DENTAL MANAGEMENT OF MEDICALLY COMPROMISED CHILDPRESENTED BY :-

DR. PAWAN K. SINSINWAR

Content • Hematologic Disorders• Hemophilia or Inherited Bleeding

Disorder.• Blood Transfusion• Anemia• Leukemia• Taking a “Blood Thinner”/Tendency

to Bleed Longer Than Normal

• Cardiovascular Disease• Heart Failure• Heart Attack• Angina Pectoris• High Blood Pressure• Heart Murmur• Mitral Valve Prolapse• Rheumatic Fever• Congenital Heart Disease• Artificial Heart Valve• Arrhythmias• Coronary Artery Bypass

Graft/Angioplasty/Stent

• Respiratory Tract Disease• Allergies or Hives• Asthma.• Emphysema/Chronic Bronchitis• Tuberculosis.• Sleep Apnea/Snoring

• Endocrine Disease• Diabetes• Thyroid Disease

• Genitourinary Tract Disease• Kidney Failure• Sexually Transmitted Diseases

• Other Conditions• Tobacco and Alcohol Use• Drug Addiction and Substance Abuse• Tumor and Cancer• Radiation Therapy and Chemotherapy• Steroids• Operations or Hospitalizations

Introduction

It is the management of patients in whom the dental treatment may need modification according to their medical condition

Because the majority of medically compromised patients need oral healthcare, a working knowledge of the multitude of medically complex conditions is critical for dental professionals.

This knowledge is necessary to help prevent, minimize, and alert clinicians to possible adverse side effects potentially associated with procedures and drugs used in dentistry.

To minimize the risk for potential complications that may

affect the physical health of medically compromised patients,

an aggressive prevention oriented program is required.

Each patient presents a unique set of challenges to the dentist,

but achieving a successful outcome can be a rewarding

experience.

Hemophilia

Deficiency of a procoagulant.

Hemophilia A (classic hemophilia) -Factor VIII, (antihemophilic factor)

Hemophilia B, (Christmas disease) -Factor IX (plasma thromboplastin component).

Hemophilia C (Rosenthal’s’ disease) Factor XI (plasma thromboplastin antecedent)

Other factor deficiencies, such as those of factors II, V, and XIII (one case per 1 million population) and

factor VII (one case per 500,000 population) are rare and are inherited as autosomal recessive traits.

TREATMENT

• Replacement of the deficient coagulation factor, through the use of purified concentrates either manufactured through recombinant technology or from pooled plasma.

• In the past, whole blood, plasma, or cryoprecipitate was used for replacement therapy.

• Factor concentrates are advantageous as they are generally accessible, easily handled and stored, virally inactivated, and commonly result in consistent hemostatic results.

• The dosage, frequency of administration, and duration of therapy depend on the activity level required, the half-life of the procoagulant, the intervention or procedure contemplated, or the location and severity of the bleeding episode.

• The half-life of factor VIII is approximately 12 hours, whereas for factor IX it is approximately 18 hours.10

FEMALE WITH BLEEDING DISORDERS

Von Willebrand Disease

• Patients with Von Wille Brand disease should undergo subtyping to determine optimal therapy.

• DDAVP may be used to achieve hemostasis in most patients with type I von Willebrand disease, where type I VWD represents a quantitative VWF deficiency with intact multimers.

• When DDAVP is used, a test dose should be administered to document an adequate hemostatic response.

• For patients with less common subtypes of VWD, patients who do not respond to DDAVP, or patients for whom DDAVP is inappropriate, or in bleeding events for which DDAVP should not be used, other therapeutic modalities may be required, including replacement with exogenous intact VWF through the use of a concentrate.

COMPLICATIONS

Inhibitors are antibodies that neutralize the replaced coagulation factor and are one of the most severe complications for patients.

Inhibitors may develop in approximately 28% of patients with severe factor VIII deficiency and in 3% to 5% of patients with severe factor IX deficiency.

Hemophilic patients with inhibitors pose considerable treatment challenges and should be managed only in conjunction with a hemophilia-comprehensive treatment center, because hemostasis is often difficult to achieve or maintain.

Other Complications

Arthritis and Degenerative joint disease secondary

to recurrent bleeding.

Blood-borne viral infections may

have been transmitted via

required blood or blood products.

Hepatitis, including both B and C and

resultant liver disease

The human immunodeficiency

virus (HIV) has also been a major

source of morbidity and mortality since

1979.

• Approximately 90% of hemophilic patients with severe factor VIII deficiency and 30% of those with severe factor IX deficiency who received factor concentrate during the at-risk period may have become infected with HIV.

• Currently available treatments of factor concentrates made through recombinant technology or pooled plasma have effectively eliminated transmission of HIV and hepatitis B and C.

• Universal precautions should be followed when treating all hemophilic patients with a history of receiving either factor concentrate.

RISKS TO DENTAL STAFF

• The risk for acquiring hepatitis B virus infection following an accidental stick with a needle used by a hepatitis B virus carrier ranges from 6% to 30%, far higher than the risk for transmission of HIV infection (less than 1%) following a stick with a needle used by an HIV-infected patient.

• A study by Klein and colleagues demonstrated a less than 0.5%

occupational risk for HIV infection among dental professionals despite their infrequent compliance with recommended infection control precautions, frequent occupational exposure to persons at increased risk for HIV infection, and frequent accidental parenteral inoculations with sharp instruments.

DEVELOPMENT OF A TREATMENT PLAN

• With recent advances in treatment, most hemophilic patients can receive outpatient dental care routinely.

• The dentist must be fully aware of the procedures that can be safely performed and those in which complications may arise.

• The dentist should confer with the patient’s physician and hematologist to formulate an appropriate treatment plan.

• The dentist should know the specific type of bleeding disorder, the severity of the disorder, the frequency and treatment of bleeding episodes, and the patient’s inhibitor status.

• The dentist should discuss with the hematologist the type of anesthetic anticipated to be administered, the invasiveness of the dental procedure, the amount of bleeding anticipated, and the time involved in oral wound healing to help establish an appropriate treatment plan including the need for replacement and adjunctive therapies.

USE OF ANTIFIBRINOLYTIC AGENTS

• Antifibrinolytic agents are an adjunctive therapy for dental management of patients with bleeding disorders and are important for prevention or treatment of oral bleeding.

• These agents include -Aminocaproic acid and Tranexamic acid .

• Hemophilic patients form loose, friable clots that may be readily dislodged or quickly dissolved, especially in the oral cavity where local fibrinolysis is increased.

