POSTTRANSPLANT LYMPHOCELES - A CRITICAL-LOOK INTO THE RISK-FACTORS, PATHOPHYSIOLOGY AND MANAGEMENT

To define better the prevalence and pathophysiology of lymphoceles fol lowing renal transplantation, we prospectively evaluated 118 consecuti ve renal transplants performed in 115 patients (96 cadaveric, 22 livin g-related, 7 secondary and 111 primary). Ultrasonography was performed post-operatively and during rehospitalizations or whenever complicati ons occurred. Perirenal fluid collections were identified in 43 patien ts (36%). Lymphoceles with a diameter of 5 cm. or greater were identif ied in 26 of 118 cases (22%). Eight patients (6.8%) had symptomatic ly mphoceles requiring therapy. The interval for development of symptomat ic lymphoceles was 1 week to 3.7 years (median 10 months). Risk factor s for the development of lymphoceles were examined by univariate and m ultivariate analysis, and included patient age, sex, source of transpl ants (cadaver versus living-related donor), retransplantation, tissue match (HLA-B/DR), type of preservation, arterial anastomosis, occurren ce of acute tubular necrosis-delayed graft function, occurrence of rej ection, and use of high dose corticosteroids. Univariate analysis show ed a significant risk for the development of lymphoceles in transplant s with acute tubular necrosis-delayed graft function (odds ratio 4.5, p = 0.004), rejection (odds ratio 25.1, p <0.001) and high dose steroi ds (odds ratio 16.4, p <0.001). When applying multivariate analyses us ing stepwise logistic regression, only rejection was associated with a significant risk for lymphoceles (symptomatic lymphoceles-odds ratio 25.08, p = 0.0003, all lymphoceles-odds ratio 75.24, p <0.0001). When adjusting for rejection, no other risk factor came close to being sign ificant (least p = 0.4). Therapy included laparoscopic peritoneal mars upialization and drainage in 1 patient, incisional peritoneal drainage in 4 and percutaneous external drainage in 3 (infected). All symptoma tic lymphoceles were successfully treated without sequelae to grafts o r patients. We conclude that allograft rejection is the most significa nt factor contributing to the development of lymphoceles. Therapy of s ymptomatic lymphoceles should be individualized according to the prese nce or absence of infection.