Poster Presentation ESA-SRB Conference 2015

Desmopressin, Oxytocin and a Failing Heart (#254)

Kharis Burns 1 2 , David Chipps 1 2
  1. Department of Diabetes and Endocrinology, Westmead Hospital, Westmead, NSW, Australia
  2. University of Sydney, Sydney, NSW, Australia

A 27-year old female G2P1 presented at 33 weeks gestation with dyspnoea and peripheral oedema. Her past history consisted of diabetes insipidus (DI), thought to be nephrogenic, diagnosed at age 7, and obesity with a prepregnancy BMI of 53kg/m2. Her mother, brother, uncle and 2 cousins were also affected by DI. She had not any endocrine review since childhood, and had maintained fluid balance by drinking 10L/day. She had not noticed any change in her fluid input or output during pregnancy.

Following admission, investigations revealed a dilated cardiomyopathy (LVEF 28%), and a 2000ml/day fluid restriction was advised, posing a significant risk of dehydration and hypernatraemia given her unrestrained polyuria (>4.5L/day). A modified water deprivation test was performed with failure to adequately concentrate the urine at 4 hours, despite hyperosmolality (table 1). However, the urine osmolality increased following administration of desmopressin 1mcg. Subcutaneous desmopressin (1mcg bd) was commenced, allowing a modified fluid restriction to 3L daily with maintenance of normal serum sodium levels and stable fluid balance.

The patient developed acute pulmonary oedema and frusemide was commenced. Desmopressin was continued. Due to acute cardiac deterioration with SVT requiring adenosine, lower segment caesarean section (LSCS) was recommended at 37/40. Oxytocin was administered intraoperatively, but was not associated with any excess antidiuretic effect (such as might occur with normal vasopressin responsiveness). Her newborn, however was noted to be hypernatraemic (Na 146-148mmol/L), with serum osmolality 320mOsm/L and urine osmolality 100mOsm/L suggestive of DI, and consistent with an autosomal dominant trait.

This patient’s management raised several challenges: the diagnosis of DI in pregnancy and the risks of dehydration; the response to vasopressin in nephrogenic DI; the need for fluid restriction in the presence of unrestrained polyuria; the potential impact of oxytocin on renal salt and water metabolism in nephrogenic DI. 1,2

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  1. Joo KW, Jeon US, Kim GH, et al. Antidiuretic action of oxytocin is associated with increased urinary excretion of aquaporin-2. Nephrol Dial Transplant 2004;19:2480-6.
  2. Moeller HB, Rittig S, RA F. Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment. Endocrine Reviews 2013;34:278-301.
  3. HA T. Biochemical tests in pregnancy. Medical Journal of Australia 2005;28.