Pleural complications in patients with coronavirus disease 2019 (COVID-19): how to safely apply and follow-up with a chest tube during the pandemic?

OBJECTIVES: Severe acute respiratory syndrome coronavirus 2, a novel coronavirus, affects mainly the pulmonary parenchyma and produces significant morbidity and mortality. During the pandemic, several complications have been shown to be associated with coronavirus disease 2019 (COVID-19). Our goal was to present a series of patients with COVID-19 who underwent chest tube placements due to the development of pleural complications and to make suggestions for the insertion and follow-up management of the chest tube. METHODS: We retrospectively collected and analysed data on patients with laboratory-confirmed COVID-19 in our hospital between 11 March and 15 May 2020. Patients from this patient group who developed pleural complications requiring chest tube insertion were included in the study. RESULTS: A total of 542 patients who were suspected of having COVID-19 were hospitalized. The presence of severe acute respiratory syndrome coronavirus 2 was confirmed with laboratory tests in 342 patients between 11 March and 15 May 2020 in our centre. A chest tube was used in 13 (3.8%) of these patients. A high-efficiency particulate air filter mounted double-bottle technique was used to prevent viral transmission. CONCLUSIONS: In patients with COVID-19, the chest tube can be applied in cases with disease or treatment-related pleural complications. Our case series comprised a small group of patients, which is one of its limitations. Still, our main goal was to present our experience with patients with pleural complications and describe a new drainage technique to prevent viral transmission during chest tube application and follow-up.

Spontaneous pneumothorax and subpleural bullae in a patient with COVID-19: a 92-day observation.

This report describes a patient with COVID-19 who developed spontaneous pneumothorax and subpleural bullae during the course of the infection. Consecutive chest computed tomography images indicated that COVID-19-associated pneumonia had damaged the subpleural alveoli and distal bronchus. Coughing might have induced a sudden increase in intra-alveolar pressure, leading to the rupture of the subpleural alveoli and distal bronchus and resulting in spontaneous pneumothorax and subpleural bullae. At the 92-day follow-up, the pneumothorax and subpleural bullae had completely resolved, which indicated that these complications had self-limiting features.

[Clinical characteristics and therapeutic experience of case of severe highly pathogenic A/H5N1 avian influenza with bronchopleural fistula].

OBJECTIVE: To summarize the clinical characteristics and therapeutic experience of A/H5N1 infected patient with intractable bronchopleural fistula. METHOD: The data of a patient with A/H5N1 infection complicated with bronchopleural fistula was collected and analyzed. RESULTS: A 44-year-old woman with pneuminian was diagnosed as A/H5N1 infection by reverse-transcription polymerase chain reaction (RT-PCR) in laboratory from the sample of secretion of respiratory tracts. She had exposed to sick or dead poultry 3 days before development of illness. She developed acute respiratory distress syndrome 7 days after onset of sickness. After comprehensive management with antiviral agents, antibiotics, convalescent serum and invasive ventilation, her clinical condition improved and turned to stable. However, 16 days after onset of illness, her clinical situation deteriorated due to ventilator-associated pneumonia, bilateral pneumothorax and persistent right bronchopleural fistula. After partly failure of beside assist thoracoscopy to fix the pleural fistula, transbronchoscopic bronchial occlusion by autoblood was explored and the air leakage stopped soon after occlusion. Three days after the autoblood clot was expectorated out and air leak recurred. Then, bronchopleural fistula on the surface of visceral pleura was successfully blocked by biogel and OB gel through pleural cavity by fibrobronchoscopy. The patient was discharged from the hospital 99 days after onset of illness (at the 94th hospital day). CONCLUSION: Bronchopleural fistula was an intractable complication for patient with A/H5N1 infection. Occlusion operation by biogel and OB gel through bronchoscopy might be an alternative choice for fixing the bronchopleural fistula.

Isolated pleural PTLD after cardiac transplantation.

