Portopulmonary hypertension in liver transplantation: Case report
DOI:
https://doi.org/10.53855/bjt.v19i1.102Keywords:
Pulmonary Hypertension, Portal Hypertension, Liver TransplantationAbstract
Introduction: The existence of pulmonary hypertension associated to portal hypertension is a relevant condition in cirrhotic patients. In the severe form, it is an absolute contraindication for liver transplantation. We report a case of portopulmonary hypertension in liver transplantation with severe hypertensive peak during reperfusion of liver graft. Case report: Female patient, 40-year-old, functional capacity ˂4 METs, ASA IV, bearer of alcoholic liver disease with portopulmonary hypertension, dialysis kidney failure and heart failure. Doppler echocardiography showed systolic pulmonary artery pressure estimated at 30mmHg, and indicated right heart catheterization. This showed 48mmHg mean pulmonary arterial pressure (MPAP). Patient underwent liver transplantation under general anesthesia and monitored with a Swan-Ganz catheter, showing MPAP 28mmHg and 24mmHg central venous pressure. The gasometry at hepatectomy was normal. The anhepatic phase had not any considerable bleeding, and slight MPAP oscillation. In the reperfusion, it was recorded a greatest MPAP variation (26-50mmHg), which lasted 40 minutes until returning to the baseline with expectant management. Until then, they were given 900ml of plasma-lyte albuminated 2% solution. The arterial blood gas after reperfusion presented metabolic and respiratory acidosis with 7.28 pH. At the end of the surgery, patient was hemodynamically stable with MPAP 30mmHg. She was referred to the ICU intubated. The total volume infused was 1650mL. The patient underwent a kidney transplant 24 hours after liver transplantation, and she was discharged without complications. Discussion: The intraoperative anesthetic management requires knowledge of the variations of pulmonary artery pressure in each stage of liver transplantation. Proper monitoring of cardiac output, stroke volume variation and pulmonary artery pressures allowed the optimization of using vasoactive drugs fluid replacement. Although water restriction is described as an adequate way to control the volume overload in the hepatic reperfusion phase, which is a factor of cardiovascular instability in those patients, in this case, the measurement of the volume restriction adopted, without using pulmonary vasodilator drug was unable to prevent the sudden increase of MPAP in the reperfusion of the graft.