ABSTRACT
Background: The incidence of venous thromboembolism (VTE) in patients with COVID-19 during hospitalization and in the post-discharge setting has been reported with wide variability. Many studies have short follow-up, reported the early phase of the pandemic, or did not report bleeding or anticoagulant dosing. Aim(s): We determined the incidence of symptomatic VTE and bleeding in patients admitted to hospital for COVID-19 and their 3-month risk of VTE post-discharge. Method(s): All patients admitted for COVID-19 at 5 regional hospitals were identified between January 1 and December 31, 2020. Data were collected from their hospital admission and for a minimum of 3 months post-discharge. Re-admissions during this period were considered as post-discharge data of the index admission. Standard thromboprophylaxis for critical care and ward patients were enoxaparin 30 mg twice daily or 40 mg once daily. Post-discharge thromboprophylaxis was not given. Patient consent was waived by the institutional research ethics board. Result(s): A total of 565 patients were included. Baseline demographics are reported in Table 1. Median length-of- stay was 9.0 days (range 5-131). 178 patients (31.5%) required critical care support and 79 patients (14%) died during index admission. 25 patients (4.4%) had VTE during hospitalization, of which 17 occurred within first 2 weeks and none occurred in those on therapeutic anticoagulation. There were no fatal bleeds. 5 patients (0.88%) developed critical site bleeding. Patient characteristics, anticoagulant use and bleeding rates during hospitalization are reported in Table 2. Among 486 discharged patients, median length of follow-up was 163 days (range 3-600): 63.5% had at least 90 days of follow-up data and 18.7% were lost to follow-up. 5 patients (1.3%) had symptomatic VTE diagnosed within 3 months after discharge. Conclusion(s): The in-hospital incidence of VTE in COVID-19 was lower but post-discharge incidence was higher than other studies. Therapeutic anticoagulation appeared protective against symptomatic VTE. (Table Presented).
ABSTRACT
INTRODUCTION: COVID-19 infection induces pulmonary endothelial injury, widespread thrombosis and microangiopathy in the gas-exchange networks resulting in ventilation-perfusion mismatch and hypoxemia. We reasoned that therapies aiming to redistribute blood flow away from gasless tissue such as prone positioning (PP) and inhaled nitric oxide (iNO) may not produce the same expected effects on gas exchange as seen in other causes of ARDS. We therefore investigated the effect of PP and iNO on gas exchange in COVID-19 ARDS. METHODS: All adult intubated patients with confirmed SARS-CoV-2 infection and respiratory failure undergoing PP and administration of iNO during April 2020 were included prospectively, provided they had no chronic pulmonary or cardiovascular disease and were hemodynamically stable. Arterial blood gases and measurements of pulmonary mechanics were taken before and after iNO administration (0- 40ppm over 20mins) whilst supine and before and after one hour in prone position. RESULTS: Six intubated patients with COVID-19 pneumonia were assessed for inclusion. One patient was excluded due to chronic pulmonary disease. Median age was 58 years (range, 50-63) and four patients (80%) were male. Median time since occurrence of symptoms was 11 days (range, 8-22), median time since intubation was 3 days (range, 1-6). Prior to PP and iNO delivery median static compliance was 45mL/cmH2O (IQR, 28-50). The median supine PaO2:FiO2 and dead space fraction (VD/VT) were 110 (IQR, 103-208) and 0.21 (IQR, 0.10-0.27), and were 131 (IQR, 100-156) and 0.19 (IQR, 0.12-0.31) after one hour prone. After the addition of iNO, the median PaO2:FiO2 and VD/VT were 111 (IQR, 110-206) and 0.25 (IQR, 0.17-0.30), and 147 (IQR, 115-176) and 0.19 (IQR, 0.14-0.32) whilst prone. CONCLUSIONS: In this cohort patients with moderate and severe ARDS due to COVID-19, we found that PP marginally improved oxygenation whilst the addition of iNO did not have a significant additional effect. We speculate that the dissociation between relatively normal lung mechanics and ventilation perfusion mismatch supports the theory of a dysregulated vasculature secondary to COVID-19 induced endothelial damage. Redistributing blood flow away from gasless tissue may not produce the same expected effects on gas exchange as seen in other causes of ARDS.