UNLABELLED: PREAMBLE: Epstein-Barr virus infection (EBV) and immunosuppression promote emergence of posttransplant lymphoproliferative disorders (PTLD) in patients undergoing organ transplantation. OBJECTIVE: We report a case of PTLD confined to the pleura. FINDINGS: The patient was a 62-year-old male who had undergone cardiac transplant in 1993 for ischemic heart disease. Seven years later, he presented with dyspnea and bilateral pleural effusions. The CT scan revealed left sided pleural base thickening. The cytology of the pleural fluid and fine needle aspirate of the pleura was both suggestive of PTLD. However, the tissue submitted for ancillary studies did not contain the diagnostic material. A clinical decision was made to withdraw immunosuppressive therapy and start rituximab. His clinical course was complicated by Pneumocystis carinii pneumonia and he died 4 months after the diagnosis of PTLD. Autopsy revealed bilateral pleural effusions with pleural nodules involving the visceral and parietal pleura of both lungs. Immunohistochemistry demonstrated B cell lineage with kappa/lambda ratio of 1. PCR studies done on the pleural nodules (postmortem specimen) revealed the presence of EBV DNA and absence of human herpes virus 8 (HHV8) DNA. In situ hybridization revealed positive staining for EBV RNA within the neoplasm. CONCLUSION: Pleural-based PTLD is rare. Cytology in conjunction with immunophenotyping and molecular studies can be useful for a definitive diagnosis. In our case, cytology sample was suggestive of PTLD. PCR studies performed on the antemortem specimen confirmed the presence of monoclonal IgH gene rearrangement, while the postmortem specimen revealed oligoclonal IgH gene rearrangement. The change from monoclonal to oligoclonal IgH gene rearrangement suggests reversion of monoclonal to polyclonal PTLD following rituximab and CHOP therapy. We also demonstrated EBV DNA and RNA in the tumor nodules, supporting EBV-induced PTLD.

Pleural posttransplantation lymphoproliferative disorder following liver transplantation.

A case of posttransplantation lymphoproliferative disorder (PTLD) involving the pleura is reported. The patient was a 57-year-old man who underwent liver transplantation 2 years prior to the development of PTLD. The PTLD was pleural-based and was first detected by radiologic studies as a pleural effusion. Transbronchial biopsy and cytologic examination of 2 pleural fluid specimens were nondiagnostic. Subsequent open-wedge biopsy revealed a monomorphic PTLD, composed of large immunoblasts with plasmacytoid differentiation. Immunohistochemical studies demonstrated B-cell lineage with expression of monotypic cytoplasmic immunoglobulin kappa light chain and CD79a, and absence of T-cell antigens. Immunohistochemical and in situ hybridization studies demonstrated Epstein-Barr virus protein and RNA, respectively. No evidence of human herpesvirus 8 DNA was detected by polymerase chain reaction. We report this case because pleural-based PTLD is rare. The diagnosis of this entity is made more difficult by the fact that PTLD is often underrepresented in pleural fluid cytology samples.

SV40, JC and BK expression in tissue, urine and blood samples from patients with malignant and nonmalignant pleural disease.

BACKGROUND: Polyomaviruses are expressed in both human tumors and immunodepressed patients. Malignant and nonmalignant pleural effusions create an environment that could favor the expression of opportunistic viral infections. We studied if SV40, JC, and BK viral DNA can be amplified from biopsies obtained from different pleural diseases. MATERIALS AND METHODS: DNA was extracted from mesotheliomas (MM), nonspecific inflammatory and tubercular pleural biopsies, blood and urinary sediments from patients with MM, and pleural effusion cytological specimens. SV40, JC and BK viral early regions were amplified by PCR and analyzed by Southern Blot hybridization with specific probes. RESULTS: SV40 was positive in 9/23 MM, 5/18 tubercular and 1/7 nonspecific inflammatory biopsies, and 5/12 pleural effusion cytological specimens. JC was positive in 2/23 MM and in 7/15 urinary sediments. All blood samples were negative and BK was also negative in all samples. CONCLUSIONS: Tissue specific factors, characteristic of MM and TB, may contribute to expression of SV40 in these diseases.