Ruoyu Zhang1, Kerstin Schwabe2,3, Marcus Krüger4, Axel Haverich4, Joachim K Krauss2,3, Mesbah Alam2. 1. Department of Thoracic Surgery, Center for Pneumology and Thoracic Surgery, Schillerhoehe Hospital, Gerlingen, Germany. 2. Section of Neurosurgery, Department of Surgery, Hannover Medical School, Hannover, Germany. 3. Center for Systems Neuroscience (ZSN) Hannover, Hannover, Germany. 4. Section of Thoracic, Cardiac, Transplant and Vascular Surgery, Department of Surgery, Hannover Medical School, Hannover, Germany.
Abstract
BACKGROUND: Although intercostal nerve injury is one of the major causes for post-thoracotomy pain, the exact mechanisms are still unclear. We sought to evaluate the electro-physiological changes of intercostal nerve injury after thoracotomy in a sheep model. METHODS: Adult sheep underwent thoracotomy in the sixth intercostal space by employing diathermy to superior border of the seventh rib. In two sheep, ribs were then spread using retractor spreading for a distance of 7 cm for 30 minutes. In the third sheep, thoracotomy was followed by harvesting intercostal muscles including the neurovascular bundle adjacent to inferior edge of the sixth rib. Thereafter, ribs were spread in the same way, but with the muscle flap dangled between the blades for intercostal nerve protection (dangling muscle flap technique). The nerve conduction velocity of the intercostal nerve was recorded before and after incision of intercostal muscles, immediately and 30 minutes after retractor placement and 30 minutes after removal of the retractor. RESULTS: In the sheep undergoing conventional thoracotomy, the physiological conductivity of intercostal nerve was completely blocked immediately after retractor placement using the same stimulation intensity or even the supra-threshold intensity. The conduction block persisted for 30 minutes during the retractor placement and further 30 minutes after removal of the retractor. In contrast, intercostal nerve conduction was not impaired throughout the experiment with the dangling muscle flap technique. CONCLUSIONS: Our experiment provides electro-physiological evidence for intercostal nerve injury after thoracotomy. The injury is primarily attributed to mechanical compression caused by the rib retractor.
BACKGROUND: Although intercostal nerve injury is one of the major causes for post-thoracotomy pain, the exact mechanisms are still unclear. We sought to evaluate the electro-physiological changes of intercostal nerve injury after thoracotomy in a sheep model. METHODS: Adult sheep underwent thoracotomy in the sixth intercostal space by employing diathermy to superior border of the seventh rib. In two sheep, ribs were then spread using retractor spreading for a distance of 7 cm for 30 minutes. In the third sheep, thoracotomy was followed by harvesting intercostal muscles including the neurovascular bundle adjacent to inferior edge of the sixth rib. Thereafter, ribs were spread in the same way, but with the muscle flap dangled between the blades for intercostal nerve protection (dangling muscle flap technique). The nerve conduction velocity of the intercostal nerve was recorded before and after incision of intercostal muscles, immediately and 30 minutes after retractor placement and 30 minutes after removal of the retractor. RESULTS: In the sheep undergoing conventional thoracotomy, the physiological conductivity of intercostal nerve was completely blocked immediately after retractor placement using the same stimulation intensity or even the supra-threshold intensity. The conduction block persisted for 30 minutes during the retractor placement and further 30 minutes after removal of the retractor. In contrast, intercostal nerve conduction was not impaired throughout the experiment with the dangling muscle flap technique. CONCLUSIONS: Our experiment provides electro-physiological evidence for intercostal nerve injury after thoracotomy. The injury is primarily attributed to mechanical compression caused by the rib retractor.
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