Abstract: PO1434
Should Sodium Monitoring Be Included in Routine Prenatal Care?
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Kharadjian, Talar, University of California San Diego, La Jolla, California, United States
- Jamshidian, Mitra, University of California San Diego, La Jolla, California, United States
- Miracle, Cynthia, University of California San Diego, La Jolla, California, United States
Introduction
The American College of Obstetricians and Gynecologists does not recommend serum chemistries as part of routine prenatal care. Our case demonstrates the clinical utility in diagnosing hyponatremia prior to symptom development in mother or newborn.
Case Description
A 39-year-old pregnant female with no known prenatal issues underwent a spontaneous vaginal delivery; the infant was initially apneic and had a witnessed seizure. His initial serum sodium was 120mEq/L, and he was treated with phenobarbital and hypertonic saline. Serum sodium corrected by 4mEq/L during the first 7 hours, and increased from 120 to 133mEq/L over the first 24 hours. Brain MRI performed on day 4 demonstrated no abnormal findings.
The mother’s baseline sodium level was unavailable. She received 1L of D5LR and 1L of LR during labor. She had urinary retention following delivery and a foley catheter immediately drained 2L of urine. Her initial postpartum sodium level was 123mEq/L without associated symptoms. Urine osmolality was 64 mOsm/kg on admission. History revealed typical daily fluid consumption of 6L. Two days prior to admission, she had abruptly increased fluid intake to 13L per day in response to contractions. Twelve hours into admission, serum sodium corrected from 123 to 134 mEq/L in the setting of a relative reduction in fluid intake to 5L. Due to concern for a chronic component of hyponatremia, free water and DDAVP were given to slow the rate of correction. With the effect of DDAVP, urine concentrated to 695 mOsm/kg, illustrating the regeneration of an osmotic gradient within 30 hours.
Discussion
Primary polydipsia served as the leading driver of acute hyponatremia in this mother and infant, appropriately associated with ADH suppression. Although well-known drivers of increased ADH secretion were present, such as urinary retention and labor pain, their effects were less significant, as evidenced by very dilute urine on presentation. She was not exposed to the antidiuretic effects of oxytocin, which is an additional consideration in the peripartum period. Higher plasma volume during pregnancy and chronic polydipsia increased the mother’s propensity to develop clinically significant hyponatremia in this case. This may have been detected earlier had serum sodium testing been included in routine prenatal care.