Effects of hypertonic saline on intracranial pressure and cerebral autoregulation in pediatric traumatic brain injury

Abstract

OBJECTIVE Hypertonic saline (HTS) is commonly used in children to lower intracranial pressure (ICP) after severe traumatic brain injury (sTBI). While ICP and cerebral perfusion pressure (CPP) correlate moderately to TBI outcome, indices of cerebrovascular autoregulation enhance the correlation of neuromonitoring data to neurological outcome. In this study, the authors sought to investigate the effect of HTS administration on ICP, CPP, and autoregulation in pediatric patients with sTBI. METHODS Twenty-eight pediatric patients with sTBI who were intubated and sedated were included. Blood pressure and ICP were actively managed according to the autoregulation index PRx (pressure relativity index to determine and maintain an optimal CPP [CPPopt]). In cases in which ICP was continuously > 20 mm Hg despite all other measures to decrease it, an infusion of 3% HTS was administered. The monitoring data of the first 6 hours after HTS administration were analyzed. The Glasgow Outcome Scale (GOS) score at the 3-month follow-up was used as the primary outcome measure, and patients were dichotomized into favorable (GOS score 4 or 5) and unfavorable (GOS score 1–3) groups. RESULTS The mean dose of HTS was 40 ml 3% NaCl. No significant difference in ICP and PRx was seen between groups at the HTS administration. ICP was lowered significantly in all children, with the effect lasting as long as 6 hours. The lowering of ICP was significantly greater and longer in children with a favorable outcome (p < 0.001); only this group showed significant improvement of autoregulatory capacity (p = 0.048). A newly established HTS response index clearly separated the outcome groups. CONCLUSIONS HTS significantly lowered ICP in all children after sTBI. This effect was significantly greater and longer-lasting in children with a favorable outcome. Moreover, HTS administration restored disturbed autoregulation only in the favorable outcome group. This highlights the role of a “rescuable” autoregulation regarding outcome, which might be a possible indicator of injury severity. The effect of HTS on autoregulation and other possible mechanisms should be further investigated.

Cerebral Autoregulation-guided Management of Adult and Pediatric Traumatic Brain Injury

“…Lung-protective ventilation, 36 early orthostatic exercises, 37 and propofol/vasopressor use 38,39 have no detrimental effect on CA. Short-term hyperventilation (PaCO 2 : 37 mm Hg→ 28 mm Hg) may improve dynamic CA, 40 hypertonic (20%) saline may or may not improve CA status, 41,42 and decompressive craniectomy may either have no effect or revert impaired CA to an intact CA pattern, primarily due to its ICP-lowering effect. 43 Unanswered Questions/Future Research Future studies may examine the effect of CA status and provocative testing on brain-tissue oxygenation and whether an intervention bundle may allow clinicians to preserve and/or reverse CA status.…”

“…Lung-protective ventilation, 36 early orthostatic exercises, 37 and propofol/vasopressor use 38,39 have no detrimental effect on CA. Short-term hyperventilation (PaCO 2 : 37 mm Hg→ 28 mm Hg) may improve dynamic CA, 40 hypertonic (20%) saline may or may not improve CA status, 41,42 and decompressive craniectomy may either have no effect or revert impaired CA to an intact CA pattern, primarily due to its ICP-lowering effect 43 …”

Approaches to neuroprotection in pediatric neurocritical care

“…A recent comparative effectiveness study of pediatric TBI patients demonstrated bolus dosing of hypertonic saline to be superior to mannitol in reduction of intracranial hypertension[ 68 ]. Some evidence suggests that hyperosmolar therapy is more likely to be effective in reducing intracranial hypertension when there is evidence of efficient cerebrovascular pressure reactivity (CVPR)[ 69 - 71 ]. Emerging research has demonstrated several biomarkers that target the blood-brain barrier or receptors of aquaporin-4 or vasopressin V1a to mitigate cerebral edema, although these are not yet standard treatment targets in clinical care[ 72 ].…”