Hemostasis

lectures 3 and 4

Assistant Professor
Ahmed Almerzoug
Hemostasis
• Hemostasis is the normal response of the body to stop
bleeding and loss of blood, keeping the blood within a
damaged blood vessel.
Hemostasis depends upon interactions between four elements:
• 1. Vessel wall
• 2. Platelets
• 3. Coagulation system (Clotting system)
• 4. Fibrinolytic system (Fibrinolysis)
Mechanism

• During hemostasis four steps occur in a rapid sequence:

• 1 .Vascular spasm:

• 2 .Platelet plug formation: platelet pluged in 15 seconds (primary hemostasis)

• 3. Blood coagulation or blood clotting: the sequential process by which the multiple coagulation factors
of the blood interact in the coagulation cascade resulting in the formation of insoluble fibrin clot
(secondary hemostasis.)

• 4. Fibrinolytic system (Fibrinolysis): to maintain the patency of blood vessels. The main enzyme
responsible for this process is the plasmin. (tertiary hemostasis.)
Primary hemostasis (platelet plug
successful primary hemostasis factors are:

• 1 .Adequate vascular response.

• 2 .Adequate platelet number.

• 3 .Adequate platelet function.

• 4 .Adequate level of the Von Willebrand's Factor ( factor

VIII). it enhances the adhesion of the platelets.
Secondary hemostasis (fibrin clot):
through coagulation cascade
Tertiary hemostasis:
Is the formation of plasminogen and then plasmin
which is the main enzyme responsible for
fibrinolysis. Activation of fibrinolysis is triggered
by the presence of fibrin, and tissue-type
plasminogen activators (t-PA) at the site of fibrin
formation. Drugs that inhibit fibrinolysis (anti-
fibrinolytic) include aminocaproic acid and
tranexamic acid.
Hemostasis can be achieved in other ways
•if the body cannot do it naturally during surgery
or medical treatment. When the body is under
shock and stress, . During surgical procedures
hemostasis can be achieved by a direct pressure,
ligation or a hemostatic agent (chemical and/or
mechanical).
Clinical assessment
• History:-Family history and duration of bleeding may indicate
whether the disorder is congenital or acquired. Coexisting illness
or drug therapy predisposing to bleeding should be sought.

•Examination :- Bruising. Purpura. Telangiectasia on lips

(indicates hereditary hemorrhagic telangiectasia). Swollen
joints/hemarthrosis. Hepatomegaly. Splenomegaly.
• Muscle and joint bleeds indicate a coagulation defect. Purpura,
prolonged bleeding from cuts, epistaxis, GI hemorrhage,
excessive post-surgical bleeding and menorrhagia suggest a
platelet disorder, thrombocytopenia or von Willebrand disease
 Investigations :-
Platelet count =150000-410000 cells / mm3 (life span 7-10 days), Bleeding
time (BT)= 1- 6 min. measure aspirin effect

Prothrombin time (PT)= 10- 15 second (measure warfarin effect)

• Partial thromboplastin time (PTT)=25-35 sec, monitor heparin therapy

• Thrombin time (TT)= 9 -13 sec. test excessive plasmin or fibrin split products
Bleeding Disorders

•Disorders of primary hemostasis

• Vessel wall abnormalities:- Hereditary hemorrhagic telangiectasia Patients present
with recurrent bleeds (particularly epistaxis) or with iron deficiency due to occult GI
bleeding. Treatment includes iron therapy and local cautery or laser therapy to prevent
lesions from bleeding.

• Platelet disorders:-Thrombocytopenia (low platelets) (aplastic anemia, chemotherapy,

radiotherapy or metastatic diseases), viral infections (HIV, CMV, rubella) or drugs.

• Increased platelet destruction; immunological (idiopathic thrombocytopenic purpura

ITP), splenomegaly or disseminated intravascular coagulopathy (DIC).
 Clinical features of platelet deficiency
• include; easy bruising and easy bleeding, petechia, ecchymosis that
can be seen on the oral mucosa and on the skin of the extremities in
addition to postoperative hemorrhage but not usually until the
platelet count falls < 20 000 cells/mm³.

• Management is by platelet infusion, which carries the risk of

infection with blood- borne agents. Where there is immune
destruction of platelets (e.g. in ITP), platelet infusions are less
effective.
Congenital bleeding disorders
• Hemophilia A (Factor VIII deficiency):

• X-linked recessive disorder; about 10 times as common as

hemophilia B.

