Unfortunately providing oral health care for the orally anticoagulated patient can sometimes provoke fear and anxiety for the general dentist and their team.
From my experience, as both pre-doctoral and postdoctoral educator, this fear and anxiety typically stems from certain gaps in the knowledge base of a subject. Although a lot of training is crammed into four years of pre-doctoral dental programs, much of it, as intimated to me by full time faculty members, is geared toward passing board exams rather than practical knowledge. Unless a provider has attended a hospital-based general practice residency or oral-maxillofacial surgery residency, gleaning both the technical and didactic skills to efficiently manage medically complex patients becomes difficult to garner once in practice. Hopefully this article will help to fill some of those knowledge gaps and eliminate the “guess-work” in treating the orally anticoagulated subset of medically complex patients.
Before reviewing treatment modalities for the management of the orally anticoagulated patient, lets discuss what it means to be “anticoagulated”? Being “anticoagulated” simply indicates being in a state in which the clotting of blood is impaired or diminished. Thus, to understand anticoagulation we need to first understand normal blood coagulation.
Blood Clotting Simplified (o.k. really simplified)
Blood clot (thrombus) formation relies on circulating blood cells known as platelets (thrombocytes). Thrombi occur when platelets are activated (change shape) in response to trauma. Activated platelets quickly stick together and to the damaged blood vessel wall to form a “platelet plug.” The platelet plug is later reinforced with strands of fibrin. Fibrin is the “scaffolding” for the blood clot matrix. Fibrin is generated from one of two processes:
1. A contact (intrinsic) pathway
2. A tissue factor (extrinsic) pathway
The contact (intrinsic) pathway is activated when there is trauma to the inside of the vascular system; all the coagulation factors are already “intrinsically” present in the circulating blood. The tissue factor (extrinsic) pathway is activated when blood escapes the vascular system; the activating coagulation factors are found “externally” from the blood vessel.
The efficiency of these two pathways can be measured with blood tests. The tissue factor pathway is measured with a prothrombin time (PT). The contact pathway is measured with a partial thromboplastin time (PTT) or activated partial thromboplastin time (aPTT). To standardize different ways a p.t. can be measured an i.n.r. (international normalized ratio) was developed. Therapeutic ranges for an i.n.r. typically range from 2.0-3.5.
These pathways can be disrupted on purpose by a physician using various medications. They can also be affected by a single disease process or comorbidity (two or more concurrent disease processes). Our discussion will focus on oral pharmaceuticals which affect thrombus formation.
Orally administrated anticoagulants can be divided into two broad groups:
1. “Anti-platelet” medications which exert an effect on platelet aggregation.
2. “Anti-coagulant” medications which exert an effect on coagulation factors and ultimately the production of fibrin.
Both medication groups are used prophylactically, either long-term or shortterm, to reduce the chance of forming a thrombus. Clinically, both are required and in some instances used in concert.
Anti-platelet medications work by inhibiting the function or formation of thromboxane. Thromboxane is required to make platelets for a platelet plug. Most anti-platelet medications bind irreversibly to platelets to exert an effect. Thus, if for some reason, you needed to have a patient discontinue anti-platelet therapy, in consultation with the patient’s physician, the waiting time before the procedure would be 8-9 days (the life span of a circulating platelet).
Finally, anti-platelet drugs are typically used for prophylaxis against arterial thrombi. These types of thrombi tend to be comprised mostly of platelet aggregates and some fibrin.
Common Anti-Platelet Medications:
• clopidogrel (Plavix)
• prasugrel (Effient)
• dipyridamole/aspirin (Aggrenox)
Patients who are recovering from percutaneous coronary intervention with stent placement, post stroke, post myocardial infarction, and coronary artery disease are likely on an antiplatelet or dual antiplatelet medication regime.
Anti-coagulation medications work by interfering with the production of coagulation factors and ultimately the endproduct of the coagulation cascade: fibrin.
Common anti-coagulation medications:
• Warfarin (Coumadin)
• Enoxaparin (Lovenox)
• Rivaroxaban (Xarelto)
• Dabigatran (Pradaxa)
• Apixaban (Eliquis)
It is worth mentioning a few facts about these medications. Warfarin works by competitively inhibiting vitamin K. The liver uses vitamin K to make several clotting factors. Warfarin takes approximately 3-5 days to reach therapeutic levels and 2-3 days to drop from therapeutic levels to non-therapeutic levels. Warfarin’s effectiveness (therapeutic level) is measured by the value of a blood test called the international normalized ration (inr). Uncoagulated blood will have an inr of 1.0. Depending on the reason for Warfarin therapy, the INR will have a therapeutic level ranging from 2.03.5. Warfarin can be reversed with IV administration of vitamin K. This can take 12 -24 hours.
