Pituitary Apoplexy in the Setting of Oral Anticoagulation Therapy With Apixaban

Background: Several medical conditions require chronic anticoagulation, but there are potential long-term complications, including intracranial hemorrhages. Pituitary apoplexy (PA), caused by infarction or bleeding into the pituitary gland, is a rare condition that commonly occurs in the setting of a pituitary adenoma. However, several reports have shown an increased risk of PA associated with anticoagulation therapy. Recent case reports have shown that even the newer oral anticoagulants may increase the risk of PA. Typically patients present with an acute headache, visual disturbances and pituitary hormonal deficiencies. Management is controversial and includes either a conservative medical treatment versus a more aggressive surgical approach. We present a case of a PA induced by Apixaban, an orally active factor Xa inhibitor. Clinical Case: This is the case of a 45 years-old male patient with prior medical history of hyperthyroidism treated with radioiodine ablation, systolic heart failure and atrial fibrillation, receiving Apixaban for stroke risk reduction. The patient presented initially to the ER after developing an acute, pulsatile frontal headache, associated with nausea and vomiting. He was treated for a suspected acute gastroenteritis and was discharged home. Two days later the patient returned to the ER, with persistent headaches unresponsive to oral analgesics. This time, the patient also complained of decreased energy, difficulty concentrating, and memory problems. He denied visual changes, galactorrhea, decreased libido or polyuria. Vital signs were unremarkable and there was no orthostatic hypotension. Physical examination showed a male in mild distress due to pain. There were no visual field defects on confrontation, no neurological deficits, and an intact mental status. Brain imaging showed hemorrhage within the pituitary gland with associated edema, compatible with PA. There was no obvious evidence of a pre-existing pituitary adenoma. Laboratory workup did not reveal any hormonal deficiencies. The patient was managed conservatively with close neurological follow up and empiric high dose dexamethasone. Headaches improved significantly after treatment and eventually resolved. After clinical improvement, the patient was discharged home on physiologic replacement of glucocorticoids with outpatient follow up and plans for re-evaluation of hormonal axis. Conclusion: Oral anticoagulants can increase the risk of PA, even in the absence of a pre-existing pituitary adenoma, as other case reports have shown. Management is controversial, and although there are agents for reversal of Apixaban effects (recombinant factor Xa), their use in PA has not been described. This case was managed conservatively with excellent results. Although we cannot exclude a pre-existing pituitary adenoma in this patient, this case shows that Apixaban increases the risk of PA.