08 hemostasis neonatal

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    12-Aug-2015

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<ol><li> 1. HEMOSTASIS By Prof Sameh Shamaa Prof Of medical Oncology and Internal medicine Mansoura Faculty Of Medicine HEMOSTASIS </li><li> 2. HEMOSTASIS Def:- stoppage of bleeding from the blood vessels Mechanisms (I) v.c of blood vessels (II) platelet plug formation (III) Blood coagulation (fibrinogen fibrin) (IV) Clot retraction (V) fibrinolysis to dissolve the clot HEMOSTASIS </li><li> 3. PRIMARY HEMOSTASIS includes the processes that result in the formation of the platelet plug. Necessary factors-: -The blood vessels : the vessel walls esp. the subendothelial layer. -The platelets -2plasma glycoproteins: -fibrinogen -Willebrand factor ,which also presents inside the platelets </li><li> 4. Mechanisms: 1-v.c of the bl. vessel. 2-Platelets adhesion to subendothelial layer, ( Willebrand factor is necessary for this stage) adhesion of platelets- 3- platelets secretion: their activation and secretion of ADP,adrenaline, noradrenaline &gt; aggregation &amp; activation of other platelets. 4-Aggregation of platelets. 5-Formation of capillary plug. HEMOSTASIS </li><li> 5. Exploration of the 1ry homeostasis 1) Important points in the history of any bleeding patients : HEMOSTASIS </li><li> 6. - Family history - Duration (recent onset or since childhood) - Duration of the bleeding episode. - Circumstance of bleeding (spontaneous, after trauma, or surgery) HEMOSTASIS </li><li> 7. Type and character of bleeding: -- Purpuric spots (capillary or platelets defect not characteristic of hemophilia) - Hematoma, hemarthrosis or large ecchymoses at the site of trauma : suggests hemophilia (coagulation defect) - Sudden severe bleeding from multiple sites after prolonged surgery or during obstetric procedures suggests acquired fibrinogen defect HEMOSTASIS </li><li> 8. 2) Investigations : HEMOSTASIS </li><li> 9. 1) Capillary resistance test of Hess 2) Platelets count 3) Bleeding time time needed for the platelet plug formation If . N. ------ Normal 1ry homeostasis . ------ platelet or vascular defect. HEMOSTASIS </li><li> 10. Capillary resistance test of Hess: sphygmomanometer cuff above the cubital fossa and raise the pressure to 100 mm Hg (or midway between systolic &amp; diastolic if systolic pressure fibrin Measured by addition of thrombin to citrated patients plasma If polonged Abnormalities of fibornogen (hypo or hyper or dysfibrinogenemia) Heparin Presence of some abnormal proteinswhich inhibits the polymerisation of monomers of fibrin. (e.g myeloma protein HEMOSTASIS </li><li> 31. (5) Deficiency of F XIII (fibrin stabilizing factor ) detected by noting the solubility of fibrin in 5M urea or 1% monochloroacetic acid (can't dissolve fibrin in the presence of factor XIII).In congenital defect of f. XIII ---&gt; dissolution of the clot in severe hemorrhage 2-Inhibitors against platelets or tissue phospholipids ---&gt; prolongation of tests of coagulation (Quick or CKT) e.g L.E but usually no hemorrhagic manifestations 3- if there is of Quick test or CKT or thrombine:- 50% of normal plasma + 50% of patient plasma (incubation at 370c for I hour) repeat the test If become normal ---&gt; factor defect if no correction ---&gt; presence of inhibitors. HEMOSTASIS </li><li> 33. PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE B.T Platelets count Quick test CKT Thrombin time Dosage of fibrinogen HEMOSTASIS </li><li> 34. PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE I- B.T, platelets ( 80.000; mm3) Thrombocytopenia 2- B.T, platelets normal Qualitative platelets abnormalities Willebrand disease congenital or acquired platelet factor tests dosage of factor VIII HEMOSTASIS </li><li> 35. PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE 3- Quick + CKT Other tests are N Acquired defect of several defect of factor common for factors (II, VII, X,V) 2 pathways ex. X or V or II 4- Quick N., CKT: either: I- Hemophilia Aor B. 2- Rarely ---&gt; defect of one factor of the contact system (XII, or XI or others) HEMOSTASIS </li><li> 36. PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE 5- Quick , CKT N isolated defect of factor VII in 3, 4..5 dosage of the factors with suspected deficiency, also search for inhibitors. Ex: - Quick, normal dosage of factors---&gt; hyperfibriongenemia which inhibit the test - Quick +CKT + no F. defect ---&gt;? Inhibitors, e.g. antiphospholipides. HEMOSTASIS </li><li> 37. PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE 6-T.T either: * heparine in the blood or in the tube. Here T.T can be corrected by adding either a-toluidine blue b-Reptilase time (incomplete thrombin not sensitive to heparin and not inhibited by antithrombin III). * If (a-b also defective) ---&gt; troubles of fibrin polymerisation :either due to abnormal fibrin (dysfibrinogenimia) or inhibition e.g by ---&gt; myeloma protein or F.D.P. HEMOSTASIS </li><li> 38. PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE 7- fibrinogen * congenital afibrinogenimia or hypofibrinogenimia Acquired hypofibrinogenimia e.g.liver cirrhosis. consumption of fibrinogen: e.g. D.I.V.C, fibrinolysis HEMOSTASIS </li><li> 39. 8-All tests ate Normal: * Capillary fragility (usually only ecchymoses ) ---&gt; measurement of cap.fragility. * deficient factor XIII * no hemostatic troubles. PRACTICAL INVESTIGATION OF HEMOSTATIC TROUBLE HEMOSTASIS </li><li> 40. Thank You HEMOSTASIS </li></ol>