haemostasis

1. HAEMOSTASIS
Presented by:
SHRUTI SUDARSANAN
JUNIOR RESIDENT 1ST YEAR
DEPT OF PEDODONTICS AND
PREVENTIVE DNETISTRY
GDC KOTTAYAM

2. CONTENTS
• INTRODUCTION
• COAGULATION VS THROMBOSIS
• VASCULAR CONSTRICTION
• FORMATION OF HAEMOSTATIC PLUG
• BLOOD COAGULATION
• CLOT RETRACTION
• INVESTIGATIONS OF HEMOSTATIC FUNCTION
• BLEEDING DIATHESIS
• DENTAL SCENARIO
• HEMOSTATIC AGENTS

3. INTRODUCTION
HEMOSTASIS : preventing blood loss
Spontaneous arrest or stoppage of bleeding from injured
blood vessel by physiologic process
• Whenever a vessel is severed or ruptured, hemostasis is
achieved by several mechanisms:
(1) vascular constriction,
(2) formation of a platelet plug, or PRIMARY HAEMOSTASIS
(3) formation of a blood clot as a result of blood coagulation,
or SECONDARY HAEMOSTASIS
(4) eventual growth of fibrous tissue into the blood clot to close
the hole in the vessel permanently.

4. COAGULATION VS THROMBOSIS
• Haemostatic plugs are the blood clots formed in healthy individuals at the site of
bleeding e.g. in injury to the blood vessel.
• PHYSIOLOGICAL
• Thrombosis is the process of formation of solid mass in circulation from the
constituents of flowing blood; the mass itself is called a thrombus.
• PATHOLOGICAL

5. 1) VASCULAR
CONSTRICTION
• Immediately after a blood vessel has been cut or ruptured  the
smooth muscle in the wall contract  reduces the flow of blood
• The contraction results from
(1) local myogenic spasm,
(2) local autacoid factors from the traumatized tissues and blood
platelets, and
(3) nervous reflexes.
(4) thromboxane A2 .

6. 2) FORMATION OF THE PLATELET PLUG
• If the cut in the blood vessel is very small the cut is often sealed by a
platelet plug, rather than by a blood clot.

7. THROMBOCYTES
• Platelets (also called thrombocytes)
• are minute discs 1 to 4 micrometers in diameter.
• They are formed in the bone marrow from megakaryocytes,
• the megakaryocytes fragment into the minute platelets either
in the bone marrow or soon after entering the blood,
especially as they squeeze through capillaries.
• The normal concentration of platelets in the blood is
between 150,000 and 300,000 per microliter.
• It has a halflife in the blood of 8 to 12 days

8. EVENTS IN PRIMARY HEMOSTASIS
PLATELET ADHESION
PLATELET GRANULE RELEASE
PLATELET AGGREGATION

10. • i) Platelet adhesion. The platelets in circulation recognise the site of endothelial injury and
adhere to exposed subendothelial collagen (primary aggregation);.
• ii) Platelet release reaction. platelet granules released are:
• a) Alpha granules containing fibrinogen, fibronectin, platelet-derived growth factor,
platelet factor 4 (an antiheparin) and cationic proteins.
• b) Dense bodies containing ADP, ionic calcium, 5-HT (serotonin), histamine and
epinephrine. As a sequel to platelet activation and release reaction, the phospholipid
complex-platelet factor 3 gets activated which plays important role in the intrinsic pathway
of coagulation.
• c) Lysosomal vesicles
• iii) Platelet aggregation. Following release of ADP, a potent platelet aggregating agent,
aggregation of additional platelets takes place (secondary aggregation). This results in
formation of temporary haemostatic plug
• However, stable haemostatic plug is formed by the action of fibrin, thrombin and thromboxane
A2

11. PLATELET ADHESION
PLATELETS
RECEPTOR=
Gp Ia-IIa (an
integrin)
COLLAGEN SUBENDOTHELIUM
Gp Ib-IX
complex
Von
Willebrand
factor
Gp Ib-IX
complex
Von
Willebrand
factor
Gp Ib-IX
complex
Von
Willebrand
factor
Gp Ib-IX
complex
Von
Willebrand
factor
Gp Ib-IX
complex
Von
Willebrand
factor

12. 3. ROLE OF COAGULATION SYSTEM OR
SECONDARY HAEMOSTASIS
• Coagulation mechanism is the conversion of the plasma fibrinogen into solid
mass of fibrin
• The clot begins to develop in 15 to 20 seconds
• Within 3 to 6 minutes after rupture of a vessel, if the vessel opening is not too
large, the entire opening or broken end of the vessel is filled with clot.
• After 20 minutes to an hour, the clot retracts; this closes the vessel still further.

