Dental Management of Patients with Bleeding Disorders by dentalhealth


									                   Dental Management of Patients
                      with Bleeding Disorders
                        Sandra D’Amato-Palumbo, RDH, MPS
                                   Continuing Education Units: 3 hours

When a patient presents with a bleeding disorder, how should dental providers proceed to manage the
complexity of the case? Management of such medically-complex patients involves “an understanding of
basic physiology of hemostasis”, which can greatly enhance one’s comprehension of most bleeding and
clotting disorders. In addition to this composite of knowledge, clinical application of recent evidence-
based recommendations can contribute to the management of these patients who may potentially require
specialized medical and or dental care.

This continuing education course will provide dental professionals with general information for managing
patients with bleeding disorders. Specifics of this course include: basic physiology of the hemostatic system;
common bleeding disorders and their etiologies; requisite laboratory testing; and current evidence-based
guidelines for the purpose of developing individualized treatment plans for such patients. Having a greater
appreciation of these essentials will enable the dental practitioner to successfully treat patients with bleeding

Conflict of Interest Disclosure Statement
•   The author reports no conflicts of interest associated with this work.

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          Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
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. 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.       The microscopic illustration of the hemostatic clot (thrombus) displays a matrix of platelets, red
blood cells, white blood cells, and fibrin. (Figure 1)

                           Figure 1. Illustration of a clot.
                           The end product of the coagulation system, which
                           shows a fibrin clot or thrombus. White threads are
                           fibrin, the structure with yellow on the surface is a
                           white blood cell, platelets are green, and the red
                           structures are red blood cells.
                           Image source: Little J, Falace D, Miller C, Rhodus N. Dental
                           Management of the Medically Compromised Patient, 7th ed.
                           Reprinted with permission of CNRI/Photo Researchers, Inc.

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

        Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
hemostasis.” 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. 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. When
a “high-intensity” anti-coagulation therapy is warranted, patients have a “five-fold” 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 complicationsas 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.

                                          Learning Objectives
Upon completion of this course, the dental professional will be able to:
• List the primary hemostatic components of blood.
• List and briefly describe the three phases of hemostasis.
• Describe the basic physiology of hemostasis.
• List and briefly describe common bleeding disorders (genetic, acquired and or medication-induced).
• Discuss the pathophysiology of common bleeding disorders.
• List and describe the associated etiologies of common bleeding disorders.
• List the frequently prescribed and OTC drugs that cause anticoagulation effects (anti-platelet and anti-
  thrombotic effects) on the hemostatic system.
• List the common blood laboratory tests to diagnose and evaluate common bleeding disorders.
• Become familiar with interpretation of common blood laboratory tests (normal and abnormal values) used
  in the dental office.

        Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
     •   Discuss the medical / dental management strategies for patients with bleeding disorders.
     •   Discuss treatment plans (assessment, diagnosis, plan, implementation and evaluation) that provide
         safety and comfort for managing patients with bleeding disorders in the dental environment.
     •   List and describe hemostatic agents (local and systemic) to prevent and or reduce the clinical bleed in
         patients with bleeding disorders during and after invasive dental procedures.
     •   Gain knowledge about the current evidence-based recommendations for the purpose of managing
         patients with disorders of coagulation while providing invasive dental procedures.

Course Contents                                                         a bleed by mechanical or chemical means or by
•   Normal Hemostasis: The Making of a Blood                            the complex coagulation [clotting] process of the
    Clot                                                                body…”6 Composing of a coordinated sequence of
•   Laboratory Assessment of Hemostasis                                 events, hemostasis consists of vasoconstriction of
•   Common Bleeding Disorders                                           the blood vessel, platelet adhesion and aggregation,
•   Blood Vessel Wall Abnormalities                                     and thrombin and fibrin synthesis. (Diagram 1) The
•   Platelet Related Bleeding Disorders                                 general sequence of events in hemostasis is briefly
      Thrombocytopenia                                                  presented by describing the three main phases:
      Thrombocytopathy                                                  vascular, platelet and coagulation phases.
•   Coagulation Factor Disorders
•   Inherited Coagulation Disorders                                     Vascular phase: Immediately, when blood
•   Patient and Clinical Assessment                                     vessels are injured, vasoconstriction of the arteries
•   Treatment Planning Considerations                                   and veins begins. Within the injured vessel wall,
•   Conclusion                                                          exposure of subendothelial tissues, collagen, and
•   Course Test                                                         basement membrane contribute to prothrombotic
•   References                                                          activites. Clotting activities include platelet
•   About the Author                                                    aggregation and adhesion via release of adenosine
                                                                        diphosphate (ADP) and von Willebrand factor (vWF).
Normal Hemostasis: The Making of a
Blood Clot                                                              Additionally, the release of a tissue factor (formerly
Hemostasis is defined as “the termination of                            known as tissue thromboplastin) during this phase

                    Diagram 1. Schematic of an Injury to Blood Vessel
                    Adapted from: Principles and Practice of Oral Medicine, 2nd edition

              Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
initiates coagulation via the extrinsic pathway.1,2,5          resulting in the primary cessation of the bleed by
At this point, the initial layer of the platelet plug is       the hemostatic plug formation.1,2,5
established at the site of the injury.
                                                               Coagulation phase: Virtually simultaneously with
Platelet phase: “Platelets are cellular fragments              the vascular and platelet phases, the extrinsic,
from the cytoplasm of megakaryocytes” that                     intrinsic and common pathways, containing
survive in the vascular system for 8–12 days.2                 12 circulating plasma proteins, (also termed
They are essential for the clotting process in the             plasma coagulation factors) are initiated. These
blood. Primary hemostatic functions of platelets               plasma proteins are produced in the liver. More
include: maintaining the health of the inner lining            specifically, of the 12 plasma proteins, factors
of the vascular wall; formation of a platelet plug             II, VII, IX and X are Vitamin-K dependent for
during vessel wall injury; and initiation of the               synthesis. The coagulation factors are activated
coagulation phase, which leads to the stabilization            in a cascade-like manner within their respective
of the platelet plug.2                                         pathways. The “faster” extrinsic pathway is
                                                               initiated by factor VII when exposed to a tissue
During the platelet phase, platelets become sticky             factor (or a membrane protein) within the injured
and adhere to the site of injury after contact                 vessel; and the intrinsic pathway is initiated
with exposed collagen and subendothelial tissue                when factor XII contacts with injury-exposed
component vWF glycoprotein Ib. Additionally,                   subendothelial tissues. Subsequently, coagulation
ADP is released by exposed subendothelial                      factors in the intrinsic pathway activate one
tissues that contributes to platelet aggregation.              another: F-XII activates F-XI; F-XI activates-IX;
A product of platelets, thromboxane, causes                    and F-IX activates F-VIII. Both pathways merge
another surge of platelet aggregation.2                        and factor X is activated, yielding the activation of
                                                               the common pathway. Subsequently, prothrombin
In summary, platelets adhere to the damaged                    is converted to thrombin; thrombin acts as a
subepithelial surface, change shape, become                    catalyst for the conversion of fibrinogen; fibrinogen
sticky, and aggregate to form a hemostatic                     is the precursor to fibrin.
platelet plug at the injured blood vessel site.
Under these normal conditions, adequate                        Fibrin is thus converted to a stringy, insoluble
numbers and function of platelets are required,                protein that forms an intricate network of minute

