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Background Mannitol and hypertonic saline (HTS) are used as boluses during episodes of raised intracranial pressure (ICP) in severe traumatic brain injury (TBI). We recently demonstrated that ICP reduction and neurological outcomes are similar with mannitol and HTS in TBI. In the current post hoc analysis, we hypothesized that this lack of difference between mannitol and HTS is due to increased urinary sodium losses after HTS. Methods In this post hoc analysis of our earlier randomized controlled trial, we analyzed serum and urine osmolarity and sodium levels in 38 patients with severe TBI over 6 days. Equiosmolar boluses of mannitol and HTS were administered whenever ICP increased above 20 mm Hg. Seven hundred sixty samples each of serum sodium, urine sodium, serum osmolarity, and urine osmolarity were analyzed during this period. Results Three hundred and one and 187 boluses of mannitol and HTS, respectively, were required to maintain ICP below 20 mm Hg. The urinary osmolarity was similar between mannitol and HTS groups (p = 0.63). The urinary sodium excretion was significantly higher in HTS group compared with mannitol group (p = 0.002). Serum sodium and osmolarity values were similar between mannitol and HTS groups (p = 0.16 and 0.31, respectively). There was no difference in the mean ICP between the groups (p = 0.31). Conclusion Increased urinary sodium loss after HTS contributes to its lack of superiority over mannitol in controlling raised ICP.

journal of neuroanaesthesiology and critical care

Urinary Sodium Loss following Hypertonic Saline Administration Curtails its Superior Osmolar Effect in Comparison to Mannitol in Severe Traumatic Brain Injury: A Secondary Analysis of a Randomized Controlled Trial