April 2022 Medical Image of the Month: COVID Pericarditis

Figure 1. A: Pericardial enhancement on thoracic CT (red arrows). B: Thoracic CT in lung windows showing mosaic attenuation (black arrows) and bilateral pleural effusions (red arrows).

Figure 2. A: Static image of parasternal short axis on transthoracic echocardiogram showing moderate, generalized pericardial effusion with right ventricular diastolic collapse (red arrow). B. Static image of parasternal long axis on transthoracic echocardiogram again showing a moderate, generalized pericardial effusion (red arrow). Lower panel: video of echocardiogram in parasternal long axis view.

A 76-year-old patient presented with fatigue and shortness of breath after missing one session of dialysis. Past medical history included end stage renal disease on hemodialysis and atrial fibrillation on anticoagulation. Initial labs showed that she was COVID positive with mild elevation in troponin and a BNP 1200. While an inpatient, she had received a few sessions of dialysis and treatment for COVID (including dexamethasone and remdesivir). Initial echo showed an ejection fraction of 60-65% with a small generalized pericardial effusion, a thickened pericardium with calcification. A few days after admission patient was suddenly noted to be hypotensive with systolic blood pressure in the 70s and altered mental status. Repeated labs showed a D-Dimer of 17,232, leukocytosis, lactic acidosis, troponin 0.556 ng/ml and arterial blood gas with metabolic acidosis. With a worsening clinical picture, repeat imaging was obtained. CT angiography of the chest was negative for pulmonary embolism; however, it showed a large pericardial effusion with reduced size of the right ventricle more so than left, concerning for cardiac tamponade (Figure 1A). CT chest also showed moderate-to-large pleural effusions with scattered mosaic attenuation of the lung parenchyma (Figure 1B). Repeat transthoracic echocardiogram had a moderate generalized pericardial effusion with right ventricular diastolic collapse concerning for pericardial tamponade (Figure 2). Her airway was secured with endotracheal intubation and vasopressors added for hemodynamic support. Pericardiocentesis was indicated however, patient’s INR was severely elevated in the setting of anticoagulation use. Efforts were made to lower INR with FFP; however, patient had a PEA arrest the following day and expired.

COVID-19 has been classically known for its detrimental lung damage; however, it has shown to cause extrapulmonary effects as well. Cardiac injury is one phenomenon that has been seen with the fulminant inflammatory state that COVID is known to cause. With a few cases reported for COVID pericarditis, it is a possible culprit when all other causes have been ruled out. Pericardial involvement can be seen in about 20% of COVID 19 cases, with effusion found in about 5% of patients (1). Concomitant myocarditis can also be found in up to 17% of patients. Having isolated cardiac involvement with COVID is rare, with most cases presenting mainly as lung involvement in addition to other organs affected as well. Clinically, patients with pericarditis typically experience chest pain and in the setting of COVID infection, an increase in inflammatory markers. Characteristic findings of pericarditis include friction rub on auscultation, diffuse ST elevations on EKG and a potential progression to pericardial effusion on echo. When a pericardial effusion becomes large enough, it can progress to cardiac tamponade (2). Having a high clinical suspicion for tamponade is crucial in a patient who has developed respiratory distress and hypotension in the setting of recent viral pericarditis. It is a clinical diagnosis and requires rapid treatment with pericardiocentesis to prevent cardiac arrest.

Sarah Youkhana, MD¹ and Maged Tanios, MD²

St. Mary Medical Center, Long Beach, CA USA

¹Internal Medicine Resident, PGY-3

²Medical Director, Critical Care Services

References

1. Diaz-Arocutipa C, Saucedo-Chinchay J, Imazio M. Pericarditis in patients with COVID-19: a systematic review. J Cardiovasc Med (Hagerstown). 2021 Sep 1;22(9):693-700. [CrossRef] [PubMed]
2. Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic Review. JAMA. 2015 Oct 13;314(14):1498-506. [CrossRef] [PubMed]

Cite as: Youkhana S, Tanios M. April 2022 Medical Image of the Month: COVID Pericarditis. Southwest J Pulm Crit Care Sleep 2022;24(4):62-3. doi: https://doi.org/10.13175/swjpccs006-22 PDF

Medical Image of the Month: COVID-19-Associated Pulmonary Aspergillosis in a Post-Liver Transplant Patient

Figure 1. Axial (A) and coronal (B) CT views before transplantation. The lung parenchyma appears normal.

Figure 2. Postoperative axial (A) and coronal (B) CT views 14 days later. Multiple consolidatory nodules with central break down seen involving both lungs, the largest 43mm x 47 mm in the lower lobe of right lung.

A previously healthy, 48-year-old woman, admitted with a working diagnosis of acute-on-chronic liver failure (Grade III) secondary to an autoimmune etiology, was found to be SARS COV-2 RTPCR positive on routine admission screening. She was initially managed with standard medical care for COVID, including steroids. She required invasive ventilation for worsening encephalopathy and when her antigen test was negative 10 days later, she underwent an urgent liver transplantation.

Her preoperative infection screen (culture of blood, bronchoalveolar lavage, urine) was negative and computerised tomography (CT) of the chest was normal (Figure 1). She was extubated on day 3 after liver transplantation. Her recovery was uneventful until the 10th postoperative day when she developed cough and oxygen desaturation. A repeat CT chest showed multiple multilobular consolidatory nodules with central breakdown involving both lung (Figure 2).  Her bronchoalveolar lavage culture grew Aspergillus fumigatus (azole sensitive) which fulfilled criteria for proven COVID-19 Associated pulmonary aspergillosis (pulmonary form) which the host criteria already met (1). Although she was aggressively managed with intravenous voriconazole and liposomal amphotericin, she subsequently succumbed to her illness.