                    Diagram 2. Coagulation Cascade

             Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
delicate structures called fibrils. At this point,         Laboratory Assessment of Hemostasis
blood cells and plasma are enmeshed in the                 Many of the bleeding disorders can be diagnosed
network of fibrils to form the clot. Therefore,            and monitored by way of laboratory testing.
fibrils are responsible for tightly binding the            When a significant disorder occurs in the
platelet plug, stabilizing the plug, and affixing it       vascular or platelet phase a clinical bleeding
to the site of injury. Resulting in a semi-solid,          problem is observed immediately after injury, or
gelatinous mass, it is termed the hemostatic               during invasive medical or dental procedures.
clot or thrombus. This definitive clot prevents            Conversely, when a significant disorder affects
excessive bleeding from the site of the injury.            the coagulation phase, the clinical bleed will
Within approximately 9 to 18 minutes, the fibrin           most likely not be observed until several hours or
clot is produced. (Diagram 2) Under these                  longer after the injury or invasive procedure.
physiological conditions, it is important to note
that if any defect or deficiency of platelets or           Various laboratory screening tests can be ordered
coagulation factors exists, disorders of the               by the dentist when the patient reports a bleeding
hemostatic system can result.1,2,5                         disorder: when the patient responds positively
                                                           to a family history of a bleeding disorder; or
Finally, anticlotting mechanisms (broadly termed           when the clinician observes a sign/symptom of
fibrin degradation products) in the fibrinolynic           a bleeding problem during the clinical exam.
pathway are activated to prevent the formation             Patients with unknown bleeding problems should
of more clots and to allow for the dissolution of          be referred to their physician or to a hematologist
the definitive clot.4,5 The expected outcome is            for further evaluation. Laboratory tests provide
accomplished: repair of the injured blood vessel           an assessment of adequate numbers of platelets,
wall results and bleeding ceases.                          proper functioning of platelets, sufficient levels

             Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
of plasma coagulation factors, and proper                    2. Without a positive medical history finding
functioning of the fibrinolytic pathway. When                   related to a bleeding disorder/platelet
evaluating defects in the hemostatic system prior               disorder, the bleeding time test is not a
to invasive treatment dental professionals should               “useful predictor” of an excessive bleed when
become familiar with the following common blood                 performing invasive dental procedures; and
laboratory tests.                                            3. The results of a prolonged bleeding time
                                                                cannot reliably identify patients who are
Common Blood Laboratory Tests                                   taking anti-platelet therapy; thus, a prolonged
Platelet Count is a routine blood laboratory                    bleeding time cannot be linked to the ingestion
test that provides a quantitative assessment of                 of aspirin or NSAIDs.10,11 Therefore, the
circulating platelets in the vascular system. A                 bleeding time test is merely a tool to screen for
normal platelet count should be within the range                platelet disorders; it is not an effective clinical
of 150,000 to 450,000 cells/mm3 of blood.8 When                 testing method for predicting the quantity of a
the platelet count is less than 100,000 cells/                  bleed associated with an increased bleeding
mm3, thrombocytopenia is diagnosed. Patients                    time in such patients.10
presenting with a platelet count between
50,000 and 100,000 cells/mm3 will predictably                Platelet Function Analyzer (PFA-100) is a
bleed mildly with severe trauma or with dental               sophisticated laboratory testing devise that is
surgical procedures. When the platelet count                 currently being used in place of the Ivy Bleeding
is less than 20,000 cells/mm3 an excessive                   Time test. Platelet function tests or platelet
and prolonged bleed is predictable; thus, this               funtion assay (PFA) evaluate the quantitative
high-risk condition will require medical attention           and qualitative function of platelets. They
prior to dental invasive procedures.2 Ultimately,            provide an assessment of platelet attachment,
thrombocytopenia can prevent the formation of a              platelet activation and platelet aggregation during
hemostatic plug, resulting in hemorrhage.                    the development of a platelet plug, or primary
                                                             hemostasis.2,12 Generally, these tests measure
The Ivy Bleeding Time laboratory test has been               the time it takes for a clot to form (platelets to
routinely used as a screening test for assessing             clump together) to prevent blood loss as the
adequacy of platelet function. Abnormal platelet             closure time. The PFA test (and other platelet
function is termed thrombocytopathy. When                    function tests) has not been shown to predict the
performed, the bleeding time test calculates the             likelihood that a patient will bleed excessively
time required for a standard skin incision to stop           during invasive procedures; although, its full
bleeding by the formation of a hemostatic plug.9             clinical utility has yet to be established.12,13
The normal range of the Ivy Bleeding Time test is
usually between 2 and 10 minutes.8                           Prothrombin Time (PT), measures the patient’s
                                                             ability to form a definitive clot by monitoring the
Over the years, this test was presumed to provide            proper functioning of the extrinsic coagulation
a measurement of bleeding risk in patients                   pathway (Factor VII) and the common pathway
by way of a prolonged bleeding time result.                  (Factors V, X, prothrombin and fibrinogen).
Consequently, its current use and application                Factors VII, X and prothrombin are Vitamin
have been deemed very limited because of its                 K-dependent for their synthesis and become
recognized unreliability to predict bleeding risk            unstable when coumarin-like drugs are
based on an abnormal test result.10,11 This test fails       prescribed.2,5,9 A normal coagulation profile
to produce quantifiable and useful information for           indicates adequate levels or percentages of
several reasons. According to an original article            clotting factors in the extrinsic and common
by authors Peterson et al,10 the following major             pathways. Generally, the laboratory testing
conclusions were drawn regarding this test:                  range is between 11–15 seconds.8 Testing
1. Given the normal results of a standard bleeding           results beyond 15 seconds indicate an abnormal
   time test one cannot exclude the possibility of           or prolonged PT. This outcome is indicative of
   a significant clinical bleed with invasive dental         deficient coagulation factors needed to form a
   procedures.                                               fibrin clot, resulting in a prolonged bleed in the

             Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
body. An active bleed caused by anticoagulation            Common Bleeding Disorders
therapy, coumarin-like drugs, is most commonly             Excessive or prolonged bleeding may result from:
monitored by the international normalized ratio            1. extremely fragile blood vessels;
(INR) laboratory test.                                     2. decreased number of platelets or impaired
                                                              platelet function;
International Normalized Ratio (INR) In 1983,              3. abnormalities in the blood clotting coagulation
the World Health Organization Committee on                    factors;
Biological Standards established a more precise            4. defects in the fibrinolytic pathway; or
laboratory testing method, the INR, to monitor             5. a combination of these.
patients taking anticoagulation drugs (warfarin
therapy). Consequently, laboratory materials               The following information provides an overview of
(thromboplastin reagents) and laboratory                   the various abnormalities in the hemostatic system.
techniques were internationally instituted for the
purpose of standardizing the assigned values.              Blood Vessel Wall Abnormalities
Patients with a normal coagulation profile result          Blood vessel wall abnormalities, or increased
in an INR value of 1.0.11,14 The “low intensity” INR       fragility of the blood vessels, are relatively common
range is between 2.0 and 3.0; and the “high-               but do not usually cause a serious bleed. When
intensity” INR range is between 2.5 and 3.5.               evaluating the laboratory tests for this condition,
What governs the intensity of anticoagulation              one can expect a normal platelet count, bleeding
therapy? The intensity is determined by the                time and coagulation times (PT and aPTT).
patient’s predisposition to abnormal clotting.             Pathophysiologically, this condition manifests
Patients diagnosed at high risk clot formation,            itself by observable extraoral and intraoral signs
will require higher intensity of anticoagulation.4         of hemorrhage: Petechiae and ecchymosis are
From a pharmacological standpoint, anticoagulant           found in the skin or on the mucous membranes,
drugs inactivate Factor VII within the extrinsic           particularly on the gingiva. Very rarely, significant
pathway by inhibiting Vitamin K action; Vitamin K          hemorrhage may occur, particularly in the joints,
is required by the liver to synthesize Factor VII.         muscles, and subperiosteal locations. Excessive
                                                           bleeding may also take the form of menorrhagia
Activated Partial Thromboplastin Time                      (abnormal long and heavy menstrual periods),
(aPTT) also measures the patient’s ability to              nosebleeds, gastrointestinal bleeding, or hematuria
effectively form a definitive clot by evaluating           (abnormal presence of blood in the urine).5
the effectiveness of the intrinsic and common
pathways of the coagulation cascade.2,5,9 It               Causes of Blood Vessel Wall Abnormalities5
tests for deficiencies in the intrinsic pathway,           • Infections (i.e. septicemia, infective endocarditis,
specifically factors VIII, IX, XI, XIII; and                 several forms of rickettsioses)
deficiencies in the common pathway, specifically           • Drug reactions (i.e. hypersensitivity vasculitis)
factors V and X, prothrombin and fibrinogen. A             • Scurvy, Henoch-Schönlein purpura
normal aPTT is usually 25 to 40 seconds.8 The              • Hereditary hemorrhagic conditions.
aPTT is the laboratory test most often used
by physicians to monitor heparin therapy and               Platelet Related Bleeding Disorders
to diagnose the hemophilias, which result in a
prolonged or increased aPTT time.2,9,11                    Thrombocytopenia
                                                           The important role of platelets in hemostasis is
Thrombin Time laboratory test assesses the                 to form the temporary hemostatic plug, primarily
conversion of fibrinogen to insoluble fibrin by            requiring a sufficient number of platelets. When
adding thrombin to the patient’s blood sample.2,8          a quantitative reduction of platelets exists, it
Specifically, this test bypasses the extrinsic,            can result in a significant cause of generalized
intrinsic and common pathways to determine the             bleeding. Patients presenting with a platelet count
stability of the clot. Normally, the range of this         of less than 100,000 cells/mm3 are diagnosed with
test is between 9 and 13 seconds.2 A prolonged             thrombocytopenia. When the platelet count is
time, in excess of 16 to 18 seconds, is considered         under 50,000 cells/mm3, bleeding will be excessive
abnormal.2                                                 postoperatively; thus, a platelet transfusion may be

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
necessary prior to invasive treatment. Moderate         or flossing may be observable, and bleeding from
to severe thrombocytopenia (less than 50,000            teeth extractions is possible. This condition is
cells/mm3) is usually manifested by petechiae in        diagnosed by a platelet count laboratory test, or by
the skin or on the mucous membranes; purpura            a complete blood count (CBC). Depending on the
or ecchymoses on the skin; spontaneous mucosal          cause, thrombocytopenia can be a consequence
bleeding; or intracranial hemorrhage.1,5 In the         of increased platelet destruction, decreased
oral cavity, bleeding gingiva is a common sign,         platelet production, decreased platelet survival, or
spontaneous bleeding associated with brushing           increased splenic sequestration.5

           Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
Thrombocytopenia is the leading cause of                    •   Acquired disordersV
bleeding disorders, as presented in the following               • Drug-Induced defects
major categories.                                                 • *Aspirin (ASA)
                                                                  • **Nonsteroidal anti-inflammatory drugs
Causes of Decreased Production of Platelets1,9                      (NSAIDS)
• Generalized diseases of the bone marrow                         • ***Clopidogrel bisulfate and Ticlopidine
   • Aplastic Anemia                                              • Alcohol in combination with aspirin or
• Drug Induced Thrombocytopenia                                     NSAIDS
   • Cytotoxic drugs                                            • Uremia
   • Alcohol                                                    • Myloproliferative disorders
   • Thiazide diuretics
• Infections: measles, HIV                                  *Aspirin and aspirin-containing drugs1 are by far
• Ineffective megakaryopoiesis                              the most common reason for platelet dysfunction,
                                                            frequently resulting in a prolonged bleeding time.
Causes of Platelet Destruction or Decreased                 Aspirin, a nonsteroidal salicylate, acts as an
Platelet Survival1,9                                        inhibitor of cyclooxengenase; thus, inhibits the
• Immunologic destruction                                   synthesis of prostaglandins and interferes with the
   • Immune Thrombocytopenic Purpura (ITP)                  production of thromboxane A2.15 The net result of
   • Infections                                             aspirin therapy is to inhibit platelet aggregation,
      • HIV, infectious mononucleosis,                      hence, the formation of a platelet plug. (Diagram 3)
   • Drug-associated                                        Aspirin therapy, prescribed or self-administered, is
      • Quinine or quinidine                                a leading drug widely used by millions of people
      • Methyldopa                                          in the U.S. for its cardioprotective properties. Its
      • Sulfonamides                                        anti-platelet action prevents thrombus formation2,13
      • Heparin                                             by impairing platelet function and by interfering
      • Gold                                                with their ability to form an intact platelet plug.
      • D-penicillamine                                     As a result, aspirin causes irreversibility of
      • Þ-aminosalicylic acid                               platelet function for the duration of their lifetime,
• Nonimmunologic destruction                                approximately 7–10 days. Use of aspirin therapy
   • Thrombotic Thrombocytopenic Purpura                    is indicated for primary and secondary prevention
   • Giant hemangiomas                                      of thromboembolism, myocardial infarction and
   • Hemolytic anemias                                      cerebrovascular accident.

