Introduction

Anticoagulant and antiplatelet agents are prescribed to patients with histories or high probabilities of thromboembolic events (blood clots). These at-risk patients include those who have suffered from deep vein thrombosis, pulmonary embolism, or nonvalvular atrial fibrillation, an arrhythmia that predisposes patients to intracardiac clot formation.

Anticoagulants include the vitamin K antagonist warfarin (Coumadin^®) and newer target-specific agents such as the direct thrombin inhibitor dabigatran (Pradaxa^®) as well as factor Xa inhibitors apixaban (Eliquis^®) and rivaroxaban (Xarelto^®). Antiplatelet agents include clopidogrel (Plavix^®), ticlopidine (Ticlid^®), and aspirin. Adverse effects associated with these drugs can result in prolonged bleeding or bruising.

Dental providers must assess the risk of bleeding (hemorrhage) and clotting (thrombosis) in this patient population. Most patients undergoing oral surgery in the office do well and have uneventful courses with minimal blood loss. Significant blood loss during oral surgery is atypical, but such bleeding may prolong postoperatively as well.

A few simple steps can prevent bleeding complications and potentially dangerous postoperative sequelae. Practitioners must understand the patient’s medical history, survey the patient’s medications and note any potential interactions, understand the physiology of blood coagulation, evaluate the surgical site, remain aware of meticulous surgical techniques, and implement calm, sound clinical judgment.

Biology of Hemostasis

• There are two main phases of hemostasis:

  • Primary or cellular phase.

  • Secondary or humoral phase.

Primary (Cellular) Phase of Hemostasis

• Begins immediately after endothelial disruption and is characterized by vasoconstriction, platelet adhesion, and formation of a soft-tissue plug.

• Temporary local constriction of vascular smooth muscle; blood flow slows down.

• Within 20 seconds of injury, circulating von Willebrand factor attaches to the subepithelium at the injury site and adheres to the glycoproteins on the surface of the platelets.

• Platelets are then activated by contact with the collagen.

• Activated platelets then bind with circulating fibrinogen, forming a platelet plug.

• This is a short-lived phase of hemostasis and the plug can be easily dislodged.

• The soft platelet plug is stabilized during secondary hemostasis to form a clot.

• Vasoconstriction and reduction in blood flow are maintained by platelet secretion of serotonin, prostaglandin, and thromboxane as the coagulation cascade is initiated.

• If the patient has a disorder of primary hemostasis, there will be an abnormality in platelets.

  • Classic symptoms are:

    • Epistaxis (nose bleed).

    • Hemoptysis (coughing up blood).

    • Gastrointestinal (GI) bleeds.

    • Hematuria (blood in urine).

    • Menorrhagia (abnormal, prolonged menstruation).

    • Petechiae (< 3 mm).

    • Purpura (3–10 mm).

    • Ecchymoses (> 1 cm).

    • Easy bruising.

  • Specific pathologies can be divided into quantitative or qualitative platelet issues.

Secondary (Humoral) Phase of Hemostasis

(▶ Fig. 11.1)

• Consists of the coagulation cascade.

• The end product of the cascade generates an active version of factor X which produces thrombin.

• Inactive factor X must be activated by:

  • Trauma that causes blood to leave the vessel (extrinsic pathway).

  • Damage to the inside of the vessel (intrinsic pathway).

• Goal is to stabilize the weak platelet plug.

• Factor X from the coagulation cascade generates thrombin from prothrombin.

• Thrombin converts fibrinogen in the platelet plug to fibrin.

• Fibrin is cross-linked to yield stable platelet-fibrin thrombus (blood clot) by factor XIII.

Disorders of the Coagulation Cascad

(▶ Fig. 11.2)

• Due to factor abnormalities.

• Clinically present with deep tissue bleeding into muscles and joints with possible postoperative bleeding.

• Examples:

  • Hemophilia A (factor VIII deficiency).

  • Hemophilia B (factor IX deficiency).

  • von Willebrand disease (the most common inherited coagulation disorder, impairs platelet adhesion).

  • Vitamin K deficiency [occurs in newborns, long-term antibiotic users, as well as in patients with malabsorption issues (i.e., alcoholics), liver failure, and large volume blood transfusions].

Typical Patient—Discontinue or Keep on Anticoagulant Medications?

• ▶ Table 11.1 shows common categories and drug names for anticoagulant and antiplatelet medications.

• For a typical dental patient using anticoagulant or antiplatelet medications, there is no need to discontinue his or her regimen(s).

• Local hemostatic measures should be sufficient to control most of the bleeding.

• These measures include:

  • Mechanical pressure with gauze.

  • Hemostatic agents (e.g., Gelfoam^® or Surgicel^®).

  • Suturing.

  • Tranexamic acid mouthwash.

Medical Conditions with Higher Risks of Bleeding

• Age more than 65 years.

• Stroke (cerebrovascular accident).

• GI hemorrhage.

• Diabetes mellitus.

• Renal insufficiency.

• Recent myocardial infarction (MI).

• Anemia.

• History of significant bleeding in a prior surgery.

• Liver disease with synthetic dysfunction.

• Hematological (bleeding) disorder (von Willebrand disease, hemophilia, etc.).

Von Willebrand Disease

• Type 1: Most common and mildest form.

  • Responds to treatment with desmopressin (DDAVP).

• Type 2: Normal amounts of von Willebrand factor, but it does not work correctly.

  • Several types (types 2A, 2B, 2 M, 2N).

• Type 3: Most severe form of von Willebrand disease.

  • No von Willebrand factor present and low levels of factor VIII.

Treatment of Hemophilia

• Replacement of factor VIII for hemophilia A.

• Replacement of factor IX for hemophilia B.

  • Clotting factor concentrates can be made from pooled human blood.

  • Clotting factors can be made from recombinant clotting factors.