Haemolytic disease of the newborn can result from Rhesus incompatibility in utero. In this disease a Rh-ve mother becomes exposed to the antigens of a Rh+ve foetus by fetomaternal haemorrhage causing her to mount an immune response against the D antigen. In her second pregnancy, repeat exposure to the D antigen activates memory cells causing a large production of IgG Anti-D antibodies that cross the placenta adhering to foetal red blood cells, which are then destroyed.
To prevent this, Rh-ve mothers are normally given exogenous Anti-D at 28 and 34 weeks gestation or after any sensitising event. The aim of this treatment as I understand it is to 'mop up' any D antigen in the maternal bloodstream, covering it in exogenous antigen so the mother's immune system does not mount its own response.
I had previously assumed that these exogenous antibodies would be IgM to avoid them crossing the placenta, however looking at the summary of product characteristics for some of the common preparations I see that they are comprised of 95% IgG. I then wondered if the exogenous antibodies had a much reduced half life, however the half life is 3-5 weeks.
Why does the exogenous IgG not cause haemolytic disease of the newborn in the exact same way that endogenous IgG would in a previously exposed woman who had not had prophylaxis? Is it dose-dependent or am I missing something entirely?