Abbreviated thoracotomy and temporary chest closure: an application of damage control after thoracic trauma.

HYPOTHESIS: Abbreviated thoracotomy, a damage-control strategy, improves survival in patients with metabolic exhaustion. DESIGN: Case series report. SETTING: University-based, level I trauma center. PATIENTS: All patients admitted to our trauma center with severe chest trauma in whom an abbreviated thoracotomy was performed between January 1, 1994, and January 1, 1998. INTERVENTIONS: Patients in whom an abbreviated thoracotomy was performed had their life-threatening thoracic injuries treated and had temporary closure of the incision. They were then resuscitated in the intensive care unit (ICU). Definitive care of injuries and formal chest closure were performed when physiological characteristics were normalized. MAIN OUTCOME MEASURES: Survival to discharge and postoperative complications. RESULTS: Of 10 787 patients admitted to the trauma center, 196 required thoracic operations. Eleven of these 196 patients underwent abbreviated thoracotomy; all patients survived to reach the ICU. Four died in the ICU within 24 hours of injury; the remaining 7 patients survived and were discharged. Based on their Trauma and Injury Severity Score, predicted mortality for our 11 patients was 59%; our mortality was 36%. Complications after abbreviated thoracotomy were similar to those seen after standard thoracotomy. CONCLUSIONS: Abbreviated thoracotomy is a useful strategy in the treatment of severe chest trauma. Its use in situations of metabolic exhaustion or planned reexploration may increase patient survival rates by expediting transfer of the patient from the operating room to the ICU, where homeostasis can be restored.

Split tolerance induced by immunotoxin in a rhesus kidney allograft model.

BACKGROUND: Renal allografts were performed in rhesus monkeys using FN18-CRM9, a potent immunotoxin capable of depleting T cells to less than 1% of baseline levels in blood and lymph nodes, as a preparative agent. We have recently reported that animals pretreated with FN18-CRM9 1 week before transplantation without further immunosuppression had prolonged graft survival time compared with control animals, and frequently became tolerant. METHODS: This report examines the alloimmune responses of recipient monkeys to the donor, including cytotoxic T lymphocyte precursor (CTLp) frequency, mixed lymphocyte response, and antidonor IgG response. RESULTS: CTLp frequencies declined significantly (P<0.01) after FN18-CRM9 treatment and renal transplantation. This decline in CTLp was initially nonspecific, as CTLp frequencies against third-party animals also declined (P<0.01). The decrease in CTLp was maintained in five of five animals tested 6 months after transplant. However, unresponsiveness was limited to the CTL arm of the immune response as antidonor IgG was detected in four of four animals tested, and the 5-day mixed lymphocyte response stimulation index and relative response were not significantly different before and after transplant. In long-term survivors (>150 days), an increase in anti-third-party CTLp was detected 1 month after grafting with third-party skin. No change was seen in the antidonor CTLp frequency after donor skin grafting, indicating that a specific defect in the antidonor CTL response had developed. CONCLUSIONS: These data suggest that FN18-CRM9 treatment of rhesus monkeys allows the development of specific down-regulation of antidonor CTL activity in renal allograft recipients.