• Mild when factor VIII level is 5-30% of the normal

• Moderate1-5% ,

• Severe less than 1% of the normal

 Hemophilia A
•

Healthy people have a factor VIII or factor IX plasma concentration of 0.50-1.50 IU/mL.
Factor VIII or factor IX concentrations can also be expressed as percentages of normal
pooled plasma (defined as 100%), with normal levels between 50% and 150%
• diagnosis is normally made after the age of 6 months when babies become more mobile and first
experience bruising. Although joints and muscles are the most common sites for hemorrhage,
bleeding can occur at almost any site. Intracranial hemorrhage is often fatal.

• Abnormal bleeding after extractions has sometimes led to the recognition of hemophilia. Dental
extractions lead to prolonged bleeding. Laboratory findings are all normal except for the
prolonged PTT and reduced levels of factor VIII.

• Management: Bleeding episodes should be treated early with intravenous factor VIII concentrate.
.

• In mild hemophilia, antifibrinolytic agents such as tranexamic acid may be adequate .

•Hemophilia B (Christmas disease):
•This is caused by a deficiency of factor IX
and is also an X-linked condition. The
disorder is clinically indistinguishable from
hemophilia A but is less common.
Replacement therapy is with synthetic factor
IX.
•Hemophilia C (Factor XI deficiency):
•Inherited as an autosomal dominant
disorder. Factor XI deficiency
results in rapid fibrinolysis. Fresh-
frozen plasma or factor XI is
required
Acquired bleeding disorders (Anticoagulant therapy)

•These are given as prophylaxis or

treatment of thromboembolic events;
they are used to treat atrial fibrillation,
IHD, MI, DVT, CVA and pulmonary
embolism. The common anticoagulant
drugs are warfarin for long-term
treatment and heparin for short-term
treatment.
Warfarin

• vitamin K antagonist , Its effect begins after 8

hours and persists for 72 hours resulting in
prolonged PT and INR.
• Reversal of warfarin's effect by discontinuing
its use, or by administering vitamin K.
 Aspirin Is the most commonly used antiplatelet
agent. Inhibits platelet aggregation (Bleeding
time increased).

Clopidogrel (Plavix) One of the commonly

used antiplatelet agents. The mechanism of
action of the agents is to prevent platelet
aggregation.
 Heparin

• It is used as a parenteral anticoagulant given SC/IV for acute

thromboembolic episodes (to prevent DVT and pulmonary emboli).
• Heparin acts immediately on blood coagulation to block the
conversion of fibrinogen to fibrin. Protamine sulfate is a drug that
reverses the anticoagulant effects of heparin by binding to it.
• The anticoagulant effect of heparin is usually lost within 6 hours of
stopping it. The PT, PTT are prolonged. Most patients are monitored
with the PTT.
END OF 1ST LECTURE
•Vitamin K deficiency
•Vitamin K is a fat-soluble vitamin that plays an
essential role in hemostasis. It is present in the diet
and also synthesized by the intestinal flora. It is
absorbed in the small intestine and stored in the
liver. The three major causes of vitamin K
deficiency are poor dietary intake, intestinal
malabsorption, and liver disease. Factors II, VII,
IX, and X, protein C and protein S all decrease
with vitamin K deficiency
• Disseminated intravascular coagulation (DIC):

• The generation of intravascular fibrin clots leading to multi-organ failure, with

simultaneous coagulation factor and platelet consumption causing bleeding. It
can be initiated by a number of mechanisms such as infections, malignancy, drug
toxicity and burns.

• Investigations: Thrombocytopenia. ● Prolonged PT and PTT due to coagulation

factor deficiency.

• Management: Therapy should be aimed at treating the underlying condition

causing DIC (e.g. IV antibiotics for septicemia). Blood products such as platelets
and/or fresh frozen plasma should be given to correct identified abnormalities.
Liver disease:
In severe liver disease, bleeding may arise from many
different causes. These include reduced synthesis of
coagulation factors or thrombocytopenia secondary to
hypersplenism. Cholestatic jaundice reduces vitamin K
absorption leads to a deficiency of factors II, VII, IX and
X. This deficiency can be treated with parenteral vitamin
K.
•Renal disease:
•Advanced renal failure is
associated with platelet
dysfunction and bleeding,
especially GI bleeding.
•Scurvy:
•Vitamin C deficiency affects the normal
synthesis of collagen and results in a bleeding
disorder characterized by petechial hemorrhage,
bruising and subperiosteal bleeding. The key to
diagnosis is the dietary history.
• Oral Findings
• Platelet deficiencies can cause petechiae or ecchymosis in oral mucosa and
promote spontaneous gingival bleeding. These disorders may be present alone or
in conjunction with gingival hyperplasia in cases of leukemia.
• Hemosiderin and other blood degradation products can cause brown deposits on
the surface of teeth due to chronic bleeding.
• People with hemophilia may have multiple bleeding events over their lifetime. The
frequency of bleeding depends on the severity of hemophilia.
• The incidence of dental caries and periodontal diseases is higher in patients with
bleeding disorders, which may be because of lack of effective oral hygiene and
professional dental care due to fear of oral bleeding
• Dental Management

