OB-GYN-L Messages for July, 1997: Re: any clues?

Re: any clues?

From: dahmd

dahmd@gate.net

Fri Jul 11 17:01:53 1997

> 1) I have often seen it claimed that uterine abnormalities may
> account for preterm delivery and or late spontaneous abortion - though I
> have also read that uterine abnormalities other than the most gross ones
> are not a particulary cause for such deliveries. In this instance though
> I am particularly puzzled how a uternie abnormality might be implicated
> in IUFD.

Malcolm-

Here's a couple of thoughts. I recently cared for a patient with a bicornuate uterus who bled off and on throughout the late first and entire second trimesters. She would come in "just sure" that she had miscarried due to clots and blood running down her leg, yet every time we did an ultrasound the baby (and a retroplacental clot) was still there. I have seen a few other cases where the presumption (after all, how can one be completely certain?) was that the uterine anomaly such as a septatd or bicornuate uterus caused an abruption or rupture of membranes, which led to fetal demise. A large but "hidden" abruption can certainly cause a fetal demise. My assumption has always been that as the placenta grows it is constrained by the abnormal uterus and shears, causing the abruption. There is also an association between fibroids and abruptio placentae, although I suspect this is a rare cause of fetal loss. Finally, preterm labor and delivery caused by a fetal anomaly can certainly cause a "fetal death" although I agree that's not really in the same context as our discussion here.

> 2) I have an unpublished case series well into three figures of
> second & third trimester losses. In no case was HbA1c ever raised in the
> absence of frank diabetes or some other indicator.

This makes sense (much more than 2c) to me. We care for a large number of women with diabetes and/or hypertension. Most women with frank diabetes *do* have other indicators that their diabetes is out of control, although it seems that you are assuming that a normal blood sugar, lack of glucosuria (insensitive in pregnancy, anyway), and absence of such things as DKA implies that diabetes has not caused the fetal loss. I've seen women present with a fetal demise who had perfectly normal blood sugars but who had markedly elevated hemoglobin A1C levels and who, on questioning, admitted extremely poor control (i.e. only took their insulin because they were coming to the hospital to investigate why their baby hadn't moved in 3 days). Still, I'll bet this is rare, and would agree that there may be little value in obtaining a hemoglobin A1C in second trimester losses from a cost:benefit perspective. Your data supports this.

Thanks for the dialogue.

Ashley D. Ashley Hill, M.D. dahmd@gate.net Orlando, FL

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