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IC was a median of 5 days . Logistic regression revealed two predictors of IC, presence of comorbidities (OR 5.4, p < 0.001) and 24-hour total transfused PRBC volume (OR 1.08, 95% CI 1.02 -1.15, p = 0.01). Findings from the Cox proportional hazards model revealed that injury severity (HR 1.41, 95% CI 1.03 -1.92, p = 0.03) and 24-hour total transfused PRBC volume (HR 1.01, 95% CI 1.00 -1.02, p = 0.001) were associated with development of IC. Conclusions: Enhanced understanding of the mechanisms that contribute to immune alterations after trauma and blood component transfusion may provide clinicians with the ability to individualize patient management and reduce complications to optimize patient outcomes.Learning Objectives: Hypertonic saline (HTS) is commonly used for hyperosmolar therapy in patients with traumatic brain injury (TBI) for intracranial hypertension. Whether hypernatremia is associated with increased renal excretion of sodium and increased urine sodium (uNa) concentrations is unknown. We evaluated uNa concentrations to examine whether a correlation between serum Na (sNa) concentrations exists in relation to uNa concentrations. Methods: Patients who suffered TBI, received HTS therapy, and had uNa concentrations measured were identified and charts were reviewed. Data collection included patient demographics, dose and duration of HTS therapy, sNa concentrations, and uNa concentrations. Correlations between the uNa closest to HTS discontinuation and the change in sNa 12-24 hr and 24-48 hr post-HTS were evaluated. Continuous variables reported as median [IQR 25:75]. The degree of correlation was analyzed using Spearman rho with a level of significance ≤ 0.05. Results: 31 patients (47[27:60] yr, 84% male, ISS 29[25:35], GCS 8[3:13]) were included in the analysis. The last uNa collected 6:50[5:54: 9:23] hr before HTS discontinuation was 166[127:249] mEq/L, and the last sNa before HTS discontinuation was 146[143:152] mEq/L. The change in sNa 12-24 hr (18:15[16:16 19:20] hr) after HTS discontinuation was significantly correlated with the uNa concentration (r=-0.59, p<0.001). This trend persisted in 26 of the 31 patients who had sNa collected 41:30 [39:00: 42:28] hr after HTS was discontinued (r=-0.29, p=0.148). There was a trend toward an association between the average HTS infusion rate (mEq/hr) to the uNa closest to HTS discontinuation (r=0.34, p=.076). No correlation was found between sCr closest to HTS discontinuation and uNa concentration. Conclusions: The degree of change in sNa concentrations following discontinuation of HTS is correlated with uNa concentrations. Increased renal excretion of Na during HTS therapy may result in higher HTS infusion needs and greater decreases in sNa and hyponatremia following discontinuation of HTS infusions.

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