Abstract
We present a systemic review of available literature on the complications of deep venous thrombosis that develops in patients presenting with acute stroke. There are several pharmacological and physical treatment options available and used. We aim to summarize the management plans currently used at different centers. In conclusion, low-dose anticoagulant therapy for ischemic stroke is recommended. In the case of intracerebral hemorrhage, pneumatic sequential compression devices should be placed initially, followed by the administration of ultra-fractioned heparin on the next day, and then oral anticoagulant therapy to replace the heparin after a week in high-risk patients. Similar prophylactic treatment recommendations are used for subarachnoid hemorrhage.
Highlights
BackgroundDeep vein thrombosis (DVT) is a serious complication in stroke patients and may lead to the devastating consequences of a pulmonary embolism
We present a systemic review of available literature on the complications of deep venous thrombosis that develops in patients presenting with acute stroke
In the case of intracerebral hemorrhage, pneumatic sequential compression devices should be placed initially, followed by the administration of ultra-fractioned heparin on the day, and oral anticoagulant therapy to replace the heparin after a week in high-risk patients
Summary
Deep vein thrombosis (DVT) is a serious complication in stroke patients and may lead to the devastating consequences of a pulmonary embolism. Both pharmacological and physical methods are used to prevent DVT. DVT commonly occurs in the setting of stroke and can be a fatal complication if it leads to pulmonary emboli. In immobilized post-stroke patients, the incidences of DVTs vary from 1075%, depending on the diagnostic method and time of evaluation [1,2]. The onset of development of a DVT after acute stroke can be as early as the second day, peaking between Days 2 and 7; if left untreated, proximal DVT have a 15% risk of death [7]. The risk of DVT/pulmonary embolism (PE) may even be higher in patients with SAH and ICH but smallest with the transient ischemic attack (TIA) [8]
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