Category: Pituitary Disorders/Neuroendocrinology

Monitor: 23

23 - CENTRAL DIABETES INSIPIDUS IN PREGNANCY COMPLICATED BY OXYTOCIN USE

Friday, Apr 26
11:30 AM – 12:00 PM

Objective :

To present a case of central diabetes insipidus (DI) in a pregnant woman requiring oxytocin infusion. 


Methods : N/A


Results :

A 40-year-old woman with idiopathic central DI for 15 years was admitted for premature rupture of membranes at 39 weeks gestation. Previous workup for the etiology of DI revealed normal anterior pituitary function and no abnormalities on pituitary MRI. The desmopressin (dDAVP) dose was 10 mcg intra-nasally 3 to 4 times daily, with the 4th dose administered at bedtime as needed. The dDAVP dose was unchanged prior to and during pregnancy. Serum sodium (Na) was stable throughout pregnancy at 136-141 mEq/L (normal range (n): 135-145 mEq/L). 


Admission labs were normal with serum Na 138 mEq/L, urine osmolality 403 mOsm/kg (n: 50-1400 mOsm/kg), urine specific gravity 1.011 (n: 1.010-1.025), and serum osmolality 286 mOsm/kg (n: 280-300 mOsm/kg). Continuous oxytocin infusion was started for induction of labor along with lactated Ringer’s infusion. She developed pre-eclampsia and was treated with a magnesium infusion. Caesarean section was performed on day 2 of hospitalization due to arrest of cervical dilation. She required the same dose of dDAVP while on the oxytocin infusion. Na levels were normal throughout labor. However, dDAVP was not given for 24 hours after Caesarean section due to mild hyponatremia (Na 133 mEq/L) and she did not develop signs of polyuria. Upon discharge, her Na stabilized at 137-142 mEq/L and the home dose of dDAVP was resumed. 


Discussion : DI affecting pregnancy is rare but it remains a challenge to manage the fluid and electrolyte shifts during gestation. While transient DI due to the placental production of vasopressinase is the most common cause of DI in pregnancy, patients with pre-existing DI require careful monitoring during pregnancy. The normal physiological changes of pregnancy include the placental production of vasopressinase, which degrades anti-diuretic hormone (ADH). Therefore, it is expected that pregnancy will lead to an increase in dDAVP doses in individuals with pre-existing DI. In addition, the use of oxytocin for labor induction also complicates DI management due to its anti-diuretic action through vasopressin V2 receptor (V2R) and aquaporin-2 (AQP2).


Conclusion :

Our case presentation illustrates the complexities in managing central DI during the peri-partum period that can be complicated by additional intravenous fluids and oxytocin administration. Our patient did not require additional dDAVP while on oxytocin which suggests that oxytocin may have low potency on V2R and AQP2. However, the constant changes in the fluid status in pregnancy require frequent monitoring of serum and urine parameters. 

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Beatrice Wong

Fellow
Icahn School of Medicine at Mount Sinai
New York, New York

I obtained my MD degree from SUNY Downstate and completed my Internal Medicine residency at Rutgers Robert Wood Johnson Medical School. I am currently an Endocrine fellow at the Icahn School of Medicine at Mount Sinai.

Emily Jane Gallagher

Assistant Professor
Icahn School of Medicine at Mount Sinai

The focus of my research is to understand the mechanisms through which systemic metabolic abnormalities increase breast cancer growth and metastases. Specifically, my work examines the role of metabolic abnormalities associated with obesity and type 2 diabetes, including hyperinsulinemia and dyslipidemia, on cancer progression I have studied how insulin and IGF-1 signaling promote breast cancer and how inhibiting this signaling affects whole body metabolism and cancer progression in pre-clinical animal studies. My recent work has focused on the role of systemic lipid abnormalities on breast cancer growth and metastases. My clinical practice is a dedicated OncoEndocrinology clinic, where I treat the endocrine complications of oncology therapies primarily metabolic and autoimmune endocrine effects of cancer therapies. Therefore, through my research and clinical practice I aim to improve uncover novel mechanisms linking systemic metabolic disorders to breast cancer progression in order to identify novel treatment options for these patients.

Khadeen C. Cheesman

Assistant Professor
Icahn School of Medicine at Mount Sinai
New York, New York

Dr. Khadeen Cheesman graduated from Columbia University College of Physicians and Surgeons in New York, New York. Following medical school she completed her residency training in Internal Medicine, and her fellowship training in Endocrinology, Diabetes and Bone diseases at the Icahn School of Medicine at Mount Sinai. During her fellowship training she developed interests in the diagnosis and management of pituitary and adrenal disorders. She has participated in several research projects related to Primary Aldosteronism, Cushing disease and Acromegaly. Most recently, she presented her research at the Endocrine Society Meeting 2016. As a faculty member, Dr. Cheesman aims to provide exceptional care to patients with a wide variety of endocrine disorders, and mentorship to fellows, residents and medical students.