Management of dental patients with bleeding disorders: Review and update

Management of dental patients with bleeding disorders: Review and update William T. Johnson, D.D.S., M.S.,* and James M. Leary, D.D.S., MS.,** Lincoln, Nebraska, and Iowa City, Iowa

Management of the dental patient who has a bleeding disorder requires an understanding of the normal hemostatic system and the patient’s specific coagulation defect. This patient group can receive quality comprehensive dental care, provided appropriate preoperative planning and evaluation with the patient’s physician or hematologist is accomplished. Emphasis should be placed on providing appropriate replacement therapy before the dental procedure, selection of conservative treatment approaches, and use of local hemostatic measures to facilitate hemostasis. (ORAL SURG ORAL MED OFCAL PATHOL 1988;66:297-303)

T he oral tissues present several physiologic con-

cerns that increase the risk of postoperative bleeding in patients who have defects of the coagulation system. First, blood flow to the oral tissues is greater than skin1 and second, the oral mucosa exhibits significant fibrinolytic activity.2 Treatment of patients with bleeding problems can be accomplished if the clinician has an understanding of normal hemostatic mechanisms, as well as of the common abnormalities that affect the coagulation system. Assessmentof the degree of hemorrhage associated with a dental procedure is also essential. Procedures that are likely to produce bleeding problems include inferior alveolar and superior alveolar nerve blocks, extractions, and surgical flap procedures. Conservative periodontal treatment (scaling and root planing) is less likely to produce postoperative bleeding. Potential problems from periodontal procedures can be minimized by supragingival scaling, followed by preventive oral hygiene procedures and allowance of several weeks for gingival shrinkage and healing before further scaling procedures.3 Endodontic procedures are unlikely to produce postoperative hemorrhage, and they offer a conservative alternative to extraction.)q4 Infiltration, intraligamental, and intrapulpal injections offer conservative methods for local anesthesia.5

*Department of Endodontics, University of Nebraska Medical Center, College of Dentistry, Lincoln, Nebraska **Department of Family Dentistry, University of Iowa, College of Dentistry, Iowa City, Iowa

THE HEMOSTATIC

SYSTEM

Hemostasis involves a complex series of reactions between the endothelial wall, platelets, and plasma that ultimately prevent blood loss by formation of a fibrin clot after injury. The initial responseto trauma is smooth muscle contraction of the vessel wall; this results in vascular constriction and reduced blood flow. This reaction is followed by platelet adherence to exposed collagen in the endothelial wall, a process enhanced by Von Willebrand’s factor. Platelet contact with collagen results in the release of arachidonic acid and activates a series of biochemical reactions in the platelets; results in the formation of prostaglandins, endoperoxides, and thromboxanes. Influenced by thromboxane AZ, which is produced by the action of cycle-oxygenase on arachidonic acid, the platelet releases adenosine diphosphate (ADP) and serotonin. The release of ADP results in further aggregation of the platelets and formation of a platelet plug, whereas serotonin causesfurther vasoconstriction.6z7 After aggregation, phospholipids (platelet factor 3) and changes in the platelet phospholipid membrane expose receptor sites for activation of the coagulation system (Table 1). This process allows concentration and localization of the clotting factors at the site of injury and prevents generalized systemic coagulation. Coagulation occurs with the conversion of fibrinogen to fibrin and can result from activation of either the extrinsic or intrinsic systems (Fig. 1). The extrinsic system is triggered by a substance elaborated by the injured tissue. In this system, tissue 297

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THE COAGULATION _ I.The Intrinsic

CASCADE

Table 1. Coagulation factors

System

XII

kmgn surface

I-

il I Ii 1

Ca++ PIat&! Factor

The Extrinsic

dill ?