Thrombocytopathy                                            Although the blood thinning properties of aspirin
Caused by a platelet disorder, thrombocytopathy             cause an increased risk of a clinical bleed, proper
is characterized by impairment in platelet function,        management usually includes maintaining patients
but adequate numbers of platelets are normally              on “low-dose” aspirin therapy (75 to 100 mg) to
present. Thrombocytopathy may be congenital                 prevent the risk of a clot-threatening event.13 The
or acquired. The PFA-100 test (or other platelet            following evidence-based outcome supports this
function tests) provides an assessment of the               practice management. Authors Ardekian et al.16
adequacy of platelet function, and contributes to           presented the results of a clinical study which
the diagnosis of the following disorders:                   quantified the “intraoperative” and “postoperative”
                                                            bleeding in dental patients taking 100 mg of
Causes of Platelet Destruction or Decreased                 aspirin daily and those who discontinued their
Platelet Survival1,9                                        aspirin regimen for seven days. Conclusions
• Inherited Disorders                                       established was that no statistical difference was
   • von Willebrand’s disease: consists of                  found regarding “excessive” bleeding between
     a platelet dysfunction and a Factor VIII               the experimental group (patients who continued
     deficiency (Refer to Inherited Coagulation             aspirin therapy) and the control group (patients
     Disorders)                                             who discontinued aspirin therapy) who underwent

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
                  Diagram 3. The effect of aspirin on platelets.

various, complex surgical procedures. Although               antiplatelet therapy deceases the risk of a
the findings in this study concluded the more                cardiovascular episode. This strategy, therefore,
complex the surgical dental procedure the more               outweighs the benefits of a decreased risk of
significant the bleed, it is recommended that                bleeding complications with surgery following
suturing and local hemostatic agents can be used             cessation of aspirin.
to control the clinical bleed.
                                                             Outside of this standard practice, when complex
Moreover, Brennan et al.13 recently presented                surgical procedures are planned, Brennan et al.13
a “new recommendation” in their medical                      indicated that more research is warranted in this
management update review article based on                    area to predict the amount of the bleed. When
similar studies which demonstrated aspirin’s                 indicated, the “discontinuation of aspirin therapy
limited effects on bleeding during routine dental            should be limited to 3 or fewer days” to reduce
extractions. When taking low–dose aspirin (up                the risk of a thromboembolic event.13 Other
to 320 mg), it is recommended patients “not                  medical and dental providers suggest a 7–10 day
discontinue the use of daily aspirin before routine          aspirin cessation protocol; for this reason, the
dental extractions (to include multiple routine              risk benefit ratio must be considered during the
extractions).”13                                             consultation with the patient’s physician.

More interesting, and supported by recent                    **Non steroidal anti–inflammatory drugs (NSAIDs)
evidence, the chemical properties of low                     cause abnormal platelet function; thus, bleeding
dose aspirin exert its antithrombotic and                    can be expected. Once the drug is discontinued
cardioprotective properties up to 320 mg taken on            thrombocytopathy is reversed within 1–5 half–
a daily basis (Beyond this dosage, aspirin “may              life’s of the drug. And, when considering aspirin
be less effective as an antithrombotic” drug.)13             and NSAIDs as pain relievers after dental
                                                             procedures, dental professionals should not
In conclusion, it is recommended that a clinical             prescribe these analgesics when optimum blood
bleed caused by routine dental extractions,                  clotting/hemostasis is desired.17
can be managed by standard local hemostatic
measures (with direct packing of gauge, from                 It is recommended that prescription anti-platelet
suturing to hemostatic agents). Additionally, it             drugs, such as ***clopidogrel (Plavix) or ticlopidine
is recommended dental professionals adhere to                (Ticlid), when prescribed with or without aspirin,
the expert opinion that the benefits of continuing           not be discontinued for minor dental surgical

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
procedures. However, more studies are needed                (inflammation of a vein); atrial fibrillation (rapid,
to examine the quantity of the bleed during major           random contractions of the atria); myocardial
or complicated surgical dental procedures.13 If             infarction (heart attack); mechanical heart valves
these anti-platelet drugs are to be discontinued, it        (artificial heart valves); carotid artery disease; or
is prudent to consult with the patient’s supervising        peripheral vascular disease. Additionally, clots
physician.                                                  form because there is an existing hypercoaguable
                                                            condition where by the blood has a tendency to
Coagulation Factor Disorders                                clot more rapidly than normal, caused by either a
                                                            blood vessel defect, clotting factor abnormality or
Anticoagulation Therapy                                     an immunologic abnormality.5
Warfarin Sodium is a coumadin derivative listed
in the drug class as an oral anticoagulant. It              When patients are on warfarin therapy to prevent
interferes with the liver’s synthesis of Vitamin            thromboembolic events, they are monitored by the
K-dependent clotting factors; resulting in                  International Normalized Ratio (INR) laboratory
depletion of blood clotting factors II, VII, IX, and        test. The recommended INR therapeutic range
X. Its therapeutic effect is to prevent further             for patents on “low-intensity” warfarin therapy is
development of the hemostatic plug; and it                  between 2.0 to 3.0, with a target goal of 2.5 INR.
prevents new thromboembolic clot formation.15               When patients are on “high-intensity” warfarin
Thrombosis is the formation of abnormal blood               therapy, the INR range is between 2.5 to 3.5, with
clots (termed thrombi) that develop within the              a target goal of 3.0 INR.2 Indications for placing
vascular system. Thrombi are carried through                patients in these ranges are determined by the
the bloodstream (termed emboli) which can                   severity of the thromboembolic condition.
potentially occlude the lumen of an artery or a
vein and shut down a vital organ. The following             Historically, anticoagulation profiles for patients
conditions increase the risk of a thromboembolic            were much higher. Thus, it was necessary to
event: deep venous thrombophlebitis                         discontinue or alter the warfarin therapy to avoid

