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Pneumomediastinum and COVID-19 Infection Rajan Pooni, Gargi Pandey, Saniath Akbar

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Pneumomediastinum and COVID-19 Infection Rajan Pooni, Gargi Pandey, Saniath Akbar Reminder of important clinical lesson BMJ Case Rep: first published as 10.1136/bcr-2020-237938 on 11 August 2020. Downloaded from Case report Broadening the differential: pneumomediastinum and COVID-19 infection Rajan Pooni, Gargi Pandey, Saniath Akbar Gastroenterology, Barts Health SUMMARY pathologies, less common diagnoses may be missed, NHS Trust, London, UK The novel coronavirus (COVID-19) has emerged as even if their radiographic findings are self- evident! a new pathogen responsible for an atypical viral We feel this is something that doctors and medical Correspondence to pneumonia, with severe cases progressing to an acute students in training can empathise with. Third, it Dr Rajan Pooni; r. pooni@ nhs. net respiratory distress syndrome. In our practice, we have is uncommon to see an adult case of a pneumome- observed patients admitted with COVID-19 pneumonia diastinum, in the absence of trauma or prolonged Accepted 24 July 2020 developing worsening hypoxaemic respiratory failure mechanical ventilation. There are only a handful prompting the need for urgent endotracheal intubation. of reports of pneumomediastinum associated with Here, we present a case of a patient admitted with COVID-19 currently in the literature.8–10 severe COVID-19 pneumonia who required continuous positive airway pressure support following acute CASE PRESENTATION deterioration. However, with the patient requiring an A- 56- year old man presented to the Emergency Department with a 14- day history of a non- increasing fraction of inspired oxygen (FiO2), a prompt CT pulmonary angiogram scan was performed to exclude an productive cough, dyspnoea and fever. His medical acute pulmonary embolism. Surprisingly, this revealed a history included type 2 diabetes mellitus, hyper- pneumomediastinum. Following a brief admission to the tension and seasonal asthma. Social history elicited intensive care unit, the patient made a full recovery and the patient was a non- smoker and did not consume was discharged 18 days post admission. alcohol. The patient’s regular medications included oral antihyperglycaemic agents, an ACE inhibitor and when required, a salbutamol inhaler. Physical examination revealed the patient was BACKGROUND in respiratory distress, with an oxygen saturation The spectrum of COVID-19 infection ranges from (SpO2) of 88% on room air and a respiratory rate mild to severe disease. Of the eight million cases http://casereports.bmj.com/ of 40 breaths/min. He was feverish at 37.9°C, with diagnosed worldwide,1 an estimated 5% are crit- 2 a blood pressure of 151/78 mm Hg and pulse of 103 ically unwell. Cases of hospitalised COVID-19 beats/min. Auscultation of the chest did not reveal pneumonia can be complicated by hypoxaemic any added sounds. Remainder of the clinical exam- respiratory failure, a common reason for admission ination was unremarkable. to intensive care unit (ICU). These patients develop Laboratory blood tests on admission revealed a an acute respiratory distress syndrome (ARDS) with normal white cell count of 8.4×109/L (4.0–10.0 × deterioration often attributed to worsening disease 9 3 10 /L), elevated ferritin at 512 µg/L (30–400 µg/L) or the so- called ‘cytokine storm’. and lactate dehydrogenase (LDH) of 348 U/L However, worsening respiratory failure in (0–249 U/L). His D- dimer was raised at 1.16 mg/L patients with COVID-19 pneumonia may have fibrinogen equivalent units (FEU) (<0.50 mg/L on September 29, 2021 by guest. Protected copyright. aetiology other than ARDS. A study from Wuhan FEU) with a C-reactive protein (CRP) of 146 mg/L analysing the characteristics of COVID-19 pneu- (<5 mg/L). Serum troponin T level was normal. Of monia found that 1% of patients had a pneumo- note, there was no lymphopenia on admission. 4 thorax on chest imaging. There is also increasing An admission chest X- ray (figure 1) displaying recognition that pulmonary embolism (PE) is a bibasal opacities suspicious for COVID-19 infection major cause of acute deterioration, with elevated was confirmed with subsequent positive reverse- hypercoagulability profiles observed in patients transcriptase PCR testing. Despite conflicting 5 6 with COVID-19 with acute respiratory failure. evidence for the efficacy of non- invasive ventilation Furthermore, superimposed bacterial infection has (NIV) in type 1 respiratory failure not attributed been attributed as the cause of mortality for 50% of to acute cardiogenic pulmonary oedema,11 based 7 patients who have died with COVID-19. on both national and local guidance,12 the patient © BMJ Publishing Group Our case highlights several learning points which Limited 2020. No commercial was started on continuous positive airway pres- re-use . See rights and readers may find interesting. First, it emphasises the sure (CPAP) support after failure on supplemental permissions. Published by BMJ. importance of ‘thinking outside the box’. Respira- oxygen therapy. The patient received antibiotic tory deterioration