Pneumomediastino em um paciente com COVID-19

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Abstract

Paciente do sexo masculino, 36 anos, sem comorbidades, foi admitido na UTI com história de febre, tosse e dispneia intensa por 14 dias. Na admissão, sua temperatura corporal era de 38°C (100,4°F), sua FR era de 30 ciclos/min, e sua SpO2 era de 93%. A TC de tórax sem contraste mostrou áreas de consolidação predominantemente periféricas em ambos os pulmões, bem como pneumomediastino (Figuras 1A a 1C). A reação em cadeia de polimerase por fluorescência em tempo real do escarro do paciente foi positiva para o ácido nucleico de SARS-CoV-2. Após quatro dias de internação, tendo sido tratado exclusivamente com medidas de suporte, incluindo oxigenoterapia, o paciente apresentou melhora parcial dos sintomas e foi realizada uma nova TC (Figura 1D), que mostrou diminuição substancial das áreas de consolidação e reabsorção do pneumomediastino. Figura 1 Cortes axiais (A e B) e coronais (C) em TC de tórax sem contraste mostrando opacidades em vidro fosco em ambos os pulmões. Observe a presença de pneumomediastino (setas). Uma imagem coronal reconstruída obtida quatro dias depois (D) demonstrou melhora nas áreas de opacidade em vidro fosco e reabsorção do pneumomediastino. As principais causas de pneumomediastino espontâneo incluem aquelas relacionadas à manobra de Valsalva e asma. 1 Os achados tomográficos do COVID-19 já foram amplamente estudados e relatados na literatura médica. 2 Até onde sabemos, pneumomediastino raramente tem sido associado à doença. 3 Conforme descrito em outras doenças, o mecanismo mais provável de formação de pneumomediastino no contexto da COVID-19 é o surgimento de um gradiente de pressão entre os alvéolos e as estruturas circundantes, levando a ruptura alveolar e vazamento de ar, que se move ao longo do feixe broncovascular até atingir o mediastino. Esse gradiente de pressão parece estar relacionado ao envolvimento heterogêneo do pulmão quando há áreas parenquimatosas normais adjacentes a áreas afetadas pela doença. 1

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Radiological Society of North America Expert Consensus Statement on Reporting Chest CT Findings Related to COVID-19. Endorsed by the Society of Thoracic Radiology, the American College of Radiology, and RSNA.

Scott Simpson, Fernando U Kay, Suhny Abbara … (2020)

Routine screening CT for the identification of COVID-19 pneumonia is currently not recommended by most radiology societies. However, the number of CTs performed in persons under investigation (PUI) for COVID-19 has increased. We also anticipate that some patients will have incidentally detected findings that could be attributable to COVID-19 pneumonia, requiring radiologists to decide whether or not to mention COVID-19 specifically as a differential diagnostic possibility. We aim to provide guidance to radiologists in reporting CT findings potentially attributable to COVID-19 pneumonia, including standardized language to reduce reporting variability when addressing the possibility of COVID-19. When typical or indeterminate features of COVID-19 pneumonia are present in endemic areas as an incidental finding, we recommend contacting the referring providers to discuss the likelihood of viral infection. These incidental findings do not necessarily need to be reported as COVID-19 pneumonia. In this setting, using the term “viral pneumonia” can be a reasonable and inclusive alternative. However, if one opts to use the term "COVID-19" in the incidental setting, consider the provided standardized reporting language. In addition, practice patterns may vary, and this document is meant to serve as a guide. Consultation with clinical colleagues at each institution is suggested to establish a consensus reporting approach. The goal of this expert consensus is to help radiologists recognize findings of COVID-19 pneumonia and aid their communication with other healthcare providers, assisting management of patients during this pandemic. Published under a CC BY 4.0 license.

