Spontaneous Massive Hemothorax As a Complication of Necrotizing
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Jung et al. J Med Case Reports (2021) 15:444 https://doi.org/10.1186/s13256-021-03032-9 CASE REPORT Open Access Spontaneous massive hemothorax as a complication of necrotizing pneumonia in a patient with severe acute respiratory syndrome coronavirus 2 induced acute respiratory distress syndrome: a case report Carolin Jung* , Hans‑Joerg Gillmann, Thomas Stueber and Lukas Hinken Abstract Background: We present an unusual bleeding complication in a patient with severe acute respiratory distress syn‑ drome in coronavirus disease 2019. Case presentation: The patient, a 63‑year‑old Caucasian man, received venovenous extracorporeal membrane oxy‑ genation support after rapid deterioration of lung function on day 6 after admission to hospital. After initial stabiliza‑ tion on lung protective ventilation and prone positioning, he started to develop mild bleeding complications until he went into occult profound hemorrhagic shock. Causative was a massive hemothorax of the right hemithorax with mediastinal shifting due to spontaneous bleeding from a pulmonal artery in a heavily remodeled right inferior lobe. Histopathological examination of the resected tissue showed signs of an organizing fbrinous pneumonia with focal parenchyma necrosis. After surviving a massive bleeding event caused by necrotizing pneumonia, the patient made a swift recovery and was discharged to rehabilitation 31 days after initial hospital admission. Conclusions: The combination of severely elevated infammatory markers and pulmonary hemorrhage should arouse suspicion of necrotizing pneumonia. In necrotizing pneumonia, the possibility of severe intrathoracic bleeding complications should be kept in mind if it comes to sudden deterioration of the patient. Keywords: COVID‑19, Necrotizing pneumonia, Hemothorax, ARDS, Case report Background pulmonary hemorrhage and severely elevated infamma- Pulmonary hemorrhage is a recurring fnding in patients tory markers and comes with a poor prognosis [2, 3]. It with severe acute respiratory syndrome coronavirus 2 can induce profound parenchyma damage and lead to (SARS-CoV-2) infections and has been reported in 17% severe complications such as spontaneous hemothorax. of cases with severe coronavirus disease 2019 (COVID- Awareness of the possibility of this complication can lead 19) on extracorporeal support [1]. Necrotizing pneu- to timely diagnostic and therapy. monia is strongly associated with the occurrence of We report a case of spontaneous hemothorax as a complication of necrotizing pneumonia in a patient with severe COVID-19, that took a favorable course after sur- *Correspondence: jung.carolin@mh‑hannover.de gical resection of the necrotic tissue. Department of Anaesthesiology and Intensive Care Medicine, Medical School Hannover, Carl‑Neuberg‑Str. 1, 30625 Hannover, Germany © The Author(s) 2021. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http:// creat iveco mmons. org/ licen ses/ by/4. 0/. The Creative Commons Public Domain Dedication waiver (http:// creat iveco mmons. org/ publi cdoma in/ zero/1. 0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Jung et al. J Med Case Reports (2021) 15:444 Page 2 of 9 Fig. 1 Timeline Case presentation white blood cell count 20,400/µl (normal range 3600– A 63-year-old Caucasian male with a background of arte- 10,000/µl), CRP 316.5 mg/l (normal range < 5 mg/l), IL-6 rial hypertension and mild obesity (BMI 30.5 kg/m2) was 420 ng/l (normal range < 7 ng/l), soluble IL-2-receptor admitted to hospital with dyspnea under COVID-19. He 1549 kU/l (normal range 223–710 kU/l), ferritin 916 µg/l initially tested positive for SARS-CoV-2 via a polymer- (normal range 27–365 µg/l), and fbrinogen > 9 g/l (nor- ase chain reaction swab conducted in the ambulatory mal range 1.8–3.5 g/l). He showed lymphocytopenia with setting. When he arrived at the primary care hospital, a cell count of 470/µl (2.3%). SARS-CoV-2-PCR diag- he displayed a reduced general condition. Admission nostic was repeated from tracheal aspirate on arrival at observations revealed: blood pressure 100/40 mmHg, our hospital and remained positive (cycle threshold 25). heart rate 115 beats/minute, peripheral oxygen satura- His medical treatment taken at home included valsar- tion 71%, body temperature 40 °C. His breathing noises tan, bisoprolol, amlodipine, and