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HAEMOSTATIC FAILURE

Failure of ahemostasis is common in critically ill patients and may be complex and
multifactorial in pathogenesis as haemostatic failure may complicated a wide range of medical
surgical and obstetric disorder definitive diagnosis and specific therapy can significantly impact
on outcome . frequently, complex test are required for defintif diagnosis but the urgency of the
situation can not always wait for he result, and therapy may be defined on clinicall evidence with
minimal laboratory information. Consultation with a clinical haemathologist strongly
recommended.
NORMAL HAEMOSTATIS
In haemostatic system is a delicatedly controlled component of the host defends system.
The role of which is to initiate haemostatis where and when required and in adequate but not in
excessive amounts. The system closely intherect with other component of the host defands
system, including the acute responses, infalmation, healing, and imunefunctions. There has been
aparadigm shift in our understanding of the haemostatic system to modulate its activity, that is
important that core aspects of the structure of functions of the system or summarized .
The convertions of blood from its fluid to solid state is an increasingly understood
physiological process. The thread of vascular constriction, platelet plugging and fibrin formation
from haenostatic pluges and provide the frame word on which haemostatic operate. An set the
scene for healing to ocure . thrombin is poten proteolytic enzyme of the coagulation squance
converting fibrinongen to fibrin soluble monomers, which subsequenyly polymerase to form the
fiblin cloth. Fibrinogen is the bulk protein of the coagulation system and fibrin is the and product
of these cacade of proteolytic activity in which precursore coagulation protein are activated to
poten roteolitic enzyme with the aid of cofactor to produce active procursore further down
coagulation amplifier . the polymerase fibrinis further acted on by factor XIII to form a stable the
fibrin cloth . the process of thrombin generation in small ammounts initially acure in relationship
to tissue factor healing cells and the process is subsequently transferred to the activated platelet
suface were amplification ocurre .
Following injury vascular constriction reduce bleeding and allows time to initiate
haeostatic. With large volume haemorage, resulting systemic hypertension is an important
physiological mechanism to minimize blood lost and facilitate stabilization of haemostatic plug
controlled or tolerated hypotension is now exapted as an important aspect of managing critical
haemorage. This vascular constriction is further accentuated by vasoconstrictors realese in
association with platelet plug formation. Vascular endothelial cell play an active part by synthesis
sinc which act at the membrane surface and interact with platelet and coagulation system.
Following the initial vascular reaction, success full haemostatic efand on adequate number of
functioning platelete, coagulation cascade function, and purely understood contribution for red
cell and leucocyte .
The coagulation system is triggered via the extrinsic pathway, by which damaged tisuues
expose tissue factor. Tissue factor is membrane bound protein presents in cells surrounding the

Leading to activation of factor X directly on the platelete surface. It the a not play a significant role In the initiation face of coagulation. The conceps of the instrinsic and extrinsic system is more of historical and laboratory significants as it is now clear that such a division is artificial but the concepts still have value in performing and accessing haemostatic laboratory test . Factor Xa interacts with te cofactor Va to Form prothrombinase complexes with the generation of a small amount of thrombine on the cell suface.vascular bad. but difuses accros to platelete in the vicinity that have adhered inproximity to the side of the TF bearing cells binding to a specific platelete surface reseptor and interacting with cofactor factor VIIIa. Factor VII a are bound to TF activating factor X . Factor IX is also activated by the TF VIIa complex.n .