Vascular medicine
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The risk of venous thromboembolism (VTE) varies throughout a woman's life and is associated primarily with underlying hormonal exposure. Alteration in hemostatic mechanisms, including resistance to activated protein C, may explain this altered risk. Initially, development of VTE with the use of contraception in young adulthood may reveal inherited thrombophilia. ⋯ Use of hormone replacement therapy later in life is associated with increased risk of VTE, and may be safest if given as an estrogen-only preparation to young postmenopausal women for less than 5 years. Universal screening for thrombophilia prior to pregnancy or initiating hormonal therapy is not recommended; however, selected testing in high-risk groups may be warranted. The lack of firm recommendations for the prevention of VTE in women highlights the need for future investigation aimed at identifying high-risk groups and evaluating the efficacy of prophylactic measures.
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Review
Delayed ischemia after subarachnoid hemorrhage: result of vasospasm alone or a broader vasculopathy?
The term vasospasm is commonly used to describe constriction of cerebral blood vessels after subarachnoid hemorrhage which results in the restriction of blood flow and ischemia in affected portions of the brain. The pathophysiological changes that underlie vascular constriction after subarachnoid hemorrhage include changes within the vessel walls themselves, alteration of the levels of several vasoactive substances, and broader pathological conditions such as immune responses, inflammation, and oxidative damage. In this review, we summarize the current state of knowledge concerning the processes that occur in cerebral blood vessels after subarachnoid hemorrhage and how they may be involved in the development of vasospasm. We also propose that, rather than merely vasospasm, the multitude of vascular effects occurring after subarachnoid hemorrhage can be best described as a post-subarachnoid hemorrhage vasculopathy.
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Review Case Reports
Vertebral artery dissection following intravascular catheter placement: a case report and review of the literature.
Vertebral artery dissections (VAD) are known to occur as a result of mechanical manipulations of the cervical region, traumatic injury, iatrogenic injury and are also known to arise spontaneously. We report a case of vertebral artery dissection following vertebral artery cannulation during a central line placement and review the literature. The patient underwent intravascular catheter placement that subsequently demonstrated arterial blood. ⋯ There were no neurological sequelae. The patient was successfully anticoagulated with warfarin but died from unrelated complications. This case report describes the rare iatrogenic event of VAD and reviews its etiology, diagnosis, complications, and management.
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Inherited abnormalities of coagulation are increasingly recognized in patients with venous thromboembolism. Common causes of hypercoagulability, also known as thrombophilia, include factor V Leiden, the prothrombin gene mutation, hyperhomocysteinemia, and antiphospholipid antibodies. ⋯ The most cost-effective approach is to initially screen for factor V Leiden, the prothrombin gene mutation, hyperhomocysteinemia, and antiphospholipid antibodies because these are the most common defects causing thrombophilia. Long-term anticoagulation is controversial but should be considered if unprovoked venous thromboembolism recurs.
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Reflex sympathetic dystrophy (RSD) syndrome has been recognized clinically for many years. It is most often initiated by trauma to a nerve, neural plexus, or soft tissue. Diagnostic criteria are the presence of regional pain and other sensory changes following a noxious event. ⋯ Besides, it has been suggested that excitation of sensory nerve fibres at axonal level causes release of neuropeptides at the peripheral endings of these fibres. These neuropeptides may induce vasodilation, increase vascular permeability, and excite surrounding sensory nerve fibres -- a phenomenon referred to as neurogenic inflammation. At the level of the central nervous system, it has been suggested that the increased input from peripheral nociceptors alters the central processing mechanisms.