14. GENERAL MECHANISM
Clotting takes place in three essential steps:
(1) In response to rupture of the vessel or damage to the blood itself, a complex
cascade of chemical reactions occurs in the blood involving coagulation factors. The
net result is formation of a complex of activated substances collectively called
prothrombin activator.
(2) The prothrombin activator catalyzes conversion of prothrombin into thrombin.
(3) The thrombin acts as an enzyme to convert fibrinogen into fibrin fibers that
enmesh platelets, blood cells, and plasma to form the clot.

15. Prothrombin activator is generally considered to be formed in two ways
1) by the intrinsic pathway that begins in the blood itself
2) by the extrinsic pathway that begins with trauma to the vascular wall and
surrounding tissues and

17. INTRINSIC PATHWAY

18. EXTRINSIC PATHWAY

19. THE COMMON PATHWAY

20. BLOOD CLOT
• The clot is composed of a meshwork of fibrin fibers running in all directions and
entrapping blood cells, platelets, and plasma. The fibrin fibers also adhere to
damaged surfaces of blood vessels; therefore, the blood clot becomes adherent to
any vascular opening and thereby prevents further blood loss.

21. REGULATION OF COAGULATION SYSTEM
• The blood is kept in fluid state normally and coagulation system kept in check by
controlling mechanisms. These are as under:
a) Protease inhibitors: e.g. antithrombin III, protein C, C1 inactivator, alpha1-
antitrypsin, alpha 2- macroglobulin
b) Fibrinolytic system. Plasmin, a potent fibrinolytic enzyme, is formed by the
action of plasminogen activator on plasminogen present in the normal plasma.

22. FIBROUS ORGANIZATION OR
DISSOLUTION OF THE BLOOD CLOT
• Once a blood clot has formed, it can follow one of two courses:
(1) It can become invaded by fibroblasts, which subsequently form connective tissue
all through the clot, or
(2) it can dissolve

23. CLOT RETRACTION

24. INTRAVASCULAR ANTICOAGULANTS
• Endothelial Surface Factors
• (1) the smoothness of the endothelial cell surface
• (2) a layer of glycocalyx on the endothelium
• (3) thrombomodulin, protein C
• Antithrombin Action of Fibrin and Antithrombin III - also inactivates the thrombin itself
during the next 12 to 20 minutes.
• Heparin

25. ANTICOAGULANTS FOR CLINICAL USE
• Heparin : Injection of 0.5 to 1mg/kg of body weight, causes the blood-clotting time to
increase from a normal of about 6 minutes to 30 or more minutes.
• this change in clotting time occurs instantaneously.
• The action of heparin lasts about 1.5 to 4 hours.
• The injected heparin is destroyed by an enzyme in the blood known as heparinase.
• Coumarins: warfarin,
• After administration of an effective dose of warfarin, the coagulant activity of the blood
decreases to about 50 percent of normal by the end of 12 hours and to about 20 percent
of normal by the end of 24 hours.
• Normal coagulation usually returns 1 to 3 days after discontinuing coumarin therapy

27. PREVENTION OF BLOOD
COAGULATION OUTSIDE THE
BODY
• Heparin is especially used in surgical procedures in which the blood must be passed
through a heart-lung machine or artificial kidney machine and then back into the person.
• Various substances that decrease the concentration of calcium ions in the blood can also
be used for preventing blood coagulation outside the body.
• a soluble oxalate compound mixed in a very small quantity with a sample of blood causes
precipitation of calcium oxalate from the plasma and thereby decreases the ionic calcium
level so much that blood coagulation is blocked.
• The citrate ion combines with calcium in the blood to cause an un-ionized calcium
compound, and the lack of ionic calcium prevents coagulation.
• Citrate anticoagulants have an important advantage over the oxalate anticoagulants
because oxalate is toxic to the body, whereas moderate quantities of citrate can be injected
intravenously.

29. INVESTIGATIONS OF HAEMOSTATIC
FUNCTION
A. Investigation of Disordered Vascular Haemostasis
1. BLEEDING TIME 3-8 minutes
2. HESS CAPILLARY RESISTANCE TEST
(TOURNIQUET TEST). Presence of more than 20
petechiae is considered a positive

30. • B. Investigation of Platelets and Platelet Function
Screening tests: i) Peripheral blood platelet count.
Ii) Skin bleeding time.
iii) Examination of fresh blood film to see the morphologic abnormalities
of platelets.
Special tests: i) Platelet adhesion tests
ii) Aggregation tests
iii) Granular release