CElf’

I/ (Prothrombln) -1 x

System

“!I

v

t x

v Cal-

ca++

TlSSlR Thromboplastin CP

PF, , Thrombr I -

Fibrin

Monomer

Factor Factor Factor Factor Factor

Factor Factor Factor Factor Factor Factor Factor

I II III IV V VII VIII IX X XI XII XIII

Fibrinogen Prothrombin Thromboplastin Calcium ions Labile factor or proaccelerin Stable factor or proconvertin Antihemophilic A Christmas factor Stuart-Prower factor Plasma thromboplastin antecedent Hageman factor Fibrin stabilizing factor

-XIII Ca” I Fibrin msrmnogen-

BLEEDING

PlasmtnI Flbrm

Fig.

1. Intrinsic

Hydrolyss

and extrinsic coagulation

systems.

thromboplastin forms complexes with factors V, VII, and X in the presence of calcium ions to convert prothrombin to thrombin. It is a rapid system, since it activates the coagulation cascadeby bypassing the contact phase of the intrinsic system. Although the amount of thrombin and fibrin formed is slight, the extrinsic system facilitates aggregation of platelets and enhances the activity of the intrinsic system.6-8 The intrinsic system is slower, but generates thrombin in sufficient quantities to convert fibrinogen to fibrin. In the intrinsic system, a circulating surface-sensitive protein, the Hageman Factor (factor XII), is activated on contact with a foreign surface. This contact (and subsequent reaction) initiates the coagulation cascade. Factor XII can be activated by contact with collagen, vascular basement membranes, activated platelets, or phospholipids from platelets. The process ultimately results in the polymerization of fibrin which is then stabilized by factor XIII. While the intrinsic and extrinsic system differ in methods of activating the coagulation system, they share a common pathway for production of fibrin. This pathway involves factors V 9 II 3,I and XIII.6-8 Fibrin deposition plays an important role, not only in hemostasis but also in wound healing. For healing to occur, the fibrin barrier must be removed. To accomplish this the fibrinolytic system must be activated. Coagulation factors XI and XII, proteolytic plasminogen activators from the endothelial wall, and tissue activators convert plasminogen to plasmin, which hydrolyzes fibrin.8s9

DISORDERS

Evaluation of patients with suspected bleeding disorders requires a complete medical history, as well as laboratory examination. Before dental procedures are initiated, the patient should be asked specifically about previous episodes of hemorrhage that may have occurred after traumatic injuries, dental procedures, and surgical therapy, as well as episodes of epistaxis and menorrhagia. In addition, the practitioner should obtain information about the patient’s family history and use of medications. Initial laboratory tests to confirm or diagnose a suspected bleeding disorder should include a platelet count, bleeding time, prothrombin time, partial thromboplastin time, thrombin clotting time, and clot stability testing.lO The bleeding time (Ivy method) is primarily dependent on normal platelet function. Clinically spontaneous subcutaneous hemorrhages are primarily related to defective platelet activity in the hemostatic system. The bleeding time and platelet count should be performed simultaneously, as both qualitative and quantitative platelet abnormalities can result in prolonged bleeding.‘O The bleeding time is usually normal when defects in coagulation factors are present; therefore, a prolonged bleeding time signifies thrombocytopenia or a platelet functional defect.“ The prothrombin time (PT) measuresthe integrity of factors V, VII, and X of the extrinsic system and factors V, II, and I of the common pathway. The partial thromboplastin time (PTT) measures the integrity of factors XII, XI, IX, VIII, and X of the intrinsic system and factors V, II, and I of the common pathway. If the prothrombin time is normal but the partial thromboplastin time is abnormal, the deficiency involves factors XII, XI, IX, VIII, and X and usually indicates hemophilia. A lengthened PT

