Re: Rh immunization in the first pregnancy
From: J. Hellriegel (jhellrie@pce.net)
Fri Mar 24 13:30:59 2000
At Fri, 24 Mar 2000, Andrzej Piela M.D. wrote:
>
>I vave had a patients conceived after two years of sterility without any
>history of gyn/pb interventions before. In the first and second
>trimester indirect Coombs testes were negative. In the 30 weeks of
>pregancy- until now uneventull- she fell weak fetal movements and in the
>same days usg revealed: ydrops fetus universalis, atrial flutter and
>preagonal CTG. She was delivered by cs and ferus died after 6 hours
>with signs of RDS. The structures on autopsy were normal. In 30 years
>of practice I hava had never seen hydrops fetus in the first opregnancy-
>what should I do next time and in the next pregnancy?
>Andrzej Piela M.D.
--
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
