In our study, CTPA was performed in a population in which we were looking for a cause to clinical deterioration, which might be due to PE, but also to mechanical ventilation-acquired pneumonia. We therefore did not necessarily select a population with a strong suspicion of PE. We did not have a systematic standardized assessment of thromboembolic events as well. Imaging was thus performed based on the evolution of clinical or laboratory parameters. Respiratory (PaO2/FiO2) or hemodynamic deterioration, or evidence of dilated right ventricle—even without acute cor pulmonale—was explored by CTPA. A rapid elevation of D-dimer despite anticoagulation, reflecting increased thrombin generation, i.e., clot formation, and fibrinolysis, was investigated. D-dimer level did not differ at baseline between patients with/without pulmonary embolism, but increased with thrombotic events during ICU stay, with D-dimers > 5 mg/L in 92% of the patients. A sudden increase in D-dimer level along with clinical deterioration was an additional argument to explore patients by CTPA.