RESUMEN
Our aim was to determine whether hyponatremia is associated with waiting list or posttransplantation mortality in children having liver transplantation (LT). METHODS: A retrospective analysis of the united network for organ sharing/organ procurement transplantation network database on pediatric LT performed between 1988 and 2016 was conducted. Hyponatremia was defined as a serum sodium of 130 mEq/L or below. Subjects were divided into 2 age groups: I (0-6 y old) and II (7-18 y old). Patient survival before and after LT, as well as graft survival, were compared in patients with and without hyponatremia. Multivariable Cox proportional hazards models were constructed for perioperative mortality. RESULTS: Data from 6606 children were available for analysis of waiting list mortality, and 4478 for postoperative mortality. The prevalence of hyponatremia at the time of registration was 2.8% and 3.7% at the time of LT. Waiting list mortality in patients with hyponatremia was significantly higher in group I (P < 0.001) but not in group II (P = 0.09). In group I, the relative risk of mortality adjusted to pediatric end-stage liver disease score was significantly associated with hyponatremia (P < 0.001). A sodium level below 130 mEq/L (hazard ration [HR] = 1.7), younger age (group I) (HR = 2.01), and need for dialysis (HR = 2.3) were independent predictors for increased waiting list mortality. There was no difference in overall postoperative patient or graft survival related to hyponatremia. CONCLUSIONS: Hyponatremia is associated with increased waiting list mortality for pediatric LT candidates, particularly in younger children. Future studies examining incorporation of age-specific serum sodium levels into organ allocation policies in children seems warranted based on our findings.
RESUMEN
In this review, we analyze the epidemiology of thromboses related to end-stage liver disease (ESLD), discuss causes of hypercoagulability, describe susceptible populations, and critically evaluate proposed prophylaxis and treatment of thromboses. Classically, ESLD has been regarded as a model for coagulopathy, and patients were deemed to be at high risk for bleeding complications. Patients with ESLD are not auto-anticoagulated, and they do not have a lower risk of portal vein thrombosis, intracardiac thrombus formation, pulmonary embolism or hepatic artery thrombosis. Though the cause of hypercoagulability is multifactorial, endothelial dysfunction likely plays a central role for all patients with ESLD. Some subpopulations, such as patients with nonalcoholic steatohepatitis and autoimmune conditions, are at increased risk of thrombotic events as are patients of Hispanic ethnicity. The science behind prophylaxis of different types of clotting and treatment of thromboses is developing rapidly. A number of medications, including low molecular weight heparin, unfractionated heparin, aspirin, vitamin K antagonists, and direct oral anticoagulants can be used, but clear guidelines are lacking. Acute intraoperative clotting can be associated with high mortality. Routine use of transesophageal echocardiography can be helpful in early recognition and treatment of intraoperative thrombosis. Heparin should be reserved for cases of intracardiac thrombus/pulmonary embolism without hemodynamic instability. In unstable patients, low dose of recombinant tissue plasminogen activator can be used. In this new era of heightened awareness of thrombotic events in ESLD patients, prospective randomized trials are urgently needed to best guide clinical practice.