Lovenox is a type of heparin known as low molecular weight heparin or “lmwh”. Lovenox exerts an anticoagulant effect by inhibiting the function of thrombin. This directly decreases the amount of fibrin produced thus affecting the formation of a thrombus. As opposed to Warfarin, lmwh has a half-life of only 12 hours. Lovenox is typically utilized in during hospital stays for prophylaxis against the formation of deep vein thrombosis and pulmonary embolism. It is also useful pre and post-operatively (see below) for bridging patients back to Warfarin or one of the newer class of anticoagulants.
Rivaroxaban, dabigatran, apixaban are newer classes of anticoagulants. They are unique, compared to Warfarin and lmwh in not requiring monitoring. They also do not currently have a reversal agent. These medications can take as much as 4 days to lose a therapeutic effect.
Anticoagulants are commonly used prophylactically against venous thrombi. Venous thrombi, opposed to arterial thrombi, are composed mainly of fibrin not platelets. Some common conditions prophylaxed with anticoagulants are mechanical heart valves, atrial fibrillation, deep vein thrombosis (dvt), pulmonary embolism (pe), and patient status post joint replacement therapy.
Considerations in Management
So how does all this information affect day to day dental procedures? Most importantly patients are being administered anticoagulant/antiplatelet therapy for a reason. Many times the risk of removing them from anticoagulation therapy could become life threatening.
Thus having a clear picture of the patient’s overall health becomes paramount for making a risk assessment for a particular procedure. However, with some forethought and purposeful surgical technique many of these patients become predictably managed in office.
For anticoagulated patients, dental procedures should be classified into two categories for expected bleeding risk.
1. Low bleeding risk procedures:
b. Supra /sub gingival removal of calculus
d. Simple extractions
2. High bleeding risk procedures:
a. Surgical extraction
b. Multiple tooth extraction
c. Major oral surgical procedures
For the low bleeding risk procedures, anticoagulant therapy or anti-platelet medicated patients present few complications from a hemostatic point of view. However, the disease states which have dictated anticoagulated / anti-platelet therapy could present due consideration prior to treatment.
For the high bleeding risk procedures, I will list some strategies in management.
As in low bleeding risk procedures, have a firm understanding of a patient’s medically history prior to treating the patient.
Finally, here in the U.S. most patients who are administered anticoagulation medications are managed by a “coagulation clinic”. If the patient must discontinue anticoagulation therapy or be bridged (see below), working with the coagulation clinic streamlines the process for both you and the patient.
For all anticoagulated patients, it is a good idea to know the patient’s INR history over the last several months. In addition to gathering a comprehensive past medical history, it is important to make a thorough physical exam as well. If the patient reports easy bruising or shows sign of easy bruising have their physician order a cbc and INR.
FIGURE 1: Ecchymotic patches easily visible on hands and arms.
FIGURE 6: Interproximal approach
FIGURE 7: Benex Extractor
FIGURE 8: Post inserted
FIGURE 9: Extractor connected to post via cable
FIGURE 11: Voila!
FIGURE 12; Atraumatic surgical site
FIGURE 13: Periotome tip
FIGURE 14: Similar in use to a manual periotome
FIGURE 15: Rotational forces following the periotome
FIGURE 16: Alveleoplasty performed against tissue without a flapped approach
FIGURE 17: Section buccal roots from clinical crown and palatal root
FIGURE 18: Separate the clinical crown and palatal root complex from the buccal roots using an elevator
Using rotational forces remove clinical crown and palatal root. Note continued use of throat pack
FIGURE 20: Crown and palatal root
FIGURE 21: palatal root / crown complex and buccal roots
FIGURE 22: Bayonet forceps retrieving buccal roots using rotational force
FIGURE 23: Example of a liver clot place at end with perio pack photo ( gc coe- pack dressing 4b)
FIGURE 24: Surgicel packed into atraumatic extraction sites
FIGURE 25: Figure of 8 sutures provide compression and stability for the socket dressing
FIGURE 26: Opposing side Surgicel dressing and figure of 8 sutures
Nu gauze soaked in topical thrombin inserted into socket covered with Perio-pack
Bridging refers to transitioning a patient from Warfarin or one of the newer thrombin inhibiting anticoagulants to LWMH. Unlike the other anticoagulants, LWMH has a very short half-life. It is administered every twelve hours via an injection into the abdomen. This is the best strategy to operate on a patient who must be off anticoagulants due to the procedure and who is at high risk of developing a thrombus. The bridging protocols are created and managed by the patient’s coagulation clinic. They will typically want to know when the surgery is scheduled and when the surgery site is stable enough to allow post-operative administration of LWMH.