• Antifibrinolytics prevent clot lysis within the oral cavity.

• They are often used as an adjunct to factor concentrate replacement.• For some dental procedures in which minimal bleeding is anticipated,

they may be used alone.

Dosages

• In children, Aminocaproic acid is given immediately before dental treatment in an initial loading dose of 100 to 200 mg/kg by mouth up to a maximum total dose of 10 g.

• Subsequently, 50 to 100 mg/kg per dose up to a total maximum dose of 5 g is administered orally every 6 hours for 5 to 7 days.

• Alternatively, for patients of approximately adult size or heavier than 30 kg, a regimen of 3 g by mouth four times daily without a loading dose may be used.

• The adult and pediatric dosage of Tranexamic acid is 25 mg/kg given immediately before dental treatment.

• The same dose is continued every 8 hours for 5 to 7 days.

Side Effects

The common side effects associated with the use of antifibrinolytics include headache, nausea, and dry mouth.

These side effects are usually tolerable and, unless severe, do not require discontinuation of the medication.

Other less common side effects have also been reported.

To avoid thrombosis, Antifibrinolytics should not be used when renal or urinary tract bleeding is present or when there is any evidence of disseminated intravascular coagulation.

Repeated use of prothrombin complex concentrate (PCC) or bypassing products (activated PCC) in patients with inhibitors should also be avoided during a course of Antifibrinolytic therapy because they may predispose to thrombotic episodes.

PAIN CONTROL

If patient apprehension is significant, sedation or nitrous oxide–oxygen inhalation analgesia and Hypnosis may be considered.

IM injections of hypnotic, tranquilizing, or analgesic agents are contraindicated due to the risk of hematoma formation.

Analgesics containing aspirin or anti-inflammatory agents (e.g., ibuprofen) may affect platelet function and should be avoided.

Acute pain of moderate intensity - Acetaminophen.

Propoxyphene hydrochloride analgesic is acceptable.

Severe pain- Narcotic analgesics are indicated.

Local Anesthesia

Absence of factor replacement, PDL injections may be used.

Infiltration can generally be administered without pretreatment with either -Aminocaproic acid or replacement therapy.

If the infiltration injection is into loose connective tissue or a highly vascularized area, then factor concentrate replacement to achieve a level of approximately 30% to 40% activity is recommended.

Proceed with caution when considering block anesthesia.

The loose, connective, nonfibrous, and highly vascularized tissue at the sites of IANB and PSA are predisposed to development of a dissecting hematoma, which potentially may cause airway obstruction and create a life-threatening bleeding episode.

A minimum of a 40% factor correction is mandatory with block anesthesia.

The dentist must carefully aspirate to ensure that the

needle has not entered a blood vessel.

If there is bloody aspirate, further factor replacement may be required, and the attending

hematologist should be notified immediately following the

operative procedure.

All patients should be observed for development of a hematoma

and immediately referred for treatment in case hematoma

forms after the administration of local anesthesia.

DENTAL MANAGEMENT

Most hemophilic patients can receive outpatient dental care routinely.

Maximum treatment should accomplished per visit to minimize the need for unscheduled factor infusions and hence cost.

Patients with inhibitors are best treated at a center with experience in dealing with this complication.

The dental procedures used in treating a patient with hemophilia do not differ significantly from those used for unaffected individuals.

Prevention of Dental Disease

A program that includes

• Tooth brushing, Flossing, • Topical fluoride exposure, • Systemic fluoride administration, • Proper diet and• Professional examination at regular intervals

are effective measures that prevent dental problems.

Rubber cup prophylaxis and supragingival scaling may be safely performed without prior factor replacement therapy.

Minor bleeding can be readily controlled with local measures, such as direct pressure with a

moistened gauze square.

If bleeding persists for several minutes, the topical application

of bovine thrombin, microfibrillar collagen and local

fibrin glue may be of value.

Periodontal Therapy

Patients who require deep scaling initially undergo supragingival scaling than tissue should be allowed to heal for 7 to 14 days, as edema and hyperemia diminish.

Subsequent treatments to remove calculus and irritants therefore decreased bleeding risk from the tissue.

If subgingival scaling is planned, replacement therapy may be considered, depending on the amount of anticipated bleeding and the severity of the factor deficiency.

It is imperative that periodontal patients be placed on a maintenance schedule for proper management.

• An abnormal frenum attachment may cause gingival recession and pocket formation. Early treatment is indicated

• Frenectomy techniques are surgically acceptable for

hemophilic patients; both factor concentrate replacement and antifibrinolytic therapy are required before frenum or other periodontal surgery.

• If a large amount of bleeding is anticipated, should be performed in a hospital environment, with the requisite preparation.

Restorative Procedures

Most restorative procedures on primary teeth are successfully completed without factor concentrate replacement using PDL injections of local anesthesia or local infiltration.

Small lesions may be restored using nitrous oxide–oxygen inhalation analgesia alone.

The use of acetaminophen with codeine may also decrease discomfort in the child.

Most operative procedures for adults may also be completed using local infiltration of anesthetic, a procedure that usually does not require factor concentrate replacement.

If a mandibular block or a posterior superior alveolar injection is anticipated, factor concentrate replacement to a level of 40% and antifibrinolytic therapy are required before injection.

If factor concentrate replacement is required, all possible restorative treatment should be completed in one visit to minimize the number of infusions required to complete the restorative treatment plan.

• A rubber dam should be used to isolate the operating field and to retract and protect the cheeks, lips, and tongue.

• A thin rubber dam is preferred because there is a decreased tendency to torque the rubber dam retainer and cause gingival tissue abrasion.

• The retainer should be placed carefully so that it is stable. • Retainers with subgingival extensions should be avoided. • Wedges and matrices can be used conventionally. • During proximal preparation, the wedge retracts the papilla, thus

protecting it. • A properly placed matrix should not cause bleeding.

• High-speed vacuum and saliva ejectors must be used with caution so that sublingual hematomas do not occur.

• Care must also be used in the placement of intraoral radiographic films, particularly in highly vascular sublingual tissues.

• The preparation of a tooth for a cast crown requires caution in gingival preparation, as does placement of retraction cord and impression material.

• Periphery wax is used on the impression tray to prevent possible intraoral laceration during tray placement. Undue trauma should be avoided in cementing or finishing a crown.

Pulpal Therapy.

