Bleeding Disorders
Hemorrhage in Oral Surgery
            What is meant by Hemorrhage ?
 Prolonged or Uncontrolled Bleeding
The amount of blood lost as a result of hemorrhage can
 range from minimal to significant quantities.

Hemorrhage can occur to a greater or lesser degree during
 all surgical procedures and it’s management depends
 upon whether the patient is hematologically normal or
 suffers from some disturbance in the normal clotting
                    Hemorrhage in Oral Surgery
   The overwhelming majority of patients who undergo oral surgical
    procedures are those who have normal haemostatic mechanism.
   Therefore, significant or major hemorrhages are not that common in
    oral surgery except in patients who have a bleeding / clotting
    disorder or those who are on anticoagulants.
   However, uncontrolled and persistent bleeding can occur in some
    healthy patients after dental extraction.
   Therefore, it is still important to achieve proper hemostasis in all
    patients during oral surgical procedures, so as to prevent excessive
    post-operative blood loss.
       Normal Mechanism of Hemostasis

 Hemostasis is a complicated process.
 It involves a number of events


1. Blood vessel
2. Blood platelet
3. Blood coagulation
4. Fibrinolysis
               Coagulation Cascade
Intrinsic system (surface contact)                      Extrinsic system (tissue damage)

         XII           XIIa                                         Tissue factor

                XI                 XIa

                       IX                        IXa             VIIa              VII

                            VIII         VIIIa

                                     X                      Xa
                                            V          Va

                                                  II                    IIa   (Thrombin)
                                           Fibrinogen                          Fibrin

Vitamin K dependant factors
          Normal Mechanism of Hemostasis
   VASCULAR PHASE : When a blood vessel is damaged,
    Vasoconstriction results.
    PLATELET PHASE : Platelets adhere to the
    damaged surface and form a temporary plug.
    COAGULATION PHASE : Through two separate
    pathways, the Intrinsic and Extrinsic, the conversion of
    fibrinogen to fibrin is complete. Fibrin tightly binds the
    platelets to form a clot

 Vessel Wall Integrity

 Adequate Numbers of Platelets

 Proper Functioning Platelets

 Adequate Levels of Clotting Factors

 Proper Function of Fibrinolytic Pathway
   All component onset at same time and close at different
   Primary(3-5 mins to onset)
     Vessel
     Platelet

   Secondary( 5-10 mins to onset)
       Coagulation
   Fibrinolysis( need 2-3 days to onset)
        Terminology in Bleeding Disorders
   Petechiae- Pinpoint hemorrhage (Platelets Disorder )
   Purpura –Larger, less regular (Platelets Disorder )
   Ecchymoses –Over 2 cm – bruise (Coagulation disorders )
   Hematoma –Blood trapped in soft tissue (Coagulation disorders )


Do not blanch with pressure
        (cf. angiomas)
       Not palpable
        (cf. vasculitis)
(Typical of Coagulation Factor Disorders)
Joint bleeding or Hemarthrosis
                               Specific Symptoms

Symptoms                     Defect of vessel or plt    Defect of coag.

Organ of frequent bleeding   Skin, mucous membrane,        muscle, joint
                                 nose, gut
  Size of purpura               Small-medium                   large
  Bleed at injury sizing        Small                          large
  Size of bleeding point        Petechiae                    hematoma
  Ecchimosis                    Superficial, small           deep, large
                                 to large
Bleeding at                      Frequent, prolonged         Not severe
    superficial wound
    Start bleeding                Immediately                 Many hrs after
    after injured
   When wound                   Recurrent bleeding             Bleeding stops
   suppressed                   when stop suppressing          permanently
    Clinical Features of Bleeding Disorders
                                   Platelet              Coagulation
                                   disorders             factor disorders
Site of bleeding                   Skin                  Deep in soft tissues
                                   Mucous membranes        (joints, muscles)
                                   (epistaxis, gum,
                                    vaginal, GI tract)
Petechiae                          Yes                   No
Ecchymoses (“bruises”)             Small, superficial    Large, deep
Hemarthrosis / muscle bleeding     Extremely rare        Common
Bleeding after cuts & scratches    Yes                   No
Bleeding after surgery or trauma   Immediate,            Delayed (1-2 days),
                                   Usually mild            Often severe
Bleeding Disorders - Bleeding Pattern
Clinical signs           Disorders of coagulation Disorder of platelets or
Petechiae                Rare                      Characteristics
Ecchymoses               Common, large             Characteristics, small

