Coronavirus disease 2019 complicated by hemothorax, pneumomediastinum, pneumothorax, and subcutaneous emphysema

Introduction

Coronavirus disease 2019 (COVID-19), is being notified as the third epidemic leading to unexplained pneumonia at the end of 2019, and it is spreading to the entire globe with more than 519 million cases, and the reported mortality is nearly 6.2 million[¹]. Currently, there is not much strong evidence from randomized clinical trials to show improved outcomes in terms of mortality with regard to the various treatment options available or prophylactic treatment, and among the many available treatment options, the role of a systemic corticosteroid has been shown to improve survival in COVID-19. Unfortunately, the widespread use of glucocorticoids can lead to secondary bacterial or fungal infections[²]. COVID-19-induced viral infections can cause acute respiratory-distress syndrome and require mechanical ventilation. As the COVID-19 pandemic progresses, various uncommon presentations or complications of COVID-19 are revealed. Complications like pneumothorax, pneumomediastinum, or hemothorax are associated with COVID-19 described in the literature. Barotrauma can be a complication of mechanical ventilation and leads to the development of pneumothorax and pneumomediastinum.

We probably present the first case of COVID-19 associated with a combination of hemothorax, pneumothorax, pneumomediastinum, and subcutaneous emphysema. We have reviewed the literature to identify cases of COVID-19-associated hemothorax and their possible mechanisms.

Case report

A 22-year-old nonsmoker male with no known comorbidities was tested positive for COVID-19 following symptoms of cough and difficulty in breathing. The patient was initially admitted to a local district-dedicated COVID hospital where he received continuous positive airway-pressure support for 10 days. He was then referred to our institute because his condition was not improving. At the time of presentation, to our emergency department, the patient was having breathlessness with the following baseline vitals: heart rate 113 beat/min, blood pressure 138/89 mmHg, respiratory rate 38 rate/min, and oxygen saturation 88% on room air, and local examination revealed subcutaneous emphysema. He was initially given oxygen support with a nonrebreathing mask at the flow rate of 15 l/min, but later, he required the support of high-flow nasal cannula at 60 l/min for maintaining the SpO₂ more than 95%. The patient was comfortable and maintained an oxygen saturation of more than 95% with a respiratory rate of 30 breath/min. Initial blood investigation revealed hemoglobin 14 g/dl, total leukocyte count 12.57 × 10⁹/mm³, neutrophil-to-lymphocyte ratio 18.4, and highly elevated inflammatory markers lactate dehydrogenase 1971 U/l, ferritin 1447.9 mg/dl, C-reactive protein 29.6 mg/ml, and interleukin-6 112.5 pg/ml and D-dimer value of more than 20 µg/ml. An anteroposterior view of the chest radiograph showed bilateral pneumothorax, pneumomediastinum, and bilateral subcutaneous emphysema (Fig. 1a). Low-molecular-weight enoxaparin was given at the dose of 1 mg/kg subcutaneously twice a day. Injection dexamethasone 6 mg once daily was given for steroid coverage. After sampling blood for culture and sensitivity analysis and as per our local ICU, antibiogram-policy injection of amoxicillin and clavulanic acid 1.5-g intravenous 12 hourly and injection of azithromycin 500 mg optical density were started as empirical antibiotics. This patient in the same local district-dedicated COVID hospital received a complete dose of injection: Remedesivir 200 mg intravenously on day 1, followed by 100 mg of Remdesivir once daily for the subsequent 5 days. We added Tocilizumab 8 mg/kg on day 2 of ICU admission considering a high inflammatory marker and persistent high oxygen requirement. We gradually weaned this patient from HFNC after gradual improvement in the patient clinical condition and shifted to a nonrebreathing mask with 15 l/min in the next 3 days. He had a persistent cough that was nonproductive and relieved by cough-suppressant medications. In the next few days, he started complaining of right-sided mild chest pain that was waxing and waning with breathing movements. Blood cultures did not reveal any significant growth, but there was leukocytosis with neutrophilia. Antibiotics were upgraded to injection Piperacillin–Tazobactum 4.5-g intravenous TDS. On the 10th day after ICU admission, the chest radiograph revealed blunting of the right costophrenic angles that progressed over the coming days (Fig. 1b, c). Diagnosis of pleural effusion was made after lung ultrasound showed the collection in the right costophrenic space. We planned to put an intercostal chest drain and following the right-sided chest-drain insertion, 1200 ml of hemorrhagic fluid was removed from the pleural cavity that was sent for analysis (Fig. 2). We immediately stopped the LMWH and other treatments were continued. After right-sided pleural fluid drainage, the patient was clinically better, but still required oxygen support along with antimicrobial coverage. Pleural fluid analysis showed hematocrit 45% (normal hematocrit 38.3–48.6%), exudative type, neutrophil predominant with adenosine deaminase of 3.8 (normal adenosine deaminase <4), and pleural fluid sent for cartridge-based nucleic acid amplification test for early diagnosis of tuberculosis, bacterial and fungal culture were found negative. Complete blood count showed hemoglobin 15.6, leukocyte elevated to 25.64/mm³, and neutrophil-to-lymphocyte ratio 17.4. Peripheral blood culture revealed Acinetobacter baumanii and antibiotics were revised according to sensitivity. This A. baumanii were sensitive to Piperacillin–Tazobactum and Meropenem, so we added Meropenem 1.5-g intravenous TDS and continued Piperacillin–Tazobactam. We considered the possibility of hospital-acquired pneumonia, which could be a cause of lung cavitation. Bronchoscopy was performed and broncho-alveolar-lavage fluid analysis did not reveal any clue for the underlying etiology. However, galactomannan tests for broncho-alveolar-lavage fluid were positive for a few Aspergillus species. So intravenous voriconazole 6 mg/kg every 12 h followed 24 h later by 4 mg/kg every 12 h, considering the possibility of invasive Aspergillus species infection. For further evaluation, an high-resolution computed tomography (HRCT) thorax was done. The oblique coronal reformatted image of a HRCT scan shows a thick-walled irregular cavity in the right lower lobe (white arrow), other changes of COVID-19 pneumonia are evident, including extensive ground-glass opacification (black arrow), with a thin line of subpleural hypodensity (black dashed arrow), consolidation collapse and bronchiectasis (white dashed arrow) (Fig. 1d), and the axial-reformatted image of an HRCT scan showing a thick-walled irregular cavity in the right lower lobe (white star), pneumothorax, ground-glass opacities, and consolidation, note the intercostal drainage tube in situ (black arrowhead) (Fig. 1e). The patient gradually improved with decreased oxygen requirement, and finally, the patient was discharged after 34 days of hospitalization. We have obtained all appropriate patient-consent forms from patient relatives. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal.

