An 89 year-old male was admitted to the ICU on April 14, 2020. The patient had a history of chronic obstructive pulmonary disease (COPD) on nocturnal oxygen therapy and no known cardiac disease. He had been hospitalized since March 30 because of COPD exacerbation. During his hospitalization his condition improved, but on April 8 he developed new-onset fever with hypoxemia and bilateral lung infiltrates. Reverse transcription polymerase chain reaction (RT-PCR) of a nasopharyngeal swab was positive for SARS-CoV-2. He was treated with hydroxychloroquine and azithromycin but was intubated on April 14 because of worsening hypoxemia.
On admission, he was sedated and mechanically ventilated with a tidal volume of 6.5 ml/kg of Predicted Body Weight at a rate of 20 breaths per minute and Positive End-Expiratory Pressure (PEEP) of 8cmH2O. Physical examination was unremarkable and he was hemodynamically stable. He had a PaO2/FiO2 of 110, respiratory system compliance 35 ml/cmH2O, airway resistance 18cmH2O/L/sec and intrinsic PEEP of 2cmH2O. Central venous pressure (CVP) was 12 mmHg and central venous oxygen saturation (ScvO2) was 76 %. Electrocardiography (ECG) showed incomplete RBBB (Fig. 1). Chest X-ray revealed signs of emphysema and bilateral infiltrates (Fig. 2).
Abnormal laboratory tests included mild leukocytosis with low lymphocyte count (800/muL) and elevated C-reactive protein (24.77 mg/dL; RR < 0.5 mg/dL), ferritin (2279 ng/mL; RR 11-307 ng/mL), interleukin-6 (52 pg/mL; RR <5 pg/mL) and d-dimer levels (1.65 mug/mL; RR < 0.89 mug/mL). A panel of lower respiratory specimen was negative, including influenza A and B, respiratory syncytial virus, corona virus, metapneumovirus, parainfluenza virus, rhinovirus, Legionella pneumophila, Myocoplasma pneumoniae, Chlamydia pneumoniae and bacteria. Urinary antigen testing for Legionella pneumophila and Streptococcus pneumoniae was also negative.
Twenty-four hours after admission the patient developed acute circulatory collapse non-responding to fluid resuscitation and high dose of vasopressors. His CVP was 18 mmHg and ScvO2 was 58 %, indicating cardiogenic or obstructive pathophysiology of shock. Differential diagnosis included myocardial infarction, acute myocarditis due to COVID-19, acute pulmonary embolism, aortic dissection, tension pneumothorax and cardiac tamponade. ECG showed new onset infero-lateral ST elevation (Fig. 3). High sensitive cardiac troponin I was 35 pg/mL (RR < 34 pg/mL). Bedside transthoracic echocardiography (TTE) revealed an anterior pericardial effusion with right ventricular diastolic collapse and mitral valve inflow variation of 30 %, while left ventricular systolic function was normal with LVEF of 60 % (Video 1). Other causes of shock were excluded by TTE. Echo-guided pericardiocentesis was immediately performed and 200 mL of serous fluid were aspirated with subsequent hemodynamic improvement (Video 2). Pericardial drainage was maintained in situ for 24 h and yielded a total of 240 mL of fluid.
The pericardial fluid tested negative for Gram stain and acid-fast bacilli smear. No growth on bacterial and fungal cultures was reported. Molecular testing for Mycobacterium tuberculosis was negative as was RT-PCR for SARS-CoV-2. Fluid cytology yielded no malignant cells. Thyroid function tests were normal. Serologic tests for Coxsackievirus, Echovirus, hepatitis viruses, cytomegalovirus, human immunodeficiency virus and autoantibodies were also negative. Treatment with colchicine was started. Following fluid drainage the patient was rapidly weaned off vasopressors. Repeat echocardiograms showed no recurrence of pericardial effusion. However, on the sixth day he developed septic shock and multi-organ failure caused by multi-drug resistant Acinetobacter baumanii and died.