Colloid Osmotic Pressure Participates on the Post-transplant Lymphocele Pathogenesis.

The aim of the study was to evaluate the role of colloid osmotic pressure in post-transplant lymphocele pathogenesis. We have analyzed total plasmatic protein and albumin levels, and electrophoresis has been completed in blood samples before transplantation and in days 3 and 14 after transplantation in 50 patients with lymphocele (Lymphocele) and 198 patients without lymphocele (control), respectively. Colloid osmotic pressure (COP) was calculated according to the Hoefs formula. Statistically significant differences were confirmed in albumin levels (42.2 respectively 44.8 g/L) before transplantation (day 0); in total protein (52.5 resp. 55.5 g/L), in albumin (30.1 resp. 32.1 g/L), and COP (15.6 respectively 17.7 kPa) in day 3; and in total protein (52.8 resp. 58.9 g/L), in albumin (30.5 respectively 35.4 g/L), in COP (16.1 respectively 21.2 kPa) in day 14. A potentially critical albumin level was established in 44.1 g/L in the blood analyzed, but its sensitivity was only 62%. The main risk element for the lymphocele formation remains the surgeon's hand. We can proclaim the role of proteins and their COP in the post-transplant lymphocele formation as one of possible pathogenetic cofactors. It is responsible for the impaired mechanisms of the reabsorption the lymph back to the tissues. Better metabolic care could help to reduce incidence of this surgical complication.

The outcomes of treatment and the etiology of lymphoceles with a focus on hemostasis in kidney recipients: a preliminary report.

BACKGROUND: The etiopathogenesis of lymphoceles remains incompletely understood. The aim of our work was to analyze the perturbations of blood coagulation process for their possible impact on the etiology of lymphoceles. Additionally we performed an evaluation of the incidence and effectiveness of treatment methods for lymphoceles. MATERIALS AND METHODS: During 2004 to 2010, we performed 242 kidney transplantations in 92 female and 150 male patients. The hemostatic parameters included concentrations of: antithrombin, plasminogen, thrombin/antithrombin complexes (TAT), prothrombin products F1+2 (F1+2), d-dimers, and plasmin/antiplasmin complexes. RESULTS: At 7 years follow-up 27 (11%) recipients had developed symptomatic lymphoceles, namely abdominal discomfort, a palpable mess in the lower abdomen, arterial hypertension, infection of the operative site with fever, lymphorrhoea with surgical wound dehiscence, decreased diurnal urine output with an elevated plasma creatinine, voiding problems of urgency and vesical tenesmus, and/or symptoms of deep vein thrombosis. We applied the following methods of treatment aspiration alone, percutaneous drainage, laparoscopic fenestration or open surgery. In two only patients did perform open surgery. Since 2008 we have not performed an aspiration alone because of high rate of recurrence (almost 100%) and abandoned open surgery in favor of a laparoscopic approach. Our minimally invasive surgery includes percutaneous drainage guided by ultrasound and a laparoscopic procedure with 100% effectiveness. The examined hemostatic parameters revealed decreased concentrations of TAT complexes and F1+2 in subjects with lymphocele showing positive predictive values of 33% and 41% respectively. The negative predictive values for TAT complexes and F1+2 were 14% and 10%, respectively, suggesting decreased blood coagulation activity among effected recipients. Altered blood coagulation processes may explain some aspects of the disturbances of postoperative obliteration of damaged lymphatic vessels and formation of pathological lymph collection afterward. CONCLUSIONS: Perturbations of blood coagulation may be one cause for a lymphocele.