Acute Stroke as a Cause for Acute Hyponatremia in a Hospitalized Patient

Introduction: Hyponatremia is a common electrolyte disturbance that affects about 35% of hospitalized patients. We are presenting a case of acute hyponatremia that developed during hospitalization. Case Description: 86-year-old woman with atrial fibrillation (AF), hypertension, HCOM s/p myomectomy, and osteoporosis was admitted for AF with RVR. She underwent a cardiac ablation and was due to be discharged home the following day. On the day of discharge she developed sudden onset Wernicke’s aphasia and a stroke code was called; she had been observed normal 15 minutes prior. Non-contrast CT head was negative for acute hemorrhage or ischemia. Labs collected at the time of the stroke code showed an acute drop in serum sodium (PNa) to 120 from 135 just 12 hours earlier. Repeat labs collected 2.5 hours later confirmed hyponatremia with a PNa of 123. Urine studies around this time showed urine sodium <20 and urine osmolality 177. She received 100cc hypertonic saline with improvement in PNa to 133 within 12 hours and resolution of symptoms, and PNa normalized to 136 by the following morning. She had increased urine output over this 12 hour period making over 4 liters of urine. To complete her workup, she underwent MRI brain which showed an acute cortical infarct in the right middle frontal gyrus. Discussion: This case demonstrates a patient who developed sudden onset severe hyponatremia due to an acute stroke. After thorough patient evaluation and chart review, there were no other apparent causes for her acute hyponatremia – she had normal intake, was not getting any hypotonic fluids, denied pain or nausea, and received no medications known to cause hyponatremia. Due to high suspicion for cardioembolic stroke due to recent AF with RVR and ablation she underwent MRI brain which confirmed an acute stroke. Hyponatremia is frequently described in patients with neurological disorders such as stroke though temporality is not always captured, and this case clearly demonstrates how rapidly hyponatremia can develop. Possible mechanisms include increased antidiuretic hormone (ADH) or brain natriuretic peptide (BNP) released in brain injury to cause SIADH or cerebral salt wasting, respectively. Interestingly this patient developed severe hyponatremia with a small infarct in a region not associated with ADH production underscoring the complexity of sodium dysregulation in neurological disorders.