Bleeding from superficial Minimal                  Persistent
Delayed bleeding         Common                    Rare

Deep hematomas           Characteristics           Rare
Hemathrosis              Characteristics           Rare
 How to D/D Primary or Secondary Hemostasis
Clinical Distinction between Disorder of Vessels and Platelets and Disorders of Blood Coagulation

              Finding                  Disorder of Coagulation         Disorder of Platelets or Vessels

Petechiae                        Rare                            Characteristic
Deep dissecting hematomas        Characteristic                  Rare
Superficial ecchymoses           Common, usually large and       Characteristic, usually small and
Hemarthrosis                     solitary                        multiple
Delayed bleeding                 Characteristic                  Rare
Bleeding form superficial cuts   Common                          Rare
and scratches                    Minimal                         Persistent, often profuse
Sex if patient                                                   Relative more common in females
                                 80-90% of inherited forms
Positive family history          occur only in male patients     Rare ( Except vWD and hereditary
                                 Common                          hemorrhagic telangiectasia)
             Coagulation Factor Disorders
   Inherited bleeding disorders       Acquired bleeding disorders
       Hemophilia A and B                 Liver disease
       Von Willebrands disease            Vitamin K deficiency/warfarin
       Other factor deficiencies           overdose
                                           DIC
                          Hemophilia A and B
                                 Hemophilia A                   Hemophilia B

Coagulation factor deficiency    Factor VIII                    Factor IX

                  Inheritance    X-linked                      X-linked
                                 recessive                     recessive

                   Incidence     1/10,000 males                 1/50,000 males

                     Severity            Related to factor level
                                 <1% - Severe - spontaneous bleeding
                                 1-5% - Moderate - bleeding with mild injury
                                 5-25% - Mild - bleeding with surgery or trauma

               Complications                 Soft tissue bleeding
Clinical manifestations (hemophilia A & B are indistinguishable)

  Hemarthrosis (most common)
     Fixed joints
  Soft tissue hematomas (e.g., muscle)
     Muscle atrophy
     Shortened tendons
  Other sites of bleeding
     Urinary tract
     CNS, neck (may be life-threatening)
  Prolonged bleeding after surgery or dental extractions
             von Willebrand disease
   The most common hereditary bleeding disorder
     Often mild and subtle symptoms
     Incidence: 1/100, male = female

     Autosomal Dominant disorder (12p)

   Clinical presentation
    Epistaxis, ecchymoses, petechiae, menorrhagia,
    post-operative bleeding
              Treatment of von Willebrand disease

   Cryoprecipitate
       Source of fibrinogen, factor VIII and VWF
       Only plasma fraction that consistently contains VWF multimers
       Correction of bleeding time is variable

   DDAVP (Deamino-8-arginine vasopressin)
       Increases plasma VWF levels by stimulating secretion from endothelium
       Duration of response is variable
       Used for type 1 disease
       Dosage 0.3 µg/kg q 12 hr IV

   Factor VIII concentrate (Humate-P)
       Virally inactivated product
                    Vitamin K deficiency
   Source of vitamin K             Green vegetables
                                    Synthesized by intestinal flora
   Required for synthesis          Factors II, VII, IX ,X
                                    Protein C and S
   Causes of deficiency            Malnutrition
                                    Biliary obstruction
                             Antibiotic therapy
   Treatment                       Vitamin K
                                    Fresh frozen plasma
                       Disorders of Platelets
   Thrombocytopenia – decreased numbers of platelets (below 100,000/mm3)
   Can lead to spontaneous bleeding, if low enough, and can be fatal if bleeding
    occurs in the G.I. Tract, respiratory system or central nervous system.
   Can be congenital or acquired; acquired is more common.
   Seen with:
       Generalized bone marrow suppression
       Acute viral infection
       Nutritional deficiencies of B12, folic acid and iron
       Bone marrow transplant
       drugs, especially heparin, and toxins, thiazide diuretics, gold, ethanol…
       Immune reactions

