks graft failure and hepatic arterial complications.
- The hepatic arterial buffer response can lower hepatic artery flow when portal vein flow is excessive.
Observation:
- A pediatric LDLT case presented with excessive portal vein flow and reduced hepatic artery flow.
- This hemodynamic imbalance occurred early post-transplant without anastomotic stenosis.
Findings:
- Portal vein flow normalized around postoperative day 8.
- Simultaneously, hepatic artery flow improved, indicating the reversibility of the condition.
Implications:
- Temporary portal pressure modulation may prevent hepatic arterial complications in at-risk LDLT patients.
- Understanding these hemodynamic shifts is crucial for optimizing outcomes in pediatric liver transplantation.
Background:
Excessive portal pressure at an early stage after living-donor liver transplantation (LDLT) can damage sinusoidal endothelial cells and hepatocytes through shear stress leading to graft failure, or hepatic arterial complications due to low hepatic artery flow from a hepatic arterial buffer response. We encountered a case in which excessive portal vein flow was observed from an early stage after pediatric LDLT. The hepatic artery flow decreased due to a hepatic arterial buffer response.
Case Report:
A 6-month-old boy with biliary atresia showed excessive portal vein flow early after LDLT with a decreasing hepatic artery flow without anastomotic stenosis from postoperative day 3. The PV flow gradually exhibited a decrease at approximately postoperative day 8 and, similtaneously, hepatic artery flow exhibited improvement.
Conclusion:
Because excessive portal pressure after LDLT is reversible, it has been suggested that it may be possible to prevent the progress of hepatic arterial complications if temporary portal pressure modulation can be performed for cases among the high-risk group for hepatic arterial complications.
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