Lobar Necrosis from Pulmonary Embolism

Ramiro Fernandez ,  Jonathan M. Tomasko ,  Daphne Edgren, et al

Am J Respir Crit Care Med 2017; 195: 685-686

A 63-year-old male heart transplant recipient with recurrent lower extremity deep vein thrombosis, receiving warfarin, with chronically reduced glomerular filtration rate (30 ml/min), presented with worsening cough and dyspnea. Laboratory testing revealed normal blood cell counts, mildly elevated C-reactive protein, and international normalized ratio of 1.8. Subsequent radiograph revealed a middle lobe cavity (Figure 1A). Bronchoalveolar fluid cultures revealed Candida albicans, but antifungal therapy cleared the organism after 2 weeks. Nevertheless, the cough persisted, and the cavity progressed over the following 6 weeks (Figure 1B). Given the uncertain etiology of the cavity and persistence of symptoms, thoracoscopic middle lobectomy was performed, during which the majority of the lobe was found to be necrotic and filled with ∼10 ml of thick brown liquefied debris. Major and minor fissures were “complete,” preventing any collateral blood supply to the middle lobe. Gross and histological examination revealed an occlusive thrombus in the pulmonary artery branch to the middle lobe. The majority of the lobar parenchyma had undergone necrosis, leading to the cavity formation, and the walls of the cavity adjacent to the minor and major fissures revealed microscopic features of alveolar damage/hemorrhage, septal thickening, and neutrophil infiltration (Figure 1C–1E), suggesting ongoing ischemic damage. Bacterial, viral, mycobacterial, and fungal cultures of the lobar tissue, as well as bronchoalveolar lavage fluid and cavity debris, were negative. Postoperatively, computed tomography pulmonary angiogram confirmed new bilateral pulmonary emboli (Figure 1F) but preserved right bronchial artery. Pulmonary infarction from segmental artery occlusion can be associated with cavitation, especially in the setting of underlying infection in up to 10% of cases (1–5), but complete lobar necrosis does not usually occur. Because the middle lobe is usually supplied by only one branch of the pulmonary artery, it may be uniquely susceptible to lobar necrosis in the setting of an occlusive thrombus within the middle lobe artery. This case, therefore, highlights the importance of pulmonary circulation in maintaining viability of lung parenchyma.

一名63岁男性心脏移植患者因反复出现下肢DVT接受华法林抗凝治疗，且有慢性肾小球滤过率降低(30 ml/min)。患者因咳嗽及呼吸困难加重就诊。实验室检查发现血常规正常，C反应蛋白轻度升高，国际标准化比值1.8。影像学检查发现中叶空洞(Figure 1A)。肺泡支气管灌洗液培养为白色念珠菌，经过抗真菌药物治疗2周后培养阴性。然而，患者仍持续咳嗽，随后6周内空洞呈进展表现(Figure 1B)。由于空洞及临床症状病因不明，进行了胸腔镜中叶切除术，术中发现，大部份中叶呈坏死表现，约有10 ml褐色浓稠的液化坏死组织。叶间裂完整，中叶没有任何侧支循环。标本的大体及组织学检查发现中叶的肺动脉分支有血栓阻塞。肺叶实质大多已经坏死，导致空洞形成，邻近叶间裂的空洞壁在显微镜下呈肺泡损伤／出血，间隔增厚，中性粒细胞浸润(Figure 1C–1E)，提示缺血性损伤持续进展。肺叶组织、肺泡支气管灌洗液及空洞坏死组织的细菌、病毒、支原体及真菌培养均为阴性。术后肺动脉CT造影确诊新发双侧肺栓塞(Figure 1F)，但右侧支气管动脉未受累。肺段动脉阻塞引起的肺梗死可伴随空洞形成，尤其是合并感染时可有多达10%的病例形成空洞，但通常不会发生肺叶完全坏死。由于中叶常常由肺动脉的单一分支供血，因而中叶动脉发生血栓阻塞时更容易出现肺叶坏死。因此，本例患者说明了肺循环对于维持肺实质活力的重要性。