Rh Sensitization

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RH Sensitization

Abstract

The Perinatal Hemolytic Disease is a disease caused by the immune passage through the placenta and maternal antibody specific classIg G for the antigen (the paternal) present in fetal red blood cells, shortening its lifetime. Haemolytic disease by the system Rh (Cc, Ee,Dd) is the prototype of maternal all immunization and fetal hemolytic disease. In around 98% of cases of maternal all immunization to erythrocyte antigens not (ABO hemolytic disease _ DHPN) are due to Rh (D), the remaining 2% atypical antigens as Kell factors, E or C (Bowman,1997).The D antigen is expressed only in red blood cells and is part of RH system with other antigens such as Cc, Ee, these alsohemolytic properties, but D is 50 times more immunogenic than the other antigens of the Rh system. The process of raising the maternal system Rh (D) is given by presence of Rh positive red blood cells in your bloodstream, either during pregnancy via maternal-fetal transfusion (which can reach 29% inlast quarter), transfusion of incompatible blood, abortion, and today, deserves the use of injected illicit drugs.

Introduction

The process of hemolysis can start as early as 16 weeks gestation (Fairs, Agbetile, Hargadon, Bourne, Monteiro, Brightling, & Pashley,2010). The D maternal antibodies react with the antigens of fetal red blood cells, which are specific, covering them, but why not turn complement hemolysis not occurs in the intravascular system and yes, through the recognition of sensitized erythrocytes by the reticulo endothelial system of the fetus, mainly spleen, and then destroyed. Installed the destruction of RBCs of the fetus it produces anemia if untreated intensifies and forces the body to try to compensate for it, releasing into circulation young RBCs that are erythroblasts and also depending on the seriousness. It is important to frame the formation of foci of extramedullary hematopoiesis (Mollisonet al, 1997).

Anemia can be intensified in such a way, leading to a fetus extremely anemic conditions that justify this hepatos plenomegaly, generalized edema, effusion of serous cavities, congestive heart failure characterizing fetal hydrops. The untreated jaundice develops for the deposition of bilirubin in the system. Central Nervous leading to acute bilirubin encephalopathy or Kernicterus late.

After discharge, these infants have a picture of anemiahiporregenerativa (low reticulocyte count by low production blood by the bone) due to own illness and the pathophysiological also for these patients receive transfusions in the neonatal period. Maternal antibodies have a half-life of 28 days, and ...
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