///2012 Abstract Details
2012 Abstract Details2018-05-01T17:55:36+00:00

Diabetes Insipidus as a Heralding Sign of Placental Abruption

Abstract Number: S-50
Abstract Type: Case Report/Case Series

Rachel M Kacmar MD1 ; Christine S Park MD2; Laurie Chalifoux MD3

Introduction: Gestational diabetes insipidus is a rare condition diagnosed in roughly 1/30,000 pregnancies(1,3) and is characterized by polydipsia and polyuria(2). While gestational diabetes insipidus is more often reported in association with pre-eclampsia, HELLP syndrome, and liver dysfunction with decreased metabolism of vasopressinase, there can be a relationship to twin pregnancy and the accompanying larger placental mass.

Case: A 31 y/o G3P0 female with 33.3 wks EGA twin pregnancy presented to the labor and delivery floor with complaints of several hours of uterine contractions. Fetal distress was noted on FHR monitoring leading to emergency cesarean delivery under general anesthesia. The intraoperative course was complicated by EBL of 2L requiring 4 doses of carboprost and placement of a B-Lynch suture. Fluid administration included 1800 ml crystalloid and 1.5 L colloid with intraoperative urine output of 300 ml. Upon emergence the patient complained of extreme thirst. Polyuria soon became evident with a urine output of 850 ml in the first 40 min, 650 ml in the following 35 min, and a total of 4.95 L during the first 4 hrs and 25 min. Upon further questioning the patient admitted to extreme thirst approximately coincident with the onset of contractions. Urine and plasma osmolalities 2 hrs post-delivery were 147 and 292 mOsm/Kg respectively. After maintenance fluids were discontinued the patient was allowed to drink to thirst, consuming 1000-1200 ml/ hr. UOP during that time was 650-1000 ml/ hr. Following administration of 2 mcg subcutaneous DDAVP the patient’s PO fluid intake decreased to 200 ml/hr and UOP decreased to < 150 ml/hr. Pituitary MRI revealed loss of posterior pituitary bright spot on pre-contrast T1 images, consistent with an absence of significant stores of vasopressin, but was otherwise unremarkable. The patient continued to demonstrate polydipsia and polyuria between doses of DDAVP and failed to respond to a challenge dose of vasopressin. A diagnosis of transient gestational diabetes insipidus secondary to elevated vasopressinase was made. The patient was treated with DDAVP for two months with complete resolution of her symptoms. During a subsequent pregnancy she again suffered post-partum hemorrhage, but no signs or symptoms of diabetes insipidus.

Discussion: There are no case reports in the literature of transient gestational DI associated with placental abruption. The increased thirst noted by the patient coincident with the onset of contractions was likely a heralding sign of abruption secondary to vasopressinase release as the utero-placental interface was interrupted. This pathology may be underdiagnosed and should be considered in patients reporting thirst and polyuria in the presence of predisposing factors.

References

1.Passannante AN, et al. Anesth Analg 1995;80(4):837-8.

2.Brewster UC, et al. Obstet Gynecol 2005;105(5pt2):1173-6.

3.Ananthakrishnan S. Endocr Pract 2009;15(4):377-8

SOAP 2012