31. • C. Investigation of Blood Coagulation
• I. Whole blood coagulation time: 4-9 minutes at 37°C.
• II. Activated partial thromboplastin time (APTT) or partial thromboplastin time with
kaolin (PTTK): 30-40 seconds
• to measure the intrinsic system factors (VIII, IX, XI and XII) as well as factors common to
intrinsic and extrinsic systems (factors X, V, prothrombin and fibrinogen).
• causes of a prolonged PTTK (or APTT) are as follows: i) Parenteral administration of heparin.
Disseminated intravascular coagulation. iii) Liver disease. iv) Circulating anticoagulants.
• III. One-stage prothrombin time (PT):10-14 seconds.
• PT measures the extrinsic system factor VII as well as factors in the common pathway
• The normal range for INR in a healthy person is 0.9 to 1.3
• causes of prolonged one-stage PT are as under: i) Administration of oral anticoagulant
ii) Liver disease, especially obstructive liver disease. iii) Vitamin K deficiency. iv) Disseminated
intravascular coagulation
• IV. Measurement of fibrinogen: The normal value of thrombin time is under 20
while a fibrinogen titre in plasma dilution up to 32
• V. Coagulation factor assays

32. • D. Investigation of Fibrinolytic System
• 1. Estimation of fibrinogen.
• 2. Fibrin degradation products (FDP) in the serum.
• 3. Ethanol gelation test.
• 4. Euglobin or whole blood lysis time.

34. BLEEDING DISORDERS
(HAEMORRHAGIC DIATHESIS)
• The tendency to bleeding may be spontaneous in the form of small haemorrhages
into the skin and mucous membranes (e.g. petechiae, purpura, ecchymoses), or
there may be excessive external or internal bleeding following trivial trauma and
surgical procedure (e.g. haematoma, haemarthrosis etc).
• I. Haemorrhagic diathesis due to vascular abnormalities.
• II. Haemorrhagic diathesis related to platelet abnormalities.
• III. Disorders of coagulation factors.
• IV. Haemorrhagic diathesis due to fibrinolytic defects.
• V. Combination of all these as occurs in disseminated intravascular coagulation
(DIC).

35. I. HAEMORRHAGIC DIATHESIS DUE TO
VASCULAR ABNORMALITIES.
Inherited
1. Hereditary haemorrhagic telangiectasia
(OslerWeber-Rendu disease)
2. Inherited disorders of connective tissue
matrix. These include Marfan’s syndrome,
Ehlers-Danlos syndrome and
pseudoxanthoma elasticum
Acquired
1. Henoch-Schönlein purpura.
2. Haemolytic-uraemic syndrome
3. Simple easy bruising (Devil’s pinches)
4. Infection
5. Drug reactions
6. Steroid purpura
7. Senile purpura
8. Scurvy

36. 2. HAEMORRHAGIC DIATHESES DUE
TO PLATELET DISORDERS
• A. Due to reduction in the number of platelets i.e. various forms of thrombocytopenias.
• B. Due to rise in platelet count i.e. thrombocytosis.
• C. Due to defective platelet functions.
• Hereditary Disorders :3 groups:
1. DEFECTIVE PLATELET ADHESION. : i) Bernard-Soulier syndrome
ii) In von Willebrand’s disease
2. DEFECTIVE PLATELET AGGREGATION: thrombasthenia (Glanzmann’s disease
3. DISORDERS OF PLATELET RELEASE REACTION: release of ADP, prostaglandins
and 5-HT is defective due to complex intrinsic deficiencies.
• Acquired Disorders 1. aspirin therapy
2. others

37. 3. COAGULATION DISORDERS
• HEREDITARY
• Classic Haemophilia
(Haemophilia A)
• Christmas Disease
(Haemophilia B)
• von Willebrand’s Disease
• ACQUIRED
• Vitamin K Deficiency
• coagulation disorder in liver
diseases, fibrinolytic defects and
• disseminated intravascular
coagulation (DIC).

38. IDIOPATHIC THROMBOCYTOPENIC
PURPURA
• An autoimmune disorder
• Reduction in normal platelet count
• Peak incidence: upto 4 yrs
ORAL MANIFESTATIONS:
Ecchymoses and frank hemorrhages
Profuse gingival haemorrhage
Petechiae on mucosa – palate- numerous tiny grouped clusters of red spots 1mm or
less in diameter

39. DENTAL MANAGEMEN
• Elective dental treatment- deferred till platelet count is above 50000/mm3
• Steroids- 1-2mg/kg – to bring up the platelet level
• Splenectomy
• Replacement therapy platelet concentrate or whole blood transfusion before
surgery
• 1 unit6000/mm3
• Improve red cell mass, coagulation factors
• Local measures of haemostasis
• IV immunoglobulin1g/kg/day twice before xtraction
• Avoid blocks and extraction
• Avoid NSAIDs and Aspirin for 7days preoperatively before any surgical

