Severe hyponatremia is rare when carbamazepine is used as monotherapy [
6], however if it does develop, it is most common in the first 3 months [
7], with a median onset of 38.5 days [
8]. Our patient had been on carbamazepine therapy for less than 30 days. The reason for her being prescribed carbamazepine is unknown, but most likely secondary to chronic pain. Our patient increased the dose herself to twice the originally prescribed amount; this might have prompted the exacerbation of the sodium imbalance, even though baseline sodium levels were not recorded. Several risk factors have been associated with the development of carbamazepine-induced SIADH, such as female sex, being over 40 years of age, use of other medications known to cause hyponatremia, menstruation, psychiatric condition, surgery, psychogenic polydipsia, low baseline serum Na
+ levels, and hypothyrodism [
3,
4,
7,
8]. In this case, our patient’s only risk factors were age above 40 years and female sex. It is unknown if KTW syndrome is a risk factor for SIADH or hyponatremia due to the rarity of this pathology. The only major symptom our patient showed was fatigue. Other factors have been attributed to the lack of symptoms in cases of slowly developing hyponatremia, as decreased uptake of taurine aims to adapt to the decrease in extracellular osmolality [
9]. In the work by Pliquett
et al. [
9], some of the symptoms in patients with moderate hyponatremia include headache and modest nausea. Our patient failed to show these symptoms, which can be attributed to her young age and the few risk factors she presented with, but if many more cases are reported, fatigue may be added to this list and can be one sign to look for hyponatremia in patients prescribed with carbamazepine. Treatment of this pathology includes fluid restriction and management of the underlying cause [
10]. The use of demeclocycline and lithium is not recommended due to the increased risk of harm versus the benefits of treatment [
11]. Our patient showed good response to management with fluid restriction and discontinuation of carbamazepine therapy. Predictors of poor response to therapy are serum osmolality > 500 mmol per kg, 24 hour urine output > 1.5 L, increase of > 2 mmol of serum Na
+ in 24 hours, and a serum Na
+ level less than the sum of UNa
+ and K
+ levels [
12]. Our patient only presented with the poor response predictor of serum Na
+ levels of 119 mmol/L, which was still less than the sum of UNa
+ and K
+ levels, but fortunately for our patient, she responded well to therapy. We did not request cerebral imaging studies due to the lack of neurologic symptoms and the lack of pertinent history of trauma or a psychiatric condition.