This is a 75-year-old patient with a history of cholecystectomy, hallux valgus, gastric ulcer and left fifth nerve pain.
He had pain in the territory of the trigeminal area on the left side that began 4 years ago and had remained controlled with gabapentin.
In the last 18 days, pain was severe in intensity and did not respond to pharmacological treatment.
The lack of control led to an urgent admission in the Neurology Service, from where they requested collaboration to the Pain Unit.
In the anamnesis, the patient reported left frontoparietal pain radiating to the palate, with very frequent sensation of electrical discharges (about 30 days), with pain intensity VAS 9-10.
At that time, the patient was being treated with intravenous metamizole gr/24 hours) and (300 mgr/24 hours) in infusion with gabapentin (1,200 mg/8 hours) and continuous intravenous tramadol (8/8 hours) intravenously.
Nerve block of 1st and 2nd left branches of the fifth pair was performed with 0.5% bupivacaine, achieving good superficial analgesia (VAS 4), although the pain persisted in the palate.
Pharmacological treatment with oxcarbacepine 300 mg/12 hours was adjusted and buprenorphine was discontinued progressively.
After 10 days, due to the good evolution of the patient, she was discharged, then VAS 0 (without any pain in the palate).
The sodium level upon leaving the hospital was within normal limits, according to an analysis performed during admission.
Pain was controlled and in a review performed 4 months after admission the patient reported no pain crisis at that time.
At the same visit, it was found that in an analysis carried out a few days before, a sodium level of 125 mgr/dl appeared. More than a month ago, treatment with an antihypertensive drug combining an angiotensin II receptor inhibitor had started.
The patient had no symptoms attributable to hyponatremia.
Due to the suspected contribution of both hydrochlorothiazide and oxcarbacepine to hyponatremia, hydrochlorothiazide was removed, according to your bedside physician.
In an ionogram requested 15 days later, the sodium value was 143 mgr/dl, with normal potassium and chloride levels.
Two months later, the patient was admitted to the emergency department with symptoms of intense asthenia and muscle weakness and a sodium value of 120 mgr/dl. She had again begun to have poorly controlled hydrochlorothiazide for one month.
Due to the good evolution of the pain in the last months, it was decided to withdraw oxcarbacepine and leave the patient only with gabapentin to control her neuropatic pain.
At this time, the dose of hydrochlorothiazide was maintained.
Symptoms attributable to hyponatremia improved immediately upon withdrawal of oxcarbacepine.
In a new analytical requested 8 days after admission the sodium level was 140 mg/dl.
