Liver transplantation in hyponatremic patients with emphasis on central pontine myelinolysis.

Patients awaiting liver transplantation may suffer from severe hyponatremia. It has been suggested that hyponatremia or its treatment might be associated with central pontine myelinolysis (CPM), a serious complication that can be seen after orthotopic liver transplantation (OLT). We undertook this study to assess the outcome of hyponatremic patients after OLT and to evaluate the risk factors in the development of CPM. A total of 379 adult OLT performed in 347 patients between March 1993 and December 1995 was studied using a prospectively-collected data base and retrospective chart review. The following risk factors for the development of CPM were analyzed: primary liver disease, nutritional status, alcoholism, diuretic use, hepatic encephalopathy, United Network for Organ Sharing (UNOS) status, preoperative serum sodium, magnesium and cholesterol levels, increase in serum sodium concentration during surgery, and immunosuppressive treatment. Overall 12 patients (3.5%) underwent OLT in a hyponatremic state (serum sodium < or = 127 meq/L). At a median follow-up of 14 months, 8 patients were alive without any neurological sequel. Six of the 12 patients developed neurological complications in the early post-operative period including CPM in 3, confusion in 2, and seizure in 1. The 3 patients who developed CPM expired within 3 months of OLT. The changes in serum sodium concentration during OLT in patients with and without CPM were 20.7 +/- 8.1 and 7.0 +/- 5.1 meq/L, respectively (p = 0.005). No other risk factor could be identified in the development of CPM. It is concluded that prognosis of hyponatremic patients after OLT is poor if they develop CPM. Slow correction of hyponatremia perioperatively may be critical in preventing this devastating complication.

Hepatic artery stenosis after liver transplantation--incidence, presentation, treatment, and long term outcome.

Little is known about hepatic artery (HA) patency and patient clinical course when the nonthrombosed HA has been revised. We undertook this study to evaluate the risk factors in the development of HA stenosis and to assess the impact of HA revision on the outcome. A total of 857 adult consecutive OLT in 780 patients performed over a 6-year period were studied. Patients who underwent revision of their nonthrombosed but stenotic HA were reviewed for patient/graft survival, method of HA revision, incidence of biliary strictures, and long-term HA patency. Overall 39 patients (5%) with 41 allografts underwent HA revision for stenosis. Median time to diagnosis was 100 days posttransplant (range 1-1220 days). HA flow at the time of OLT was found to be the only significant variable of an anastomotic stenosis. No risk factor could be identified for the graft HA stenosis. Treatment methods included resection of the stenotic segment with primary reanastomosis (n = 17), aortohepatic iliac artery graft (n = 11), interposition vein graft (n = 4), vein patch angioplasty (n = 2), interposition artery graft (n = 1), and percutaneous transluminal balloon angioplasty (n = 6). Postrevisional HA patency was demonstrated in 32 (78%) cases. At a median follow-up of 25 months, 26 patients (67%) were asymptomatic with good liver function. Nine patients had developed biliary strictures. Seven patients had undergone retransplantation and 8 patients had died. The actuarial patient and graft survivals at 4 years in the patients with revised HA were 65% and 56%, respectively. HA stenosis requiring revision is an infrequent occurrence after OLT. Long-term patency of the revised HA is good. Revision of the HA may help prevent biliary strictures and allow for good long-term graft function in the majority of patients.