Sites of Bleeding in Thrombocytopenia
   Skin and mucous membranes
     Petechiae
     Ecchymosis
     Hemorrhagic vesicles
     Gingival bleeding and epistaxis

   Menorrhagia
   Gastrointestinal bleeding
   Intracranial bleeding
    Classification of Platelet Disorders
   Quantitative disorders         Qualitative disorders

       Abnormal distribution          Inherited disorders (rare)
       Dilution effect                Acquired disorders
       Decreased production                Medications
                                            Chronic renal failure
       Increased destruction
                                            Cardiopulmonary bypass
            Acquired Thrombocytopenia with
               Shortened Platelet Survival
   Associated with bleeding        Associated with thrombosis

       Immune-mediated                 Thrombotic thrombocytopenic
        thrombocytopenia (ITP)           purpura
       Most drug-induced               DIC
        thrombocytopenias               Heparin-associated
       Most others                      thrombocytopenia
           Acquired Platelet Defects-Thrombocytopenia
                                                  Increased platelet destruction
   Sequestration                                     Immune thrombocytopenia
       Hypersplenism                                       Acute and chronic ITP
       Hypothermia                                         Drug-induced immune thrombocytopenia
       Burns                                               Post-transfusion purpura
   Impaired platelet production                            Allergy and anaphylaxis
       Aplastic anemia                               Non-immune thrombocytopenia
       Myelodysplastic syndrome                            Thrombocytopenia of infection
       Marrow infiltrative process                         Thrombotic microangiopathic disorders:
       Osteopetrosis                                        HUS, TTP
       Nutritional deficiency states                       Platelets in contact with foreign material
        (iron, folate, viatmin B12, anorexia                Congenital heart disease
        nervosa)                                            VWD
       Drug or radiation-induced                     Combined platelet and fibrinogen consumption syndromes
        thrombocytopenia                                    DIC
                                                            Virus-associated hemophagocytic
    Autoimmune Thrombocytopenia Purpura
Idiopathic (primary)
   By exclusion Dx , no identifiable underlying case

   Collagen vascular diseases
   Lymphoproliferative disorders
   Solid tumors
                 Features of Acute and Chronic ITP

Features                          Acute ITP            Chronic ITP

Peak age                          Children (2-6 yrs)   Adults (20-40 yrs)
Female:male                       1:1                  3:1
Antecedent infection             Common                Rare
Onset of symptoms                 Abrupt               Abrupt-indolent
Platelet count at presentation    <20,000              <50,000
Duration                          2-6 weeks            Long-term
Spontaneous remission            Common(80%)           Uncommon
             Initial Treatment of ITP

Platelet count   Symptoms        Treatment
    (per µl)

>50,000           None

20-50,000         Not bleeding   None
                  Bleeding       Glucocorticoids