• If the procedure has limited invasiveness and the patient has a mild
bleeding disorder, only slight or no modification will be required.

• In patients with severe bleeding disorders, the patient’s physician

should be consulted before invasive treatment is undertaken. In
patients with drug-induced coagulopathies, drugs may be stopped or
the doses modified. For irreversible coagulopathies, replacement of
missing factors may be necessary.
Pain management
• Anesthetic infiltration and intraligamentary anesthesia
are potential alternatives to nerve block in many cases.
An anesthetic with a vasoconstrictor should be used
when possible. Alternative techniques, including
sedation with diazepam or nitrous oxide–oxygen
analgesia.
• Patients undergoing extensive treatment requiring
factor replacement may be treated under general
anesthesia in a hospital operating room.
• Oral Surgery

• For coagulopathies, transfusion of appropriate factors to 50% to

100% of normal levels is recomonded. In patients with hemophilia,
additional postoperative factor maintenance may be required after
extensive surgeries.

• The patient’s hematologist should be consulted before planning, and

patients with severe disease should be treated in specialty centres.
• Local hemostatic agents and techniques such as pressure, surgical
packs, and may assist in the local delivery of hemostatic agents, such
as topical thrombin and vasoconstrictors.
If ASA has to be withdrawn, this should be done at least 10
days before surgery.
For patients taking warfarin, most oral surgical procedures
can be performed without altering the warfarin dose if the
INR is less than 3.0
Patients taking heparin are often those who are on
hemodialysis due to end-stage renal disease. Heparin has a
short half-life (about 5 hours) and patients can often be treated
safely on the days between dialysis.
Periodontal Procedures
• Patients with coagulopathies may neglect their oral health due to fear of bleeding
during tooth brushing and flossing, which leads to increased gingivitis,
periodontitis and caries.

• Periodontal probing, supragingival scaling and polishing can be done normally

without the risk of significant bleeding, if these procedures are done carefully.

• For severely inflamed tissues, initial treatment with chlorhexidine mouthwashes

and gross debridement is recommended to reduce tissue inflammation before deep
scaling. Factor replacement may be required before extensive periodontal surgery
and use of nerve blocks.

• Post-treatment antifibrinolytic mouthwashes are usually effective in controlling

protracted bleeding.
• Restorative and Endodontic Procedures
• General restorative procedures do not pose a significant risk of
bleeding. Care should be taken to avoid injuring the gingiva while
placing rubber dam clamps, matrices and wedges. A rubber dam
should be used to prevent laceration of soft tissues by the cutting
instruments.
• Saliva ejectors and high-speed suction can injure the mucosa in the
floor of the mouth and cause hematoma or ecchymosis; thus, they
should be used carefully.
• Endodontic therapy is preferred over extraction whenever possible in
these patients. Endodontic therapy does not usually pose any
significant risk of bleeding and can be performed routinely.
Endodontic surgical procedures may require factor replacement
therapy.
• Prosthodontic Procedures
• These procedures do not usually involve a
considerable risk of bleeding. Trauma should be
minimized by careful post-insertion adjustments.
Oral tissue should be handled delicately during the
various clinical stages of prosthesis fabrication to
reduce the risk of ecchymosis. Careful adjustment of
prostheses is needed to reduce trauma to soft tissue.
•Orthodontic Procedures
•Orthodontic therapy can be carried out without
bleeding complications, although care should
be taken that appliances do not impinge on soft
tissues and emphasis should be put on
excellent, atraumatic oral hygiene.
•Choice of Medications
• When used for prolonged periods, ASA and nonsteroidal
anti-inflammatory drugs (NSAIDS) can increase the effect of
warfarin. Penicillins, erythromycin, metronidazole,
tetracyclines and miconazole also have potentiating effects on
warfarin. Care should be taken when prescribing these drugs
to patients with bleeding tendencies or those receiving
anticoagulant therapy.
END