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as the only finding indicates a factor VII deficien6,10-12 CY. The results obtained from the prothrombin time must be related to a control value. The normal PT is usually 12 to 14 secondsand-as a general guideline for dental procedures-the PT should be less than 1% of the control value. The normal partial thromboplastin time is less than 45 seconds.It is important to note that PTT is relatively insensitive to changes in the intrinsic coagulation system. A 70% decrease in factor levels may still provide normal results; small changes in the PTT, therefore, may be of significance.*,‘I The thrombin clotting time measures the rate of fibrin formation when thrombin is added to plasma. Normal plasma has a thrombin time of 15 to 18 seconds.Abnormal results usually occur with times greater than 30 secondsor in the failure of a clot to form.6 Clot stability testing is used to determine factor XIII activity. Normal clots are stable in 5 molar urea or 1% monochloroacetic acid. Clots from patients with a factor XIII deficiency will dissolve. Factor XIII activity is not reflected in the other initial tests.6slo When evaluating patients for suspected bleeding disorders, the clinician must remember normal coagulation results do not rule out a mild bleeding disorder, 20% to 25% of a clotting factor is sufficient to normalize the PTT or PT. In addition, the initial tests should serve as a guide in ordering specific clotting factor assays.‘O Hemostatic disorders can be inherited or acquired, but most disturbances fall into the acquired category. The acquired disorders can be drug-induced or result from liver, kidney, and other systemic diseases. The drug-induced hemostatic disorders generally affect platelet function or cause thrombocytopenia. Of the drugs that affect platelet function, aspirin is the most common.* Aspirin and nonsteroidal antiinflammatory agents inhibit the cycle-oxygenase pathway and production of thromboxane AZ, which is essential for platelet aggregation. This inhibitory effect of aspirin can occur after a 300 to 600 mg dose, last for the life span of the platelets (9 to 12 days), and be measurable for several days after ingestion.6 A normal platelet count with prolonged bleeding time indicates a functional disturbance that involves the platelets or the inherited Von Willebrand’s disease. Other common drugs that inhibit platelet function include dipyridamole (Persantine), propranolol (Inderal), antihistamines, theophylline, phenothiazines, tricyclic antidepressants (Elavil),

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furosemide (Lasix), penicillins, gentamicin, and corticosteroids.6 Platelet function can also be altered in kidney disease. With chronic renal disease, metabolic waste products, succinic and phenolic acids, coat the platelets and block the binding sites necessary for hemostasis. In addition, the loss of protein may deplete the coagulation factors.” Should dental treatment of a patient with a qualitative platelet disorder be required, platelet concentrate infusions equal to six donor units should be given and the bleeding time should be monitored before therapy.‘O In addition, local hemostatic measures may be employed to enhance clot formation. These may include the application of pressure packs, placement of sutures, the use of electrocautery, the use of splints and dressings, and/or the application of local hemostatic agents. Astringents such as aluminum chloride act by precipitating protein; are used for capillary bleeding and their action is limited to the surface of contact. Vasoconstrictors such as epinephrine (1: 1,000) have been advocated for control of bleeding from arterioles and capillaries; however, systemic absorption and cardiovascular reactions limit topical use.13Absorbable hemostatic agents include Gelfoam, oxidized cellulose (Oxycel), Surgicel, and Avitene. They are used in conjunction with suturing and ligation and when suturing and ligation are impractical. Gelfoam is a water-insoluble gelatin sponge that acts by disrupting the platelets and establishes a framework with fibrin to create a clot. The oxidized cellulose preparation, Oxycel, and the oxidized regenerated cellulose preparation, Surgicel, have an affinity for hemoglobin that leads to an artificial clot. Oxycel retards epithelial healing, however Surgicel has the advantage of not interfering with epithelization and can be used as a surface dressing. These materials are not adhesive and the cellulose preparations exhibit an acidity that inactivates topical thrombin.13 Topical thrombin is useful in capillary and venous bleeding from inaccessible areas. It acts by directly converting the fibrinogen in the blood to fibrin. It can be applied in powder form or dissolved in isotonic sodium chloride and applied to Gelfoam. Application of microcrystalline collagen, Avitene, is useful in the oral environment in that it can be rapidly molded to the required size and shape or spread over a bleeding surface as it adheres to moist surfaces. Avitene appears to provide a fibrillar mesh in which platelets become physically entrapped; this aids aggregation and the chemical reactions necessary for hemostasis. Evidence indicates that Avitene is superior to other agents (such as gelatin foam and oxycellulose) in