<20,000           Not bleeding   Glucocorticoids
                  Bleeding       Glucocorticoids
                                       Treatment of ITP in Adults
    Approach                                Treatment                                        Notes
      Initial        Steroids (prednisone 1-1.5 mg/kg/d po tapered over   Useful acutely, but long term s/e
                     wks vs.dexamethasone 40 mg po x 4d)                   Fc receptor on Mɸ
                                                                          anti-plt Ab production
                     Anti-Rh(D) Ig 75μg/kg/d IV                           For Rh(D) +pts
                                                                          Ab-coated RBCs overwhelm Mɸ Fc
                     IVIG(1g/kg/d IV x 2-3d)                              If plt <5000 despite steroids
                                                                          Blacks Fc receptors on Mɸ
                                                                          anti-plt Ab production
   Refractory        Splenectomy                                           Plt clearance
                     Rituximab (anti-CD20)                                 Plt clearance, Ab against B cell
                     Danazol, vincristine                                  Plt clearance
                     Azathioprine, cyclophosphamide                       Immunosuppressants
                                                                           anti-plt Ab production
                     AMG531,AKR-501, eltrombopag                          Thrombopoiesis stim. proteins
    Bleeding         Aminocaproic acid                                    Inhibits plasmin activation
                     Methylprednisolone 1g/d IV x 3d                      See above
                     IVIG                                                 See above
Chronic refractory   Autologous HSCT                                      Investigational
        Practical Aspects for the management of
   What is an adequate platelet count for procedures?
       Routine Dentistry >10 000
       Dental Extraction >30 000
       Regional Dental Block >30 000
       Minor Surgery >50 000
       Major Surgery>80 000
       Epidural is okay at platelet count 50 000 for patient with ITP
   The target platelet count for a bleeding patient is generally >40
   Prophylactic platelet transfusions for platelets < 10 000
                 Heparin-Induced Thrombocytopenia
Feature                  Type I                             Type II

Mechanism                Direct effect of heparin           Immune(Ab)-mediated
                                                            IgG vs platelet factor 4-heparin complex

Incidence                20%                                1-3%

Onset                    After 1-4 d of heparin therapy     After 4-10d; but can occur early (<24h)with
                                                            history of prior exposure within last 100d
                                                            ( felt to be secondary to persistent Ab)
                                                            Can occur after heparin discontinue.

Platelet nadir           > 100,000/μl                       30-70,000/μl,  >50%

Sequelae                 None                               Thrombotic events (HITT) in 30-50%
                                                            Rare hemorrhagic complications

Management               Can continue heparin and observe   Discontinue heparin
                                                            Alternative anticoagulation (lepirudin or
           Liver Disease and Hemostasis

1.   Decreased synthesis of II, VII, IX, X, XI, and fibrinogen
2.   Dietary Vitamin K deficiency (Inadequate intake or
3.   Dysfibrinogenemia
4.   Enhanced fibrinolysis (Decreased alpha-2-antiplasmin)
5.   DIC
6.   Thrombocytoepnia due to hypersplenism
  Management of Hemostatic Defects in Liver
Treatment   for prolonged PT/PTT
        Vitamin K 10 mg SQ x 3 days - usually ineffective

        Fresh-frozen plasma infusion
        25-30% of plasma volume (1200-1500 ml)
        immediate but temporary effect

Treatment   for low fibrinogen
        Cryoprecipitate (1 unit/10kg body weight)

Treatmentfor DIC (Elevated D-dimer, low factor VIII,
        Replacement therapy
    Vitamin K deficiency due to warfarin overdose
                    Managing high INR values

Clinical situation Guidelines

INR therapeutic-5 Lower or omit next dose;
                          Resume therapy when INR is therapeutic

INR 5-9; no bleeding       Lower or omit next dose;
                           Resume therapy when INR is therapeutic
                           Omit dose and give vitamin K (1-2.5 mg po)
                           Rapid reversal: vitamin K 2-4 mg po (repeat)

INR >9; no bleeding        Omit dose; vitamin K 3-5 mg po; repeat as necessary
                           Resume therapy at lower dose when INR therapeutic

Chest 2001:119;22-38s (supplement)
   Vitamin K deficiency due to warfarin overdose
            Managing high INR values in bleeding patients

Clinical situation         Guidelines

INR > 20; serious bleeding Omit warfarin
                                   Vitamin K 10 mg slow IV infusion
                                   FFP or PCC (depending on urgency)
                                   Repeat vitamin K injections every 12 hrs as needed

Any life-threatening bleeding        Omit warfarin
                                     Vitamin K 10 mg slow IV infusion
                                     PCC ( or recombinant human factor VIIa)
                                     Repeat vitamin K injections every 12 hrs as needed

Chest 2001:119;22-38s (supplement)
                 Hemorrhage in Oral Surgery
   Hemorrhage following Oral Surgical procedures can occur
    due to Local or Systemic causes.

