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MECHANISM OF HAEMOSTASIS ,
FIBRINOLYSIS AND METHOD TO
CONTROL HAEMORRHAGE
DR. BIPUL BORTHAKUR
PROFESSOR AND HOD ,
DEPARTMENT OF ORTHOPAEDICS, SMCH
HAEMOSTASIS
• Means prevention of blood loss.
• Definition:- spontaneous arrest or stoppage of
bleeding from injured blood vessel by
physiological process.
• Is precisely orchestrated process involving
platelets, clotting factors, and endothelium that
occurs at the site of vascular injury and
culminates in the formation of a blood clot, which
serves to prevent or limit the extent of bleeding.
Function of haemostasis :-
maintain blood in fluid state
 arrest bleeding following trauma
 removes platelet plug when healing is complete
THREE PROCESS :-
 I) vasoconstriction
 II) formation of temporary haemostatic plug
 III) formation of definitive haemostatic plug
I) VASOCONSTRICTION:-
 IMMEDIATE:- direct effect of injury
 LATE :- by release of 5HT by bound platelets to
the collagen
II) FORMATION OF TEMPORARY HEMOSTATIC
PLUG:-
PROCESS :- (a) platelet adhesion
(b) platelet activation
(c) platelet aggregation
(d) temporary haemostatic plug
(A)PLATELET ADHESION:-
• done by VWF
• degranulation of platelet occurs
• Helped by fibronectin and other components of
extra cellular matrix.
• Calcium is required
(B) PLATELET ACTIVATION :-
• Platelet secretsADPs & thromboxane
A2activate other platelets and cycle continues
(C) PLATELET AGGREGATION :-
• activate platelet becomes sticky and stuck to
other and aggregates to form platelet plug.
• Platelet activating factors released by neutrophils,
monocytes and platelets cell membrane lipids
also increases the process
• (D) FORMATION OF TEMPORARY
HAEMOSTATIC PLUG:-
Platelet adhesion  platelet aggregation 
platelet plug formation
FORMATION OF DEFINITIVE
HAEMOSTATIC PLUG
• Temporary haemostatic plug converts into
definitive haemostatic plug by blood
coagulation
BLOOD COAGULATION:-
• When a vessel is ruptured , procoagulants
from the area of tissue damage become
activated clot formation occurs
• CLOTTING TAKES PLACE IN THREE STEPS:-
• 1st STEP:-
rupture/damage of blood vessels
complex cascade of chemical reactions occur 
prothrombin activator
• 2nd STEP:-
Prothrombin is converted into thrombin by
prothrombin activator.
Prothombin is formed by the liver .
Vitamin k required by the liver for normal
activation of prothrombin
3rd STEP:-
fibrinogen converted to fibrin by thrombin.
Thrombin acts on fibrinogen to remove four low
molecular weight peptides from each molecule of
fibrinogen forming one molecule of fibrin
monomer.
Fibrin monomer polymerise to form reticulum of
blood clot
• FORMATION OF PROTHROMBIN ACTIVATOR :-
Prothrombin considered to be formed in two
ways.
1> Extrinsic pathway :- begins with trauma to
vascular wall and surrounding tissues
2> Intrinsic pathway:- begins in the blood
• STEPS OF EXTRINSIC PATHWAY:-
1> Release of tissue factor :- traumatised tissue
releases tissue factor.
2> Activation of factor X :- tissue factor
activates factor VII into VIIa, which along with
ca+2 activates factor X.
3> Effects of Xa to form prothrombin activator:-
Xa combines with tissue factor & factor V to
form complex called prothrombin activator.
EXTRINSIC PATHWAY
STEPS OF INTRINSIC PATHWAY
• 1) blood trauma causes activation of factor XII
and release of platelet phospholipids
• 2) activation of factor XI by activated factor XII
• 3) activation of factor IX by activated factor XI
• 4) activation of factor X
INTRINSIC PATHWAY
FIBRINOLYSIS
• It is a process by which blood clot is prevented
from growing and becoming pathological.
• Prevents excessive fibrin deposition
• It is a physiological process.
• Can be dangerous if it were to expand beyond
boundary.
• Prevents clot formation but doesnot destroys
the clot
• This process requires a substance called
plasmin or fibrinolysin, which breaks down
fibrin and interferes with its polymerization.
• Clot stimulates tissue plasmin activator
• Plasminogen is found in blood in inactivated
state by tissue plasminogen activator.
METHODS TO CONTROL
HAEMORRHAGE
• HAEMORRHAGE :- Extravasation of blood from
vessels, is most often the result of damage to blood
vessels or defective clot formation.
