Re: Diabetes Insipidus and hydramnios

From: James Smeltzer (James.Smeltzer@wellstar.org)
Mon Jul 21 16:07:13 2008


Hi!

A syndrome of Diabetes insipidus OF PREGNANCY has been seen frequently. It turns out that oxytocinase - made in gram quantities by the placenta - also can inactivate arginine vasopressin. Women with this syndrome have virtually entirely normal pregnancies, except for the consumption of over 5 gallons of fluid per day - with which they spontaneously self-treat. They can rapidly get into trouble with shock, hyperosmolar coma and hypernatremia if they cannot drink ad lib. Saline can obviously make matters worse in a hurry. There does seem to be an increased risk of preeclampsia and acute fatty liver noted by some - possibly causally related to fetal growth restriction seen here (http://ndt.oxfordjournals.org/cgi/content/full/18/10/2193)

Since their babies are usually normal, I do not believe that maternal DI is a cause for what you see. Perhaps the DI of pregnancy - easily and safely treated with nasal desmopressin spray (one 4 times per day - not inactivated by placental oxytocinase) is associated with PIH because both are caused by the placenta.

A much more likely alternative explanation is FETAL DIABETES INSIPIDUS - such as induced by maternal lithium use in pregnancy, (Maternal lithium therapy and neonatal morbidity. Zegers B, Andriessen P.Eur J Pediatr. 2003 May;162(5):348-9. Epub 2003 Feb 28). or sporadic ("...Markedly elevated fetal urine output of 18 mL/hour (tenth to 95th percentile at 26 weeks, 4-7 mL/hour) was present in one fetus that was subsequently found to have diabetes insipidus..." Fetal urine output in hydramnios. Kirshon B. Obstet Gynecol. 1989 Feb;73(2):240-2.

If the maternal DI is a result of inherited DI(http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=125700) - a dominant trait, paradoxically - then the fetus could be affected as well (half the time having the gene). If the fetus is affected, then the hydramnios is a potential subtle marker for presence of this inability to concentrate urine in the fetus. Since the SGA is minor, it is likely unrelated, but possibly a harbinger of PIH.

If the maternal central DI is variant of hypopituitarism, as suggested by the thyroid deficiency, it is possible that there is a degree of Addison's syndrome exposed by the stress of pregnancy, which could result in fetal growth restriction from hypotension. It is also possible that the DDAVP needs to be increased (for both, see: Clomiphene-induced pregnancy in a patient with diabetes insipidus and hypothyroidism. Chelvam P, Puraviappan, Ahmad Z. Med J Aust. 1979 Sep 22;2(6):316-7.

"A patient with diabetes insipidus and hypothyroidism developed anovular menstrual cycles. Ovulation, which was followed by pregnancy, was induced by the administration of clomiphene. In the later stages of pregnancy, an increase in the dosage of vasopressin was necessary to achieve a satisfactory control of the symptoms of diabetes insipidus. Labour was induced before the estimated date of confinement by the intravenous administration of oxytocin and an intra-partum haemorrhage necessitated delivery by the lower-segment caesarean section. The post-partum period was uneventful. Lactation was suppressed on request from the patient."

On the other hand, animal models suggest excess maternal water ingestion plus DDAVP can produce hypOnatremia in the fetus - and presumably self-treatment by the fetus through polyuria of excess free water. Kujovich JL. Von Willebrand disease and pregnancy. J Thromb Haemost. 2005;3: 246-253 (see pdf 1523VWD in Oct) Roberts TJ, Nijland MJ, Curran M, Ross MG: Maternal 1- deamino-8-D-arginine-vasopressin-induced sequential decreases in plasma sodium concentration: ovine fetal renal responses. Am J Obstet Gynecol 1999;180:82-90.

If the etiology of the DI is known, and it is hereditary: Check the DDAVP dose and evaluate the baby for DI after birth. If not, then also check an AM cortisol (which should be high in pregnancy) and ACTH (also higher). If they are not, cover for addison's.

If the baby has DI, it would be good to know since they can get into trouble easily because they can not drink ad lib. If the mother has any chance of being addisonian, I would cover her for C/Section and delivery with glucocorticoids.

Interesting case. let us know what the baby has.

Hope this helps Jim Smeltzer

--
James S. Smeltzer, MD, FACOG, SMFM
Consultant, Maternal Fetal Medicine
Wellstar Physicians' Group
Northwest Women's Care
787 Campbell Hill St
Marietta GA 30060
James.Smeltzer@wellstar.org
VM 678-290-3035
Off 770-528-0260
Page 404-318-3451

>>> Annibale Mazzocco <annigiu@tiscali.it> 7/20/2008 4:43 AM >>> Hello: I have a 32-year-old patient, first pregnancy, at 23 weeks affected by central diabetes insipidus + hypothyroidism, now in treatment with minirin (3-4 puff /day) + eutirox 150 mg 7day. She is being treated by the endocrinological center of my hospital in Montebelluna ûTreviso, Italy. In the first trimester she underwent a first trimester combined screening with a risk for T21 of 1/9297. I performed the anomaly scan at 20 w+5d and found normal morphology, fetal growth at 25Æ centile , Amniotic Fluid at borderline (max fold 79 mm, AFI 180 mm). I suggested a new endocrinological consultation, also to gain time on the subject, and a new control after two week. At 23 +0 I found fetal growth at 10 centile (AC: 168, DBP: 53, HC: 292, F: 36, HL: 31), morphology still normal, hydramnios: AFI 238, max fold: 90. Uterine artery Doppler normal with medium IR 0,44, normal Doppler in UA. The endocrinologist didnÆt change the therapy in any way. I didnÆt find anything in Pub med about diabetes insipidus in pregnancy complicated with hydramnios and fetal grow restriction. Have you had cases like this? Do you have data about diabetes insipidus and hydramnios and fetal growth restriction, or on the other hand, do you think that these are casual concomitant factors ? Thank you so much Annibale Treviso Italy

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