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Antithrombotic drugs are those used to slow down blood clot formation, including antiplatelet agents and anticoagulants. Dentists commonly encounter patients who are on antithrombotic drugs, as these drugs are used to manage common conditions. For example, the direct oral anticoagulant drugs (DOACs) are frequently prescribed for management of atrial fibrillation, which affects approximately 5% of the Australian population aged 55 and over (1). As a result, the DOACs were within the top 100 drugs dispensed on the PBS in 2018 in Australia (2). Increased risk of oral bleeding is thus a common complication dentists may have to manage. The risk of post-extraction bleeding is increased three-fold in patients taking anticoagulants compared with those not taking these drugs (3, 4). Understanding the principles of haemostasis, how to balance the risk of bleeding against the risk of clotting, and how to manage these patients is thus an integral part of dentistry.
There is currently little published guidance on the management of anticoagulant and antiplatelet medication in patients admitted with epistaxis. The routine practice of withholding such medication in an attempt to control the epistaxis is common in the UK. However, this practice is not evidence-based, is often unnecessary, and can be associated with significant morbidity. This study introduces a treatment algorithm for oral anticoagulant and antiplatelet therapy in epistaxis patients, validated through a completed audit cycle.
Methods:
One hundred patients admitted with epistaxis to the University Hospital Southampton NHS Foundation Trust were studied via a two-audit cycle covering the implementation of a new treatment algorithm formulated jointly by the otolaryngology and haematology departments.
Results:
On admission, 58 per cent of patients were taking some form of anticoagulant or antiplatelet medication. The number of patients having such medication withheld decreased significantly between the two audits, for all drugs studied (i.e. aspirin, clopidogrel and warfarin). There was no significant increase in re-bleeding or re-admission rates between the audits.
Conclusion:
Implementation of this treatment algorithm would help standardise management for epistaxis patients taking anticoagulant or antiplatelet drugs, and should reduce morbidity associated with unnecessary routine discontinuation of such medication.
This chapter explores the complex relationship of stroke with polyarteritis nodosa (PAN) and microscopic polyangiitis (MPA). MPA is a systemic necrotizing vasculitis that clinically and histologically involves capillaries, venules, or arterioles without granulomata, and is associated with necrotizing crescentic glomerulonephritis and hemorrhagic pulmonary capillaritis, which are the main causes of mortality and morbidity. Hemorrhagic strokes occur more frequently than ischemic infarction in MPA. Immunohistochemical studies from muscle and nerve biopsies showed that macrophages and T cells, mostly CD8+, are involved in the pathogenesis of PAN. Neurological symptoms and signs are a major and common feature of PAN, occurring in nearly three-quarters of patients. A close relationship between the use of corticosteroids and stroke exists in PAN. From a therapeutic point of view, antiplatelet drugs, which inhibit platelet thromboxane production, might reduce the risk of corticosteroid-induced, antiplatelet drugs in PAN. The use of aspirin and corticosteroids prospectively prevents stroke recurrence.
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