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CASE STUDY The 89-year-old resident of a nursing home was admitted to the Emergency Department with acute, severe dyspnea and hypotension. Due to fast respiratory deterioration rapid sequence intubation was performed in the ambulance with full personal protection regimen in place. At admission patient was fully conscious with excessive respiratory effort. Despite the fluid resuscitation and high doses of catecholamines, patient’s hemodynamic was not stable, with mean artery pressure (MAP)<60mmHg and heart rate of 90/min generated by implantable cardiac pacemaker. Apart from severe hypoxemia refractory to 100% oxygen therapy and increased body temperature (37.4°C), laboratory tests revealed significant leukopenia (1.96 K/ul), lymphocytopenia (0.42 K/ul), high lactate dehydrogenase (371 U/L), high AST (55 U/L), elevated CRP (50.2 mg/L) and procalcitonin (10.5 ng/mL). Due to the strong suspicion of COVID19 a single nasopharyngeal swab for SARS-CoV2 RT-PCR was obtained. Chest Computed Tomography (CT) demonstrated bilateral infiltrates more severe in the right lung with small pleural effusion, massive consolidations in the lower lobe and peribronchial consolidations with patchy ground-glass opacities in the middle lobe. The left lung was less affected with consolidations mainly in the lower lobe. Mediastinal and hilar lymphadenopathy was not observed [Figure 1]. Consequently, the estimated probability of COVID19 was below 70% as per British Society of Thoracic Imaging guidelines (BSTI). According to administrational procedures patient was transferred to the Department of Pneumonology designated for COVID19 screening. Blood samples for standard microbiology cultures were collected. Despite aggressive treatment with meropenem, azithromycin and hydroxychloroquine as well as invasive mechanical ventilation patient’s condition remained unstable meeting criteria of severe Acute Respiratory Distress Syndrome (ARDS) with FiO2 1,0, PEEP 12 cmH2O and calculated PaO2/FiO2 ratio 50.1 [1]. Due to resistant hypotonia patient was maintained on norepinephrine and dobutamine infusion with and positive fluid balance. Laboratory tests repeated within 24 hours showed low WBC count (0.82 K/ uL), a two-fold increase in creatinine, hypoalbuminemia 32 g/L and severe acid-base balance disorders with mixed respiratory-metabolic acidosis pH 7.25. The first RT-PCR test for SARS-CoV2 (nasopharyngeal swab) proved negative, therefore patient was transferred to the ICU and no longer isolated in accordance with the hospital safety protocol. In the following hours patient’s condition deteriorated. Blind bronchoalveolar lavage (BAL) samples for standard microbiological diagnosis were collected, while echocardiography showed no obvious heart pathology with estimated left ventricular ejection fraction of 45%. In order to maintain MAP 65mmHg, in addition to norepinephrine and dobutamine adrenaline infusion was started. As soon as hemodynamic stabilized, lung recrutation was performed according to the ARDS-net protocol, but no significant improvement in oxygenation was achieved. Maximal SpO2 value with FiO2 =1.0 after recrutation maneuver was 88-90%. During four-day ICU stay we observed only a slight increase in WBC count (maximal 3.19 K/μL), persistent anuria and severe mixed acid-base disorders. All microbiological samples were found negative. Significant deterioration of patient’s condition prompted retesting for COVID19 and sample from the blind BAL was harvested on day 6. In the next few hours patient died because of the multiorgan failure. CPR was not attended. A SINGLE NEGATIVE SARS-COV2 RT-PCR TEST DOES NOT EXCLUDE COVID-19 IN PATIENT WITH SEVERE ARDS, CASE STUDY