IMPORTANCE Infection in neonates remains a substantial problem. Advances for this population are hindered by the absence of a consensus definition for sepsis. In adults, the Sequential Organ Failure Assessment (SOFA) operationalizes mortality risk with infection and defines sepsis. The generalizability of the neonatal SOFA (nSOFA) for neonatal late-onset infection-related mortality remains unknown. OBJECTIVE To determine the generalizability of the nSOFA for neonatal late-onset infection-related mortality across multiple sites.

The influence of barbiturate anesthesia and minor surgical incisions on renal function was assessed in trained, chronically catheterized rats. In addition, renal hemodynamic changes during recovery from ether anesthesia and surgery were examined. Administration of pentobarbital in the chronic animals was associated with a marked reduction in arterial pressure (108 +/- 5 vs. 85 +/- 2 mmHg, P less than 0.01), renal blood flow (8.28 +/- 0.50 vs. 6.20 +/- 0.53 ml X min-1 X 100 g body wt-1, P less than 0.01), and glomerular filtration rate (1.30 +/- 0.10 vs. 0.97 +/- 0.11 ml X min-1 X 100 g body wt-1, P less than 0.01). Responses to Inactin were essentially identical. Small skin incisions during barbiturate anesthesia caused blood pressure to rise, but did not significantly change renal function parameters from already reduced values. In rats studied 2 h after ether anesthesia and surgical placement of catheters, arterial pressure was elevated compared with the same rats studied 4-7 days later (127 +/- 3 vs. 109 +/- 3 mmHg, P less than 0.005). Renal blood flow (5.80 +/- 0.37 vs. 8.90 +/- 0.93 ml X min-1 X 100 g body wt-1, P less than 0.01) and glomerular filtration rate (0.81 +/- 0.07 vs. 1.05 +/- 0.08 ml X min-1 X 100 g body wt-1, P less than 0.001) were markedly depressed during the recovery from surgery. It is concluded that barbiturate anesthesia depresses renal function in rats. This impairment should be considered when interpreting experiments that must be performed under anesthesia. In addition, the "conscious" preparation commonly used for renal studies in rats, i.e., one involving experimentation 2-3 h after ether anesthesia and surgery, is associated with a severe depression of renal hemodynamics.

Studies demonstrating the antagonism by prostaglandins (PGs) of antidiuretic hormone (ADH) action led to the proposal that renal medullary PGs may act to attenuate the physiologic effects of ADH via a negative-feedback loop. Therefore, we examined urinary PG excretion, an indicator of renal PG synthesis, in rats with hereditary diabetes insipidus (DI) utilizing gas chromatography-mass spectrometry. The DI rats, devoid of ADH, excrete much less prostaglandin E2 (PGE2) than normal Long-Evans rats (39 +/- 5 vs. 228 +/- 53 ng/24 h, means +/- SE, P less than 0.005). DI and normal rats were treated for 35 days with ADH while separate groups of DI and normal controls received vehicle only. The ADH treatment increased urinary PGE2 excretion in DI rats to 233 +/- 35 ng/24 h whereas PGE2 excretion was unaffected by vehicle treatment. ADH treatment in normal rats similarly increased PGE2 excretion from 215 +/- 49 to 410 +/- 63 ng/24 h (P less than 0.05). To determine whether the rise in PGE2 excretion is the result of the rise in papillary osmolality, we subjected DI rats to dehydration, which increased urine osmolality from 130 +/- 10 to 302 +/- 12 mosmol/kg H2O but left urinary PGE2 unaffected. We conclude that ADH stimulates renal medullary PGE2 synthesis in vivo.

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We augmented our standard extracorporeal membrane oxygenation laboratory protocol to include antifactor Xa assays, thromboelastography, and antithrombin measurements. We performed a retrospective chart review to determine outcomes for patients placed on extracorporeal membrane oxygenation (ECMO) prior to and after the initiation of our anticoagulation laboratory protocol. A total of 663 consecutive ECMO runs were evaluated from January 1, 2007 to June 30, 2018. Of these patients, 252 were on ECMO prior to initiation of the anticoagulation laboratory protocol on September 1, 2011, and 411 patients were on ECMO after initiation of the protocol. There were no major changes to our extracorporeal membrane oxygenation circuit or changes to our transfusion threshold during this continuous study period. Transfusion utilization data revealed statistically significant decreases in almost all blood components, and a savings in blood component inflation-adjusted acquisition costs of 31% bringing total blood product cost-savings to $309,905 per year. In addition, there was an increase in survival to hospital discharge from 45 to 56% associated with the initiation of the protocol (p = 0.004). Our data indicate that implementation of a standardized ECMO anticoagulation protocol, which titrates unfractionated heparin infusions based on antifactor Xa assays, is associated with reduced blood product utilization, significant blood product cost savings, and increased patient survival. Future prospective evaluation is needed to establish an antifactor Xa assay-driven ECMO anticoagulation strategy as both clinically superior and cost-effective.