• At times, pulp exposures in primary and permanent teeth may be avoided if carious dentin is not entirely removed in one procedure (indirect pulp therapy).

• A pulpotomy or pulpectomy is preferable to extraction.

• Most vital pulpotomy and pulpectomy procedures can be successfully completed using local infiltration anesthesia.

• Nitrous oxide–oxygen inhalation analgesia may also help alleviate discomfort.

• If the pulp of a vital tooth is exposed, an intrapulpal injection may be used safely to control pain.

• Bleeding from the pulp chamber does not present a significant problem in that it is readily controlled with pressure from cotton pledgets.

• If pulp tissue is necrotic, local anesthetic is usually unnecessary.

Oral Surgery

Preoperative evaluation and postoperative management of the hemophilic patient undergoing extractions must be coordinated with the hematologist.

The surgical procedure, including the anesthetic technique, the degree of anticipated surgical trauma, and the expected duration for healing.

The hematologist can then determine the amount and duration of factor concentrate replacement and adjunctive therapies required for surgery and postoperative management.

Patients with inhibitors should only be treated in a hospital setting by those experienced in their management.

For simple extractions of erupted permanent teeth and multirooted primary teeth, a 30% to 40% factor correction is administered within 1 hour before dental treatment.

Antifibrinolytic therapy should be started immediately before or after the procedure and should be continued for 5 to 10 days.

The patient should be placed on a clear liquid diet for the first 72 hours.

For the next week, a soft, pureed diet is recommended.

During this time, the patient should not use straws, metal utensils, pacifiers, or bottles.

After 10 days, the patient may begin to consume a more normal diet. Specific postoperative instructions should be provided to the patient and parent.

Factor concentrate is extremely costly, therefore all extractions should be completed in one appointment if possible.

After extractions direct topical application of hemostatic agents, such as thrombin or microfibrillar collagen hemostat (Avitene), may assist with local hemostasis.

The socket should be packed with an absorbable gelatin sponge (e.g., Gelfoam, Pharmacia and Upjohn Co., Kalamazoo, MI).

Microfibrillar collagen or topical thrombin or fibrin glue may then be placed in the wound.

Direct pressure with gauze should then be applied to the area.

Stomahesive may be placed over the wound for additional protection from the oral environment.

The use of sutures should be avoided unless suturing is expected to markedly enhance healing, in which case resorbent sutures are recommended.

The patient must be given specific and thorough postoperative instructions.

For surgical extractions of impacted, partially erupted, or unerupted teeth, a higher factor activity level may be targeted before surgery.

The hematologist may also elect to administer factor replacement to the patient postoperatively.

Antifibrinolytic therapy should be started immediately before or after the procedure and continued for 7 to 10 days.

For simple extractions of single-rooted primary teeth (i.e., incisors and canines), one must evaluate the amount of root development present to determine whether factor replacement therapy is required.

If there is complete root development, factor replacement therapy may be required, whereas if there is only partial root formation, antifibrinolytic therapy along with local hemostatic agents may be all that is required.

The normal exfoliation of primary teeth does not usually result in bleeding or require factor replacement.

Bleeding in these circumstances can generally be controlled with direct finger and gauze pressure maintained for several minutes.

The direct topical application of an adjunctive agent may also help with local hemostasis.

If there is continuous slow bleeding, antifibrinolytic therapy may be initiated.

In rare circumstances, most commonly when the gingival tissue is repeatedly traumatized during exfoliation, use of factor replacement therapy may be required.

In this circumstance, dental evaluation should be performed and consideration given to removal of the exfoliating tooth if repeated trauma cannot be avoided.

Surgical Complications

Bleeding may occur 3 to 4 days postoperatively.

Both systemic and local treatment should be used for hemostatic control.

Sufficient replacement factor should be administered to control recurrent bleeding.

It is not prudent to protect a loose clot.

The typical clot in this situation is characterized as a “liver clot” and is dark red, usually protruding from the surgical site, and often covers the surfaces of several teeth.

Following adequate replacement with factor concentrate, usually to a 30% to 40% activity level, the abnormal clot should be removed and the area cleansed to help isolate the source of bleeding.

The socket should then be repacked and use of antifibrinolytic agents considered.

Antibiotic Prophylaxis

Total joint replacement, is often performed in patients with severe hemophilia to restore function and alleviate pain associated with degenerative arthritis due to multiple hemarthroses.

Antibiotic prophylaxis is required before invasive dental procedures.

The American Heart Association recommendations for bacterial endocarditis prophylaxis, 2007, are commonly followed.

If the patient is immunocompromised because of HIV infection, intravenous antibiotic prophylaxis may be considered.

Orthodontic Treatment

Early recognition of an orthodontic problem is important to eliminate complex orthodontic problems.

Both interceptive and full-banded orthodontics may be performed if required.

Care must be taken in the adaptation and placement of bands to prevent laceration of oral mucosa.

Accidental scratch or minor laceration responds to applied pressure for 5 minutes.

The use of preformed orthodontic bands and brackets

Longer-acting wires and springs require less frequent adjustment of orthodontic appliances.

Oral hygiene is particularly important to avoid inflamed, edematous, and hemorrhagic gingival tissues.

A water irrigating device may be helpful for home dental care.

Dental Emergencies

Oral trauma is a common during childhood.

Management of bleeding injuries, including hematomas, in patient

with a bleeding disorder require a combination of factor replacement

and antifibrinolytic therapy, as well as treatment with local

hemostatic agents.

Blood loss from the oral cavity is easily underestimated or

overestimated.

The patient’s hemoglobin may be checked to ensure that the patient

is not anemic in these circumstances.

THANK YOU

SICKLE CELL ANEMIA

• Patients with sickle cell anemia have an autosomal recessive hemolytic disorder that occurs predominantly in persons of African descent but is also found among Italian, Arabian, Greek, and Indian people.

• Patients with sickle cell anemia produce hemoglobin S instead of the normal hemoglobin A.• Hemoglobin S has a decreased oxygen-carrying capacity. • Decreased oxygen tension causes the sickling of cells. • These patients are susceptible to recurrent acute infections, which result in an “aplastic crisis” caused by

decreased red blood cell production and in subsequent joint and abdominal pain with fever. • Over time there is a progressive deterioration of cardiac, pulmonary, and renal function.• Many factors can precipitate a sickle cell crisis, including acidosis, hypoxia, hypothermia, hypotension,

stress, hypovolemia, dehydration, fever, and infection. • Radiographic changes are associated with sickle cell anemia. • There is a generalized radiolucency and loss of trabeculae with prominent lamina dura, caused by increased

erythropoietic demands that result in expansion of the marrow spaces. • Bone growth may be decreased in the mandible, resulting in retrusion, and the teeth may be

hypomineralized. • Occasionally, patients with sickle cell anemia have infarcts in the jaw, which may be mistaken for a

toothache or osteomyelitis. • The patients experience dental pain with absence of pathology.

