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.