Within the body’s vascular system, blood flows in its liquid state while clotting components of the hemostatic system circulate in their inactive forms. Once activated, the hemostatic components undergo a series of reactions to produce a clot at the site of an injured blood vessel, resulting in repair of the injury. If this healthy hemostatic system becomes defective, by means of a hypercoaguable condition or a bleeding disorder, abnormal clotting or blood loss is predictable, respectively. Consequently, hemostasis can be considered an unstable system. Having a working knowledge of the hemostatic system is vital for understanding pathophysiology while managing patients with bleeding or clotting problems.
Physiologically, hemostasis is the body’s mechanism designed to prevent blood loss by forming a clot within injured blood vessels. When activated, the hemostatic system involves a number of intricate and biochemical events, including three main phases: the vascular phase, the platelet phase and the coagulation phase.2,3 The vascular phase involves vasoconstriction of arteries and veins, exposure of collagen, and release of specialized tissue factors that activate platelets to the injured area. The platelet phase involves platelet adhesion and aggregation of platelets (thrombocytes) to form a fragile, jelly-like temporary clot, termed a hemostatic platelet plug. This platelet plug strives to seal the injured area(s) or gap(s) in the vessels to temporarily prevent blood loss. The coagulation phase involves activation of a “cascade” of twelve clotting factors (or plasma coagulation factors) that ultimately produce strands of fibrin. Fibrin binds the platelet plug to form the permanent, tight clot, termed the hemostatic clot. To maintain equilibrium, the body’s fibrinolytic system is activated: anticlotting mechanisms in the fibrinolytic system prevent the expansion of the final clot; cause dissolution of the existing clot; and complete the repair of the injured vessel.2,4,5 The microscopic illustration of the hemostatic clot (thrombus) displays a matrix of platelets, red blood cells, white blood cells, and fibrin (Figure 1).
Alterations in the hemostatic system result in a myriad of bleeding disorders. Disorders of the body’s hemostatic system can lead to serious clinical clotting or bleeding consequences. Regarding bleeding disorders, they can be acquired, inherited or drug-induced. Characterized by a group of distinct conditions, bleeding disorders can affect the “ability of blood vessels, platelets, and coagulation factors to maintain hemostasis.”2 Major causes of bleeding result in the body’s inability to form a hemostatic plug or a clot, affecting the platelet phase and/or the coagulation phase, correspondingly.
For the platelet phase, common causes of bleeding include decreased platelet count and/or abnormal platelet function. For the coagulation phase, common causes of bleeding can include deficiencies in the clotting factors. When treating dental patients with bleeding disorders, dentists and dental hygienists should possess an awareness of common bleeding disorders as well as an awareness of a patient’s predisposition to bleeding during restorative, periodontal or surgical procedures.
Affecting up to 150 patients in a dental practice of 2000 adults, potential bleeding disorders will be encountered.2 Common drug-induced causes of bleeding disorders seen in dental practices include patients on anticoagulation or antiplatelet therapy. Patients on “low-intensity” anticoagulation therapy are at a 1% risk for a major bleed and an 8% risk for a minor bleed during multiple invasive dental procedures.2 When a “high-intensity” anti-coagulation therapy is warranted, patients have a “five-fold”2 risk for bleeding. Anti-coagulation therapy is widely prescribed for individuals with a history of mechanical heart valves, secondary myocardial infarction, cerebral vascular accidents, or thrombophlebitis. Additionally, millions of patients who are on anti-platelet therapy to prevent cardiovascular disorders or inflammatory joint disorders will likely cause bleeding problems during invasive dental procedures.
The most common inherited bleeding disorder is von Willebrand’s disease, which affects platelet function and, in some cases, causes a clotting factor deficiency (Factor VIII). Of the common genetic disorders Hemophilia A (a factor VIII deficiency) occurs in about 80% of all inherited coagulation disorders, and Hemophilia B (a factor IX deficiency) occurs in about 13%. Affecting a smaller percentage of the population in the United States, these inherited conditions require extreme care and possibly specialized treatment planning to prevent a clinical bleed during invasive dental procedures.
Depending on the cause, medical and dental management may differ for any one of the bleeding disorders. Therefore, it is imperative dental professionals conduct comprehensive clinical assessments and communicate with the patient’s supervising physician to develop appropriate treatment planning strategies to treat such patients.
Inevitably, dentists and dental hygienists will treat a considerable number of patients with bleeding problems in the dental environment; although, many clinicians may perceive these patients’ bleeding complications as a significant challenge. Hence, this continuing education course plans to address such challenges, including: knowledge about the hemostatic system; interpretation of laboratory testing; an overview of underlying causes of common bleeding disorders; clinical management options to address the risk of bleeding during and after invasive dental procedures; and the presentation of current recommendations regarding managing patients on anti-coagulation and anti-platelet therapy. Acquiring knowledge of these essentials will greatly enhance the management of patients with bleeding disorders in the dental office.