Case Presentation:
A 29-year old primigravida at 39.1 weeks gestation presented in spontaneous labor. The patient had no significant past medical history except for gestational diabetes, which was controlled with diet. The patient had an uncomplicated antenatal course and followed routinely with a midwife. The patient was interested in in-home delivery with the assistance of her midwife. While the patient was in the first stage of active labor, she began to have a tonic-clonic seizure which prompted the midwife to call 911 and take the patient to the hospital. At the hospital, initial vital signs were HR 98, BP 126/70, Temp 98.9, RR 20. Physical examination showed an alert but lethargic gravida woman. The physical exam was unremarkable, except for tachycardia and a physiologic murmur. vaginal examination showed that she was completely effaced and dilated. Given that she was on the second stage of labor, the decision was made to have a vacuum-assisted vaginal delivery.  The patient was placed on the delivery table in the operating-room in case an emergent c-section was required. During the labor, the patient seized for approximately one minute. She was immediately given Ativan 2mg IV and Magnesium Sulfate 2g IV. Urgent investigations were ordered including urinalysis, basic metabolic panel, and complete blood count. Approximately four minutes later she delivered a baby boy, but while she during suturing, she had another episode of a tonic clinic seizure, also lasting approximately a minute. An additional Ativan 2mg IV was given.
The urinalysis was remarkable for a few RBC’s and low urine gravity. Urine Osmolality was 87 mosm/Kg and urine sodium was 19 mmol/L. The basic metabolic panel showed a potassium of 3.6 mmol/L, sodium concentration of 115 mmol/l, serum osmolality of 256 mosm/kg, and blood sugar of 92 mg/dL.  Furthermore, a CT scan was negative for any acute intracranial abnormality. A baby boy was delivered with hyponatremia, with a plasma sodium concentration of 117 mmol/L. These clinical symptoms and laboratory were suggestive for severe hyponatremia due to polydipsia leading to multiple episodes of seizure.
After determining the hyponatremia was the cause of the patient’s seizures, the patient was given 100ml of 3% normal saline as an IV bolus, followed by a continuous rate of 2 mmol/L. Sodium levels were measured every 6 hours. Over the next three days, the patient remained seizure free and her sodium level improved to 129mmol/L. She began to follow commands intermittently but still remained lethargic. On Day 4 the patient became more alert and she was oriented to place and person but not time or situation.  She was transferred out of the MICU on Day 5 and soon thereafter discharged from the hospital.