chlorthalidone as well as were reduced, and there were rattling noises over his atorvastatin and mirtazapine. Te patient did not smoke lungs bilaterally. He was cooperative and orientated, and or consume alcohol regularly. He is married and has showed no focal neurological defcit. His renal function been working as a specialist in internal medicine until his markers were elevated [creatinine 1.66 mg/dl, estimated recent retirement. glomerular fltration rate (eGFR) 45 ml/minute], and the He received therapeutic anticoagulation with unfrac- liver function markers were in the normal range. He was tionated heparin (UFH). Monitoring of anticoagulation admitted to intensive care unit (ICU) 5 days later owing was done by measurement of activated partial throm- to worsening of respiratory symptoms. After 1 day of boplastin time (aPTT) every 6 hours with a target of noninvasive ventilation, the patient decompensated into 50–60 seconds. Preexisting treatment with acetylsalicylic global respiratory insufciency, and endotracheal intuba- acid was continued. Sedation proved to be difcult even tion was required. Because of persistent global respira- under a multimodal intravenous sedative regime. First tory insufciency under exhausted conservative therapy, signs of pulmonary hemorrhage were noticed on day 11. the patient was transferred to our university hospital for Because of a suspected hyperinfammatory syndrome [4], venovenous extracorporeal support (vvECMO) in severe dosage of dexamethasone was increased from 6 to 18 mg acute respiratory distress syndrome (ARDS). Computed per day. For a detailed depiction of events, see timeline tomographic (CT) imaging before transferal showed dif- (Fig. 1 and Additional fle 1). fuse bilateral ground-glass opacities. On admission at Over the following days, the patient continuously pro- our hospital, his acute phase reactants were elevated: duced extensive aqueous and slightly bloody discolored Jung et al. J Med Case Reports (2021) 15:444 Page 3 of 9 tracheal secretion. Chest x-ray on day 15 in supine posi- acid. Te patient had a normal platelet count until the day tion showed a progressive extensive opacity projecting to he developed hemorrhagic shock. At the time of the mas- the right inferior lobe (Fig. 2). Tis corresponded with a sive bleeding event, aPTT ranged between 38 and 50 sec- heavy decline in pulmonary gas exchange. A diagnostic onds. Occurrence of bloody discolored tracheal secretion bronchoscopy on the same day revealed hemorrhagic was thought to be the result of a possible aspiration event pneumonia with extremely vulnerable mucosa and plenty of blood in the hypopharynx due to nasal bleeding. Since of viscous mucus as well as extensive coagulum in seg- the bloody discolored tracheal secretion remained per- ment 9. After removal of the coagulum, gas exchange sistent and was of very aqueous consistence, the working improved at frst. Because pulmonary hemorrhage diagnosis changed to lung edema. Te patient required remained persistent and gas exchange declined yet again large amounts of sedatives and was repeatedly dishar- alarmingly, the patient underwent a second bronchos- monic to the respirator, so that we suspected a self- copy on the following day. Here, another extensive coag- inficted lung injury as causal to the potential lung edema. ulum in right lung segment nine was cautiously and, due On day 18, when the patient was in manifest shock, to high risk of bleeding, incompletely recovered. Depend- serum transaminases were severely elevated, indicative of ence of extracorporeal support remained very high, and a severe liver damage. Renal parameters displayed acute the patient became increasingly unstable. On day 17, the kidney injury KDIGO stage 2. Focused assessment with patient developed profound hemorrhagic shock (Table 1) sonography revealed a large pleural efusion in the right without evident source of bleeding. Te patient required hemithorax; transthoracic echocardiography led to the extensive doses of norepinephrine, epinephrine, and conclusion of hypovolemic shock. After stabilization of vasopressin as well as a massive transfusion of red blood the patient, a CT scan of head, thorax, abdomen, and pel- cells, plasma, and platelets for stabilization. At the same vis was done, revealing a massive hemothorax in the right time, a severe acute decrease of pulmonary compliance hemithorax with complete compression of the ipsilateral