BACKGROUND: Coronavirus disease-2019 (COVID-19) is associated with hypercoagulability and increased thrombotic risk in critically ill patients. To our knowledge, no studies have evaluated whether aspirin use is associated with reduced risk of mechanical ventilation, intensive care unit (ICU) admission, and in-hospital mortality. METHODS: A retrospective, observational cohort study of adult patients admitted with COVID-19 to multiple hospitals in the United States between March 2020 and July 2020 was performed. The primary outcome was the need for mechanical ventilation. Secondary outcomes were ICU admission and in-hospital mortality. Adjusted hazard ratios (HRs) for study outcomes were calculated using Cox-proportional hazards models after adjustment for the effects of demographics and comorbid conditions. RESULTS: Four hundred twelve patients were included in the study. Three hundred fourteen patients (76.3%) did not receive aspirin, while 98 patients (23.7%) received aspirin within 24 hours of admission or 7 days before admission. Aspirin use had a crude association with less mechanical ventilation (35.7% aspirin versus 48.4% nonaspirin, P = .03) and ICU admission (38.8% aspirin versus 51.0% nonaspirin, P = .04), but no crude association with in-hospital mortality (26.5% aspirin versus 23.2% nonaspirin, P = .51). After adjusting for 8 confounding variables, aspirin use was independently associated with decreased risk of mechanical ventilation (adjusted HR, 0.56, 95% confidence interval [CI], 0.37-0.85, P = .007), ICU admission (adjusted HR, 0.57, 95% CI, 0.38-0.85, P = .005), and in-hospital mortality (adjusted HR, 0.53, 95% CI, 0.31-0.90, P = .02). There were no differences in major bleeding (P = .69) or overt thrombosis (P = .82) between aspirin users and nonaspirin users. CONCLUSIONS: Aspirin use may be associated with improved outcomes in hospitalized COVID-19 patients. However, a sufficiently powered randomized controlled trial is needed to assess whether a causal relationship exists between aspirin use and reduced lung injury and mortality in COVID-19 patients.

BACKGROUND: Over 6 million esophagogastroduodenoscopy (EGD) procedures are performed in the United States each year. Patients having anesthesia for advanced EGD procedures, such as interventional procedures, are at high risk for hypoxemia. METHODS: Our primary study aim was to evaluate whether high-flow nasal cannula (HFNC) oxygen reduces the incidence of hypoxemia during anesthesia for advanced EGD. Secondarily, we studied whether HFNC oxygen reduces hypercarbia or hypotension. After obtaining written informed consent, adults having anesthesia for advanced EGD, expected to last longer than 15 minutes, were randomly assigned to receive HFNC oxygen or standard nasal cannula (SNC) oxygen. The primary outcome was occurrence of one or more hypoxemia events during anesthesia, defined by arterial oxygen saturation <92% for at least 15 consecutive seconds. Secondary outcomes were occurrence of one or more hypercarbia or hypotension events. A hypercarbia event was defined by a transcutaneous CO2 measurement 20 mm Hg or more above baseline, and a hypotension event was defined by a mean arterial blood pressure measurement 25% or more below baseline. RESULTS: Two hundred seventy-one adult patients were enrolled and randomized, and 262 patients completed study procedures. Eight randomized patients did not complete study procedures due to changes in their anesthesia or endoscopy plan. One patient was excluded from analysis because their procedure was aborted after 1 minute. Patients who received HFNC oxygen (N = 132) had a significantly lower incidence of hypoxemia than those who received SNC oxygen (N = 130; 21.2% vs 33.1%; hazard ratio [HR] = 0.59 [95% confidence interval {CI}, 0.36–0.95]; P = .03). There was no difference in the incidence of hypercarbia or hypotension between the groups. The HR for hypercarbia with HFNC oxygen was 1.29 (95% CI, 0.89–1.88; P = .17), and the HR for hypotension was 1.25 (95% CI, 0.86–1.82; P = .25). CONCLUSIONS: HFNC oxygen reduces the incidence of hypoxemia during anesthesia for advanced EGD and may offer an opportunity to enhance patient safety during these procedures.

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BACKGROUND: There is a paucity of data on the underlying procoagulant–anticoagulant balance during extracorporeal membrane oxygenation (ECMO). We hypothesized that adult ECMO patients would have an imbalance between procoagulant and anticoagulant factors, leading to an abnormal underlying thrombin generation (TG) pattern. METHODS: Twenty adult venoarterial (VA) ECMO patients had procoagulant and anticoagulant factor levels measured temporally on ECMO day 1 or 2, day 3, and day 5. In heparin-neutralized plasma, underlying TG patterns, and sensitivity to activated protein C were assessed using calibrated automated thrombogram. TG parameters including lag time, peak TG, and endogenous thrombin potential (ETP) were compared against 5 normal plasma controls (3 males and 2 females) obtained from a commercial supplier. Thrombomodulin (TM) was added to some samples to evaluate for activated protein C resistance. RESULTS: Procoagulant factors (factor [F] II, FV, and FX) were mostly in normal reference ranges and gradually increased during the first 5 ECMO days (P = .022, <.001, <.001). FVIII levels were elevated at all time points and did not change (P = .766). In contrast, FXI was in the low-normal range but did not increase during ECMO (P = .093). Antithrombin (AT) and protein C levels were below normal but increased during the first 5 ECMO days (P = .002 and P = .014). Heparinase-treated samples showed prolonged lag time, increased peak TG, and increased ETP compared to controls; mean difference in lag time on ECMO day 1 or 2 = 6.0 minutes (99% confidence interval [CI], 2.8–9.2), peak TG = 193.4 (99% CI, 122.5–264.3), and ETP = 1170.4 (99% CI, 723.2–1617.6). After in vitro TM treatment, differences in TG parameters were accentuated and ECMO samples appeared insensitive to TM treatment; mean difference in lag time on ECMO day 1 or 2 = 9.3 minutes (99% CI, 6.2–12.4), peak TG = 233.0 (99% CI, 140.9–325.1), and ETP = 1322.5 (99% CI, 764.8–1880.2). Similar differences in TG parameters were observed on ECMO days 3 and 5. CONCLUSIONS: Contact activation occurs during ECMO, but procoagulant factor levels are generally preserved. Although heparin-neutralized TG is delayed, peak TG and ETP are supranormal in the setting of high FVIII and low AT and protein C levels. Resistance to TM is also apparent. These changes demonstrate a possible mechanism for hypercoagulability during adult VA ECMO.

Critically ill patients with coronavirus disease 2019 (COVID-19) have been observed to be hypercoagulable, but the mechanisms for this remain poorly described. Factor VIII is a procoagulant factor that increases during inflammation and is cleaved by activated protein C. To our knowledge, there is only 1 prior study of factor VIII and functional protein C activity in critically ill patients with COVID-19. Here, we present a case series of 10 critically ill patients with COVID-19 who had severe elevations in factor VIII activity and low normal functional protein C activity, which may have contributed to hypercoagulability.