• CLASSIFICATION
• ACCORDING TO SOURCE OF BLEEDING
• CAPILLARY :- BLEEDING IS RAPID, BRIGHT RED COLOR
• VENOUS :- STEADY FLOW, DARK RED COLOR
• ARTERIAL :- SPURTING BLOOD, PULSATING FLOW , BRIGHT
RED COLOR
BASED ON TYPES OF HAEMORRHAGE :-
• REVEALED HAEMORRHAGE:-
 EXTERNAL HAEMORRHAGE
 RESULTS FROM SOFT TISSUE INJURY
• CONCEALED HAEMORRHAGE:-
 INTERNAL HAEMORRHAGE
 RESULTS FROM BLUNT OR PENETRATING TRAUMA
 MORE DANGEROUS THAN REVEALED HAEMORRHAGE
• INITIALY CONCEALED BUT LATER REVEALED:-
 EXAMPLE – HEMATURIA, HAEMATEMESIS, MELAENA
ON THE BASIS OF TIME:-
• PRIMARY:- at the time of trauma
• REACTIONARY:- within 24 hours of trauma/surgery
• SECONARY:- within 7 to 14 days of trauma/surgery
ON THE BASIS OF VOLUME OF BLOOD LOSS:-
• MILD:- blood loss <500ml
• MODERATE:- blood loss 500ml -1L
• SEVERE:- blood loss > 1L
ON THE BASIS OF PERCENTAGE OF BLOOD LOSS
• CLASS I :- upto 15%
• CLASS II :- upto 15 -30%
• CLASS III :- upto 30-40 %
• CLASS IV :- more than 40%
• HAEMORRHAGE ASSESSMENT:-
FRACTURE BLOOD LOSS
-> PELVIS 2L
-> FEMUR 1.5 L
-> TIBIA/FIBULA 500ml -750ml
METHODS OF ACHIEVING
HAEMOSTASIS
1. MECHANICAL :-
(A) PRESSURE :-
 immediate measure for capillary or venous bleeding
 this would control most haemorrhage
 PRESSURE POINTS :-
.Temporal artery for scalp
.Carotid artery for neck
.Brachial artery for upper limb
.Femoral artery for lower limb
(B) HAEMOSTAT:- directly occlude bleeding vessels
(C) SUTURES AND LIGATION :- severed blood vessels may be tied
with ligatures
(D) CLIPS
(E) ELEVATION
(f) SPLINTING
(G) TOURNIQUETS
2. CHEMICAL METHODS :
• ADRENALINE
• THROMBIN
• SURGICEL
• GELATIN SPONGE
• NATURAL COLLAGEN SPONGE
3. THERMAL AGENTS :-
• CAUTERY
• ELECTROCAUTERY
• LASERS
• CRYOSURGERY
4. SUPPORTIVE MEASURES :-
• I.V. fluids
• whole blood transfusion
• fresh frozen plasma
• cryoprecipitates
5. SPECIAL MEASURES :-
• ANTI SHOCK GARMENTS –
pneumatic and non pneumatic
THANKYOU.

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Mechanism of haemostasis , fibrinolysis and method to control haemorrhage

  • 1. MECHANISM OF HAEMOSTASIS , FIBRINOLYSIS AND METHOD TO CONTROL HAEMORRHAGE DR. BIPUL BORTHAKUR PROFESSOR AND HOD , DEPARTMENT OF ORTHOPAEDICS, SMCH
  • 2. HAEMOSTASIS • Means prevention of blood loss. • Definition:- spontaneous arrest or stoppage of bleeding from injured blood vessel by physiological process. • Is precisely orchestrated process involving platelets, clotting factors, and endothelium that occurs at the site of vascular injury and culminates in the formation of a blood clot, which serves to prevent or limit the extent of bleeding.
  • 3. Function of haemostasis :- maintain blood in fluid state  arrest bleeding following trauma  removes platelet plug when healing is complete THREE PROCESS :-  I) vasoconstriction  II) formation of temporary haemostatic plug  III) formation of definitive haemostatic plug
  • 4.
  • 5. I) VASOCONSTRICTION:-  IMMEDIATE:- direct effect of injury  LATE :- by release of 5HT by bound platelets to the collagen II) FORMATION OF TEMPORARY HEMOSTATIC PLUG:-
  • 6. PROCESS :- (a) platelet adhesion (b) platelet activation (c) platelet aggregation (d) temporary haemostatic plug (A)PLATELET ADHESION:- • done by VWF • degranulation of platelet occurs • Helped by fibronectin and other components of extra cellular matrix. • Calcium is required
  • 7. (B) PLATELET ACTIVATION :- • Platelet secretsADPs & thromboxane A2activate other platelets and cycle continues (C) PLATELET AGGREGATION :- • activate platelet becomes sticky and stuck to other and aggregates to form platelet plug. • Platelet activating factors released by neutrophils, monocytes and platelets cell membrane lipids also increases the process
  • 8. • (D) FORMATION OF TEMPORARY HAEMOSTATIC PLUG:- Platelet adhesion  platelet aggregation  platelet plug formation
  • 9.
  • 10. FORMATION OF DEFINITIVE HAEMOSTATIC PLUG • Temporary haemostatic plug converts into definitive haemostatic plug by blood coagulation BLOOD COAGULATION:- • When a vessel is ruptured , procoagulants from the area of tissue damage become activated clot formation occurs
  • 11. • CLOTTING TAKES PLACE IN THREE STEPS:- • 1st STEP:- rupture/damage of blood vessels complex cascade of chemical reactions occur  prothrombin activator • 2nd STEP:- Prothrombin is converted into thrombin by prothrombin activator. Prothombin is formed by the liver . Vitamin k required by the liver for normal activation of prothrombin
  • 12.