• Dental appointments should be short to reduce potential stress on the patient. • The importance of an aggressive preventive program cannot be understated,

and such a program should have the goal of maintaining excellent oral health and decreasing the possibility of oral infection.

• Dental treatment should not be initiated during a sickle cell crisis. • If emergency treatment is necessary during a crisis, only treatment that will

make the patient more comfortable should be provided. • Patients with sickle cell anemia may have skeletal changes that make

orthodontic treatment beneficial. • Special care must be taken to avoid tissue irritation, which may induce

bacteremia's, and the disease process may compromise the proposed treatment. • Careful monitoring is a necessity when proposing elective orthodontic

treatment in patients with sickle cell anemia.

• Many patients with sickle cell anemia have defective spleen function or undergo a spleenectomy, which leaves them more vulnerable to infection because immunoglobulin production is decreased and phagocytosis of foreign antigens is thus impaired.

• Most patients with sickle cell anemia are taking low-dose daily prophylactic antibiotics, and the need for additional antibiotics for dental procedures is debatable.

• Some authors have recommended the use of antibiotics for all dental procedures, whereas others recommend the administration of additional antibiotics when there is obvious dental or periodontal infection.

• The selection of an antibiotic is usually similar to that in cases of heart defect. • The use of local anesthetics with a vasoconstrictor is not contraindicated in patients with sickle cell anemia. • Some textbooks do recommend against the use of vasoconstrictors, although there is no evidence to support

this practice. • Similarly, the use of nitrous oxide is not contraindicated in these patients. • Care must be taken in treating patients with sickle cell anemia to avoid diffusion hypoxia at the completion of

the dental procedure. • The restoration of teeth, including pulpotomies, is preferable to extraction.• Pulpectomy in a nonvital tooth is reasonable if the practitioner is fairly confident that the tooth can remain

noninfected. If the tooth is likely to persist as a focus of infection, then extraction is indicated.

• The use of general anesthesia for dental procedures must be approached cautiously in consultation with the hematologist and anesthesiologist.

• Previously, the standard protocol was to perform a direct transfusion (immediate introduction of whole blood or blood components) or an exchange transfusion (repetitive withdrawal of small amounts of blood and replacement with donor blood until a large portion of the patient blood has been exchanged) before general anesthesia.

• The goal of the transfusion is to increase the patient’s hemoglobin level to higher than 10 g/dL and to decrease the hemoglobin S level below 40%.

• Transfusions do not provide complete protection against venous complications, but they may temporarily improve the patient’s condition and reduce the hazards of surgery.

• The current thinking is to weigh the risks associated with transfusion prior to anesthesia induction. Suggested guidelines for performing a prophylactic transfusion before general anesthesia have been proposed.

• Patients with a hemoglobin level of less than 7 g/dL and a hematocrit of less than 20% may require a transfusion.

• Pediatric patients are usually less likely to have post-transfusion complications than are adults. • A high frequency of hospitalizations is indicative of a more severe anemia, and such patients may require

transfusion before surgery. • Minor surgeries may not require a transfusion.

LEUKEMIA• Malignancy is second only to accidents as the leading cause of death in children.

• Leukemias are hematopoietic malignancies in which there is a proliferation of abnormal leukocytes in the bone marrow and dissemination of these cells into the peripheral blood.

• The abnormal leukocytes (blast cells) replace normal cells in bone marrow and accumulate in other tissues and organs of the body.

• Leukemia is classified according to the morphology of the predominant abnormal white blood cells in the bone marrow (Table 24-1). These types are further categorized as acute or chronic, depending on the clinical course and the degree of differentiation, or maturation, of the predominant abnormal cells.

• In the United States, about 6550 new cases of cancer are diagnosed each year in children under the age of 15.

• Acute leukemia is the most common malignancy in children, with about 2500 new cases diagnosed annually in the United States.

• Thus acute leukemia accounts for about one third of all childhood malignancies; of these, approximately 80% are lymphocytic (acute lymphocytic leukemia, or ALL).

• Chronic leukemia in children is rare, accounting for less than 2% of all cases. • Leukemia affects about one of every 29,000 children each year in the United

States. • The peak incidence is between 2 and 5 years of age. • Although the cause of leukemia is unknown, ionizing radiation, certain chemical

agents, and genetic factors have been implicated. • For example, children with chromosomal abnormalities (Down syndrome and

Bloom syndrome), children with an identical twin who has leukemia, and children with immunologic disorders have an increased risk for leukemia.

• In the US leukemia rates for white children are nearly double that for black children.48 The clinical manifestations of acute leukemia are caused by the infiltration of leukemia cells into tissues and organs.

• Infiltration and proliferation of leukemia cells in the bone marrow lead to anemia, thrombocytopenia, and granulocytopenia.

• Because these cytopenias develop gradually, the onset of the disease is frequently insidious.

• The history at presentation may reveal increased irritability, lethargy, persistent fever, vague bone pain, and easy bruising.

• Some of the more common findings on initial physical examination are pallor, fever, tachycardia, adenopathy, hepatosplenomegaly, petechiae, cutaneous bruises, gingival bleeding, and evidence of infection.

• In approximately 90% of the cases of acute leukemia a peripheral blood smear reveals anemia and thrombocytopenia.

• In about 65% of cases the white blood cell count is low or normal, but it may be greater than 50,000 cells/mm3.

• When a new case of leukemia is diagnosed, the patient is hospitalized and therapy is directed toward stabilizing the patient physiologically, controlling hemorrhage, identifying and eliminating infection, evaluating renal and hepatic functions, and preparing the patient for chemotherapy.

• These interventions proceed while the definitive studies to determine the exact type of leukemia are undertaken.

• These include performing a bone marrow aspiration to obtain marrow for microscopic analysis, special cytochemical staining, immunophenotyping by flow cytometry, and cytogenetic analysis.

• The goal of treatment is to induce and maintain a complete remission, which is defined as resolution of the physical findings of leukemia (e.g., adenopathy, hepatosplenomegaly, petechiae) and normalization of peripheral blood counts and bone marrow (less than 5% blasts).

