Effect of Hypernatremia on Outcomes After severe Traumatic Brain Injury: A Nationwide Inpatient Sample analysis.

OBJECTIVE: Induced hypernatremia is frequently used to reduce intracranial pressure in patients with severe traumatic brain injury (TBI). This technique is controversial, and some studies have independently associated hypernatremia with worse outcomes after TBI. We sought to investigate this potential association in a large healthcare database. METHODS: The Nationwide Inpatient Sample was used to obtain data on all adults who had been discharged from 2002 to 2011 with a primary diagnosis of TBI who required mechanical ventilation, intracranial pressure monitoring, or craniotomy/craniectomy. Patients with diabetes insipidus were excluded. The patients with hypernatremia were assigned to the hypernatremia group, and the rest were assigned to the control group. The primary outcome was in-hospital mortality, and the secondary outcomes included the length of stay, nonroutine hospital discharge, total hospital charges, tracheostomy, and gastrostomy placement. RESULTS: A total of 85,579 patients without a diagnosis of hypernatremia (control group) and 4542 patients with a diagnosis of hypernatremia (hypernatremia group) were identified. When controlling for age, comorbidities, gender, and cerebral edema, hypernatremia was associated with an increased rate of in-hospital mortality (odds ratio, 1.51; 95% confidence interval, 1.39-1.65), a longer mean length of stay (23.65 vs. 12.12 days; P < 0.001), an increased rate of nonroutine hospital discharge (odds ratio, 2.58; 95% confidence interval, 2.28-2.92), and greater mean total hospital cost ($227,112 vs. $112,507; P < 0.001). The patients with hypernatremia also had greater rates of tracheostomy and gastrostomy placement. CONCLUSIONS: Hypernatremia was associated with poorer outcomes in patients with severe TBI. This finding warrants further investigation in a prospective, randomized study.

Outcomes of Liver Transplantation Using Pediatric Deceased Donor Livers: A Single-Center Analysis of 102 Donors.

BACKGROUND: The outcome of pediatric deceased donor liver transplantation (LT) has not been well studied, especially pediatric deceased donor livers used in adult transplantation. This study aimed to evaluate the efficacy of LT using pediatric deceased donor livers and compare the outcomes between pediatric-to-pediatric LT and pediatric-to-adult LT. METHODS: A retrospective review of LT using pediatric deceased donor livers from June 2013 to August 2016 was performed. The patients were divided into the pediatric-to-pediatric LT group and pediatric-to-adult LT group based on the ages of the recipients. The survival and incidence of early vascular complications (VCs) were observed between the two groups. We also analyzed the risk factors of early VCs in pediatric LT and the effect of donor hypernatremia on the prognosis of recipients. RESULTS: There were 102 cases of LT using pediatric deceased donor livers in our hospital from June 2013 to August 2016, 83 pediatric-to-pediatric LT (recipients' age ≤13 years) and 19 pediatric-to-adult LT (recipients' age ≥19 years). The ratio of early VC was similar in the two groups (19.3% vs. 10.6%, P = 0.514). Low body weight of recipient was an independent risk factor of early VC in pediatric LT (odds ratio: 0.856, 95% confidence interval: 0.752-0.975, P = 0.019). The 1-year cumulative survival rates of grafts and patients were 89.16% and 91.57% in pediatric-to-pediatric LT and 89.47% and 94.74% in pediatric-to-adult LT, respectively (all P > 0.05). In all cases, patients using donors with hypernatremia (serum sodium levels ≥150 mmol/L) had worse graft survival (χ2=4.330, P = 0.037). CONCLUSIONS: Pediatric-to-pediatric LT group has similar graft and patient survival rates with those of pediatric-to-adult LT group. Low body weight of recipients is an independent risk factor of early VC in pediatric LT. Patients using donors with hypernatremia have worse graft survival.

Autoimmunity to the sodium-level sensor in the brain causes essential hypernatremia.

Na(x) is the sodium-level sensor of body fluids in the brain involved in sodium homeostasis. Na(x)-knockout mice do not stop ingesting salt even when dehydrated. Here we report a case with clinical features of essential hypernatremia without demonstrable hypothalamic structural lesions, who was diagnosed as a paraneoplastic neurologic disorder. The patient had autoantibodies directed against Na(x), along with a ganglioneuroma composed of Schwann-like cells robustly expressing Na(x). The removal of the tumor did not reduce the autoantibody levels or relieve the symptoms. Intravenous injection of the immunoglobulin fraction of the patient's serum into mice induced abnormalities in water/salt intake and diuresis, which led to hypernatremia. In the brains of these mice, cell death was observed along with focal deposits of complement C3 and inflammatory infiltrates in circumventricular organs where Na(x) is specifically expressed. Our findings thus provide new insights into the pathogenesis of hypernatremia relevant to the sodium-level-sensing mechanism in humans.