  • 13. 3rd STEP:- fibrinogen converted to fibrin by thrombin. Thrombin acts on fibrinogen to remove four low molecular weight peptides from each molecule of fibrinogen forming one molecule of fibrin monomer. Fibrin monomer polymerise to form reticulum of blood clot
  • 14. • FORMATION OF PROTHROMBIN ACTIVATOR :- Prothrombin considered to be formed in two ways. 1> Extrinsic pathway :- begins with trauma to vascular wall and surrounding tissues 2> Intrinsic pathway:- begins in the blood
  • 15. • STEPS OF EXTRINSIC PATHWAY:- 1> Release of tissue factor :- traumatised tissue releases tissue factor. 2> Activation of factor X :- tissue factor activates factor VII into VIIa, which along with ca+2 activates factor X. 3> Effects of Xa to form prothrombin activator:- Xa combines with tissue factor & factor V to form complex called prothrombin activator.
  • 17. STEPS OF INTRINSIC PATHWAY • 1) blood trauma causes activation of factor XII and release of platelet phospholipids • 2) activation of factor XI by activated factor XII • 3) activation of factor IX by activated factor XI • 4) activation of factor X
  • 19.
  • 20. FIBRINOLYSIS • It is a process by which blood clot is prevented from growing and becoming pathological. • Prevents excessive fibrin deposition • It is a physiological process. • Can be dangerous if it were to expand beyond boundary. • Prevents clot formation but doesnot destroys the clot
  • 21. • This process requires a substance called plasmin or fibrinolysin, which breaks down fibrin and interferes with its polymerization. • Clot stimulates tissue plasmin activator • Plasminogen is found in blood in inactivated state by tissue plasminogen activator.
  • 22.
  • 23.
  • 24. METHODS TO CONTROL HAEMORRHAGE • HAEMORRHAGE :- Extravasation of blood from vessels, is most often the result of damage to blood vessels or defective clot formation. • CLASSIFICATION • ACCORDING TO SOURCE OF BLEEDING • CAPILLARY :- BLEEDING IS RAPID, BRIGHT RED COLOR • VENOUS :- STEADY FLOW, DARK RED COLOR • ARTERIAL :- SPURTING BLOOD, PULSATING FLOW , BRIGHT RED COLOR
  • 25. BASED ON TYPES OF HAEMORRHAGE :- • REVEALED HAEMORRHAGE:-  EXTERNAL HAEMORRHAGE  RESULTS FROM SOFT TISSUE INJURY • CONCEALED HAEMORRHAGE:-  INTERNAL HAEMORRHAGE  RESULTS FROM BLUNT OR PENETRATING TRAUMA  MORE DANGEROUS THAN REVEALED HAEMORRHAGE • INITIALY CONCEALED BUT LATER REVEALED:-  EXAMPLE – HEMATURIA, HAEMATEMESIS, MELAENA
  • 26. ON THE BASIS OF TIME:- • PRIMARY:- at the time of trauma • REACTIONARY:- within 24 hours of trauma/surgery • SECONARY:- within 7 to 14 days of trauma/surgery ON THE BASIS OF VOLUME OF BLOOD LOSS:- • MILD:- blood loss <500ml • MODERATE:- blood loss 500ml -1L • SEVERE:- blood loss > 1L
  • 27. ON THE BASIS OF PERCENTAGE OF BLOOD LOSS • CLASS I :- upto 15% • CLASS II :- upto 15 -30% • CLASS III :- upto 30-40 % • CLASS IV :- more than 40%
  • 28. • HAEMORRHAGE ASSESSMENT:- FRACTURE BLOOD LOSS -> PELVIS 2L -> FEMUR 1.5 L -> TIBIA/FIBULA 500ml -750ml
  • 29. METHODS OF ACHIEVING HAEMOSTASIS 1. MECHANICAL :- (A) PRESSURE :-  immediate measure for capillary or venous bleeding  this would control most haemorrhage  PRESSURE POINTS :- .Temporal artery for scalp .Carotid artery for neck .Brachial artery for upper limb .Femoral artery for lower limb (B) HAEMOSTAT:- directly occlude bleeding vessels
  • 30. (C) SUTURES AND LIGATION :- severed blood vessels may be tied with ligatures (D) CLIPS (E) ELEVATION (f) SPLINTING (G) TOURNIQUETS
  • 31. 2. CHEMICAL METHODS : • ADRENALINE • THROMBIN • SURGICEL • GELATIN SPONGE • NATURAL COLLAGEN SPONGE
  • 32. 3. THERMAL AGENTS :- • CAUTERY • ELECTROCAUTERY • LASERS • CRYOSURGERY
  • 33. 4. SUPPORTIVE MEASURES :- • I.V. fluids • whole blood transfusion • fresh frozen plasma • cryoprecipitates
  • 34. 5. SPECIAL MEASURES :- • ANTI SHOCK GARMENTS – pneumatic and non pneumatic