• A new term minimal residual disease (MRD) has been applied when using multiple parameter flow cytometry and less than 0.1% blasts are found.

• Remission with MRD is better prognostically than the old definition of remission.

• The basic principle of treatment of ALL is substantially different from that of acute myelogenous or nonlymphocytic leukemia (ANLL).

• In general, the treatment of ANLL is very intense and results in profound bone marrow hypoplasia, but the treatment duration is usually short (less than 1 year).

• For ALL, the treatment is less intense but more prolonged (21⁄2 to 31⁄2 years).

• Overall, the treatment regimens vary considerably depending on prognostic factors and the parameters being evaluated by the strategists’ cooperative group (e.g., Children’s Oncology Group).

• The initial phase of treatment, induction, incorporates the use of a combination of antileukemic drugs at staggered intervals during a 4-week regimen (Table 24-2).

• This combination of drugs should rapidly destroy the leukemic cells, yet maintain the regenerative potential of the nonmalignant hematopoietic cells within the bone marrow.

• About 95% of patients with ALL will be in complete remission at day 28 of therapy.

• The second phase of ALL treatment, consolidation, attempts to consolidate remission and intensify prophylactic central nervous system (CNS) treatment.

• Prevention of CNS relapse uses intrathecally administered chemotherapy (methotrexate with or without cytosine arabinoside and hydrocortisone) to destroy leukemic cells within the CNS.

• This chemotherapeutic agent is instilled directly into the lumbar spinal fl uid because most antileukemic drugs do not readily cross the blood-brain barrier.

• Intensive intrathecal chemotherapy to prevent CNS relapse has replaced cranial irradiation for patients in the good and intermediate-risk groups of ALL patients.

• However, both cranial irradiation and intrathecal chemotherapy are still used to prevent CNS relapse in high-risk ALL patients.

• The third phase of treatment, interim maintenance, uses a combination of agents that are relatively nontoxic and require only monthly visits to the outpatient clinic.

• In most cases, another phase, delayed intensifi cation, follows interim maintenance. • This serves to intensify antileukemic therapy again after a short period of less

intensive therapy. The addition of a late phase of intensive therapy substantially improves survival in patients with ALL.

• Following delayed intensification, therapy continues for 2 years for girls and 3 years for boys (maintenance phase), with chemotherapeutic agents given as in interim maintenance.

• The prognosis for a child with acute leukemia has improved dramatically over the past several decades.

• Thirty five years ago, there would have been little need to discuss dental treatment for a child with leukemia because the disease was invariably fatal, in most cases within 6 months of diagnosis.

• Today, with the development of new and better antileukemia drugs, the use of intensive combination drug therapy, the incorporation of radiation therapy, and improvements in diagnostic techniques and general supportive care, the overall survival for all children with ALL is now about 80%.

• Pretreatment prognostic factors identify patients who are likely to benefit from either standard or more intensive therapy.

• Factors that identify patients who are likely to benefit from the type of therapy just outlined, which causes relatively minimal toxicity, are patient age between 1 and 10 years, a white blood cell count of less than 50,000/mm3, lymphoblast morphology that is not of the Burkitt type, and the absence of certain cytogenetic abnormalities [t(4;11); t(9;22)] (also known as the Philadelphia chromosome) or hypoploidy in the lymphoblast.

• The presence of either the TEL-AML1 fusion [t(12;21)(p13;q22)] or the simultaneous trisomies of chromosomes 4, 10, and 17 in the lymphoblasts correlates with an improved prognosis and may qualify these children for less strenuous therapy.

• Children with ALL who are at particularly high risk are those who are younger than 1 year of age at diagnosis, have a high white blood cell count, or have the cytogenetic abnormalities mentioned above.

• More intrusive treatment regimens are used for these patients.

• The early response to induction chemotherapy is also a strong predictor of outcome for patients with ALL.

• Current clinical trials in leukemia are using flow cytometry and molecular techniques to detect blast cells not visible morphologically in bone marrow aspirates.

• Quantification of this MRD is being used as an additional tool to direct therapy so that children can receive risk based adjusted therapy.

• The prognosis for children with acute myelogenous leukemia (AML) has improved significantly over the past several years, with event-free survivals of approximately 50% (at 3 years) for children receiving chemotherapy and somewhat higher percentages for patients undergoing allogeneic hematopoietic stem cell transplantation from a matched sibling after achieving remission with chemotherapy.50

• The treatment regimens are intrusive and result in profound bone marrow suppression.• These patients have severe prolonged neutropenia, necessitating long hospitalizations.

They often have serious infections and severe mucositis.

ORAL MANIFESTATIONS OF LEUKEMIA

• Pathologic changes in the oral cavity as a result of leukemia occur frequently. • Oral signs or symptoms suggestive of leukemia have been reported in as many

as 75% of adults and 29% of children with leukemia. • The lower incidence of oral manifestations in children can be attributed in part

to the early age at diagnosis and the high percentage of ALL in the pediatric age group.

• The incidence of ALL peaks at 3 years of age, when preexisting inflammatory and degenerative changes are comparatively less frequent.

• Abnormalities in or around the oral cavity occur in all types of leukemia, and in all age groups.

• However, oral pathoses are more commonly observed in acute leukemias than in chronic forms of the disease.

• Oral findings suggestive of leukemia are also more common in AML than in ALL.

• The most frequently reported oral abnormalities attributed to the leukemic process include regional lymphadenopathy, mucous membrane petechiae and ecchymoses, gingival bleeding, gingival hypertrophy, pallor, and nonspecific ulcerations.

• Manifestations seen occasionally are cranial nerve palsies, chin and lip paresthesias, odontalgia, jaw pain, loose teeth, extruded teeth, and gangrenous stomatitis.

• Each of these findings has been reported in all types of leukemia. Regional lymphadenopathy is the most frequently reported finding.

• Gingival abnormalities, including hypertrophy and bleeding, are more common in patients with AML, whereas petechiae and ecchymoses are more common in those with ALL.

• Like the systemic manifestations of leukemia, oral changes can be attributed to anemia, granulocytopenia, and thrombocytopenia, all of which result from the replacement of normal bone marrow elements by undifferentiated blast cells, or to direct invasion of tissue by these leukemic cells.

• Very high circulating white blood cell numbers in the peripheral blood can lead to stasis in small vascular channels.

• The subsequent tissue anoxia results in areas of necrosis and ulceration that can readily become infected by opportunistic oral microorganisms in patients with neutropenia.

