A 57-year-old man (height: 177 centimeters, weight: 86 kilograms) presented with a fever of 38.5 C for 4 days accompanied by fatigue and dyspnea, and he visited the clinic on February 4, 2020. He had an 8-year history of hypertension without other diseases. He disclosed a history of contact with a confirmed case.
As he was febrile, the screening test for COVID-19 was performed immediately. Chest-computed tomography (CT) showed diffuse ground-glass opacities in the periphery of bilateral lungs, which represented the characteristic imaging for pneumonia of COVID-19 (Figure 1). Blood tests revealed that the white blood cell count was 4.92 x 109 cells/L (normal: 4.0-10.0 x 109 cells/L), lymphocyte (LY) was 1.1 x 109 cells/L (normal: 1.1-3.2 x 109 cells/L), C-reactive protein (CRP) was 118.24 mg/L (normal: <5 mg/L), and pathogenic findings of common respiratory viruses and influenza A and B viruses were negative (Figure 2). He was diagnosed with suspected COVID-19.
On admission, he had a body temperature of 38.8 C, blood pressure (BP) of 140/80 mmHg, RR of 20 breaths/min, and a heart rate (HR) of 98 beats/min. SpO2 was 84% without oxygen supply. He was supported with high flow oxygen (50 L/min, FiO2 60%) and treated with antimicrobial and antiviral drugs, including levofloxacin (oral, early stage), moxifloxacin (intravenous, later), and ribavirin. Considering the changes noted on chest CT, the patient was diagnosed with acute respiratory distress syndrome (ARDS), and methylprednisolone (40-160 mg/day intravenously from February 4 to February 9) and gamma-globulin (10 g/day intravenously from February 5 to February 10) were administered. On February 7, the Centers for Disease Control confirmed that the patient's oropharyngeal swab test for SARS-CoV-2 was positive; thus, the patient was diagnosed with COVID-19 (severe case), ARDS, and hypertension. During the treatment course, the patient's body temperature returned to normal. Meanwhile, PaO2 improved gradually and CRP levels decreased to 50.3 mg/L on February 9. However, the patient's respiratory distress and fatigue did not relieve, and CRP levels increased to 124.2 mg/L on February 11 (Figure 2).
On February 12, PaO2 fell to 58 mmHg. Non-invasive mechanical ventilation was performed, and another course of methylprednisolone was administered. We suggested a change to invasive mechanical ventilation because there was no improvement in respiratory distress after 2 h, but his family refused. PaO2 and CRP seemed to improve with increasing FiO2 (up to 100%) and the use of methylprednisolone, but the clinical manifestation persisted, and, on February 15, PaO2 could not be maintained; it fell to 35 mmHg, the SpO2 was at 45%, the RR at 50 breaths/min, and confusion occurred. Invasive mechanical ventilation was authorized, but ventricular fibrillation occurred after endotracheal intubation. Cardiopulmonary resuscitation (CPR) and defibrillation were performed immediately, during which no blood pressure and heartbeat were detected for 12 min. The patient recovered but was in a deep coma. We adjusted the ventilator settings to a pressure synchronized intermittent mandatory ventilation (P-SIMV) mode with a maximum airway pressure (Pmax) of 18 cmH2O, positive end expiratory pressure (PEEP) of 15 cmH2O, FiO2 of 100%, and frequency of 18 breaths/min. We changed to a superior antibiotic after blood test results showed leukocytosis (26.17 x 109 cells/L), lymphopenia (0.52 x 109 cells/L), and elevated CRP levels (170.2 mg/L) (Figure 2). However, on February 17, the urine volume was 1,100 mL, and renal failure occurred, with elevated blood urea nitrogen (25.24 mmol/L, normal: 3.2-7.1. mmol/L) and creatinine (395.2 mumol/L, normal: 44.0-133.0 mumol/L) levels (Figure 2). We adjusted the ventilator to pressure-assist/control mode with PEEP of 11 cmH2O and FiO2 of 100%, and we operated continuous renal replacement therapy (CRRT) once. On February 18, renal function improved, and the urine volume reached 4,400 mL. Over this period, the patient progressed to a critical case, and bedside continuous chest digital radiography (DR) was used for monitoring. We observed faded imaging and restoration of organic function after treatment (Figure 1).
On February 24, the patient's condition remained stable and the ventilator setting was changed to P-SIMV mode. The HR was 90 beats/min, BP was 132/78 mmHg, RR was 20 breaths/min, and SpO2 was 96% (FiO2 was 60%). Considering the policy of centralized management for better treatment, the patient was to be transferred to a superior hospital on February 25. We prepared an ambulance equipped with a limited ventilator, which was a PCV model with a Pmax of 25 cm H2O and FiO2 of 100%, but it did not offer the possibility to apply PEEP and a critical care specialist; we also estimated and prepared for other potential risks. However, after 10 min in the ambulance, the patient's SpO2 suddenly fell to 0%, the HR slowed down to 20 beats/min, and he also presented with severe cyanosis and respiratory distress. CPR was performed, and the ambulance returned immediately. A specialized ventilator was used again with Pmax of 30 cmH2O, PEEP of 15 cmH2O, and FiO2 of 100%. Although the chest DR showed progress on February 27 (Figure 1), the patient's condition worsened, and he died on March 4.