COVID-19 infection shows a propensity to dysregulate the immune system and decreases T-cell lymphocytes. The dysfunctional immune system with a direct damage of respiratory epithelium by the viral infection facilitates superadded bacterial and fungal infections (2).  The use of corticosteroids and antiinterleukins in the therapy elevates the risk. Immunosuppression in an organ transplanted patient can complicate this further. Though patients with invasive fungal disease (IFD) are diagnosed and classified based on host factors, clinical factors and mycological evidences, CAPA essentially need not present with all the typical host and clinical elements (3). A high index of suspicion is essential for an early diagnosis of this condition.

Anandajith Kartha P¹, Zubair Umer Mohamed¹, Dinesh Balakrishnan², S Sudhindran²

Department of ¹Anaesthesiology and Critical Care, ²Gastrointestinal Surgery and Solid Organ Transplantation, Amrita Institute of Medical Sciences and Research Centre, Amrita Vishwa Vidyapeetham, Kochi, Kerala, India

References

1. Koehler P, Bassetti M, Chakrabarti A, et al. Defining and managing COVID-19-associated pulmonary aspergillosis: the 2020 ECMM/ISHAM consensus criteria for research and clinical guidance. Lancet Infect Dis. 2021 Jun;21(6):e149-e162. [CrossRef] [PubMed]
2. Herold S, Becker C, Ridge KM, Budinger GR. Influenza virus-induced lung injury: pathogenesis and implications for treatment. Eur Respir J. 2015 May;45(5):1463-78. [CrossRef] [PubMed]
3. Donnelly JP, Chen SC, Kauffman CA, et al. Revision and Update of the Consensus Definitions of Invasive Fungal Disease From the European Organization for Research and Treatment of Cancer and the Mycoses Study Group Education and Research Consortium. Clin Infect Dis. 2020 Sep 12;71(6):1367-1376. [CrossRef] [PubMed]

Cite as: P AK, Mohamed ZU, Balakrishnan D, Sudhindran S. Medical Image of the Month: COVID-19-Associated Pulmonary Aspergillosis in a Post-Liver Transplant Patient. Southwest J Pulm Crit Care. 2021;23(4):98-99. doi: https://doi.org/10.13175/swjpcc029-21 PDF 

Medical Image of the Month: Diffuse White Matter Microhemorrhages Secondary to SARS-CoV-2 (COVID-19) Infection

Figure 1.  An axial, maximal intensity projection (MIP), susceptibility weighted image (SWI) of the brain demonstrates numerous, punctate foci of susceptibility artifact in the genu (red arrow) and splenium of the corpus callosum (blue arrows). Other foci of susceptibility artifact are seen in the juxtacortical white matter (green arrows). These foci are consistent with microhemorrhages.

Clinical Scenario: A 59-year-old woman with hypothyroidism presented to the emergency room with progressive shortness of breath for 2 weeks.  Upon arrival, she was markedly hypoxic necessitating use of a non-rebreather to maintain her oxygen saturations above 88%. A chest radiograph demonstrated extensive, bilateral airspace disease. She was diagnosed with SARS-CoV-2 (COVID-19) pneumonia and started on the appropriate therapies. Approximately 48 hours into her hospitalization, she required intubation with mechanical ventilation due to her progressive hypoxemic respiratory failure.  She was intubated for approximately 5 weeks with a gradual improvement in her respiratory status, but not to the point where she was a candidate for a tracheostomy.  Despite being off sedation for an extended period, she remained unresponsive.  A CT of the head without contrast did not demonstrate any significant abnormalities.  An MRI of the brain was subsequently performed and demonstrated diffuse juxtacortical and callosal white matter microhemorrhages (Figure 1). Given her persistent encephalopathy and marked respiratory failure, her family elected to pursue comfort measures.

Discussion: In a recent retrospective analysis of brain MRI findings in patients with severe COVID-19 infections, 24% of the patients had extensive and isolated white matter microhemorrhages. White matter microhemorrhages with a predominant distribution in the juxtacortical white matter and corpus callosum are nonspecific and thought to be related to hypoxia.  Alternatively, small vessel vasculitis possibility related to a SARS-CoV-2 infection may result in this pattern of microhemorrhagic disease.  Diffuse axonal injury (DAI) is another etiology for microhemorrhagic disease distributed in the juxtacortical white matter and corpus callosum. However, DAI is secondary to a deceleration-type injury in the setting of trauma which is not present in most patients presenting with a SARS-CoV-2 infection. The prognosis of this condition remains to be determined.

Kelly Wickstrom, DO¹, Nicholas Blackstone MD², Afshin Sam MD¹, Tammer El-Aini MD¹

¹Banner University Medical Center – Tucson Campus, Department of Pulmonary and Critical Care, Tucson, AZ USA

²Banner University Medical Center – South Campus, Department of Internal Medicine, Tucson, AZ USA

References

1. Kremer S, Lersy F, de Sèze J, et al. Brain MRI Findings in Severe COVID-19: A Retrospective Observational Study. Radiology 2020: 297: E242-E251. [CrossRef] [PubMed]
2. Radmanesh A, Derman A, Lui Y et al. COVID-19-associated Diffuse Leukoencephalopathy and Microhemorrhages. Radiology. 2020 Oct;297(1):E223-E227. [CrossRef] [PubMed]

Cite as: Wickstrom K, Blackstone N, Sam A, El-Aini T. Medical Image of the Month: Diffuse White Matter Microhemorrhages Secondary to SARS-CoV-2 (COVID-19) Infection. Southwest J Pulm Crit Care. 2021;22(2):56-7. doi: https://doi.org/10.13175/swjpcc001-21 PDF