Background and Aim:We aimed to develop a clinical prediction model for pulmonary thrombosis (PT) diagnosis in hospitalized COVID-19 patients. Methods: Non-intensive care unit hospitalized COVID-19 patients who underwent a computed tomography pulmonary angiogram (CTPA) for suspected PT were included in the study. Demographic, clinical, analytical, and radiological variables as potential factors associated with the presence of PT were selected. Multivariable Cox regression analysis to develop a score for estimating the pre-test probability of PT was performed. The score was internally validated by bootstrap analysis. Results: Among the 271 patients who underwent a CTPA, 132 patients (48.7%) had PT. Heart rate >100 bpm (OR = 4.63 [95% CI: 2.30-9.34]; P < 0.001), respiratory rate >22 bpm (OR = 5.21 [95% CI: 2.00-13.54]; P < 0.001), RALE score ≥4 (OR = 3.24 [95% CI: 1.66-6.32]; P < 0.001), C-reactive protein (CRP) >100 mg/L (OR = 2.10 [95% CI: 0.95-4.63]; P = 0.067), and D-dimer >3.000 ng/mL (OR = 6.86 [95% CI: 3.54-13.28]; P < 0.001) at the time of suspected PT were independent predictors of thrombosis. Using these variables, we constructed a nomogram (CRP, Heart rate, D-dimer, RALE score, and respiratory rate [CHEDDAR score]) for estimating the pre-test probability of PT. The score showed a high predictive accuracy (area under the receiver-operating characteristics curve = 0.877; 95% CI: 0.83−0.92). A score lower than 182 points on the nomogram confers a low probability for PT with a negative predictive value of 92%. Conclusions: CHEDDAR score can be used to estimate the pre-test probability of PT in hospitalized COVID-19 patients outside the intensive care unit. Relevance for Patients: Developing a new clinical prediction model for PT diagnosis in COVID-19 may help in the triage of patients, and limit unnecessary exposure to radiation and the risk of nephrotoxicity due to iodinated contrast.

Background: We aimed to develop a clinical prediction model for pulmonary embolism (PE) diagnosis in hospitalized COVID-19 patients. Methods: Hospitalized non-intensive care unit COVID-19 patients who underwent a computed tomography pulmonary angiogram for suspected PE were included. Demographic, clinical, laboratory and radiological variables were selected as potential factors associated with the presence of PE. Multivariable Cox regression analysis to develop a score for estimating the pretest probability of PE was used. The score was internally validated by bootstrap analysis.Results: Among the 271 patients who underwent a computed tomography pulmonary angiogram, 132 patients (48.70%) had PE. Heart rate >100 bpm (OR 4.63 [95% CI 2.30–9.34]; p<0.001), respiratory rate >22 bpm (OR 5.21 [95% CI 2.00–13.54]; p<0.001), RALE score ≥4 (OR 3.24 [95% CI 1.66–6.32]; p<0.001), C-reactive protein  >100 mg/L (OR 2.10 [95% CI 0.95–4.63]; p = 0.067), and D-dimer >3.000 ng/mL (OR 6.86 [95% CI 3.54–13.28]; p<0.001) at the time of suspected pulmonary thrombosis were independent predictors of PE. Using these variables, we constructed a nomogram (CHEDDAR score [C-reactive protein, HEart rate, D-Dimer, RALE score, and Respiratory rate]) for estimating the pretest probability of PE in an individual patient. The score showed a high predictive ability (AUC 0.877; 95% CI: 0.83−0.92). A score lower than 182 points on the nomogram confers low probability of PE with a negative predictive value of 92%. Conclusions: CHEDDAR score can be used to estimate the pretest probability of PE in hospitalized COVID-19 patients outside intensive care unit.

Background To compare the severity of pulmonary embolism (PE) and the long-term complications between patients with and without COVID-19, and to investigate whether the tools for risk stratification of death are valid in this population. Methods We retrospectively included hospitalized patients with PE from 1 January 2016 to 31 December 2022. Comparisons for acute episode characteristics, risk stratification of the PE, outcomes, and long-term complications were made between COVID and non-COVID patients. Results We analyzed 116 (27.5%) COVID patients and 305 (72.4%) non-COVID patients. In patients with COVID-19, the traditional risk factors for PE were absent, and the incidence of deep vein thrombosis was lower. COVID patients showed significantly higher lymphocyte count, lactate dehydrogenase, lactic acid, and D-dimer levels. COVID patients had PE of smaller size (12.3% vs. 25.5% main pulmonary artery, 29.8% vs. 37.1% lobar, 44.7% vs. 29.5% segmental and 13.2% vs. 7.9% subsegmental, respectively; p < 0.001), less right ventricular dysfunction (7.7% vs. 17.7%; p = 0.007) and higher sPESI score (1.66 vs. 1.11; p < 0.001). The need for mechanical ventilation was significantly higher in COVID patients (8.6% vs. 1.3%; p < 0.001); However, the in-hospital death was less (5.2% vs. 10.8%; p = 0.074). The incidence of long-term complications was lower in COVID cohort (p < 0.001). PE severity assessed by high sPESI and intermediate and high-risk categories were independently associated with in-hospital mortality in COVID patients. Conclusion The risk of in-hospital mortality and the incidence of long-term complications were lower in COVID-19. The usual tools for risk stratification of PE are valid in COVID patients.