• A person with severe thrombocytopenia, having lost the capacity to maintain vascular integrity, is likely to bleed spontaneously.

• Clinical manifestations are petechiae or ecchymoses of the oral mucosa or frank bleeding from the gingival sulcus (Figs. 24-3 and 24-4).

• The propensity for gingival bleeding is greatly increased in persons with deficient oral hygiene, because accumulated plaque and debris are significant local irritants.

• Direct invasion of tissue by an infiltrate of leukemic cells can produce gingival hypertrophy. Such gingival changes can occur despite excellent oral hygiene.

• Infiltration of leukemic cells along vascular channels can result in strangulation of pulpal tissue and spontaneous abscess formation as a result of infection or focal areas of liquefaction necrosis in the dental pulp of clinically and radiographically sound teeth.

• In a similar fashion, the teeth may rapidly loosen as a result of necrosis of the periodontal ligament.

• Skeletal lesions caused by leukemic infiltration of bone are common in childhood leukemia. • The most common finding is a generalized osteoporosis caused by enlargement of the Haversian

canals and Volkmann canals. • Osteolytic lesions resulting from focal areas of hemorrhage and necrosis and leading to loss of

trabecular bone are also common.• Evidence of skeletal lesions is visible on dental radiographs in up to 63% of children with acute

leukemia.• Manifestations in the jaws include generalized loss of trabeculation, destruction of the crypts of

developing teeth, loss of lamina dura, widening of the periodontal ligament space, and displacement of teeth and tooth buds (Fig. 24-5).

• Because none of the oral changes is a pathognomonic sign of leukemia and all can be associated with numerous local or systemic disease processes, a diagnosis of leukemia cannot be based on oral findings alone.

• Such changes should, however, alert the clinician to the possibility of malignancy as the underlying cause.

DENTAL MANAGEMENT OF PATIENTS WITHLEUKEMIA

• Before any dental treatment is administered to a child with leukemia, the child’s hematologist/oncologist or primary care physician should be consulted.

• The following information should be ascertained:• 1. Primary medical diagnosis• 2. Anticipated clinical course and prognosis• 3. Present and future therapeutic modalities• 4. Present general state of health• 5. Present hematologic status• It is also important to establish, by consultation with the patient’s

physician, when dental treatment may be most propitious, and to schedule the patient’s treatment accordingly.

• The proposed procedures should be discussed to determine if they are appropriate.

• For a child whose first remission has not yet been obtained, or one who is in relapse, all elective dental procedures should be deferred.

• However, it is essential that potential sources of systemic infection within the oral cavity be controlled or eradicated whenever they are recognized (e.g., immediate extraction of carious primary teeth with pulpal involvement).

• Routine preventive, restorative, and surgical procedures can usually be provided for a patient who is in complete remission yet is undergoing chemotherapy.

• The time when such procedures may be completed without complications will depend on the specifi c agents administered and the time of administration.

• Before the appointment— preferably the same day—a blood cell profile (complete blood count) and platelet count should be taken to confirm that the patient is not unexpectedly at undue risk for hemorrhage or infection.

• A patient who has been in complete remission for at least 2 years and no longer requires chemotherapy may be treated in an essentially normal manner.

• A preappointment blood workup is not necessary.• Pulp therapy on primary teeth is contraindicated in any patient with a history of leukemia.• Endodontic treatment for permanent teeth is not recommended for any patient with leukemia

who may have a chronic, intermittent suppression of granulocytes. • Even with the most exacting technique, an area of chronic inflammatory tissue may remain in

the periapical region of endodontically treated teeth. • An area of low-grade, chronic inflammation in a healthy patient is generally well tolerated,

but in an immunosuppressed, neutropenic patient the same area can act as an anachoretic focus with devastating sequelae.

• The decision to perform an endodontic procedure on a patient who has been in prolonged complete remission and who is not undergoing chemotherapy must be made by the dentist.

• A platelet level of 100,000/mm3 is adequate for most dental procedures (Table 24-3).

• Routine preventive and restorative treatment, including nonblock injections, may be considered when the platelet count is at least 50,000/mm3.

• With inadequate oral hygiene, unhealthy periodontal tissues, and the presence of local irritants, hemorrhage from the gingival sulcus may be observed when platelet counts are between 20,000 and 50,000/ mm3.

• Such hemorrhaging is usually noted only after manipulation of the tissues, such as during toothbrushing.

• .

• If the platelet count is lower than 20,000/mm3, all the intraoral mucosal tissues may show clinical evidence of spontaneous hemorrhaging (e.g., petechiae, ecchymoses, or frank hemorrhage).

• No dental treatment should be performed at such a time without a preceding prophylactic platelet transfusion.

• Good oral hygiene must be maintained while the platelet count is at this level, but it may be necessary to discontinue the use of a toothbrush and to substitute cleaning with moist gauze wipes, supplemented by frequent saline rinses.

• The absolute neutrophil count (ANC) is an indicator of the host’s ability to suppress or eliminate infection.

• It is calculated using the following formula:• ANC (% of neutrophils % of bands) total white x count 100

• The clinical significance of the ANC is presented in Table 24-4. • If the ANC is less than 1000/mm3, elective dental treatment should be

deferred. • A leukemic patient with a low ANC may require prophylactic broad-

spectrum antibiotic therapy before certain dental procedures. • The patient’s physician should be consulted regarding the appropriate

drugs and dosages. • Infection and hemorrhage are the primary causes of death other than

resistant disease or relapse in children with leukemia. • Therefore the primary objective of dental treatment in a child with

leukemia should be the prevention, control, and eradication of oral inflammation, hemorrhage, and infection.

• Frequently, initial oral manifestations of bleeding or infection are observed in association with an unhealthy periodontium.

• In patients with leukemia who are neutropenic or who are being treated with corticosteroids, the true degree of periodontal inflammation or infection may be masked, because the cardinal signs of inflammation may not be apparent.

• There is a much greater propensity for gingival bleeding when the periodontium is unhealthy.

• When oral hygiene is neglected and local irritants are present, spontaneous hemorrhaging from the gingival sulcus may be observed if the patient is thrombocytopenic.

• It is imperative that a patient who is diagnosed as having leukemia be enrolled in a good preventive dental care program in which special emphasis is placed on the initiation and maintenance of a comprehensive oral hygiene regimen.

• The use of a soft nylon toothbrush for the removal of plaque is recommended, even if the patient is thrombocytopenic.