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
the risk of an excessive bleed (hemorrhage)                           debridement with slight to moderate
during and post invasive surgical and non-                            inflammation.) Proceed with attention
surgical procedures. Rationale for this practice:                     to control bleeding with standard local
Since Coumadin has a slow onset of action                             hemostatic measures.
and a half-life of 36 hours it requires complete               •   If the INR is greater than 2.5:
withdrawal of the drug two to three days prior to                   • When performing complex surgical
the invasive procedure. Consequently, patients’                       procedures or subgingival debridement
coagulation profiles resulted in suboptimal                           with severe inflammation, consult with the
therapeutic levels, and possibly, placed patients                     patient’s physician to allow the INR to drift
at risk for a thromboembolic event.                                   down to a safe INR range between 2-2.5.
                                                                      Proceed with attention to control bleeding
The current literature cautions dental practitioners                  with standard local hemostatic measures.
not to discontinue warfarin therapy due to the                      • Considerations for transiently interrupting the
risk of producing a thromboembolic event,                             anticoagulation therapy must be discussed
increasing the morbidity and mortality risks for                      with the patient’s physician.
the patient. After a 2007 comprehensive and
critical review of English-language, randomized                High intensity INR 2.5-3.54
clinical trials, by Aframanian et al.,18 as part of the        • Consult with the patient’s physician and obtain
World Workshop of Oral Medicine IV, the authors                   recent INR laboratory results prior to the
produced a “Class I” recommendation which                         invasive dental procedure.
was supported by scientific evidence and expert                • When performing non-surgical (subgingival
opinion: It is recommended that for patients who                  debridement with sight to moderate
fall “within the therapeutic range of an INR of 3.5               inflammation) and simple surgical procedures
or below, warfarin therapy need not be modified                   maintain INR in the 2.5-3.5 range; proceed
or altered for simple single dental extractions.”                 with attention to standard local hemostatic
Aframanian et al. also concluded that the                         measures to limit and control bleeding.
“more complicated and invasive oral surgical                   • When performing complex surgical procedures
procedures”, coupled with a higher range of the                   or subgingival debridement with severe
INR (3.5 and greater), one should consult with                    inflammation consult with the patient’s
the prescribing physician to consider bleeding                    physician; it may be safe to proceed in the
management options. Hence, patients with an                       lower ranges of INR 2.5-3.0 with attention to
INR above the therapeutic range of 3.5 are at an                  local hemostatic measures. Considerations
“increased risk of prolonged bleeding.”18                         for transiently interrupting the anticoagulation
                                                                  therapy must be discussed with the patient’s
More specifically, the following clinical guidelines              physician.
summarize dental management strategies                         • Consider use of low molecular weight heparin
for patients on Coumadin therapy who are                          preparations to bridge the patient through
anticoagulated in the “low intensity” and “high                   the invasive procedure as a substitute
intensity” therapeutic ranges, and who are                        anticoagulant.
scheduled for various simple and complex
surgical and non-surgical procedures:                          It can be concluded that most simple and
                                                               routine invasive dental procedures can be safely
Low intensity INR 2.0-3.04                                     performed when the INR is ≤ 3.0/3.5; and it is
• Consult with the patient’s physician and obtain              advised not to proceed when the INR value
  recent INR laboratory results prior to the                   is out of range or when complex, surgical and
  invasive dental procedure.                                   non-surgical procedures are planned.4,18,19 When
• If the INR is between the range of 2.0-3.0:                  allowing for higher normal therapeutic ranges of
   • When performing most invasive non-                        INR during invasive dental procedures, consider
     surgical or simple surgical procedures,                   operator experience. Under these conditions, it is
     one can proceed if the INR is within                      prudent to consult with the patient’s supervising
     therapeutic range 2.0-3.0. (Non-surgical                  physician; obtain results of an INR laboratory test
     invasive procedures can include subgingival               within 24 hours of the invasive dental procedure;

             Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
and be prepared to use hemostatic measures to                standard heparin usually consists of IV
manage the expected clinical bleed for all planned           infusions in a hospital setting which requires
dental procedures. Equally compelling and                    monitoring with the aPTT laboratory test. LMWH
widely accepted, presented by authors Jeske and              preparations are administered subcutaneously on
Suchko, is the fact that “the risk of experiencing           an out-patient basis. Their dosage is calculated
a thromboembolism outweighs the risk of                      based on the patient’s body weight and is given
experiencing excessive postoperative bleeding.”19            on an every 12-hour basis.2

While the current recommendations should be                  When considering substituting LMWH
tailored towards the patients’ individual needs,             preparations, dalteparin (Fragmin), for Coumadin
dental professionals must consider the following             when a dental surgical or nonsurgical procedure
dental implications when treating anticoagulated             is planned, one must consult with the patient’s
patients:                                                    physician to strictly and safely manage the
• Identify the fundamental cause of the bleeding             medication schedules. The following short-
    disorder for which anticoagulation therapy is            term heparinization schedule is recommended:
    indicated.                                               Coumadin is discontinued 4 days prior to the
• Consider operator experience with complex                  invasive dental procedure and Fragmin is started.
    invasive dental procedures.                              During this 4-day period Fragmin is administered
• Consider preexisting infection and or the                  every 12 hours. An evening dose of Fragmin
    degree of inflammation of the soft tissues.              is administered on day 4; the invasive dental
• Consider the extensiveness of the invasive                 procedure is scheduled 12 hours after the evening
    procedure, especially significant soft tissue and        dose of Fragmin. On the morning of the dental
    bone trauma.                                             procedure Fragmin is held back. During the
• Consider bleeding management strategies and                evening of the surgical procedure both Fragmin
    the availability of local hemostatic measures            and Coumadin are resumed and continued until
    when the risk of a bleed is expected.                    the INR is within the therapeutic range of 2.0-3.5.
• Consider the probable risk of inducing a                   At this point, Coumadin is continued and Fragmin
    thromboembolic event when discontinuing                  is discontinued.4
    or altering the anticoagulant drug; thus,
    resulting in coagulation profiles that are in the        Inherited Coagulation Disorders
    suboptimal therapeutic range.                            A number of congenital blood clotting factor
• Implement a heightened awareness when                      deficiencies exist; but three diseases account
    treatment planning: consider the complexity of           for more than 90% of all inherited coagulant
    the invasive dental procedure; seek medical              deficiencies. Deficiencies for discussion include:
    advice from the patient’s physician; and retrieve        Hemophilia A, Hemophilia B, and von Willebrand’s
    the results of the most recent INR test.4,20             disease. These diseases can present with mild
                                                             to severe forms, which parallels the degree of
Heparin: Managing dental patients on standard                deficiency of the blood coagulation factor.
heparin and low molecular weight heparin
(LMWH) is important when providers need to                   Hemophilia A, or also known as classic
control bleeding during and following invasive               hemophilia, is caused by a defect or a deficiency
dental procedures. Standard heparin itself is                in the activity or the amount of factor VIII,
not considered an anticoagulant but serves as                respectively. This hemophilia is a hereditary
the catalyst that inhibits plasma thrombin as                blood disorder that is transmitted as an X-linked
well as coagulation factors IX, X, XI, XII and               recessive trait, thus, predominately affecting
plasmin; thus, preventing the conversion of                  males over females. Its incidence rate is
fibrinogen to fibrin. LMWHs exert their potentiating         about 1 in 5,000 male births.1,2,5 The severity
anticoagulant effects more so on factor Xa.2                 of this condition is related to the degree of the
                                                             deficiency of factor VIII; therefore, the greater the
These drugs are used as a prophylaxis                        deficiency of the blood level factor the greater
antithrombic agent and in the treatment of                   the bleed. Regarding hemostasis, minimally
thromboembolic disorders. Treatment with                     30% of factor VIII is required for normal activity.

             Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
Approximately 60% of individuals with hemophilia            and extravascular respectively. Although, both
A possess a severe degree of deficiency, which              purified and recombinant factor IX products
is less than 1% of factor VIII.1,2,5,21 (Table 4) It        (or high-purity FIX [factor IX] products ) are
is diagnosed by a positive family history, a                recommended for the prevention or treatment of
history of bleeding episodes and a prolonged                bleeding in patients with hemophilia B. Clinical
aPTT test with a normal PT test, along with                 features of hemophilia B are similar to hemophilia
inadequate levels of factor VIII. These series              A; they include: deep tissue hemorrhage in joints,
of laboratory tests indicate a defective intrinsic          brain, and muscles.1,5,21,22
coagulation pathway. When considering the
treatment planning for these patients, the dental           von Willebrand’s Disease (vWD) is a disease
professional should consult with the patient’s              that includes a composite of two disorders:
hematologist. Usually, treatment for a minor                1. An inherited disorder of platelet adhesion,
bleed includes hemostatic dental products, local               which involves a deficiency and or a qualitative
pressure, and or cold compresses; treatment for                defect in von Willebrand’s tissue factor (vWF);
an expected major bleed includes administration                and, in some cases,
of factor concentrates termed purified factor VIII          2. Deficient or low levels of Factor VIII. Hence,
products.1,21,22                                               this bleeding disorder leads to “a combined
                                                               defect in platelet plug formation and fibrin
Clinical characteristics of Hemophilia A include:              formation.” 21
bleeding into joints (hemarthrosis), commonly
affecting knees, elbows and ankles; bleeding into           vWD is one of the most common inherited
soft tissues exhibiting extensive ecchymoses;               bleeding disorders; it presents itself clinically by
bleeding into a closed space such as muscle can             spontaneous bleeding from “mucous membranes,
lead to life-threatening blood loss; intracranial           excessive bleeding from wounds, menorrhagia,
bleeding; and bleeding into other sites such as             and a prolonged bleeding time in the presence
gastrointestinal and urinary tracts.1,21                    of a normal platelet count.” 2,21 In most cases it is
                                                            transmitted as an autosomal dominant disorder,
Hemophilia B, also known as Christmas disease               grouped into 3 major variants: Type I (deficiency
or plasma thromboplastin component deficiency,              in vWF), Type II (qualitative defect in vWF),
is transmitted in a sex-linked recessive fashion            and Type III (both Type I and II defects), from a
similar to Hemophilia A. It is a bleeding disorder          mild form to a severe form.23 vWD is diagnosed
caused by a deficiency or defective factor IX               by a positive family history; history of a serious
within the intrinsic pathway of the coagulation             bleed from trauma or surgical procedures;
system.1,2,5 (Table 4) Not as prevalent as                  spontaneous bleeding from mucous membranes,
Hemophilia A, Hemophilia B accounts for 10–15%              and laboratory tests showing prolonged aPTT,
of all hemophiliacs. It is diagnosed by a positive          abnormal assay results (a decrease in factor VIII
family history, a history of bleeding episodes              level); prolonged bleeding time and or abnormal
and a prolonged aPTT test with a normal PT                  platelet function.1,2,5,23
test, along with inadequate levels of factor
VIII. Replacement therapy for factor IX is more             Bleeding management options depend on the
variable because factor IX is distributed within            clinical condition of the patient and the type of
and outside of the blood system, intravascular              vWD that is diagnosed (Type I, II or III). Such

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
options include: Desmopressin, adequate plasma             careful treatment planning to include hemostatic
levels of Von Willebrand’s factor , and factor VIII        approaches are important elements in minimizing
concentrates (FVIII).2,22                                  the bleed during and after invasive dental
Management and treatment of dental patients
with inherited bleeding disorders present unique           Patient and Clinical Assessment
challenges to the dental practitioner. Firstly,            Assessment should include a systematic approach
knowledge about the bleeding disorder and its              of collecting, organizing, and evaluating all patient
coagulation defect are necessary. Secondly,                data. Data must be retrieved from the personal,
consultation with the patient’s hematologist               medical and dental histories, the pharmacological
should direct the dental professional to perform           history, laboratory testing, and inspection of the
the invasive dental procedure in the dental office         extra and intraoral structures. This subjective and
or in the hospital setting. This decision should be        objective evidence is vital to the development of a
based upon the severity of the patient’s condition         proper treatment plan and dental management of
as well as the possible need for infusion of factor        patients with bleeding disorders when performing
replacement therapy.24 Lastly and extremely                invasive dental procedures. All of these required
critical, treatment planning must focus on                 pieces of information are essential when
individualized bleeding management strategies.             considering the legal and ethical responsibilities
(Tables 5 and 6) Hence, comprehensive                      health care providers must exercise when caring
patient assessment, analysis of laboratory tests,          for their patients.
collaboration with the supervising physician, and

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
Examining the medical history questionnaire                combinations of herbal therapies that can affect
is the first step in identifying whether or not it         the hemostatic pathways.
includes questions regarding the suspect or
history of bleeding disorders. Questions should            Following the patient and clinical assessments,
include the following: the determination of a              dental professionals should perform a thorough
known history or a family history of a bleeding            extraoral and intraoral examination to identify
disorder, history of bleeding episodes related             deviations from normal that are indicative of
to a dental procedure, areas of petechiae,                 bleeding disorders. Long-standing history of
purpura and ecchymosis, easy brusiability,                 clinical findings in patients with mild to severe
frequent nose bleeds (epitaxis), blood in the urine        bleeding disorders often results in: petechiae,
(hematuria), clotting problems, bleeding in the            ecchymosis, spontaneous gingival bleeding, and
joints (hemarthrosis), deep muscle hematomas,              hemorrhages into the soft tissues. The most
excessive menstrual bleeding, alcohol abuse                common oral finding associated with bleeding
problems, cirrhosis of the liver, and unusual              disorders is petechiae, which present as tiny
bleeding following an injury or a surgical                 purple or red, 1 to 2 mm spots that appear
procedure.1,2,5,9 A verbal inquiry or follow-up            as a result of minute hemorrhages within the
approach can include who, what, where, when,               dermal layers. Their locations are most often
why, or how questions. Such questions that                 on the mucosal surfaces.26 Ecchymosis, larger
pertain to bleeding disorders can include:                 than petechiae, are flat, reddish blue or purplish
• What is the bleeding disorder?                           discolorations of the skin or mucosa.26 These
• What is the etiology of the bleeding disorder?           hemorrhagic lesions result from spontaneous
• What are the hemorrhagic signs and                       leakage of blood into the surrounding tissues
    symptoms? Location of the hemorrhagic signs            (extravasation). This severe bleeding results
    and symptoms?                                          from trauma, including surgery, by underlying
• What prescription medications, OTC dugs and              blood vessels or by fragility of the vessel walls.1
    or supplements are being taken?                        In severe disorders, gingival bleeding may
• What are the results of the blood laboratory             spontaneously occur.
• Who is the supervising physician, cardiologist           Based on the outcome of the patient’s histories
    or hematologist?                                       and oral examination, positive findings relative
• When was the bleeding disorder diagnosed?                to the suspicion of a bleeding disorder should
    (bleeding history and or family history)               warrant a physician consultation and a laboratory
• What bleeding complications have been                    screening evaluation. Hence, a proper diagnosis
    encountered?(specifically, spontaneous                 can be made and optimal dental care can be
    bleeding with injury or a prolonged bleed              provided.
    related to dental or medical surgeries)
• How is the bleed medically or dentally                   Treatment Planning Considerations
    managed?                                               Appropriate management for patients with
                                                           bleeding disorders who require routine invasive
Included in the pharmacological history the                dental procedures, including subgingival
dental provider should query the patient about             debridement (scaling and root planing), restorative
prescription medications that cause bleeding               procedures or simple surgical procedures,
tendencies, specifically Coumadin therapy,                 consists of the following:
aspirin, nonsteroidal anti-inflammatory drugs,
or heparin therapy. Just as important, patients               Step 1: Take accurate, comprehensive
should be asked about taking over-the-counter                 histories: personal, medical, dental, and
drugs containing aspirin; and they should be                  pharmacological. Perform a thorough extra
questioned about supplements and herbs that                   and intraoral examination to identify lesions
may exacerbate the bleed when patients are                    indicative of a bleeding disorder. When a
taking anticoagulants.25 There are more than                  known bleeding disorder is evident, understand
200 over-the-counter aspirin-containing drugs                 the pathophysiology and its related impact on
available to individuals as well as multiple                  dental treatment. When an unknown bleeding

