Background context: Previous reports have shown that 15% of patients who undergo sequential anterior, then posterior, surgical corrections for spinal deformities demonstrate evidence of acute lung injury. By analyzing the bronchoalveolar lavage (BAL) fluid from these patients for evidence of acute inflammation, we might gain some insight into the etiology of this acute lung injury.
Purpose: To elucidate the etiology of acute lung injury after corrective surgery for adult spinal deformities.
Study design/setting: Fifteen adult patients with scoliosis scheduled for elective sequential anterior then posterior corrective (A/P) spinal deformity surgery.
Patient sample: Consecutive adult patients with scoliosis scheduled for elective corrective surgery with the author (OBA).
Outcome measures: Patients were assessed for postoperative respiratory complications by oxygen requirements, continued mechanical ventilation, and radiological evidence of diffuse bilateral interstitial or alveolar infiltrates. An acute pulmonary inflammatory response included the presence of inflammatory cells and elevated cytokines in BAL fluid.
Methods: BAL were performed after induction of anesthesia but before surgery, at the completion of surgery, and on the morning after surgery with the patient still intubated. BAL fluid was analyzed for inflammatory cells and cytokine interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) levels. Patients were assessed postoperatively for increased pulmonary vascular resistance, radiological evidence of diffuse bilateral alveolar infiltrates, and the requirement for ventilatory support beyond the first postoperative day (POD1).
Results: The cell counts of BAL fluid demonstrated significant increases in neutrophils, lymphocytes, and lipid laden macrophages (LLMAC) with surgery. The concentration of the cytokines IL-6 and TNF-alpha also increased with surgery. The elevations in BAL inflammatory cells and cytokine levels correlated positively with increased pulmonary vascular resistance and the requirement for mechanical ventilation.
Conclusions: After A/P spine fusions, patients have evidence of an acute inflammatory pulmonary injury. Several etiologies exist for this finding, including blood and fluid infusions, direct trauma to the lung, a systemic inflammatory response, and the embolization of fat and bone-marrow debris. The presence of LLMAC in the lungs of these patients and the finding that the patient with the requirement for the longest ventilatory support also had the highest BAL LLMAC count, suggest that the embolization of fat and bone debris released from the spine during surgery may be at least partially responsible for the lung injury. Further studies on the mechanism of lung injury during this procedure are warranted.