A 75-year-old male patient was admitted to Zhejiang Provincial People's Hospital on 23 November 2018 after two-week-history of post-exercise dyspnea and chest pain. Physical examination revealed decreased breath sound, increased tactile fremitus on the affected side, and dullness to percussion of the left lung. Chest computed tomography (CT) showed diffuse thickening and calcification of the pleura on both sides, pleural effusion and atelectasis on the left side (Figure 1A and B). After hospitalization, the patient received a thoracentesis on November 26, 2018. The pleural fluid was bloody exudate, and no tumor cells were found in the exfoliated cells of the pleural fluid sample. According to the imaging findings, we tracked the patient's occupational history and learned that the patient had a history of close contact with asbestos for 30 years. The diagnosis of pleural mesothelioma needs to be ruled out clinically, and it is planned to be transferred to surgery for open pleural biopsy. At the same time, laboratory examination revealed elevated plasma D-dimer (26190Ug/L), combined with the patient's chest pain, dyspnea symptoms, and a large amount of pleural effusion, the possibility of pulmonary embolism should be considered. Then, the computed tomography pulmonary angiography (CTPA) was performed for the patient, and the results showed that there was embolism in the right pulmonary artery branch (Figure 2). After the diagnosis of pulmonary embolism, we immediately used anticoagulant drugs for the patient. Because anticoagulants are easy to cause massive hemorrhage, no open pleural biopsy was performed. After anticoagulation therapy, the patient's symptoms of pleural effusion and dyspnea were improved and the patient discharged on December 18, 2018.
However, after being discharged from the hospital, the patient was still admitted to the hospital several times due to chest pain and dyspnea, and the reexamined chest CT still showed a large amount of pleural effusion on the left side (Figure 3A and B). When he was hospitalized again on July 8, 2019, there was no obvious abnormality in plasma D-dimer and CTPA, which ruled out the possibility of recurrent pulmonary embolism. We also considered the possibility of pneumonia and tuberculous pleurisy, but repeated pleural effusion and sputum culture did not show any positive results and there was no evidence for tuberculosis. Because of the long-term bloody pleural effusion, the possibility of lung cancer is also considered. The patient's pleural fluid was sent for pathological examination for many times, but no tumor cells were found. PET-CT examination showed diffuse thickening of the bilateral pleura with calcification, mainly on the left side. FDG metabolism was increased, and malignant tumors were considered (Figure 4). We consider that this patient may have malignant mesothelioma. Later, the patient underwent an ultrasound-guided pleural biopsy, and the pathological examination revealed fibroblast-like spindle cells arranged in bundles or chaotic shapes (Figure 5A and B). The results of immunohistochemistry were: CK(Pan)(+), WT1(+), GATA3(+), P63(-), TTF-1(-), EMA(-), CD117(-), DOG1(-), Calretinin(-), CK5/6(-), CD34(-), ERG(-), SMA(-), Desmin(-), S100(-), MiTF(-), HMB45(Melanoma)(-), MyoD1(-), Caldesmon(-), D2-40(-), CEA(-), Vimentin(-) (Figure 6). Combined with the above examination results, the final diagnosis was sarcomatoid pleural mesothelioma. However, two days later, the patient suddenly developed a coma, facial cyanosis, and sudden cardiac arrest. And the blood pressure, oxygen saturation cannot be measured at that time. We consider that the cause of cardiac arrest may be an acute myocardial infarction or acute pulmonary embolism. After tracheal intubation, electric defibrillation and chest compression, the patient discharged voluntarily. The patient died after being discharged from the hospital 2 days later.
Mediastinal windows of computed tomography (A and B) confirm the previously noted bilateral pleural thickening, calcification. There is associated left lobe Pleural effusion and atelectasis.