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
disorder is suspected, refer the patient to                When considering the management of a
his physician or a hematologist to establish               clinical bleed during various invasive dental
a diagnosis. Definitive diagnosis of the                   procedures, hemostatic measures can include
bleeding/clotting disorder can be established              the following systemic or local applications:
by the physician or hematologist by ordering               hemostatic irrigant; absorbable gelatin sponge
the “Prolonged Clotting Time Profile”11                    containing a thrombin solution; gauze-soaked
laboratory tests.                                          squares and or mouthrinses with fibrin or
                                                           tranexamic acid (TXA); aminocaproic acid
Step 2: Consult with the supervising                       (EACA); vasoconstrictors in local anesthetics;
physician to obtain additional information                 surgical techniques and sutures; ice packs;
about the patient’s disorder or bleeding                   and or a combination of these measures
history. Continue to investigate and or to                 (Table 7).2,4,18,24,27
obtain medical clearance to treat. Secondly,
retrieve and evaluate the blood laboratory                 Regarding patients on warfarin therapy,
test results while scheduling the appointment              pharmacological evidence driven by a
within 24 hours of the results.                            current, comprehensive literature review by
                                                           investigators Patatanian and Fugate concluded
Step 3: Develop an appropriate treatment                   the following outcomes regarding the use
plan: establish whether or not the invasive                of hemostatic mouthwashes on patients
dental procedure will be carried out in                    with various INR target ranges: Based on
the dental office or in a hospital-based                   several small clinical studies, tranexamic acid
dental facility. Possibly, prior to invasive               and epsilon aminocaproic acid hemostatic
treatment, consider blood and or clotting                  mouthwashes are shown to be effective and
factor replacement therapy for patients                    safe in this selective population; although,
with hemophilia; and, patients with platelet               TXA is “6–10 times more potent than EACA.”27
disorders may require platelet transfusion                 Neither hemostatic agent is prepared as
therapy. In addition, other medical                        a solution for local delivery; however, the
interventions may be required beyond infusion              pharmacist can prepare this hemostatic
therapies for the respective disorders; for                prescription as an aqueous preparation
example, fibrinolytic defects, vascular defects            as indicated by the dental provider.27
or modification of anticoagulant therapy                   Supporting this literature review is a Class
may require specialized medical care.                      I recommendation by Aframanian et al.,
When performing the invasive procedure,                    based on a Level of Evidence A, by multiple
recommendations include: minimizing tissue                 randomized controlled trials. The use of a
trauma; consider hemostatic systems for                    2-day regimen of a 4.8% tranexamic acid
predictable extensive bleeding during and                  mouthwash is helpful in achieving adequate
after complex surgical procedures; consider                clotting in patients on oral anticoagulation
alternative pain control techniques other than             therapy after the simple oral surgical
nerve-block anesthesia, especially for patients            procedures.18
with coagulopathies; emphasize periodontal
health to minimize gingival inflammation                   More importantly, when selecting a hemostatic
which can result in increased bleeding; and                therapy that achieves adequate hemostasis
or consider using a combination of local                   when performing invasive dental procedures
hemostatic systems to manage bleeding                      on patients with bleeding disorders one must
episodes. Specialty dental procedures                      consider the following elements:
(restorative, endodontic or surgical) can
adhere to these fundamental guidelines in                  • The specific bleeding disorder
their approach to manage bleeding episodes,                • The need for a hemostatic agent and or
but most importantly, various invasive oral                  intervention
procedures carry a range of bleeding risk2,17,23,24        • The type of local and or systemic hemostatic

         Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
• The need for a consultation with the                Conclusion
  patient’s supervising physician to determine        As health care providers we are ethically and
  the need for coagulation factor replacement         legally obligated to provide the highest standards
  as indicated                                        of care for our dental patients, while actively
• The severity of the bleeding disorder               maintaining appraisal of the literature. Most
• The specific invasive dental procedure that         importantly, it is our responsibility to continue
  will induce a bleed intraoperatively and            our professional journey as life–long learners,
  postoperatively.23                                  especially for the treatment of medically-
                                                      compromised patients.

        Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
In this continuing education course, learning            decision making when selecting a dental or
encompassed both the basic physiological events          hospital treatment site. Generally, comprehensive
of hemostasis and the pathophysiological events          assessment of data, including laboratory
associated with thrombohemorrhagic disorders.            tests; diagnosis of the condition; individualized
Knowledge of these essentials is important               treatment planning with regards to controlling
for proper treatment planning and dental                 the bleed; and careful manipulation of tissues
management of such patients. Additionally,               during implementation is tantamount to successful
complex cases of clotting and bleeding disorders         management of dental patients with bleeding
most likely require physician consultation,              disorders.
interpretation of laboratory testing, and prudent

           Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
Course Test Preview
To receive Continuing Education credit for this course, you must complete the online test. Please go to and find this course in the Continuing Education section.

1.   Based on the three phases of hemostasis, the development of a hemostatic plug is the result
     of which phase in the hemostatic system:
     a. The vascular phase
     b. The platelet phase
     c. The coagulation phase
     d. The fibrinolytic phase

2.   Common causes of a bleed during the platelet phase include:
     a. Thrombocytopathy
     b. Thrombocytopenia
     c. Deficiencies in the plasma coagulation factors
     d. Both (a) and (b) only

3.   Twelve circulating plasma proteins, (also termed plasma coagulation factors) are found in
     which pathways:
     a. Intrinsic and extrinsic pathways
     b. Platelet and coagulation pathways
     c. Common pathway
     d. Both (a) and (c) only

4.   Which plasma coagulation factor is non-existent in the coagulation phase?
     a. Factor III
     b. Factor IV
     c. Factor V
     d. Factor VI

5.   Which plasma coagulation factors are Vitamin K-dependent and pharmacologically (anti-
     coagulants) depressed by indirect means?
     a. Factors II, III, IV, and V
     b. Factors II, VII, IX and X
     c. Factors VII, VIII, IX and X
     d. Factors X, XI, XII, and XIII