Local anesthetics with epinephrine 1:50,000 – 1:200,000 can help control bleeding in the surgery site due to the vasoconstriction afforded by the epinephrine. However, care must be exercised when dealing with patients who are receiving anticoagulants for post myocardial infarction, atrial fibrillation, and in some cases stroke. A consult with the patient’s physician prior to treatment is recommended.
Atraumatic Surgical Techniques
Precise incisions and compression sutures (FIGURES 2-5) will help to minimize bleeding. This patient’s INR was 2.7 at the time of surgery.
The use of periotomes minimizes the trauma to both the soft tissue and surrounding alveolus. Periotomes are best used interproximally with apical pressure and buccal lingual movement of the blade handle. It is useful to support the buccal and lingual alveolus with the opposing thumb and forefinger.
The use of extraction devices can be quite useful. This is the Benex sytem from Meissinger. The system works by inserting a steel post into the tooth. A tensioned pulley supported by a plastic platform resting against adjacent teeth provide a cornally vecotred force to remove the tooth atruamitcally from the socket. (FIGURES 7-12)
Piezo electrics surgery devices, such as the Acteon Solo, are essential when performing oral surgical procedures on anticoagulated patients. Piezo electric surgery tips vibrate at a frequency which allows for accurate incising of bone but will not incise soft tissue.
This provides an enormous amount of latitude in surgical approach. The high frequency vibration of the tips with water irrigation against the alveolus produces a “coagulum” via cavitation which significantly decreases the amount of bleeding in the surgery site. The case below details multiple extractions for a patient at high risk for developing emboli; mechanical heart valve, history of DVT, history of PE, and AFIIB! INR day of surgery was 3.8. (FIGURES 13-16)
Sectioning molars to remove them as individual roots also works well to control trauma to the hard and soft tissues.
The remaining molars removed along with the buccal roots which were sectioned from one another as well and then removed as single rooted teeth. (FIGURES 21-23)
The use of hemostatic packings with compression sutures even in simple extractions is always prudent. Plan for post-operative bleeding. The goal of packing the socket is threefold:
1. To provide pressure hemostasis directly in the surgical site
2. To provide stability/reinforcement to thrombi attempting to form
3. Hemostatic properties of packing chemically aid in thrombus formation
There are several dressings suitable for packing a fresh socket:
1. Gelfoam: resorbable animal based cellulose
2. Surgicel: resorbable plant based cellulose
3. Collagen plug: resorbable (fast) collagen plug
4. Nu gauze: sterile dressing, nonresorbable a. Topical thrombin
b. GC Coe-Pak surgical dressing
As mentioned earlier of equal and sometimes greater importance than being oral anticoagulants is why a patient is taking oral anticoagulants. Be prudent in the use of vasoconstrictor containing local anesthetics. Epinephrine can exasperate, and in some cases induce atrial fibrillation. Epinephrine can also induce or worsen an anginal episode.
Be sure to use throat packs whenever possible. Throat packs provide excellent isolation, greatly decrease the chances of aspiration of teeth/tooth fragments, securely grasp crowns (compared to latex/vinyl gloves, and absorb saliva and blood from the oral cavity.
Finally, when discussing patient management with our medical colleagues it is important to keep in mind we are the operating surgeons, not them. If an anticoagulated patient requires oral surgery, they require oral surgery. The physician’s role is to provide us with learned advice as to the patients’ medical health. It is up to us to take that information and make an informed decision as to the best course of action: do not treat at all, treat in office, refer to a specialist or university residency program for management.
Hopefully this article has added to your management skills for the orally anticoagulated patient and simplified the decision making process in determining the best course treatment.
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Dr. Haghighi graduated from CWRU School of Dentistry. He completed a one year general practice residency program at the University of Rochester Medical Center and attended a two year fellowship in geriatric dentistry at University Hospitals of Cleveland. He is the past department chair of surgery, St. John Medical Center, Longview Washington. Dr. Haghighi has lectured extensively on the management of dental patients with complex medical histories and on various dental Implantology topics. He is the clinical director for Surgikor Dental Implants www.surgikorimplants.com. You may reach Dr. Haghighi at firstname.lastname@example.org.
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