40. HAEMOPHILIA
COAGULATION DEFECTS AETIOLOGY AND TRANSMISSION LAB FINDINGS
HAEMOPHILIA A or Classic
haemophilia
(80% cases)
Factor VIII deficiency,
X-linked recessive trait
Platelet count: normal
BT: normal
PT: normal
PTT: prolonged
HAEMOPHILIA B or Christmas
Disease
(15% cases)
Factor IX deficiency,
X-linked recessive trait
Platelet count: normal
BT: normal
PT: normal
PTT: prolonged
HAEMOPHILA C Factor XI deficiency
Autosomal recessive
Platelet count: normal
BT: normal
PT: normal
PTT: prolonged
Von Wiillebrand’s disease Von Willebrand factor deficiency
(plasma, platelet, endothelial
cells)also acts as carrier of factor
VIII.
Autosomal dominant
Platelet count:normal
BT: prolonged
PT: normal
PTT: prolonged (if factor VIII<
30%)

41. ORAL MANIFESTATIONS
• Haemorrhage from many sites
• Gingival haemorrhage may be prolonged and massive
• Mouth lacerations
• Presence of mandibular pseudotumour
TREATMENT of Haemophilia A
• Replacement with product containing factor VIII or recombinant factor VIII
• Minor h’age  40%
• Severe bleeding or Major surgery  80-100%
• Mild to moderate haemophila  DDAVP
• Haemophilacs with inhibitors to factor VIII  PCC and recombinant factor 7
TREATMENT OF Haemophila B
FACTOR IX replacement

42. TREATMENT OF Haemophila C
Fresh frozen plasma
Treatment of von willebrands disease
Cryoprecipitate
DDAVP Nasal spray or IV preparation

43. DENTAL CONSIDERATIONS
• Significant apprehension of patient: sedation or nitrous oxide- oxygen inhalation anaesthesia
analgesics
• When GA Oral intubation > Nasal intubation
• IM inj, avoided
• In pts who require deep scaling, initially do supragingivally then call after 7-14 days after proper
healing
• Factor replacement before frenectomy and other surgeries
• Electrosurgery
• Small carious lesions can be restored, matrix and wedges
• Antibiotic prophylaxis b4 xtrctn
• Use of topical haemostatic agents
• fixed> removable
• Careful adaptation and cementation of bands: usually preformed bands and brackets are used

44. DENTAL PROCEDURES WITH HIGH RISK FOR
BLEEDING IN CHILDREN WITH BLEEDING DISORDERS
• Extractions
• IANB
• Pulp therapy
• Class II restorations
• RCT

45. ANTICIPATORY GUIDANCE FOR CHILDREN
WITH BLEEDING DISORDERS
• Parents should be educated
• Firm rubber or plastic filled teething ring helps the child erupt their teeth through
the gingiva. Freezing the ring  vasoconstriction and prevent oozing from gingiva
• Cold water while brushing
• Proper brushing technique
• Gingival massage
• Haemarthrosis of elbow joint electric tooth brush

46. HEMOSTATIC AGENTS IN DENTISTRY
Dr. Amit Mani , Dr. Raju Anarthe , Dr. Preeti Kale , Dr. Shalakha Maniyar , Dr. Sekharmantri Anuraga

47. A

48. EFFECTIVENESS OF HEMCON DENTAL DRESSING VERSUS CONVENTIONAL METHOD
OF HAEMOSTASIS IN 40 PATIENTS ON ORAL ANTIPLATELET DRUGS
Tejraj P. Kale,* Amit Kumar Singh, S.M. Kotrashetti, And Abhishek Kapoor
Objectives:
• The purpose of the study was to evaluate the effectiveness of the HemCon Dental Dressing
(HDD) in controlling post extraction bleeding and to ascertain its role in healing of
extraction wounds, as compared to control
Results:
All HemCon treated sites achieved haemostasis sooner (mean = 53 seconds) than the control
sites (mean = 918 seconds)

49. REFERENCE
• Guyton And Hall Textbook Of Medical Physiology – 3rd South East Asia Edition
• Textbook Of Pathology- Harsh Mohan – 8th Edition
• Mcdonald And Avery’s Dentistry For The Child And Adolescent: Second South Asia
Edition
• Pediatric Dentistry Shobha Tandon Volume 2
• Galore International Journal Of Health Sciences And Research Vol.3; Issue: 4; Oct.-
Dec. 2018
• Pubmed: National Centre For Biotechnology And Information