Perioperative Complications in Swan Neck Deformity Repair Case Report

Background

Excessive vagal stimulation in the intraoperative and perioperative periods can lead to bradycardia, asystole, and death. Painful stimulus or excessive pressure on the vagus nerve can lead to bradycardia. Increased stretch from a mechanical standpoint can also lead to more vagal nerve firing and input.

Case Summary

This case investigates the disease process of a 69-year-old female who presented to the surgical team following multiple failed conservative treatments for cervical chin on chest spinal deformity, requiring three months of hospitalization. Given the expected airway edema and swallowing dysfunction, surgical risks were high, and the patient was informed of potential complications. She consented for surgery and was educated on risks and benefits, including the possibility of requiring a tracheostomy and a Percutaneous Endoscopic Gastrostomy placement. The patient underwent a closed reduction of cervicothoracic spinal deformity, anterior cervical C4-5 osteotomy, C4-C7 corpectomies, C3-T1 anterior cervical fusion, posterior cervical C5-6 osteotomy, C2-T6 laminectomies, posterior cervical instrumented fusion C2-T8, and left L4 hemilaminectomy for placement of drains. On post op day 6, the patient requested PEG and tracheotomy placement. On post op day 10, the patient compounded a necrotizing soft tissue infection of the anterior neck that required emergent washout. The wound displayed profuse black fluid upon incision which along with imaging and crepitus on physical exam led to the diagnosis of acute necrotizing fasciitis. The patient also acquired persistent cervical esophageal perforation with a non-healed fistula and was taken to the OR two days later for tracheotomy revision and esophageal perforation repair. On post op day 20, the patient developed a neck hematoma requiring OR incision and drainage. On post op day 30, the patient was being turned by nursing to clean cervical wounds and became unresponsive. The patients became bradycardic, then developed asystole with no palpable pulses. After a few seconds, telemetry showed sinus rhythm and vitals became stable. Cardiology was consulted and attributed the patient’s episodes of asystole to pressure on the carotid sinus causing stimulation of the vagus nerve. The care team was instructed to minimize turning the patient to avoid further asystole. Local anesthesia was advised for future procedures. With an arrhythmia lasting longer than 90 seconds, pacemaker placement was indicated and performed.

Discussion

The interprofessional team effort allowed us to quickly identify the cause and treatment, which were vagal nerve compression and pacemaker placement, respectively. There are several explanations as to what contributed to the vagal stimulation. These include anatomical reconstruction, postoperative infection, neck hematoma, esophageal perforation, or mechanical ventilation stimulation. These may have caused vagal nerve stretching, causing increased vagal sensitivity. Above all, the increased vagal stimulation mostly occurred due to the drastic change in the patient’s anatomy, going from an extreme hyper flexed cervical position to hyperextension. This causes stretching and pulling on the structures in that region, which includes the vagus nerve. As anesthesia providers, it is crucial to recognize these possible complications and be able to adapt to care for these patients inside and outside of the operating room.