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Management of Bleeding in Dentistry New
Management of Bleeding in Dentistry New
bleeding in dentistry
Content
• Introduction
• Diagnosis
Introduction
• Bleeding disorders characterized by abnormal platelet function or blood vessel walls that
result in increased bleeding.
• Dentists must be aware of the impact of bleeding disorders on the management of their
patients.
• Proper dental and medical evaluation of patients is therefore necessary before treatment,
especially if an invasive dental procedure is planned
Diagnosis
• Patient evaluation and history should begin with standard medical questionnaires.
• Patients should be queried about any previous unusual bleeding episode after surgery or
injury, spontaneous bleeding and easy or frequent bruising.
• For the purpose of history-taking, a clinically significant bleeding episode is one that:
1. continues beyond 12 hours
2. causes the patient to call or return to the dental practitioner or
3. to seek medical treatment or emergency care
4. results in the development of hematoma or ecchymosis within the soft tissues
5. or requires blood product support
• The patient should be asked for any history of significant and prolonged bleeding after dental
extraction or bleeding from gingivae.
• Many bleeding disorders, such as hemophilia and von Willebrand’s disease, run in families;
therefore, a family history of bleeding disorders should be carefully elicited.
• A complete drug history is important.
• If a patient is taking anticoagulant drugs, it will be important to consult his or her physician
before any major surgical procedure
• Drugs of abuse, such as alcohol or heroin, may also cause excess bleeding by causing liver
damage resulting in altered production of coagulation factors
• A general examination of the patient might indicate a tendency to bleed. Multiple purpurae of
the skin, bleeding wounds, evident hematomas or swollen joints may be evident in patients
with severe bleeding defects.
PHYSICAL EXAMINATION :-
• The P/E should focus on whether bleeding symptoms are associated primarily with the mucous
membranes or skin (mucocutaneous bleeding) or with the muscles and joints(deep bleeding).
• The examination should determine the presence of petechiae, ecchymoses, hematomas, hemarthroses,
or mucous membrane bleeding.
• Patients with defects in platelet-blood vessel wall interaction (VWD or platelet function defects)
usually have mucocutaneous bleeding.
• Individuals with a clotting factor deficiency of factor VIII or IX (hemophilia A or B) have symptoms of
deep bleeding into muscles and joints.
• Individuals with disorders of the collagen matrix and vessel wall may have loose joints and lax skin
associated with easy bruising (Ehlers-Danlos syndrome).
Lab investigations
Bleeding time
• measures platelet plug formation in vivo
• normally between 3 and 10 minutes
• Prolonged bleeding times are found in patients with platelet function defects
Prolonged bleeding times are found in patients with platelet function defects:-
• Performed using blood collected into citrate, which neutralizes calcium ions and prevents
clotting.
• The prothrombin time (PT)
• The partial thromboplastin time (PTT)
• The thrombin time (TT)
• Correction tests
• Factor assays
• Special tests of coagulation
Coagulation tests:-
• Congenital
• Hemophilia A and B
• von Willebrand’s disease
• Other factor deficiencies (rare)
• Acquired
• Liver disease
• Vitamin K deficiency, warfarin use
• Disseminated intravascular coagulation
Platelet disorders
Quantitative disorder (thrombocytopenia)
• Immune-mediated
• Idiopathic
• Drug-induced
• Collagen vascular disease
• Sarcoidosis
• Non-immune-mediated
• Disseminated intravascular coagulation
• Microangiopathic hemolytic anemia
• Leukemia
• Myelofibrosis
Qualitative disorder
• Congenital
• Glanzmann thrombasthenia
• von Willebrand’s disease
• Acquired
• Drug-induced
• Liver disease
• Alcoholism
Vascular disorders
• Scurvy
• Purpura
• Hereditary hemorrhagic telangiectasia
• Cushing syndrome
• Ehlers-Danlos syndrome
Fibrinolytic defects
• Streptokinase therapy
• Disseminated intravascular coagulation
Coagulation factor deficiencies
Hemophilia
• Hemophilia A is due to a deficiency of clotting factor VIII or antihemophilic factor or
Hemophilia B is due to deficiency of clotting factor IX (hemophilia B).
• Inherited X-link disorder
• Prevelance 1 in 5000 in male population
Hemophilia A- X linked
• Clinical features:-
• 1. Factor replacement
• Bleeding is treated by administration of factor VIII concentrate by intravenous
infusion.
• Minor bleeding: the factor VIII:C level should be raised to 20-30%
• Severe bleeding: the factor VIII:C should be raised to at least 50%
• Major surgery: the factor VIII:C should be raised to 100% preoperatively and
• maintained above 50% until healing has occurred.
2. Synthetic vasopressin (Desmopressin)
• An analogue of vasopressin
• Intravenous, subcutaneous or intranasal
• Produces a rise in factor VIII:C in mild hemophilia
• It avoids the complications associated with blood products
• It is ineffective in severe haemophilia
3. Tranexamic acid is a synthetic derivative of lysine, available for topical and
systemic usage. However, nausea is a common adverse effect.
• Local anesthetic regional blocks, lingual infiltrations or injections into the floor of
the mouth must not be used in the absence of Factor VIII replacement because of
the risk of hemorrhage hazarding the airway and being lifethreatening.
• All fibrin glue contains human or animal components, which has made a
number of physicians and patients being hesitant to use this treatment
particularly for patients who are receiving recombinant factor concentrates or
have never received blood products derived from humans.
◾ Hereditary coagulation abnormality
caused by either:
1. Reduced level of vWF
2. Abnormality in vWF
Liver disease
◾ Treatunderlying cause
◾ Supportive therapy with fresh frozen plasma (FFP) and platelets
concentrates
◾ Cryoprecipitate may also required
Instructions to be given to patients after
procedures