Discussion

Acute respiratory-distress syndrome is most commonly associated with COVID-19, and few patients are asymptomatic or may present with mild symptoms. In COVID-19 pneumonia, the most commonly involved lung portion is the lower lobe, especially the posterior segment, and it is radiologically presented as ground-glass opacities and consolidations[³]. The findings like lung cavitation, pleural effusion, lymphadenopathy, and pericardial effusions are less commonly observed[⁴]. Our patient has a pneumothorax, pneumomediastinum that could be due to barotrauma as the patient was initially on continuous positive airway-pressure treatment. The feared complications like pneumothorax and pneumomediastinum following endotracheal intubation and mechanical ventilation[⁵] but even without barotrauma, pneumothorax, or pneumomediastinum, or rarely both, can be present in the context of COVID-19[⁶]. The underlying mechanism could be due to severe lung injury and diffuse alveolar damage that lead to the development of spontaneous pneumothorax complicating severe acute respiratory syndrome[⁷]. These changes, in addition to possible overdistention of the alveoli by using mechanical ventilation, may put patients at risk for developing pneumothorax. This case also develops hemothorax and the underlying mechanism could not be identified. The presence of chest-wall injury may lead to hemothorax[⁸]. The presence of lung tumors, pulmonary emboli, arteriovenous malformations, endometriosis, or the use of anticoagulants may lead to a rare presentation like spontaneous hemothorax[⁹]. The risk of bleeding is relatively high in COVID-19 patients, especially in those who have received therapeutic anticoagulation treatment, and associated with an increased risk of mortality. Now, it is well established that COVID-19 causes coagulopathy, and has been associated with bleeding and/or clotting diathesis in the setting of a prothrombotic state. This has made them vulnerable to hemorrhagic complications such as frank disseminated intravascular coagulation. But, in our patient, the coagulation profile was normal with no rise in PT, APTT, or decrease in platelet count. Due to some logistic issues, we could not subject the patient to CT pulmonary angiography to rule out pulmonary embolism. But none of the published case reports identified PTE as the cause of hemothorax. There were few case reports of COVID-related hemothorax during acute infection[^1011121314]. All the case reports found the different mechanisms of bleeding for hemothorax and it is summarized in [Table 1]. In COVID-19 patients following the use of anticoagulant therapy, microvascular damage of pulmonary capillaries may be one of the causes of hemothorax[¹⁰]. Another study found bleeding from the intercostal artery, and rupture of the vascular aneurysm as a cause of hemothorax in COVID-19[¹¹¹²] (Table 1). Ebrahimpour et al.[¹³] found that COVID-19 induces angioinvasion and leads to the occurrence of alveolar hemorrhage and hemothorax. Jung et al.[¹⁴] found necrotizing pneumonia with pulmonary vasculopathy and bleeding from the pulmonary artery. Considering pulmonary cavity on imaging with raised leukocyte count and normal procalcitonin, we kept the possibility of fungal infection, and the patient well responded with antifungal treatment. The pulmonary cavity is defined as an air-filled space formed within an area of consolidation, mass, or nodule, through liquefication of the necrotic portion of the lesion and the discharge of this necrotic material via the bronchial airway. It has both infective (mycobacterial, bacterial, fungal, etc.) and noninfective etiology (neoplastic, autoimmune or infarct, etc.). Pulmonary cavitation is the uncommon radiological presentation of COVID-19 and only a few case reports were published[¹⁵¹⁶]. Although the exact mechanism of cavitation in COVID-19 pneumonia is unknown, it may be related to diffuse alveolar damage, intra-alveolar hemorrhage, and necrosis of parenchymal cells based on prior autopsy reports[¹⁷].

Conclusion

This is the first case report that highlights the occurrence of a combination of hemothorax, pneumomediastinum, pneumothorax, and surgical emphysema in a young COVID-19 patient. The current case indicates the complexity and variety of pneumonia complications caused by COVID-19 infection. We need to be very judicious for use of anticoagulant and positive-pressure therapy, otherwise, it may lead to all these complications. The current case indicates the complexity and variety of pneumonia complications caused by COVID-19 infection. For any patient with a severe form of COVID-19, the physicians and radiologists should be aware of the occurrence and potentially fatal outcomes like hemothorax, pneumothorax, and pneumomediastinum, and it should be systematically searched and approached as a part of medical management.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.