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control of bleeding from various wound models, does not affect the quality of healing, and is resorbed postoperatively.14In addition epsilon-amino-caproicacid (EACA), Amicar, may be administered systemically to prevent loss of the clot. EACA exhibits a specific inhibitory action that prevents iibrinolysis by blocking the conversion of plasminogen to plasmin and results in clot stabilization. A 100 mg/kg loading dose is given preoperativeiy and the drug is continued to 8 to 10 days postoperatively at a dose 50 mg/kg every six hours.‘5 Drugs, such as thiazide diuretics, chloramphenicol, guinine, guinidine, ethanol, and estrogens, can also induce thrombocytopenias.12 The normal platelet count ranges from 200,000 to 400,000/mm3. Thrombocytopenias may be classified as severe (10,000 to 20,000) or mild (60,000 to 100,000). No dysfunction or clinical bleeding is expected with counts higher than 50,000/mm3. The diagnosis of a drug-induced thrombocytopenia is made on the basis of a decreased platelet count and a correlation between the onset of thrombocytopenia and drug administration. Treatment involves removing the patient from the involved drug; this usually results in a return to normal platelet counts over a 7 to 14-day period.16 Thrombocytopenias can also be associated with autoimmune diseases,chronic lymphocytic leukemia, lymphomas, or can accompany infectious mononucleosis and other viral infections. The diagnosis of the relatively common idiopathic (autoimmune) thrombocytopenia purpura is made on the basis of exclusion and results from peripheral platelet destruction. Thrombocytopenia is the only abnormal finding. Should dental treatment of a patient who exhibits thrombocytopenia be necessary, platelet concentrate infusions should be given to provide a platelet count of at least 50,000/mm3. Block injections are contraindicated with a platelet count below 30,000/mm3. Local hemostatic measures should be applied when indicated and epsilon-amino-caproic-acid given for 8 to 10 days.” Acquired coagulation defects can result from liver disease or a vitamin K deficiency. All coagulation factors, with the exception of a portion of Factor VIII, are synthesized in the liver. Four of thesefactors II, VII, IX, and X-require vitamin K for attachment of a calcium-binding site to the factor during synthesis. Liver disease can be differentiated from a vitamin K deficiency, since liver disease results in a deficiency in factor V as well as the vitamin K-dependent factors.6 Anticoagulant therapy for prevention of recurrent thrombosis is frequently employed in patients with

Oral Surg September 1988

myocardial infarction, cerebrovascular accidents, thrombophlebitis, and after cardiovascular surgery. The coumarin drugs are vitamin K antagonists that interfere with synthesis of factors II, VII, IX, and X and prolong the prothrombin time.6~“~‘2Within a patient population, there is a wide variation in the dose required to maintain the same intensity of anticoagulant therapy. The onset of action is 8 to 12 hours; the maximum effect occurs at 36 hours. Activity can persist for 72 hours after the drug is discontinued. The therapeutic range is 1% to 2% times the control prothrombin time.18 Spontaneous bleeding is rare in this range, but increaseswhen the prothrombin time is 2% times the control value. Patients who require dental procedures that produce hemorrhage generally require adjustment of the anticoagulant dosage to allow for a prothrombin time 19’~times that of the contro1.19Administration of vitamin K, to adjust the prothrombin time and reverse the effects of the coumarin drugs, is not appropriate since the vitamin does not affect the rate of synthesis of the coagulation factors by the liver, and vitamin K may keep the prothrombin level high for 2 weeks (or longer) after dental treatment.*O Following dosage adjustment, several days are necessary to decreasethe prothrombin time, and this must be verified before dental treatment. After the dental procedure, the patient should immediately resume his normal drug dosage, since there is a delay in re-establishing effectiveness. Local hemostatic measures are indicated. EACA is contraindicated, as fibrinolysis is the only natural defense mechanism for inappropriate thrombosis. Ninety percent of the inherited hemostatic disorders consist of hemophilia A, hemophilia B, and Von Willebrand’s disease. The hemophilias are inherited disorders caused by a decreased activity or absence of coagulation factor VIII or IX. Hemophilia A (factor VIII deficiency) is most common. It occurs in 70% to 80% of the affected persons, whereas hemophilia B (Christmas disease,or factor IX deficiency) accounts for 6%.19 With the hemophilias, vascular constriction and the platelet systems are normal, but, due to a deficiency or absence of a clotting factor,5 the blood coagulation system does not function normally. The severity of the disease is dependent on the amount of factor present. Normal plasma contains 1.Ounits of a factor per milliliter-a level that is defined as 100%. Deficiencies of a factor are expressedas a percentage (0.75 units/ml = 75%).‘O Patients with a factor VIII deficiency are categorized according to the percentage of active factor present. Antigenic assay for factor VIII protein

