The use of 23.4% hypertonic saline for the management of elevated intracranial pressure in patients with severe traumatic brain injury: a pilot study.

BACKGROUND: Oncotic agents are a therapeutic mainstay for the management of intracranial hypertension. Both mannitol and varied concentrations of hypertonic saline (HTS) have been shown to be effective at reducing elevated intracranial pressure (ICP). We compared the safety and efficacy of 23.4% HTS to mannitol for acute management of elevated ICP after traumatic brain injury (TBI). METHODS: After approval from our institutional review board, the records of patients admitted with severe TBI who received mannitol or HTS were reviewed. Demographic and physiologic data were recorded. ICP, cerebral perfusion pressure, reduction of ICP after dose administration, serum sodium, osmolality, and magnitude of dose response during the subsequent 60 minutes were analyzed. Efficacy was determined by comparison of proportion of patients with any response and mean change in ICP after dosing with either agent. Safety was determined by recording any new postinfusion electrolyte or neurologic anomalies. Data were compared using chi2 test, accepting p < 0.05 as significant. RESULTS: Twenty-two patients with severe TBI received 210 doses of either mannitol or HTS. All patients suffered severe blunt injury (mean Injury Severity Score 28 +/- 11). HTS patients had a significantly higher ICP at the initiation of therapy than that of mannitol group (30.7 +/- 7.94 mm Hg vs. 28.3 +/- 8.07 mm Hg, respectively). There was no difference in initial cerebral perfusion pressure. Mean ICP reduction in the hour after administration of 102 doses of mannitol and 108 doses of HTS was greater for patients receiving HTS (9.3 +/- 7.37 mm Hg vs. 6.4 +/- 6.57 mm Hg, respectively; p = 0.0028, chi2). More patients responded to HTS (92.6% HTS vs. 74% mannitol; p = 0.0002, chi2). There was no significant difference between groups in the duration of ICP reduction after dose administration (4.1 hours vs. 3.8 hours, respectively). No adverse events after administration of either agent were identified. CONCLUSION: Based on this retrospective analysis, 23.4% HTS is more efficacious than mannitol in reducing ICP. If these results are confirmed in a prospective, randomized study, 23.4% HTS may become the agent of choice for the management of elevated ICP after TBI.

Split cord malformation with associated type IV spinal cord perimedullary arteriovenous fistula. Case report.

The authors describe the case of a 62-year-old woman with a Type II split cord malformation (SCM). At the initial time of workup, the authors observed an associated Klippel-Feil deformity at the level of the SCM and a low-lying conus medullaris; however, they discovered an associated Type IV perimedullary spinal cord arteriovenous fistula (AVF) only after the patient continued to deteriorate following a spinal cord untethering procedure. Although prominent blood vessels have been reported within the median cleft of SCMs, an angiographically and surgically proven perimedullary AVF has not previously been described. The potential coexistence of SCM and perimedullary AVF has significant clinical implications and its recognition is critically important prior to surgical treatment.

Tumor necrosis factor alpha expression and protein levels after fluid percussion injury in rats: the effect of injury severity and brain temperature.

OBJECTIVE: Tumor necrosis factor alpha (TNFalpha) is elevated in some models of traumatic brain injury (TBI). However, it is unclear how TNFalpha messenger ribonucleic acid (mRNA) expression and protein levels are affected by injury severity and posttraumatic temperature modification. This study determined the regional and temporal profile of TNFalpha levels after moderate and severe TBI and assessed the effects of posttraumatic hypothermia or hyperthermia on this proinflammatory cytokine. METHODS: Adult male Sprague-Dawley rats were subjected to sham procedures (no injury), moderate fluid-percussion TBI (1.8-2.2 atm), or severe fluid-percussion TBI (2.4-2.6 atm). After 1 to 72 hours of survival, animals were killed, and brain samples, cerebrospinal fluid, and serum were harvested for enzyme-linked immunosorbent assay quantification of TNFalpha levels. In a subsequent study, a 3-hour period of posttraumatic hypothermia (33 degrees C) or hyperthermia (39.5 degrees C) was applied, followed by immediate killing and cytokine assay. Another group was subjected to moderate TBI (1.8-2.2 atm), followed by killing at 15 minutes or at 1, 3, or 24 hours for TNFalpha reverse transcriptase-polymerase chain reaction analysis. RESULTS: A significant increase in TNFalpha mRNA and protein levels in cellular lysates of injured cortex and ipsilateral hippocampus was noted by 1 hour after TBI; it was sustained to 3 hours, followed by a rapid decline. Increased injury severity was associated with increased protein levels at remote injury sites and in the injured cerebral cortex at 72 hours. Posttraumatic hypothermia significantly reduced TNFalpha mRNA expression in the hippocampus compared with that in normothermic rats. In contrast, no temperature effects on TNFalpha protein levels were documented. CONCLUSION: Rapid and marked increase in TNFalpha mRNA expression and protein levels follows moderate and severe TBI. Injury severity and posttraumatic temperature play a modest but significant role on TNFalpha expression and protein levels. These findings suggest that the effects of posttraumatic temperature on histopathological and behavioral outcome primarily may involve secondary mediators that do not operate directly through their effect on TNFalpha.