Re: Rh immunization in the first pregnancy
From: steve (steve@dhngwe2.db.healthlink.org.za)
Sat Mar 25 15:35:11 2000
And to all of the listed aetiologies below you should add syphilis
>
> Unless I do not understand the situation you descrive, you have not
> demonstrated that the hydrops is due to Rh immunization. There are
> multiple etiologies for hydrops. The following may be helpful.
>
> Hydrops fetalis is the final common pathway for a variety of
> pathophysiologic processes, including (1) increased capillary
> permeability to water and protein, (2) decreased lymph flow, (3)
> congestive heart failure and elevated blood volume, or (4) decreased
> albumin synthesis. There is increasing doubt that congestive heart
> failure is a common cause of hydrops; the placenta transfers water
> efficiently from the maternal to the fetal circulations. Also, hydrops is
> not universally associated with any cardiac anomaly. When cardiac anomaly
> is associated with hydrops fetalis, there may also be lymphatic anomalies
> causing lymphatic obstruction or other fetal problems causing capillary
> injury and "leak." There is also no evidence to support the theory of
> congenital abnormality in albumin synthesis. Once there is third-spacing
> of intravascular fluid, the fetoplacental circulations are generally
> affected in parallel; therefore fetal hydrops is almost always reflected
> in placental hydrops. However, the placenta is without lymphatic
> circulation, and if the primary locus of extravascular fluid is within the
> lymphatic system (due to obstruction or other reduction of lymphatic
> drainage), the placenta may not show significant edema. Generalized
> fetoplacental hydrops is most commonly due to excessive fetal erythrocyte
> destruction (e.g., Rh and blood group incompatibilities, some congenital
> viral syndromes), decreased erythrocyte production (e.g., congenital viral
> infection or aneuploidy) or fetoplacental hemorrhage. Fetoplacental
> hemorrhage may be caused by rupture of velamentous vessels or vasa previa,
> umbilical cord hemorrhage, or in our experience, most commonly after any
> villous damage (ischemia or inflammatory). Once there is fetal anemia
> sufficient to injure capillaries, experimental models have demonstrated
> capillary efflux of both protein and water. Fetal hydrops may also
> develop as a result of placental lesions (e.g., chorangioma or venous
> obstruction). Placental findings in hydrops fetalis include variable
> villous dysmaturity (i.e., histology less mature than expected for
> gestational age), increased cytotrophoblast mitoses, thickened trophoblast
> basement membranes, increased fibrinoid necrosis, and hemosiderosis, which
> may involve extraplacental membranes, villous macrophages, endothelia, and
> the trophoblast basement membrane. Increased amounts of both intravillous
> and extravillous calcification are seen with cardiac failure, intrauterine
> fetal death, or when there is less fetal demand for calcium, as in
> osteogenesis imperfecta.
>
> --
> John Hellriegel, MD, PhD
Dr. S.H. Raymond
Head of Department of O & G
Empangeni Hospital
EMPANGENI
South Africa 3880
Ph. (27)+(35)7721111
Fax (27)+(35)7922596