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reveals normal factor values; this indicates a functionally deficient molecule and not an absence of factor VIII production. 2’ A factor activity level less than 1% is considered severe, whereas 5% to 30% activity reflects mild hemophilia and may escape detection. Because the vascular and platelet systems are intact, serious bleeding rarely follows minor trauma in mild hemophilia, and superficial cuts in skin or oral mucosa usually stop bleeding with the application of pressure in the patient with severe hemophilia. With more severe injuries, both categories require replacement therapy. Factor VIII can be administered as plasma (1.0 units/ml), cryoprecipitate (5 to 10 units/ml or 80 to 100 units/bag of 10 to 15 ml), or lyophilized factor VIII (250 to 500 units/bottle of 20 to 30 ml).‘O Plasma administration has the disadvantage of factor VIII dilution during infusion, as well as volume constraints that may lead to a circulatory overload. Plasma and cryoprecipitates are recommended for patient with mild hemophilia to minimize the risk of hepatitis transmission associated with factor VIII concentrates. Cryoprecipitate is prepared by subjecting freshly drawn blood of a normal donor to rapid freezing and slow thawing. As the plasma thaws, a precipitate rich in fibrinogen, Von Willebrand factor, and factor VIII forms. This precipitate is separated from the plasma by centrifugation, then refrozen until needed. Although cryoprecipitates are not usually separated by blood type, this can be accomplished.22The lyophilized factor VIII concentrates have the disadvantage of containing anti-A and anti-B immunoglobulins from numerous pooled donors, which may induce hemolysis in patients who have blood types other than 0, and present a significant risk for transmission of hepatitis.‘O With the exception of local anesthesia and surgical procedures, there are few dental procedures that produce significant bleeding. Local anesthesia can be administered safely with the use of infiltration, intraligamental, and intrapulpal techniques, if the tissue is firm and confined. The inferior alveolar and posterior superior alveolar block injections should be administered only after replacement therapy of factor VIII, because of the possibility of a dissecting hematoma. The recommended level of replacement therapy varies with authors, and ranges from 30%4to 75%.l” For more extensive dental procedures-such as multiple extractions-and major flap procedures, the level of factor VIII should be raised to the 50% to 75% leve1.10x23 Since factor VIII has a half life of 8 to 12 hours, uncomplicated procedures may not require further replacement therapy. The more extensive procedures

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may require further infusions at 12- to 24-hour intervals. Local hemostatic measures, such as the application of topical thrombin or Avitene, to promote platelet aggregation and formation of a hemostatic plug are indicated in patients with hemophilia. EACA should also be administered to prevent the early loss of the clot. Stabilization of the fibrin clot with an antifibrinolytic drug may reduce the need for further factor VIII infusions.24 Analgesics that contain aspirin and the nonsteroidal anti-inflammatory agents are contraindicated, as they alter platelet function. Routine, comprehensive, and quality dental care can be provided to the patient with hemophilia on an outpatient basis if the practitioner is familiar with the type and severity of the factor deficiency and plans accordingly. An exception is the patient with hemophilia who has inhibitors. Development of antibodies (or inhibitors) to factor VIII occurs in 5% to 20% of the patients with factor VIII deficiency and presents a major problem in treatment.” Elective dental procedures are contraindicated in this group of patients with hemophilia. Inhibitors are detected when the patient’s plasma is mixed with normal plasma and the normal plasma fails to correct the partial thromboplastin time. lo When inhibitor titers are low, infusion of large amounts of factor VIII concentrate can overwhelm the antibodies and a circulating level of factor VIII can be maintained by a continuous infusion. However, the administration of factor VIII produces an anamnestic antibody response 3 to 5 days after introduction that may compromise further treatment. For patients with high inhibitor titers, prothrombin complex concentrates (factors II, VII, IX, and X), which exhibit an unknown mechanism to bypass factor VIII inhibitor, can be given.‘O Prothrombin complex concentrates are available in activated and nonactivated forms; but the activated concentrates exhibit a slightly better successrate.25,26 The prothrombin complex concentrate contains 500 to 1000 units of prothrombin, factor X, factor IX, and variable amounts of factor VII in a volume of 25 ml. This complex is administered over a 30- to 60-minute period and exhibits a short duration of action. Therefore, dental treatment should be performed immediately after infusion. Local hemostatic measures are indicated; however, EACA is contraindicated. Inappropriate thrombosis is a potential complication with prothrombin complex concentrates, and fibrinolysis is the only defense mechanism against the formation of unwanted clots. Other methods of treating patients with inhibitors include plasmapheresis, which has been advocated in patients to reduce the antibody titer,27l28 and a