6.   Factor VII is located in which of the following pathways?
     a. Common pathway
     b. Fibrinolytic pathway
     c. Extrinsic pathway
     d. Intrinsic pathway

7.   Which blood laboratory test monitors patients on warfarin therapy?
     a. Ivy Bleeding Time
     b. PFA 100
     c. INR
     d. aPTT

           Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
8.    Which blood laboratory test monitors patients on heparin therapy and assess defects in the
      intrinsic pathway of the coagulation system?
      a. Thrombin time
      b. PT
      c. INR
      d. aPTT

9.    Patients with a platelet count of less than ____________ manifest thrombocytopenia.
      a. 150,000/mm3
      b. 100,000/mm3
      c. 50,000/mm3
      d. 20,000/mm3

10.   Which of the following ranges is recommended for “low intensity” Warfarin therapy?
      a. 1.0 to 2.0
      b. 2.0 to 3.0
      c. 3.0 to 3.5
      d. 3.5 and greater

11.   “High intensity” Warfarin therapy (2.5-3.5) is indicated for which of the following
      a. Mechanical prosthetic heart values
      b. Prevention of recurrent MI
      c. Prophylaxis of venous thrombosis
      d. Both (a) and (b) only

12.   Aspirin and aspirin-containing drugs exert their anti-thrombotic action by irreversibly
      inhibiting which of the following hemostatic components?
      a. Adequate amounts of plasma coagulation factors
      b. Adequate function of platelets (aggregation and stickiness)
      c. Adequate numbers of platelets
      d. Adequate amounts of fibrin

13.   Based on a literature review by Armenian et al, it is recommended that patients who fall
      “within the therapeutic range of an INR of _________ or below, warfarin therapy need not be
      modified or altered for simple single dental extractions.”
      a. 2.0
      b. 2.5
      c. 3.0
      d. 3.5

14.   Inherited blood coagulation disorders include all of the following, EXCEPT:
      a. Hemophilia A
      b. Hemophilia B
      c. Immune Thrombocytopenic Purpura (ITP)
      d. von Willebrand’s disease

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
15.   Patients with hemophilia B have varying degrees of which of the following plasma
      coagulation factor deficiencies?
      a. Factor VII
      b. Factor VIII
      c. Factor IX
      d. Factor X

16.   Two defects exist in patients with von Willebrand’s disease, affecting normal hemostasis
      and resulting in a potential clinical bleed. Which of the following components comprise of
      this hemorrhagic condition?
      a. Factor VII and platelets
      b. Factor VIII and platelets
      c. Factor IX and platelets
      d. Factor VIII and factor I5

17.   Which stringy, insoluble protein is responsible for tightly binding the platelet plug to form
      the hemostatic clot?
      a. Prothrombin
      b. Thrombin
      c. Fibrinogen
      d. Fibrin

18.   Which common oral manifestation is present as tiny purple or red, 1 to 2 mm spots that
      appear as a result of minute hemorrhages?
      a. Petechiae
      b. Hematuria
      c. Ecchymosis
      d. Epitaxis

19.   When taking low-dose aspirin (40 to 320 mg) during invasive dental procedures, it is
      recommended patients _______________ before routine dental extractions or its equivalent
      a. Do not continue use of daily aspirin
      b. Alter anti-platelet drug therapy
      c. Continue use of daily aspirin
      d. Consult with the patient’s supervising physician

20.   When considering a local hemostatic agent to control a clinical bleed during invasive
      procedures, which of the following is NOT an appropriate choice for patients with a
      bleeding disorder?
      a. tranexamic acid mouthrinse
      b. absorbable gelatin sponge containing a thrombin solution
      c. oral administration of epsilon aminocaproic acid
      d. nerve-block anesthesia

            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012
1. Bick R. Disorders of Thrombosis. 3rd ed. Philadelphia: Lippincott, Williams & Wilkins; 2002. p. 1-15;
    31-37; 59-60; 69, 71; 82; 91; 121-124; 129-33.
2. Little J, Falace D, Miller C, Rhodus N. Dental Management of the Medically Compromised Patient.
    7th ed. St Louis: Mosby Elsevier; 2008. p. 396-432.
3. Terezhalmy GT, Lichtin AE. Antithrombotic, anticoagulant, and thrombolytic agents. Dent Clin North
    Am. 1996 Jul;40(3):649-64.
4. Sonis S, Fazio R, Fang L. Oral Medicine Secrets. Philadelphia: Henley and Belfus Inc.; 2003.
5. Cotran R, Kumar V, Collins T. Pathologic Basis of Disease. 6th ed. Philadelphia: W. B Saunders;
    1999. p. 119-130; 633-40.
6. Mosby’s Pocket Dictionary of Medicine, Nursing, & Allied Health. 2nd ed. St. Louis: Mosby; 1994:
    p. 483.
7. DeLong L, Burkhart N. General and Oral Pathology. Philadelphia: Lippincott Williams & Wilkins;
    2008: 229-32.
8. Detmer WM, McPhee SJ, Nicoll D, Chou TM. Pocket Guide to Diagnostic Tests. First ed. East
    Norwalk: Appleton & Lange; 1992. p. 54; 113; 115; 120; 129.
9. Sonis S, Fazio R, Fang, L. Principles and Practice of Oral Medicine. 2nd ed. Philadelphia: W. B.
    Saunders Company; 1995. p. 242-61.
10. Peterson P, Hayes TE, Arkin CF, Bovill EG, Fairweather RB, Rock WA Jr, Triplett DA, Brandt JT.
    The preoperative bleeding time test lacks clinical benefit: College of American Pathologists’ and
    American Society of Clinical Pathologists’ position article. Arch Surg. 1998 Feb;133(2):134-9.
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About the Author

Sandra D’Amato-Palumbo, RDH, MPS
                   Sandra is a tenured Associate Professor in the Dental Hygiene Program, Division of
                   Health Professions at the University of New Haven in Connecticut. She has been a
                   full-time faculty member in the program since 1996, spanning the freshman, junior
                   and senior-level curriculum, including the clinical, community-based and academic
                   areas. Her areas of expertise reflect the following courses taught in the Program:
                   Introduction to Dental Hygiene I and II, Dental Hygiene Clinical Concepts III-V,
                   Dental Hygiene Research, Oral Medicine, Senior Internships, Senior Projects, Oral
                   Pathology and the Community-Based Program. In addition to her academic teaching
schedule, Sandra continues to serve on various state and local advisory committees; continues to lecture
at state-wide and national conferences; and maintains consultant positions in the state of Connecticut.
Currently, Sandra is a research scholar at the University of Connecticut Health Center, School of Dental
Medicine and School of Medicine, where she conducts research on hemodialysis patients. Sandra has
been an active member of the New Haven Dental Hygienists’ Association and the Delta Lambda Chapter
of Sigma Phi Alpha Dental Hygiene Honor Society.


            Crest® Oral-B at Continuing Education Course, Revised January 17, 2012

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