• As long as the gingiva remains in a healthy state and its manipulation by brushing does not induce significant hemorrhage, it is not appropriate to discontinue the use of a toothbrush because of the platelet level alone. The practicality of flossing must be assessed on an individual basis. It is important that significant local irritants, including orthodontic appliances, be removed.

• Scaling and subgingival curettage should not necessarily be perceived as elective dental treatment in all patients.

• This is especially true if the anticipated clinical course may place the patient at high risk for hemorrhage and infection.

• Patients with classic leukemic gingivitis experience varying degrees of discomfort. The use of warm saline rinses several times each day may assist in the relief of symptoms.

• Erosive or ulcerative lesions are common in children with leukemia. • These lesions are often associated with the use of certain chemotherapeutic

agents (see Table 24-2), especially methotrexate and the anthracycline antibiotics daunomycin and doxorubicin.

• The lesions may be an early indicator of drug toxicity. After administration of the drug is discontinued and the ANC has recovered, these lesions usually disappear within a few days.

• Treatment is directed toward the relief of discomfort (Table 24-5).• In a patient who is granulocytopenic, trauma may result in the occurrence of

ulcerative lesions, especially along the lateral border of the tongue and buccal mucosa.

• The clinical course of these ulcerations is generally benign, although the time necessary for healing may be prolonged.

• Use of topical obtundents for pain may be the only treatment indicated. • Infrequently, deep lesions will bleed spontaneously or as a result of

trauma. • Local measures, such as the topical application of either bovine thrombin

or Avitene, and the placement of an oral adhesive for protection, may be benefi cial.

• In a patient who is physically debilitated or who is in relapse, septic, and severely granulocytopenic, ulcerative lesions require close observation.

• Such lesions may serve as a nidus for the proliferation of microorganisms, which can lead to potentially fatal viral, fungal, or bacterial infection.

• Therefore specimens from these ulcerative lesions should be cultured and subsequent sensitivity testing performed, and antibiotic therapy should be initiated or modifi ed accordingly.

• Candidiasis is common in children with leukemia.• They are especially susceptible to this fungal infection because of • (1) general physical debilitation, • (2) immunosuppression, • (3) prolonged antibiotic therapy, • (4) chemotherapy, and • (5) poor oral hygiene. • The following topical use of nystatin can be particularly beneficial: • Nystatin oral suspension, 100,000 U/mL • Swish 5 mL for 5 minutes and then swallow • Repeat every 6 hours; continue for 48 hours after lesions disappear

• In more resistant cases of oral candidiasis, fluconazole may be useful, administered once daily either orally or intravenously (in young children 6 mg/kg on day 1, then 3 mg/kg to a maximum of 12 mg/kg per day; in older children and adults 200 mg on day 1, then 100 mg).

• For patients who are thrombocytopenic or at risk for intermittent episodes of thrombocytopenia because of chemotherapy or active disease, the dentist should avoid prescribing drugs that may alter platelet function, such as salicylates (aspirin) and nonsteroidal anti-inflammatory drugs.

SOLID TUMORS

• Solid tumors account for approximately half of the cases of childhood malignancy.

• The most common tumors include brain tumors, lymphoma, neuroblastoma, Wilms tumor, osteosarcoma, and rhabdomyosarcoma.

• Because many of the malignancies can involve bone marrow and their treatment with chemotherapy and radiation can suppress marrow function, many of the complications seen in acute leukemia are also seen with these patients.

• Bleeding diatheses and the propensity to infection are the most notable medical complications seen.

• In general, the dental management of patients with solid tumors is similar to that of patients with acute leukemia.

VIRAL HEPATITIS

• Viral hepatitis is an infection that produces inflammation of liver cells, which may lead to necrosis or cirrhosis of the liver. Acute hepatitis classically presents with lethargy, loss of appetite, nausea, vomiting, abdominal pain, and ultimately jaundice. Acute viral hepatitis may be caused by any of the following: hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis delta virus (HDV), and two forms of non-A, non-B hepatitis virus (NANB)—parenterally transmitted NANB or hepatitis C virus (HCV), and enterically transmitted

• NANB or hepatitis E virus. Infection with hepatitis A virus results in an acute febrile illness with jaundice, anorexia, nausea, and malaise.

• Most HAV infections in infants and children cause mild, nonspecifi c symptoms without jaundice. HAV is spread by the fecal-oral route and is endemic in developing areas. Spread occurs readily in households and day-care centers, where symptomatic illness occurs primarily among adult contacts of children. No HAV carrier state exists, and the presence of immunoglobulin G–anti-HAV indicates past infection and lifelong immunity to HAV.

• The risk for transmission in a dental setting is low. Hepatitis B transmission is of major concern to the dentist. Members of the dental profession assume a risk for acquiring HBV that is at least three times higher than that in the general population. An additional concern, beyond that of acquiring HBV, is the potential of becoming an asymptomatic yet infectious carrier of HBV and of having the capability of transmitting the disease to patients and dental staff members and family.

• HBV is transmitted from person to person by parenteral, percutaneous, or mucous membrane inoculation. It can be transmitted by the percutaneous introduction of blood, administration of certain blood products, or direct contact with secretions contaminated with blood containing HBV. Infection may also result from inoculation of mucous membranes, including sexual transmission. Wound exudates contain HBV, and open-wound to openwound contact can transmit infection. There can also be vertical transmission from an infected mother to her baby, and this frequently leads to chronic infection.

• A medical history is unreliable in identifying patients who have HBV infection, because approximately 80% of all HBV infections are undiagnosed. However, the medical history is useful in identifying groups of patients who are at higher risk of being undiagnosed carriers. Among populations at high risk for HBV infection are patients undergoing hemodialysis, patients requiring frequent large-volume blood transfusions or administration of clotting factor concentrates, residents of institutions for the mentally disabled, and users of illicit injectable drugs. In 2006, an estimated 46,000 people in the United States became infected with HBV, and an estimated 1.25 million chronically infected people live in the United States. Overall, chronic liver disease from hepatitis B claims 5000 lives a year in the United States.39 Chronic active hepatitis develops in more than 25% of carriers and often progresses to cirrhosis. Furthermore, HBV carriers have a risk of developing primary liver cancer that is between 12 and 300 times higher than that of uninfected individuals.