may not always be due to PE or cover with coamoxiclav and clarithromycin. To cite: Pooni R, Pandey G, Akbar S. BMJ Case Rep worsening infection; uncommon diagnoses such as Following less than 12 hours of CPAP support, 2020;13:e237938. pneumomediastinum should be considered. Second, the patient was de-escalated to non- invasive doi:10.1136/bcr-2020- it highlights the importance of thorough scrutiny supplemental oxygen. Over the next 3 days, the 237938 of chest radiographs. In considering only certain patient improved clinically with reducing oxygen Pooni R, et al. BMJ Case Rep 2020;13:e237938. doi:10.1136/bcr-2020-237938 1 Reminder of important clinical lesson BMJ Case Rep: first published as 10.1136/bcr-2020-237938 on 11 August 2020. Downloaded from Figure 3 Coronal cross section of CT pulmonary angiogram showing a pneumomediastinum (see red arrows). Figure 1 Admission chest X- ray. Subtle bibasal opacities and air INVESTIGATIONS bronchograms (more prominent R>L) (see red arrows). The admission chest X-ray (figure 1) showed subtle bibasal air space opacities consistent with COVID-19 pneumonia. When the patient deteriorated on day 5, a repeat chest radiograph was initially reported as being unchanged from admission (figure 2). requirements (FiO2 of 24%) and downtrending laboratory inflammatory markers (CRP falling to 75 mg/L). On further scrutiny of the scan post CTPA, this did show curvi- On day 5 of admission, the patient showed signs of acute linear lucencies around the mediastinum and heart border, respiratory distress requiring increasing supplemental oxygen suggesting extraluminal air in the mediastinum and pericardium. This finding was missed by the medical team and radiology. therapy at 10–15 L/min to maintain SpO2 above 90%. This also coincided with worsening blood tests; a lymphocyte count of With the presumption that we did not see any obvious X-ray 0.6×109/L, LDH of 521 U/L, D- dimer of 2.42 mg/L FEU and findings to explain the ongoing hypoxia, a decision was made to a CRP of 137 mg/L. A repeat chest X- ray (figure 2) was inter- proceed to CTPA. This showed no intraluminal filling defects preted and reported as showing no interval change when however revealed a moderate pneumomediastinum without a compared with admission (figure 1). Subsequently, the patient pneumopericardium (figures 3 and 4). A transthoracic echocar- was restarted on CPAP support with antibiotic therapy escalated diogram demonstrated a normal left ventricular ejection fraction to piperacillin–tazobactam. with no evidence of pericardial effusion or tamponade. Over the next 48 hours, while on CPAP, the patient continued DIFFERENTIAL DIAGNOSIS to have an increasing oxygen requirement (FiO2 rising from 35% to 60%). A decision was made to perform a CT pulmonary Patients with COVID-19 pneumonia can become progressively angiogram (CTPA) to investigate for an acute PE as a cause of hypoxic coinciding with worsening biochemical (as in our case) http://casereports.bmj.com/ the patient’s worsening hypoxia. While the CTPA showed no and prognostic markers, that is, D- dimer. Chest X- rays typically PE, it did reveal to our surprise a moderate pneumomediastinum show worsening consolidation and/or an ARDS picture; this was (figures 3 and 4). not the case with the repeat chest X-ray for our patient. On the presumption, there was no obvious radiographic abnormality to Following further episodes of marked desaturations (SpO2 explain the worsening hypoxia and the raised D- dimer, it was below 75%) and increasing oxygen requirements (to an FiO2 of 100%), the patient was admitted to ICU for high-dependency appropriate to investigate for a PE. This is in concordance with monitoring. Over this 24 hours ICU admission, the patient did the advice from the European Society of Radiology and the not require endotracheal intubation and was managed on CPAP European Society of Thoracic Imaging, who advocate the use of with low- pressure settings. on September 29, 2021 by guest. Protected copyright. Figure 2 Repeat chest X- ray at day 5. Curvilinear opacities seen along Figure 4 Axial cross section of CT pulmonary angiogram showing a superior mediastinum and heart border, suggestive of extraluminal air pneumomediastinum (see red arrows). Note the patchy opacities and (see red arrows). the linear scarring of both lungs due to COVID-19. 2 Pooni R, et al. BMJ Case Rep 2020;13:e237938. doi:10.1136/bcr-2020-237938 Reminder of important clinical lesson BMJ Case Rep: first published as 10.1136/bcr-2020-237938 on 11 August 2020. Downloaded from CT imaging in the diagnosis of PE in patients with COVID-19 retching which our patient did not have problem of. Although pneumonia with limited disease extent, requiring supplemental reported in the literature, it is uncommon for NIV, particularly oxygen therapy.13 Cross- sectional imaging also has the added for short periods, to cause pneumomediastinum (and is more advantage of revealing pathologies which are either poorly visu- likely to be seen with mechanical ventilation).19 Indeed, there alised on a chest X- ray or missed, which in our case revealed a is a direct correlation between positive airway pressure and the pneumomediastinum.
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