Oto Takahiro, Rabinov Marc, Griffiths Anne P, Whitford Helen, Levvey Bronwyn J, Esmore Donald S, Williams Trevor J, Snell Gregory I
Heart and Lung Transplant Unit, The Alfred Hospital, Monash University, Melbourne, Victoria, Australia.
J Thorac Cardiovasc Surg. 2005 Nov;130(5):1446. doi: 10.1016/j.jtcvs.2005.07.025.
Primary graft failure remains a significant cause of morbidity and mortality after lung transplantation, and its mechanism is not understood. Previously 2 case reports described fatal primary graft failure due to donor-related unexpected pulmonary embolism. This study investigated the incidence, early outcome, and risk factors of unexpected pulmonary embolism in lung transplantation.
An exploratory retrograde donor lung flush before implantation to diagnose pulmonary embolism (emboli group) or no pulmonary embolism (no-emboli group) was performed in 74 of 122 consecutive lung transplantations.
The incidence of macroscopic unexpected pulmonary embolism was 38% (28% clot and 9% fat). In the emboli group, significantly decreased oxygenation (P < .05), increased pulmonary vascular resistance (P < .001), an increased proportion of opacity on chest radiograph (P = .03), prolonged intubation (P < .001) and intensive care unit stay (P < .01), and decreased 1-year survival (P = .03) were seen after transplantation. In multivariate analysis, pulmonary embolism was an independent risk factor for prolonged intubation (hazard ratio, 2.42; P < .01). In logistic regression, death due to trauma with fracture and a smoking history of more than 20 pack-years were significant donor risk factors for pulmonary embolism (adjusted odds ratio, 8.77 and 5.64; P = .02 and .04, respectively). No deleterious effects of the exploratory flush were seen.
Unexpected pulmonary embolism is relatively common, is potentially predicted by donor history (but not by arterial blood gas analysis or chest radiograph), and is associated with primary graft failure. Donor lungs with risk factors of pulmonary embolism should undergo an exploratory flush. When pulmonary embolism is diagnosed, further therapeutic strategies must be considered.
原发性移植肺功能衰竭仍然是肺移植术后发病和死亡的重要原因,其机制尚不清楚。此前有2例病例报告描述了因供体相关意外肺栓塞导致的致命性原发性移植肺功能衰竭。本研究调查了肺移植中意外肺栓塞的发生率、早期结局及危险因素。
在122例连续肺移植中的74例中,于植入前进行了探索性逆行供肺冲洗以诊断肺栓塞(栓塞组)或无肺栓塞(无栓塞组)。
肉眼可见的意外肺栓塞发生率为38%(28%为血栓,9%为脂肪)。在栓塞组中,移植后出现氧合显著下降(P <.05)、肺血管阻力增加(P <.001)、胸部X线片上不透明比例增加(P =.03)、插管时间延长(P <.001)和重症监护病房停留时间延长(P <.01),以及1年生存率降低(P =.03)。多因素分析显示,肺栓塞是插管时间延长的独立危险因素(风险比,2.42;P <.01)。在逻辑回归分析中,因创伤伴骨折死亡和吸烟史超过20包年是肺栓塞的重要供体危险因素(校正比值比分别为8.77和5.64;P分别为.02和.04)。未观察到探索性冲洗的有害影响。结论:意外肺栓塞相对常见,可通过供体病史(而非动脉血气分析或胸部X线片)进行潜在预测,且与原发性移植肺功能衰竭相关。具有肺栓塞危险因素的供肺应进行探索性冲洗。当诊断为肺栓塞时,必须考虑进一步的治疗策略。