   In healthy patients the postoperative bleeding is mainly due
    to local causes.

   Local causes of hemorrhage originate in either Soft Tissue
    or Bone.
    Local causes of hemorrhage in oral surgery –
                         Soft tissue bleeding
   Soft tissue bleeding is either arterial, venous, or capillary in nature.
   Arterial bleeding is bright red and spurting in nature.
   Arteries in the soft tissues at risk during oral surgical procedures
    are the lies posterior portion of hard palate) greater palatine artery
    and the buccal artery (lies lateral to the retromolar pad)
   Venous blood is dark red in color and flows steadily and heavily
    especially if the vein is large.
    Capillary bleeding is bright red in color and is more of a minimal
Local causes – Osseous (Bony) bleeding in oral surgery
Troublesome bone bleeding originates either from nutrient
  canals in the alveolar region, central vessels, such as the
  inferior alveolar artery, or from central vascular lesions
  (Hemangioma or Vascular malformation)
    Systemic causes of hemorrhage in oral surgery
   Some patients with heriditary conditions such as hemophilia, Von
    Willebrand’s disease are susceptible for hemorrhage following oral
    surgical procedures.
   Patients with thrombocytopenia, are at risk of prolonged bleeding
    after surgery.
   Patients with uncontrolled hypertension.
   Patients with H/O prosthetic heart valve replacement, Stroke
    (Cerebrovascular accident) e.t.c., take oral anticoagulants like
    Aspirin or Warfarin to prevent the occurrence of a thromboembolic
   These patients are also at risk of prolonged severe bleeding during
    and after an oral surgical procedure.
        Types of Hemorrhage - Primary Hemorrhage
 This occurs during the surgery, as a result of injury like
  cutting or laceration of the artery or bleeding from bone.

 This also occurs when surgery is done in an infected area
  with a lot of granulation tissue.

 It can also occur after a very short period of time
  immediately after surgery.
 This type of bleeding is really normal and can be controlled
             Intermediate / Reactionary Hemorrhage

 This type of bleeding occurs within a few hours after surgery.

 This type of bleeding occurs as a result of failure of coagulation to
  occur (as in patients with systemic bleeding problems or those on

 Patients who have unknowingly disturbed / dislodged the clot are
  also prone for this type of bleeding.
                 Secondary Hemorrhage

 This occurs after 7 to 10 days after surgery. This is mainly due
  to partial division of blood vessel in combination with
  infection of the wound (Like patient’s who undergo radical
  neck dissection e.t.c.,).

 This type of bleeding is not very frequently encountered after
  oral surgery procedures.
        Management of Primary Hemorrhage in Normal patients

        The management of bleeding during surgery (Primary bleeding)
         can be achieved by the following means,

(i)      Securing / ligation of blood vessels with silk sutures.
(ii)     Use of pressure swab to achieve hemostasis.
(iii)    Use of electrocautery to achieve hemostasis.
(iv)     Use of hemostatic agents like bone wax, surgicel,e.t.c.,
(v)      Hypotensive anaesthesia (G.A) and use of vasoconstrictors in
         Local Measures ( Synthetic Materials)
   There are several materials that are commercially available that are
    used locally for achieving adequate hemostasis.
 Surgical (Oxidised Regenerated Cellulose)
 Gelfoam with activated thrombin
 Gelfoam with activated thrombin

 Avitene (Microfibrillar Collagen)
   Etik Collagen (Packed collagen)
   Tranexamic acid 5%
   Tranexamic acid 5% in Syringe
   Irrigation of wound with Tranexamic acid
   Suturing the wound
   Pressure with oral packs
Local Measures: Surgicel (Oxidised
      Regenerated Cellulose)
Local measures: Gelfoam with activated thrombin
Local Measures: Avitene (Microfibrillar Collagen)
Local Measures: Etik Collagen (Packed collagen)
Local Measures: Tranexamic acid 5%
Local Measures: Tranexamic acid 5% in Syringe
Local Measures: Irrigation of wound with Tranexamic acid
Local Measures: Suturing the wound
Local Measures: Pressure with oral packs
Management of Intermediate Hemorrhage in Normal patients

      The management of bleeding that occurs immediately after
       surgery (Reactionary bleeding) involves proper examination of
       the surgical wound to identify the site of bleeding (i.e ) from
       bone or soft tissue.

