Primary Hyperaldosteronism From Adrenocortical Adenoma Presenting as Seizures and Stroke

Abstract

Background: Primary hyperaldosteronism, which is unregulated secretion of aldosterone from the adrenal gland, is a common cause of resistant hypertension. Hyperaldosteronism can lead to life threatening cardiovascular and neurological complications emphasizing the crucial need for timely identification and management. We present a case of a young patient who suffered complications as a result of primary hyperaldosteronism. Clinical Case: A 35 year old female with a past medical history of resistant hypertension on four anti-hypertensive medications, primary hyperaldosteronism with known adenoma, CKD stage III, and hyperlipidemia presented to the hospital due to multiple seizures. She was found to be encephalopathic and required intubation for respiratory failure. Her systolic blood pressure was elevated to 250 mmhg. CT scan of the head showed a small left temporal hemorrhage and an MRI brain was revealing of bilateral thalamic infarcts. No neurosurgical intervention, antiplatelet or anticoagulation was recommended. She was admitted to the ICU and started on nitroprusside infusion. CT scan of the abdomen showed a 17 mm right adrenal nodule unchanged from prior imaging. Due to concern for pheochromocytoma, she was started on alpha blockade and subsequently beta blockade therapy. After stabilization of patient’s blood pressure, extubation, and improvement in mental status, she was discharged on new anti-hypertensive medications including spironolactone given her hypokalemia. Further endocrine evaluation was pursued. Work up included urine and plasma catecholamines which were not indicative of pheochromocytoma. Morning cortisol level was within normal limits. Plasma aldosterone level was 30, plasma renin was 0.90 with an aldosterone/renin ratio of 33 suggestive of primary hyperaldosteronism. Though the patient had known primary hyperaldosteronism with an adenoma, she had poor follow up and did not comply with initial recommendation of surgical removal of adenoma prior to her stroke. After medical stabilization following her stroke, a laparoscopic right adrenalectomy was performed. Pathology showed an adrenal cortical adenoma with no evidence of pheochromocytoma. Post-surgical systolic blood pressures were less than 120 mmhg. She was able to come off of spironolactone with plans to gradually discontinue other antihypertensive medications. Conclusion: This case emphasizes the importance of testing for primary hyperaldosteronism particularly in young patients with resistant hypertension. Furthermore, primary hyperaldosteronism should be considered as an underlying etiology for young patients who suffer from strokes particularly in the setting of hypertension. Given the reversibility of primary aldosteronism from an adrenocortical adenoma with surgery, life threatening complications such as cerebrovascular accidents can be prevented.