PubMed · 13012589
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F A INDA. 1953. Bleeding peptic ulcer.. https://pubmed.ncbi.nlm.nih.gov/13012589/
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Von Willebrand disease (vWD) is an inherited bleeding disorder with a prevalence of approximately 1% in the general population. The bleeding occurs in this disorder primarily because of abnormalities in platelet adhesion, due to a primary deficiency or defect in the von Willebrand factor (vWF) often with a concomitant decrease in factor VIII (FVIII) levels. The mainstay of treatment for the majority of patients with vWD is desmopressin, which releases vWF from endothelial cells. For patients in which desmopressin is neither suitable or recommended, coagulation factor concentrates containing both vWF with FVIII are the alternative therapeutic option for controlling bleeding. Joint disease is an uncommon but disabling complication of vWD. The arthropathy results from recurrent bleeding into a joint, with the ankle and hip being the joints most often affected, particularly in patients with type 3 vWD. Without adequate treatment, persistent bleeding into joints can result in pain, joint degeneration, swelling and loss of range of motion (ROM). There is some evidence to suggest that joint bleeding and subsequent joint damage might be prevented by early prophylaxis. A soon to open clinical trial by the Von Willebrand Disease Prophylaxis Network (vWD PN) aims to further explore this treatment concept. This article addresses the prophylaxis of vWD, with a particular focus on joint disease.
PURPOSE: To briefly review the risks, in patients presenting for surgery, associated with the available antiplatelet agents, and to present the principles that should guide the evaluation of these risks and how to manage them. METHODS: A narrative review of the current medical literature in English and French. MAIN FINDINGS: Antiplatelet agents [mainly acetylsalicylic acid, clopidogrel and glycoprotein (GP) IIb/IIIa inhibitors] are used increasingly to prevent arterial thrombosis. Clinicians are confronted with the hemorrhagic risk associated with the continuation of antiplatelet agents throughout surgery or, conversely, with the thrombotic risk associated with their discontinuation. Most experts recommend surgery while maintaining acetylsalicylic acid for most vascular procedures and in several additional settings where the bleeding risk has been shown (or is likely) to be low. It is commonly recommended that clopidogrel be stopped five days before surgery to allow replacement of half the platelet pool. This approach has been associated with thrombotic events in patients waiting for urgent myocardial revascularization. In this context, aprotinin may reduce blood losses and transfusion requirements. Withdrawal of the competitive GPIIb/IIIa inhibitors at the beginning of surgery will decrease the risk of bleeding, less so for abciximab owing to its avid binding to platelet receptors. Platelets should not be transfused prophylactically, but only to those few patients with abnormal bleeding thought to be related to the persisting effect of antiplatelet therapy. CONCLUSIONS: Unfortunately, data regarding the management of antiplatelet agent-treated patients undergoing surgery, especially non-cardiovascular, are scarce. Further clinical trials must be conducted to guide the clinical management of these patients.