Effects of Yunanan Baiyao adjunct therapy on postoperative recovery and clinical prognosis of patients with traumatic brain injury: A randomized controlled trial

Background: Effective therapies are needed to prevent the secondary injury and poor prognosis associated with emergency craniotomy of traumatic brain injury (TBI). Hypothesis/Purpose: The wound-healing medicine Yunnan Baiyao (YB) and Xingnaojing (XNJ) adjunct-therapy may improve the outcome of orthodox mono-therapy (OT). Study design: Randomized controlled trial. Methods: Eighty patients with moderate-to-severe TBI received emergency craniotomy (within 12 h after TBI) at the Chinese PLA General Hospital before being randomly assigned to 4 different treatments (n = 20) for 7 days: 1) OT; 2) OT+XNJ (i.v. 20 ml/daily); 3) OT+low dose-YB (oral, 1,000 mg/day); 4) OT+high dose-YB, 2,000 mg/day). Results: GCS score was improved more quickly and became significantly higher in XNJ, L-YB, h-YB groups than in OT group (p<0.01). Serum S100B peaked higher but declined more slowly in OT group than in other groups (p<0.01). On postoperative Day 7, S100B was 20% below baseline in YB and XNJ groups but remained 19% above baseline in OT group which also lost 38% of superoxide dismutase (SOD) activity on Day 3 and recovered 69% of SOD on Day 7 whereas the YB and XNJ groups lost 16%similar to 23% of SOD activity on Day 3 and recovered 92%similar to 99% of SOD on Day 7 (p<0.01). Clinical prognosis (Glasgow Outcome Scale and Karnofsky Performance Scale) were significantly better (25%similar to 30%) in the XNJ, L-YB and h-YB groups than in OT group 3 months post-surgery and were correlated with serum S100B and SOD. Conclusions: YB and XNJ adjunct therapies improved postoperative recovery and clinical prognosis in patients with moderate-to-severe TBI partly through divergent regulation of S100B and SOD pathways.

Automated summary

Adjunct therapies with YB and XNJ can improve postoperative recovery and clinical prognosis in patients with moderate-to-severe TBI, possibly through divergent regulation of S100B and SOD pathways.