Hostile endometrium is a common cause of implantation failure.. How do we assess Endometrial Receptivity
in IVF??
Embryo transfer (ET) forms the
ultimate procedure in the program of ART. The person who does the ET must have
adequate information regarding the dimension of uterus, the length of cervical
canal; difficulty in negotiating the internal OS and the angle between the
cervical canal and body of the uterus. All these should have been recorded
after a preliminary hysteroscopy during which one would also exclude other disturbing
features like the presence of synechiae, small myoma, adenomatous polyps,
foreign bodies and large areas of bald endometrium etc.
The sonologist must report on
collection of fluid in the uterine cavity during the course of stimulation
protocol; if such a thing is reported, the fluid has to be aspirated and sent
for bacteriological examination either by culture or by PCR examination for
inflammatory conditions caused by Chlamydia and tuberculosis. Chronically
infected tubes might swell up during stimulation protocol forming a
hydrosalpinx and such fluid might be propelled into uterine cavity by
increasing peristalsis stimulated by elevated estrogen levels. Mucoid fluid
usually suggests chronic infection of genital tract.
Thickness of endometrium is a
very important feature to reckon with for the success of ET. An endometrial
thickness of less than 7mm on the day of HCG is most unlikely to produce a
pregnancy. It must be appreciated that in a natural uniovular cycle of a woman,
the Serum E2 at the time of ovulation is
around 250 pg/ml and the endometrial thickness may be anywhere between 8 and 14
mm. On the other hand in a cycle of controlled ovarian hyperstimulation (COH)
the S,E2 level may rise up to anywhere between 1000 and 3000 pg/ml at the time
of HCG administration; but one frequently gets disappointed to see that the
endometrium does not necessarily grow in parallel with the increasing Serum E2
level. The causes of endometrial growth lag may be many. Chronic infections
like tuberculosis can produce destruction of basal endometrium because of which
the endometrium may never grow to optimal thickness. Exogenous estrogen
administered orally or intramuscular may not reach the endometrium at all. It
may be taken up by the liver, metabolized and eliminated before it reaches the
uterus. On suppositories reach the endometrium directly by diffusion, thus
increasing the endometrial thickness and receptivity without increasing the
level of these hormones in the serum.
Quite frequently Doppler blood
flow velocity study of endometrium is seen to be at a very low level without any
demonstrable cause. The absence of a multi-layered endometrium associated with
uterine artery pulsatility index (PI) of more than 3 at the time of HCG
injection is an ominous sign. The absence of sub-endometrial blood flow should
give a warning regarding endometrial vascularisation and increase implantation.
But, such an observation has not been supported by most of the workers. When
both endometrial thickness and vascularity are subnormal, it is wise to
postpone ET to a cold cycle for a frozen embryo transfer (FET). The cause of
endometrial deficiency has to be evaluated and any therapeutic measures
available shuld be instituted. A good protocol for hormone replacement therapy
may be substituted.
Hyper-echogenic endometrium on
the day of administration of HCG may be a contraindication for ET. Highly
echogenic endometrium appears white. During the follicular phase of menstrual
cycle endometrium appears dark between the endometrium lining the myometrium
and that lining the endometrial cavity. During luteal phase of the endometrium,
echogenicity increases giving a whitish, smudgy appearance. This kind of change
may be seen as early as the fourth day of P exposure.
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