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العنوان
Management of Coagulation Defects in Relation to Massive Blood Transfusion
المؤلف
Shaaban,Mohamed Aziz Mahmoud
هيئة الاعداد
باحث / Mohamed Aziz Mahmoud Shaaban
مشرف / Raafat Abdel-Azim Hammad Ismail
مشرف / Dalia Abdel-Hamid Nasr ElDeen
مشرف / Sahar Mohamed Talaat Taha
الموضوع
massive blood transfusion-
تاريخ النشر
2010
عدد الصفحات
211.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
التخدير و علاج الألم
تاريخ الإجازة
1/1/2010
مكان الإجازة
جامعة عين شمس - كلية الطب - Anesthesiology
الفهرس
Only 14 pages are availabe for public view

from 211

from 211

Abstract

In patients with trauma and those who undergo major surgery, multiple breaches of vascular integrity result in bleeding, and in some cases, exsanguination. Fluid (volume) replacement with crystalloids or colloids is usually the initial measure to stabilize systemic circulation by compensating for hypovolemia. When the blood loss is considered major (hemoglobin concentration below 6–10 g/dl), erythrocyte (RBC) concentrates are transfused to sustain hemoglobin levels (i.e., oxygen-carrying capacity). The transfusion of ten or more erythrocyte units (i.e., replacement of one blood volume) within 24 h is generally considered as massive transfusion in adults.
Fluid resuscitation after massive hemorrhage in major surgery and trauma may result in extensive hemodilution and coagulopathy, which is of a multifactorial nature. Although coagulopathy is often perceived as hemorrhagic, extensive hemodilution affects procoagulants as well as anticoagulant, profibrinolytic, and antifibrinolytic elements, leading to a complex coagulation disorder. Reduced thrombin activation is partially compensated by lower inhibitory activities of antithrombin and other protease inhibitors, whereas plasma fibrinogen is rapidly decreased proportional to the extent of hemodilution. Adequate fibrinogen levels are essential in managing dilutional coagulopathy. After extensive hemodilution, fibrin clots are more prone to fibrinolysis because major antifibrinolytic proteins are decreased.
Hospitals must have a major haemorrhage protocol in place and this should include clinical, laboratory and logistic responses. Protocols should be adapted to specific clinical areas. It is essential to develop an effective method of triggering the appropriate major haemorrhage protocol.
Fresh frozen plasma, platelet concentrate, and cryoprecipitate are considered the mainstay hemostatic therapies. Purified factor concentrates of plasma origin and from recombinant synthesis are increasingly used for a rapid restoration of targeted factors. Future clinical studies are necessary to establish the specific indication, dosing, and safety of novel hemostatic interventions.