الفهرس 
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Abstract
Heparin is a negatively charged mucopolysaccharide polymer named glycosoamino-glycan which is an anticoagulant released by mast cells and basophils during the normal clotting process. Heparin is widely used for the treatment and prophylaxis of thromboembolic disease in medical and surgical patients.
Heparin induced thrombocytopenia (HIT) is one of the most serious adverse events associated with the drug. HIT is an immune mediated prothrombotic complication that occurs with un-fractionated heparin and to lesser extent with low molecular weight heparin.
The fundamental paradox of HIT results from platelet -activating immune response triggered by the act of heparin with a specific platelet protein called protein factor 4(PF4).
Heparin causes mild platelet aggregation in vivo especially in patients with activated platelets results in increased platelet sequestration in spleen & thrombocytopenia.Thrombocytopenia can be triggered via immune and non immune mechanism.
Clinically HIT can be differentiated to HIT type I, a benign non immune condition and HIT type II an immune mediated syndrome caused by antibody to the PF4/heparin complex.
Thrombocytopenia in HIT type I is usually mild and platelet counts rarely decrease below 100,000/dl Heparin administration should be continued & no specific therapy is required.
Immune mediated HIT is a disorder initiated by immunological response to heparin exposure and characterized by an absolute or relative thrombocytopenia with paradoxically increased incidence of thrombosis and heparin should be discontinued.
Acute multiple strokes and pulmonary embolism has been detected in few cases of patients receiving heparin after prophylaxis of orthopedic surgery. neuro-imaging has detect occlusion of the right common carotid artery.
The major antigen responsible for this syndrome is PF4, which is synthesized by megakaryocytes and stored in platelet α-granules. Upon platelet activation, PF4 is released and binds anionic glycosamino-glycans on cell surfaces. The main function of PF4 is to inhibit the formation of megakaryocytes and angiogenesis, as well as
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Summary
modulating the immune response. Considerable amounts of PF4 are released after trauma, inflammation, surgical trauma, and in neoplasm.
In HIT type II, heparin infusion displaces PF4 and produces structural changes on it, leading to the formation of a PF4/heparin complex. This complex is recognized as a ’foreign’ antigen and triggers an immune response, which is characterized by the release of IgG antibodies that bind to the PF4/heparin complexes with subsequent clustering of the platelet Fc-receptors (FcχRIIa, FcχRIIIa) resulting in platelet activation. This may lead to overt arterial thrombosis, historically, called ”the white clot syndrome”.
The thrombocytopenia in HIT is usually moderate in severity, with a median platelet count being between 50 and 80 × 109/L, although the nadir platelet count can remain at a level considered normal(i.e. > 150 × 109/L) but having dropped by 50% or more with respect to the pre-heparin value. The platelet count starts to rise 2 to 3 days after discontinuing heparin and usually returns to normal within 4 to 10 days. The antibody disappears within 2 to 3 months after cessation of heparin therapy.
As regards the laboratory tests, HIT-antibodies can be demonstrated in vivo by functional tests and immunoassay.
The aim of the work is to detect incidence of heparin induced thrombocytopenia in patient undergoing coronary artery bypass graft (CABG) or valvular surgery in a number of Egyptian patients.
The study included patients undergoing cardiac surgery To spot light on heparin induced thrombocytopenia after coronary artery bypass graft (CABG) or valvular surgery mostly the non immune type which appears in 1 to 4 days post operative or the immune type which appears lately.
The method included post operative patients undergoing cardiac surgery weither (CABG) or valvular surgery by documenting the platelet count in the first, second, and before discharge days to clarify the presence or absence of heparin induced thrombocytopenia in these patients after cardiac surgery and observing the occurance of bleeding ,or any other complications.
We have 47 cases underwent cardiac surgery 26 male and 21 female ;20 CABG and 27 valvular, 31 smoker and 16 non smoker cases;12 of them had DM and 35 are non diabetic;13 of them had HTN and 34 are non hypertensive.
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In our study about 9 cases of total 47 cases was found to have HIT in percentage of about 19.15% and 38 cases was free from HIT.