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synthetic vasopressin analogue (DDAVP), which has been shown to produce a transient increase in factor VIII activity.29 Hemophilia B (or Christmas disease) is a deficiency in factor IX and cannot be clinically distinguished from hemophilia A. Factor IX replacement therapy is the same as that of factor VIII, and inhibitors to factor IX are rare. Unlike factor VIII, which is maintained within the circulatory system, factor IX enters the extravascular spaces. Because of this, factor IX exhibits a two-phase disappearance. There is a rapid initial disappearance (with a half-life of 4.5 hours) that occurs as an equilibrium with the extravascular spacesis achieved. The second phase disappearance (with a biologic half-life of 32 hours) then occurs.3oReplacement therapy for mild deficiencies of factor IX consists of fresh frozen plasma (one unit factor IX/ml) or prothrombin-complex concentrates (factors II, VII, IX, and X). With plasma, infusions can begin 24 to 36 hours before the scheduled procedures due to the long factor IX halflife. This allows multiple units of plasma to be given without overloading the circulatory system. A factor level of 20% to 30% of normal should be obtained. The use of cryoprecipitate offers no advantage over plasma, since factor IX is not concentrated in the cryoprecipitate. The lyophilized factor IX concentrates exhibit significant quantities of factors II and X and variable amounts of factor VII, and have the potential for inappropriate thrombosis as well as the risk of transmitting hepatitis. Replacement therapy for severe factor IX deficiencies consists of raising the plasma level of factor IX to 30% to 50% of normal by use of prothrombin complex concentrates.1° Local hemostatic measures are indicated and EACA can be used with plasma replacement therapy, but is contraindicated with prothrombin complex concentrates. Von Willebrand’s disease is characterized by a deficiency or defect in the plasma protein-Von Willebrand Factor-which mediates the adherence of platelets to the injured vessel wall and subsequent aggregation to form a hemostatic plug.22Von Willebrand factor also plays a role in stabilizing the coagulate activity of factor VIII. Von Willebrand factor is necessary for agglutination of platelets when the antibiotic ristocetin is mixed with plasma. In patients lacking this factor, the addition of ristocetin will not produce visible platelet agglutination. The addition of factor VIII to this mixture, however, will allow for agglutination. Treatment should consist of replacement therapy with plasma or cryoprecipitate. Cryoprecipitate has the advantage of containing more Von Willebrand factor activity when