(i)    If bleeding is from bone then the hemostatic agents like bone
       wax or gelfoam is usually used.

(ii)   If bleeding is from soft tissues then, ligation / cauterization of
       blood vessels along with the use of hemostatic agents like
       surgicel and suturing of the wound is carried out.
Management of Secondary Hemorrhage in Normal patients

   The management of this type of bleeding that occurs a few days
    after surgery involves the removal of any debris from the wound
    surface that promotes the infection of the wound.

   Identify the source of bleeding and treat as would be done in a
    patient with secondary bleeding.

   Surgical stents can be placed over extraction sockets for stabilization
    of clot and prevention of wound contamination.
Management of Hemorrhage in patients with bleeding
   disorders / and those on anticoagulant therapy
   The usual protocol involved in the treatment of this group of
    patients consists of pre-operative blood investigations and
    preoperative correction of the underlying deficiency (Replacement
    of Clotting factors / platelets) if any in these patients.

   Subsequently, after this appropriate local measures are used to
    decrease the chances of post-operative bleeding.
    Management of Hemorrhage in patients with
          Uncontrolled Hypertension.
   This group of patients need appropriate medical consultation for
    initiation of medical treatment to decrease their Blood Pressure.

   Thus once their B.P is controlled, then the bleeding decreases and
    with local measures the hemorrhage is controlled.
     Approach to Post-operative bleeding
1.    Is the bleeding local or due to a hemostatic failure?
        1.   Local: Single site of bleeding usually rapid with minimal coagulation test
        2.   Hemostatic failure: Multiple site or unusual pattern with abnormal coagulation
2.    Evaluate for causes of peri-operative hemostatic failure
        1.   Preexisting abnormality
        2.   Special cases (e.g. Cardiopulmonmary bypass)
3.    Diagnosis of hemostatic failure
        1.   Review pre-operative testing
        2.   Obtain updated testing
                Laboratory Evaluation of Bleeding
CBC and smear       Platelet count                     Thrombocytopenia
                    RBC and platelet morphology        TTP, DIC, etc.

Coagulation         Prothrombin time                   Extrinsic/common pathways
                    Partial thromboplastin time        Intrinsic/common pathways
                    Coagulation factor assays          Specific factor deficiencies
                    50:50 mix                          Inhibitors (e.g., antibodies)
                    Fibrinogen assay                   Decreased fibrinogen
                    Thrombin time                      Qualitative/quantitative
                                                           fibrinogen defects
                    FDPs or D-dimer                    Fibrinolysis (DIC)

Platelet function   von Willebrand factor              vWD
                    Bleeding time                      In vivo test (non-specific)
                    Platelet function analyzer (PFA)   Qualitative platelet disorders
                                                        and vWD
                    Platelet function tests            Qualitative platelet disorders

                    PLATELET COUNT

 NORMAL              100,000 - 400,000 CELLS/MM3

 < 100,000            Thrombocytopenia

 50,000 - 100,000     Mild Thrombocytopenia

 < 50,000             Severe Thrombocytopenia
            BLEEDING TIME

             AND FUNCTION


Measures Effectiveness of the Extrinsic Pathway

 10-15 SECS ( INR : 1 )

 Measures Effectiveness of the Intrinsic Pathway

          25-40 SECS
           THROMBIN TIME

 Time for Thrombin To Convert
  Fibrinogen          Fibrin
 A Measure of Fibrinolytic Pathway

    9-13 SECS

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