Hemostasis And Blood Coagulation

Prof. M.C. Bansal MBBS ., MS., MICOG . , FICOG.

Fonder principal & Control, Jhalwar Medical College & Hospital Jhalawar

Ex principal & Controller MGMC & Hospital Sitapura ., Jaipur.

Normal Blood Coagulation

intra vascular coagulation is linked with three different interrelated systems.

1. Coagulation System .

2. Coagulation Inhibitory System .

3. Fibrinolytic System .

Events in Hemostasis Hemostasis means prevention of blood

loss after blood vessel is severed or ruptured.

It is achieved by a complex mechanism . 1, Vascular constriction. 2, Formation of Platelet plug . 3, Clot formation by coagulation

process switched on by trauma, 4, Eventual fibrosis in clot closed to the

hole in blood vessel.

Vascular constriction

It is brought about by -- a. Local auto acid factor released from

traumatized tissue ., b. spontaneous and its own Spasm of

myofibrils of blood vessel. c . Nervous reflex ---traumatized

sensory nerve endings convey to higher center and efferent nerves carry action orders to myofibrils .

d. Thromboxane A produced by Platelets .

Formation Of Platelet Plug Small holes are immediately closed by platelet plugs. Platelet Cytoplasm has many active factors like Actin,

myocine molecules , thromboplastin , Adenoplasmin Reticulum , Golgi apparatus ( synthesize Various enzymes and store Ca ++ ), Mitochondria and enzyme system capable to produce ATP, ADP , Prostgandins , fibrin stabilizing factor and growth factor.

Growth factor growth of and repair of vascular endothelium myofibrils and fibroblasts needed for blood vessel repair.

Platelet membrane is coated with glycoprotein which prevent their adherence to healthy endothelium .but once endothelium is damaged the platelets quickly and abundantly adhere to damaged endothelium and exposed collegen fibers in the vessel wall there by plugging the hole / defect.

Platelet membrane also contain phospholipids.

3rd mechanism of hemostasis---clot formation

It starts to develop with in 15-20 seconds of injury to blood vessel .

clotting process activating substances are released from traumatized tissue , vascular endothelium, platelets and plasma proteins.

If vascular hole is small , it is plugged with in 2-3 minutes but in case of large defect it may take 20 minutes to 1 hour .

The clot formed in damaged followed by repaired site retracts and further closes the vessel.

Platelets also play an important role in clot retraction .

Fibrous Organization / dissolution of clot

Once the clot is formed , blood vessel defect is repaired the clot is invaded by fibroblasts ( promoted by Growth factor produced by platelets ) . This continues till complete organization of clot in to fibrous tissue is completed with in 1-2 weeks .

Extra vagated blood is also clotted similarly and is dissolved by fibrinolysis activity.

Prevention of blood clotting in normal blood vessels – mechanism of Intra vascular anti coagulation

The smoothness of vascular endothelium prevents platelet adhesion and contact activation of intrinsic clotting cascade.

A layer of Glycocalyx on endothelium repels platelets and intrinsic factor to contact .

Protein bound to endothelium called Trombomodulin binds with Thrombin and slows the process of clotting and their complex molecule “ Thrombomodulin-thrombin “ activates protein C ., inhibits factor V and VIII.

Prevention of blood clotting in normal blood vessels – mechanism of Intra vascular anti coagulation-----

In damaged / rough endothelium –Glycocalyx and Thrombomodulin is lost hence both factor XII, platelet adhesion and intrinsic factor initiate the clotting cascade .

Anti Coagulants are also present in blood itself ----They remove thrombin from the blood.

1 Fibrin fibers . 2 Alpha globulin also called antithrombin III or

antithrombin Co factor. This prevents excessive clot formation .

3 free Thrombin combines with fibrin fibers and anti thrombin III , so free thrombin is no more available to fibrinogen to form fibrin clot

.Heparin –secreted by mast cells , its physiological role is limited and insignificant , but pharmacological use is very common in clotting disorders in clinical practice.

Lyses of Blood clot Plasma proteins contain euglobin called

Plasminogen when activated changes into Plasmin ( Fibrinlysin ) . It is proteolytic like trypsin enzyme .

It digests fibrin fibers , fibrinogen , factor V , VIII , IX and prothrombin , causing dissolution of clot .

After few days of trauma when bleeding is stopped , repair work / healing process starts Endothelium librates a powerful activator called tissue plasminogen activator (t-PA ) , which converts plasminogen in to plasmin to remove the undesired clot to facilited neo vascularisation and patency of blood vessel necessary for tissue perfusion .

Normal Values Of Blood Coagulation Profile

Test Value

Bleeding Time – Duke’s Method Ivy’s Method

1-3 Mins1-9 Mins

Coagulation Time- Wright’s Tube Method

Lee & White’s Methods

3-7 Mins4-9 Mins

Clot Observation Test (Weiner’s) 6-12 Mins

Clot Retraction Time 30 Mins

Fibrindex Or Thrombin Test Formation Of A Clot In 1 Min

Prothrombin Time 11-17 Mins

Thrombin Time 10-15 Secs

Platelet Count 1.5-4 Lacs/Cumm

Fibrin Degeneration Products 0-5 Micro G/Ml

Euglobin Clot Lysis Time 2-4 Hours

Fibrinogren 300-600 Mg%

D-dimer 0-200 Mg/Ml

Collection Of Blood Samples For Lab Tests

Test Method Of Collection Of Blood In Test Tube / Vial

Amount Of Blood

Hb% Or PCV EDTA Vial 2 Ml

ABO & Rh Group Plain (Clotted) And 3.8% Sodium

Citrate Solution

2 Ml & Few Drops

Vdrl Plain (Clotted) 2ml

Direct / Indirect Coomb’s Test

Plain (Clotted) 2ml

Prothrombin Time 0.5 Ml Of 3.8 % Sodium Citrate

Solution

4.5 Ml

Fibrinogen EDTA Vial 2ml

Platelet EDTA Vial 2ml

Edp Special Tubes Supplied With Kits

Eclt Citrate Solution 4.5 Ml

D-dimer EDTA Vial 2 Ml

Conditions causing excessive Bleeding

Deficiency of one / more blood clotting factors .

Vit. K . Deficiency . Hemophillia . Thrombocytopenia. Liver disease ==not able to produce

clotting factors . DIC

Thrombo –Embolic Conditions Abnormal that develops in blood

vessel being loosely attached may get detached and flow in circulation –get lodged at distance is called Embolus ( in pulmonary or aortic circulation ---chocks the end arteries).the affected area / organ does not get O2 resulting in Acute Ischemia and infarction .

Causes Of Thrombi-Embolism Roughened breeched endothelium in blood

vessels ---arteriosclerosis , atheroscerosis , infection , traumatic .

Blood flow is very slow or stagnant . Intra venous therapy cannulatios left in situ for a

longer time , trombophlebitis . Intravenous thrombosis ----Central sinus vein ,

deep veins of calf and pelvis . Intramural thrombus in heart chambers . Its incidences increases in pregnancy ,

puerperium LSCS ( hyper coagulability state of pregnancy , tissue trauma, inflammation , dehydration , prolong bed rest ) , pelvic surgery