Oral Surg September 1988

compared to factor VIII concentrates.‘h Ten bags of cryoprecipitate are generally required for the adult patient and should be given immediately before treatment procedures. This shortens the bleeding time for up to 12 hours and increases the plasma level of factor VIII activity.22 Reinfusions at 4- to 12-hour intervals may be necessary in conjunction with surgical procedures. Local hemostatic agents and EACA are indicated. Other rare inherited diseases that affect platelet function include thrombasthenia, storage pool disease, and Bernard-Soulier syndrome. Thrombasthenia is characterized by a normal platelet count, normal platelet adhesion, a prolonged bleeding time, poor or absent clot retraction, abnormal platelet retention, and weak or absent aggregation. This disease is the only platelet function disorder with poor or absent clot retraction.6 The abnormality is attributed to the lack of thrombasthenin, which is a glycoprotein on the platelet surface.6 Storage pool disease exhibits a normal platelet count, a variably prolonged bleeding time, and deficient platelet aggregation. The lack of platelet aggregation is thought to be the result of a deficiency in ADP in the dense platelet granules or in the release mechanism.6 Bernard-Soulier syndrome is characterized by a prolonged bleeding time, abnormal prothrombin consumption, and giant platelets. Platelet adhesiveness is decreasedand they do not bind coagulation factors V, XI, and thrombin; this probably accounts for the abnormal prothrombin consumption.6 The platelets do not aggregate when stimulated by ristocetin and can be differentiated from Von Willebrand’s disease in that addition of factor VIII does not correct the defect.“j It has been proposed that this disorder results from an abnormal interaction of the platelet with the subendothelium because of the lack of a specific membrane glycoprotein receptor for the Von Willebrand factor. Clinical treatment to correct these disorders involved platelet concentrate infusions, local hemostatic measures, and EACA. SUMMARY

Treatment of patients with bleeding disorders presents a unique challenge to the dental practitioner. Knowledge of the specific coagulation defect is essential for proper management and requires close consultation and coordination with the patient’s physician or hematologist. Before providing dental treatment, the clinician should evaluate the coagulation defect, the potential of the procedure to produce hemorrhage, and determine the need for replacement therapy. The conservative approach to local anesthesia and therapy is recommended with this patient

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Management of dental patients with bleeding disorders

group, and special attention to the application of local hemostatic measuresis critical. Aspirin and the nonsteroidal anti-inflammatory-containing analgesics should be avoided. Postoperative bleeding should be treated aggressively and without delay. Since the majority of bleeding disorders are acquired, the clinician should also be aware that the first indication of a coagulation defect may occur after a dental procedure. In these cases, a complete medical history, laboratory testing, and consultation with the patient’s physician or hematologist are necessary to arrive at a diagnosis. In general, quality comprehensive dental care can be provided to dental patients with hemostatic defects when there is an understanding of the coagulation system. Evaluation, planning, and consultation with the patient’s physician or hematologist are essential elements in treatment of this patient group. REFERENCES

1. Squier CA, Nanny D. Measurement of blood flow in the oral 2. 3.

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mucosa and skin of the Rhesus monkey using radiolabeiled microspheres. Arch Oral Biol 1985;30:3 13-8. Walsh PN, Rizza CR, Evans BE, Aledort LM. The therapeutic role of epsilon amino caproic acid for dental extractions in hemophilias. Ann NY Acad Sci 1975;240:267-76. Saari JT. Periodontic/endodontic treatment. In: Powell D, ed. Recent advances in dental care for the hemophiliacs. Los Angeles: Hemophilia Foundation of Southern California, 1979;6 i-2. Evans BE. Dental treatment for hemophilias: evaluation of dental program (1975-1976) at the Mount Sinai Hospital International Hemophilia Training Center. Mt Sinai J of Med 1977;44:409-37. Evans BE, Aiedort LM. Hemophilia and dental retreatment. J Am Dent Assoc 1978;96:827-34. Miale JB. Laboratory medicine hematology. 6th ed. St. Louis: C.V. Mosby Company, 1982;772-859. Bowie EJW, Owen CA. The hemostatic mechanism. In: Kwaan HC, Bowie EJW, eds. Thrombosis. Philadelphia: W.B. Saunders, i982;7-23. Myers AM. Evaluation of the hemorrhage prone patient. Postgraduate Medicine 1980;67: 16 i-9. Robbins KC. Fibrinoiysis. In: Kwaan HC, Bowies EJW, eds. Thrombosis. Philadelphia: W.B. Saunders. 1982:23-8. Goldsmith JC. Medical management of dental patients with bleeding disorders. J Iowa Med Sot i981;291-7. Hussev CV. Fobian JE. Wilson SD. Acute coanuiation disorders. 6th ed. In: Condon RE, Nyhus LM, eds. Manual of surgical therapeutics. Boston: Little, Brown and Company, 1985;299-3 13. Toliefsen DM, ed. Disorders of hemostasis. In: Osiand MJ, Saitman RJ, eds. Manual of medical therapeutics. Boston: Little, Brown and Company, 1986;271-84. Hemostatics and Astringents, Accepted Dental Therapeutics, 40th ed. Chicago: Council on Dental Therapeutics, American Dental Association, 1984;334-42.