• For detection of acute or chronic HBV infection, the serologic test for hepatitis B surface antigen (HepBsAg) is most commonly used. The antibody to surface antigen (HepBsAb or anti-HepBsAg) is protective and indicates a resolved natural infection or successful vaccination. Antibody to the core antigen (HepBcAb or anti-HepBc) indicates exposure to natural hepatitis B virus but can be present in either resolved or chronic infection. The hepatitis Be antigen (HepBeAg) is a useful marker for infectivity. Patients who test positive for HepBeAb and HepBsAg are most likely to transmit the disease. If the patient still shows a positive test result for HepBsAg 6 months after an acute HBV infection, the patient is considered to be chronically infected.

• The availability of a safe, effective hepatitis B vaccine affords the dentist and staff additional protection against acquiring HBV infection. HBV vaccine is recommended for all health care personnel. The vaccine is derived using recombinant DNA and therefore does not have the potential to transmit the disease. When administered in a three-dose injection regimen (0, 1, 6 months), the recombinant

• DNA vaccine induced protective antibody (anti-HepBs) in 95% to 100% of adults.

• A fulminant type of hepatitis occurs with infection by HDV but only with coexisting or simultaneous infection with HBV. HDV is defective in that it requires HBV for outer coat proteins (HepBsAg), as well as requiring HBV for replication. Transmission is similar to that of HBV, by parenteral, percutaneous, or mucous membrane inoculation.

• According to Cottone,40 HDV infection occurs in two primary modes:

• The first is simultaneous infection with HBV and HDV.• When simultaneous infection occurs, the acute clinical course of

hepatitis often is limited with resolution of both hepatitis B and HDV infections. The second mode of transmission, acute delta super-infection, involves those with chronic Hepatitis B infection. In this

• situation, the patient already has a high titer of circulating HepBsAg; thus HDV can rapidly replicate. These patients are more likely to have a serious and possibly acute fulminant form of hepatitis that more often leads to chronic HDV.

• Hepatitis C (formerly known as parenterally transmitted NANB hepatitis) is of great concern to the dentist, because it can be transmitted by needle stick (risk of about 1.8% with a range of 0% to 10%) and no immunization is available. Patients at risk for hepatitis C include those who received blood transfusions or organ transplants before 1992, those who received clotting factors before 1987, those on long-term dialysis, and most commonly those who have experimented with illicit intravenous drugs regardless of how many times or how long ago. Of those infected, chronic infection develops in 70% to 85%, and chronic liver disease develops in about 70%. Although only 3% of infected people die of liver failure, hepatitis C is the leading reason for liver transplantation in adults in the United States. In 1989, parenterally transmitted NANB was identifi ed as HCV. Subsequently, three genotypes have been identifi ed. Diagnosis is made by detection of antibody to hepatitis C virus (anti-HCV) in the serum and can be confirmed by radioimmunoblot assay. Polymerase chain reaction (PCR) testing can be done in a qualitative fashion to confirm diagnosis or in a quantitative fashion to assess response to treatment. Treatment, when indicated, includes administration of interferon or pegylated interferon with or without ribavirin. Response rates vary from 50% for type 1 infection to 80% for types 2 and 3.

CARDIOVASCULAR DISEASE

Heart Failure

• Heart failure is not a disease per se but rather a clinical syndrome complex that results from an underlying cardiovascular problem such as coronary heart disease or hypertension. The underlying cause of heart failure should be identified and its potential significance assessed. Patients with untreated or symptomatic heart failure are at increased risk for myocardial infarction (MI), arrhythmias, acute heart failure, or sudden death and generally are not candidates for elective dental treatment.

• Chair position may influence a patient’s ability to breathe, with some patients unable to tolerate a supine position. Vasoconstrictors should be avoided, if possible, in patients taking digitalis glycosides (digoxin) because the combination can precipitate arrhythmias.

• Stress reduction measures also may be advisable

Heart Attack

• A history of a heart attack (MI) within the very recent past may preclude elective dental care because during the immediate postinfarction period, patients have increased risk for reinfarctions, arrhythmias, and heart failure. Patients may be taking medications such as antianginals, anticoagulants, adrenergic blocking agents, calcium channel blockers, antiarrhythmic agents, and digitalis. Some of these drugs may alter the dental management of patients because of potential interactions with vasoconstrictors in the local anesthetic, drug adverse effects, or other considerations. Stress and anxiety reduction measures may be advisable.

Angina Pectoris

• Brief substernal pain resulting from myocardial ischemia, commonly provoked by physical activity or emotional stress, is a common and significant symptom of coronary heart disease. Patients with angina, especially unstable angina, are at increased risk for arrhythmias, MI, and sudden death. A variety of vasoactive medications, such as nitroglycerin, beta-blocking agents, and calcium channel blockers, are used to treat angina. Vasoconstrictors should be used cautiously. Patients with unstable or progressive angina are not candidates for elective dental care (see Chapter 4). Stress and anxiety reduction measures may be appropriate

High Blood Pressure

• Patients with hypertension (blood pressure greater than 140/90 mm Hg) should be identified by history and confirmed by blood pressure measurement. Patients with a history of hypertension should be asked if they are taking or are supposed to be taking antihypertensive medication. Failure to take medication is often the cause of elevated blood pressure in a patient who reports being under treatment for high blood pressure.

• Current blood pressure readings and any symptoms that may be associated with hypertension, such as visual changes, dizziness, and headaches, should be noted. Some antihypertensive medications, such as the nonselective beta-blocking agents, may require cautious use of vasoconstrictors.

• Stress and anxiety reduction measures also may be appropriate (see Box 1-1). Elective dental care should be deferred for patients with blood pressure ≥180/110.

Heart Murmur

• A heart murmur is caused by turbulence of blood fl ow that produces vibratory sounds during the beating of the heart. Turbulence may result from physiologic (normal) factors or pathologic abnormalities of the heart valves, vessels, or both. The presence of a heart murmur may be of signifi cance in the dental patient in that it may be an indication of underlying heart disease.

• The primary goal is to determine the nature of the heart murmur; consultation with the patient’s physician is often necessary to make this determination. Previously, the

• American Heart Association recommended antibiotic prophylaxis for many patients with heart murmurs caused by valvular disease (e.g., mitral valve prolapse, rheumatic heart disease); however, on the basis of accumulated scientific evidence, recently revised guidelines have omitted this recommendation. If a murmur is due to a specific cardiac condition (e.g., previous endocarditis, prosthetic

• heart valve, complex congenital cyanotic heart disease),• the American Heart Association recommends antibiotic• prophylaxis for most dental procedures