Mechanism of haemostasis , fibrinolysis and method to control haemorrhage
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Dec 21, 2020
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About This Presentation
Mechanism of haemostasis , fibrinolysis and method to control haemorrhage by Dr Bipul Borthakur
Size: 1.42 MB
Language: en
Added: Dec 21, 2020
Slides: 35 pages
Slide Content
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 A2activate 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
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:- 1 st STEP:- rupture/damage of blood vessels complex cascade of chemical reactions occur prothrombin activator 2 nd 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
3 rd 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> E xtrinsic 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 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