Background Managing patients with concomitant intracranial bleeding (ICB) and symptomatic pulmonary embolism (PE) is challenging and there are no guidelines. Methods: We identified patients with intermediate or high-risk PE and concomitant ICB referred to our institutional PE response teams. A literature review was performed to evaluate the effectiveness and risks of various treatment strategies for this challenging clinical conundrum. Results: Two patients with subdural hematoma, symptomatic intermediate-high risk PE and deep vein thrombi were identified in our institutions. Both patients were treated with lytic-free mechanical thrombectomy combined with inferior vena cava (IVC) filter implantation. This allowed for an anticoagulation-free period, during which surgical drainage was performed. Anticoagulation was safely started several days after neurosurgery. A literature review identified 148 similar cases. There was significant risk of in-hospital mortality due to PE in patients who were left untreated. Early anticoagulation was associated with elevated risks of hematoma expansion, extracranial bleeding and residual risk of PE mortality. Patients undergoing surgical or lytic-free mechanical thrombectomy all survived to discharge without bleeding complications. Conclusions: Combining thrombolytic-free mechanical thrombectomy with an IVC filter allows for effective PE treatment and temporary avoidance of anticoagulation whilst patients undergo definitive neurosurgery for concomitant ICB. Such an approach seems safer, less invasive and more clinically effective compared to other strategies reported in the literature.
Predisposing factors for venous thrombosis can be identified in the majority of patients with established venous thromboembolism (VTE). However, an obvious precipitant may not be identified during the initial evaluation of such patients. In the present case, a 47-year-old female presented to the emergency department of our hospital after ingesting multiple drugs. She had no VTE-related risk factors or previous episodes, nor any family history of VTE. After admission to the intensive care unit sudden hypoxemia developed, and during the evaluation cerebral, renal, and splenic infarctions with pulmonary embolisms were diagnosed. However, the sources of the emboli could not be identified by transthoracic echocardiography or computed tomography angiography. Protein C deficiency was identified several days later. We recommend that hypercoagulable states be taken into consideration, especially when unexplained thromboembolic events develop in multiple or unusual venous sites.