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Effects of thoracic nerve block on perioperative lung injury, immune function, and recovery after thoracic surgery
Wei Zhang1, Xuhui Cong1, Liyuan Zhang1
1Department of Anesthesiology and Perioperative Medicine, Center for Clinical Single Cell Biomedicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, P. R. China.
Background:
To investigate the effects of thoracic nerve block on perioperative lung injury, immune function, and recovery after thoracic surgery METHODS: A total of 120 patients with lung cancer were randomly allocated into three groups: general anesthesia group (GAL group), thoracic paravertebral nerve block (TPVB) combined with general anesthesia (TPL group), and TPVB (with paravertebral dexmedetomidine) combined with general anesthesia group (TDL group); 120 patients with esophageal cancer were randomly allocated into three groups: general anesthesia group (GAE group), TPVB combined with general anesthesia group (TPE group), and thoracic epidural block combined with general anesthesia group (TEE group). Lung injury and immune function were evaluated. Hemodynamic changes, early recovery in post-anesthesia care unit, pain, 6-min walking test (6MWT), drug consumption, and life quality were also observed. The duration in the PACU of patients was retrospectively analyzed. The effect of dexmedetomidine on lung injury was established in vitro.
Results:
The lung injury, including injury scores, apoptosis, and inflammation, were decreased in the TDL group compared with the GAL group and TPL group. The ratio of CD4+ /CD8+ cells at the end of surgery was higher in the TPE group than in the GAE group. More stable hemodynamic was found in TPL group and TPE group. Acute pain was alleviated and the 6MWT was enhanced by TPVB with or without dexmedetomidine. Anesthetic consumption was decreased by thoracic nerve block.
Conclusions:
Thoracic nerve block, especially TPVB with or without paravertebral dexmedetomidine, can enhance recovery after thoracic surgery. Protection against independent lung injury and cellular immune dysfunction may be a potential mechanism.
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