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Polydipsia and Ureteral Obstruction Causing Hyponatremic Acute Encephalopathy
Abstract Number: RF5BH-68
Abstract Type: Case Report Case Series
Maternal hyponatremia quickly affects the fetus since, “placental homeostasis determines electrolytes equilibrium between mother and fetus”1. There are few reports of severe maternal hyponatremia presenting as neonatal seizure.1,2 We present a unique case of polydipsia during labor and urinary tract obstruction from a large fetus resulting in maternal encephalopathy and neonatal seizure.
A 29-year-old G1P0 at term presented to labor and delivery after failed home delivery with a midwife. Labor duration was 16 hours with ruptured membranes and 4 hours of active pushing. She appeared exhausted on arrival and barely responded to questions. Pre-delivery catheterization drained < 50 mL of urine. Forceps-assisted vaginal delivery of a 4965g viable infant was complicated by shoulder dystocia and postpartum hemorrhage of 1L. She underwent laceration repair in the operating room where 1 L of urine was drained. Light sedation was discontinued when she became unresponsive to verbal and tactile stimulation. Vital signs were normal, and labs resulted in normal glucose and hemoglobin of 9.4 g/dL. Unresponsiveness was presumed to be from exhaustion. An hour after surgery, the patient became combative and tachycardic. It was reported that her newborn seized in the setting of a sodium of 114 mEq/L. Maternal labs were significant for hyponatremia at 124 mEq/L and a lactate of 11.0 mmol/L. Retroactive testing of the OR sample revealed a sodium level of 116 mEq/L. A CT scan showed a dilated bladder with hydroureteronephrosis. Placement of a catheter drained copious urine. She was transferred to intensive care for treatment of sepsis from endometritis and hypervolemic hyponatremia. It was discovered that she had consumed several liters of water with electrolyte additive during labor but had not urinated. Her hyponatremia autocorrected over several hours and encephalopathy resolved with no memory of delivery. Hyponatremia was presumed to be due to polydipsia during labor with hypervolemia developing from urinary tract obstruction from her large fetus.
In one study, 26% of mothers who consumed > 2500 mL of fluids during labor were hyponatremic at a sodium ≤ 130 mEq/L after delivery.3 Several case reports describe ureteral obstruction by the uterus during pregnancy.4,5 This case illustrates the unique combination of polydipsia during labor leading to severe hyponatremia with ureteral obstruction by a large fetus causing hypervolemia. As fluid intake during labor becomes more common, intake and output should be noted so that electrolyte imbalances may be anticipated.
1. Valerio, E., et al. (2015) Maternal Health, Neonatology, and Perinatology, 1:25
2. West, C.R. & Harding, J.E. (2004) Journal of Paediatric Child Health 40(12): 709-710.
3. Moen, V. et al. (2009) BJOG 116: 552-561.
4. Brandes, J.C. & Fritsche, C. (1991) American Journal of Kidney Diseases 18(3): 398-401
5. Irani, M. et al. (2016) J Obstet Gynaecol Res 42(6): 734-737