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COVID-19 with spontaneous pneumomediastinum

Changyu Zhou, Chen Gao, Yuanliang Xie … (2020)

A 38-year-old man from Wuhan, China, was admitted to the Central Hospital of Wuhan (Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China), on Jan 20, 2020, with a 1-day history of fever without dizziness, cough, and headaches. On presentation, his temperature was 38·1°C. Laboratory tests showed a C-reactive protein concentration of 0·56 mg/dL (normal range 0·00–0·60] mg/dL). Complete blood count showed elevated leukocytes (10 060 cells per μL [normal range 3500–9500 cells per μL]), neutrophils (7550 cells per μL [1800–6300 cells per μL]), and monocytes (990 cells per μL [100–600 cells per μL]), while the lymphocyte count (1490 cells per μL) was in the normal range (1100–3200 cells per μL). The patient was negative for influenza A and B viruses, adenovirus, respiratory syncytial virus, and parainfluenza 1, 2, and 3 viruses. Chest CT showed multiple ground-glass opacities in the lower lobes bilaterally. The patient was given antibacterial, antiviral, and corticosteroid treatments (moxifloxacin [0·4 g/day] for 5 days, followed by ribavirin [0·5 g/day] and methylprednisolone [40 mg/day] for 5 days) via intravenous drop infusion. However, after 10 days, the patient had persistent fever (highest temperature 38·5°C), cough, and shortness of breath. The patient was diagnosed with coronavirus disease 2019 (COVID-19) on the basis of RT-PCR analysis of sputum samples. On day 11, the patient developed exertional angina with cardiac palpitations along with respiratory wheezing. Chest CT revealed multiple ground-glass opacities with bilateral parenchymal consolidation and interlobular septal thickening. Spontaneous pneumomediastinum and subcutaneous emphysema were also observed (figure ). Figure Chest CT showed spontaneous pneumomediastinum (arrow), subcutaneous emphysema, and bilateral ground-glass opacities of the lung Corticosteroid treatment was stopped, while ribavirin was continued at the same dosage for 14 days. Supplemental oxygen, antibiotics, antitussives, and bronchodilators were also added to the regimen, which included theophylline (0·2 g/12 h), ambroxol (45 mg/12 h), and cefoperazone–tazobactam (2 g/8 h) via intravenous drip infusion, as well as recombinant human interferon alfa-1b via aerosol (three times daily) for 14 days. By day 25, the patient's temperature had recovered to normal (36·5°C), his cough had improved, and his breathing was normal. RT-PCR analysis of COVID-19 was negative. Chest CT revealed resolution of previous pneumomediastinum and a reduction of parenchymal consolidation with pulmonary fibrosis and pneumatocele in the inferior left lower lobe. Repeat RT-PCR was negative on day 30, and the patient was discharged for outpatient follow-up. Although the precise mechanism of pneumomediastinum is unknown, spontaneous pneumomediastinum is usually a self-limiting disease. However, it can potentially cause severe circulatory and respiratory pathology. Therefore, the occurrence of spontaneous pneumomediastinum in COVID-19 patients should be monitored closely as a potential indicator of worsening disease.

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Pneumomediastinum, subcutaneous emphysema, and pneumothorax after a pulmonary function testing in a patient with bleomycin-induced interstitial pneumonitis*

Mariana Araujo, Frederico Fernandes, Fernando Kay … (2013)

Spontaneous pneumomediastinum is an uncommon event, the clinical picture of which includes retrosternal chest pain, subcutaneous emphysema, dyspnea, and dysphonia. The pathophysiological mechanism involved is the emergence of a pressure gradient between the alveoli and surrounding structures, causing alveolar rupture with subsequent dissection of the peribronchovascular sheath and infiltration of the mediastinum and subcutaneous tissue with air. Known triggers include acute exacerbations of asthma and situations that require the Valsalva maneuver. We described and documented with HRCT scans the occurrence of pneumomediastinum after a patient with bleomycin-induced interstitial lung disease underwent pulmonary function testing. Although uncommon, the association between pulmonary function testing and air leak syndromes has been increasingly reported in the literature, and lung diseases, such as interstitial lung diseases, include structural changes that facilitate the occurrence of this complication.