Case Presentation:
28 year old male with no past medical history presented to an urgent care centre with one day history of right facial palsy which treated as Bell’s palsy with a prednisone taper. Two days later, he again presented to the ED with progressive bilateral upper and lower extremity weakness. Past medical history was significant for two similar episodes of weakness in the previous month, each lasting 2‐3 days with spontaneous resolution. On exam the patients blood pressure was 153/92 mm Hg. Neurologic exam revealed right lower motor neuron facial nerve palsy, 3/5 strength in bilateral upper and lower extremities with intact reflexes and sensations. Potassium was 1.3 mEq/liter and bicarbonate was 32 mEq/liter. CT brain and MRI brain were normal. His quadriparesis and facial weakness resolved with aggressive correction of hypokalemia. Persistent hypertension with hypokalemia and metabolic alkalosis prompted further work up of hyperaldosteronism. He had a low plasma rennin activity (0.1ug/L/hr) and normal plasma aldosterone concentration (13.6 ng/dl). Aldosterone plasma rennin ratio(APR) was 136 and elevated but aldosterone level was less than 15 ng/dl. 24 hour urine potassium and urine aldosterone were elevated. A saline suppression test revealed a persistent plasma aldosterone level >10ng/dl diagnostic of hyperaldosteronism. Adrenal vein sampling revealed right adrenal hypersecretion. CT adrenal with contrast showed a 3 x 2.6 x 3.1 cm right adrenal nodule. He underwent a robotic right adrenalectomy and biopsy showed right adrenocortical adenoma. Patient had a definitive cure and hypertension and hypokalemia completely resolved.
Discussion:
Primary hyperaldosteronism can have varied presentations with subtle findings. There have been a few reports of primary hyperaldosteronism presenting as quadriparesis. Six cases of bulbar palsy and one case of peripheral‐type facial palsy have been reported in China but to the best of our knowledge, no cases have been reported in the US. In our case, the time frame of resolution of symptoms with the correction of hypokalemia makes Bell’s palsy less likely. The right lower motor neuron facial palsy could have been related to the patient’s severe hypokalemia.
Conclusions:
Clinicians should be aware of the varied presentations of hyperaldosteronism. In patients with early onset hypertension, hypokalemia and metabolic alkalosis, hyperaldosteronism should be considered. Even in the presence of normal serum aldosterone concentration every effort should be made to rule out hyperaldosteronism and further step wise work up should be pursued. Primary hyperaldosteronism is associated with higher cardiovascular morbidity and mortality than age‐ and sex‐matched patients with essential hypertension and early diagnosis and treatment can impact patient outcomes.