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14. Evans BE. Use of Avitene as a local hemostatic agent in oral surgery for hemophiliacs. In: Powell D, ed. Recent advances in dental care for hemophiliacs. Los Angeles: Hemophilia Foundation of Southern California, 1979;79-8 I. 15. Lucas ON, Albert TW. Epsilon aminocaproic acid in hemophiliacs undergoing dental extractions: a concise review. ORAL &CC ORAL GED &AL PATHOL 198 I ;5 I :I 15-20. 16. Catalan0 PM. Platelet and vascular disorders. In: Rose LF, Kaye D, eds. Internal medicine for dentistry. St. Louis: The C.V. Mosby Company, 1983;400-8. 17. Cohen SG. Platelet disorders. In: Rose LF. Kave D, eds. Internal medicine for dentistry. St. Louis: The C-V. Mosby Company, I983;425-6. 18. Bick RL. Anticoagulant and antiplatelet therapy. In: Murano G, Bick RL, eds. Basic concepts of hemostasis and thrombosis. Boca Raton: CRC Press, 1984;246-56. 19. Little JW, Faiace DA, Dental management of the medically compromised patient, St. Louis: The C.V. Mosby Company, 1980;176-88. 20. Reeve LW. Hemorrhage. In: McCarthy FM. Emergencies in dental oractice. 3rd ed. Philadelphia: W.B. Saunders, i979;56%95. 21. Rosenshein M. Disorders of the coagulation mechanism. In: Rose LF, Kaye D, eds. Internal medicine for dentistry. St. Louis: The C.V. Mosby Company, 1983;408-14. 22. Green D. Von Wiiiebrand’s disease. Postgraduate Medicine 1980;67:241-5. oral surgical management, I. 23. Kelly WD. Outpatient/inpatient In: Powell D, ed. Recent advances in dental care for the hemophiliacs 1.0s Angeles: Hemophilia Foundation of Southern California, 1979;69-70. 24. Vinckier F, Vermyien J. Dental extractions in hemophilia: reflections on 10 year’s experience. ORAL SURF ORAL MED ORAL PATHOL 1985;59:6-9. 25. Redding SW, Stiesier KM. Dental management of the classic hemophiliac with inhibitors. ORAL SURG ORAL MED ORAL PATHOL

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26. Zech R, Strother SV. Maintenance of hemostasis during exodontia in two hemophiliacs with factor VIII inhibitors. J Oral Maxiiiofac Surg 1983;41:53-6. 27. Cobcroft R, Tamagnini G, Dormandy K. Serial piasmapheresis in haemophiiiac with antibodies to FVIII. J Ciin Path 1977;30:763-5. 28. Francesconi M, Korninger C, Thaler E, Niessner H, Hacker P, Lechner K. Piasmapheresis: its value in the management of patients with antibodies to factor VIII. Haemostasis 1982;i 1:79-86. 29. Eastman JR, Nowakowski AR, Tripiett DA. DDAVP: review of indications for its use in treatment of factor VIII deficiency and report of a case. ORAL SURG ORAL MED ORAL PATHOI. 1983;56:246-5 1. 30. Kasper CK. Hereditary disorders of coagulation. In: Powell D, ed. Recent advances in dental care for the hemophiliacs. Los Angeles: Hemophilia Foundation of Southern California, 1979;16-28. Reprint requests to: Dr. William T. Johnson Department of Endodontics University of Nebraska Medical Center College of Dentistry 40th and Holdrege Lincoln, Nebraska 68583-0740