Venous thromboembolism

• Cerebral infarction following administration of andexanet alfa for anticoagulant reversal in a patient with traumatic acute subdural hematoma
• Response to "Additional Associated Factors for Venous Thromboembolism in Patients with Traumatic Brain Injury"
• Factors related to morbidity and mortality of meningiomas resection‑associated venous thromboembolism (Review)
• Streamlining care in two neurosurgical practices in a rural trauma center
• Factors Associated with Venous Thromboembolism Development in Patients with Traumatic Brain Injury
• Risk of intracranial hemorrhage with direct oral anticoagulation versus low molecular weight heparin in the treatment of brain tumor-associated venous thromboembolism: A meta-analysis
• The risk of intracranial hemorrhage in glioma patients receiving anticoagulant treatment for venous thromboembolism: a bayesian network meta-analysis
• Comparison of the Efficacy and Safety of Rivaroxaban and Low Molecular Heparin in Preventing Venous Thromboembolism in Inpatient Cancer Patients

Venous thromboembolism risk factors.

Thromboembolic diseases are of major clinical concern due to their high prevalence and consequences, which are often fatal. Venous thromboembolism (VTE) is estimated to be the third most common cardiovascular disorder after coronary heart disease and stroke ¹⁾.

Approximately 500,000 cases of venous thromboembolism (VTE) are reported annually in the United States.

Deep-Vein Thrombosis (Deep-vein thrombosis) and pulmonary embolism (PE) are two clinical manifestations of VTE. In fact, VTE is essentially a massive PE, causing death in 70% within the first hour following the onset of symptoms.

VTEs are associated with longer hospitalizations, a decreased likelihood of being discharged home, and overall increases of hospital resource utilization and cost in inpatient and outpatient settings. VTE patients generate greater charges in the outpatient setting and are more likely to become readmitted at 6, 12, and 18 months after surgery, demonstrating a significant socioeconomic impact long after occurrence ²⁾.

see Venous thromboembolism in high-grade glioma

see Venous Thromboembolism in Spontaneous Intracerebral Hemorrhage

During aneurysm coiling

An inflammatory reaction is usually present, mainly in the superficial veins and, for this reason this pathology is called most of the time thrombophlebitis. In fact, the inflammatory reaction and the white blood cells play a role in the resolution of venous clots.

Whether an ischemic stroke is due to a noncardiogenic or cardiogenic source, the mechanism of causing a stroke is the same. Both sources are involved with the development of thrombi or emboli that move from their original source to the brain blocking blood flow in the process. Known as Virchow’s triad, venous stasis, vascular injury, and hypercoagulability are major components in the development of thrombi.

A blood clot forms due to blood changes in which cellular material, such as red and white blood cells and platelets, become bound together by fibrin strands. Deep-Vein Thrombosis (Deep-vein thrombosis), forming in the veins of the lower limbs, are the most common emboli associated with pulmonary emboli.

Nonspecific; pain, tenderness, swelling, discoloration (paleness or redness) in lower extremities.

Cerebral venous sinus thrombosis

see Pulmonary Embolism.

Asymptomatic cerebral thromboembolic events can be detected by Diffusion-weighted magnetic resonance imaging after ACDF. The incidence of such events remains very rare despite the direct manipulation and associated alteration of common carotid artery flow dynamics ³⁾.

see Venous thromboembolic prophylaxis.

Venous thromboembolism treatment.

Venous thromboembolism outcome.