SAT-072 Recurrent Hypokalemic Paralysis: A Case of Delayed Diagnosis of Primary Hyperaldosteronism

Introduction: Acute hypokalemic paralysis is a relatively rare, potentially life threatening but treatable cause of acute myopathy. Rapid diagnosis with appropriate treatment is critical. Herein, we present a case of hypokalemic paralysis due to primary hyperaldosteronism. Case report: A 54-year-old Caucasian male with history of HIV on Genvoya (elvitegravir/cobicistat/emtricitabine/tenofovir), well controlled HTN on Amlodipine 10 mg and Valsartan 160 mg daily, and pre-diabetes presented to hospital with muscle twitching followed by acute flaccid paralysis of legs. He denied having nausea, vomiting, diarrhea or the use of laxative, diuretics and licorice. No predisposing factors for paralysis were present and there was no family history of periodic paralysis. Over the last 6 months prior to presentation, he had multiple such episodes of generalized weakness and losing the ability to stand up, which typically lasted for few minutes to hours and resolved spontaneously. He had experienced two episodes of pre-syncope. He had multiple ER visits for these episodes, he was started on potassium chloride (unknown dose), but the cause for hypokalemia was not investigated. At presentation, his vitals were stable. Physical exam was significant for generalized decrease in muscle strength (4/5 in all extremities). His laboratory tests revealed: hypokalemia of 2.4 mmol/L (n.3.5-5.1) and alkalosis with bicarbonate of 36mmol/L (n.22-29). Serum magnesium, TSH and cortisol level were normal. His trans-tubular potassium gradient was elevated at 8.4, and urine pH was elevated at 8.0 (n.5-7). With aggressive IV potassium chloride replacement his symptoms resolved. Endocrine investigations revealed elevated aldosterone level (PAC) 42ng/dl (n.4-31) and undetectable plasma renin activity <0.1 ng/ml/hr (n.0.2-1.6). Based on these labs, primary hyperaldosteronism was diagnosed and confirmed by saline suppression test. CT abdomen was negative for adrenal mass. Conclusion: Based on pathophysiology, hypokalemic paralysis is divided into 2 groups: hypokalemic periodic paralysis due to acute shift of potassium into cells, and hypokalemic non-periodic paralysis resulting from a large total body deficit of potassium. 25% of cases of hypokalemic paralysis are secondary to hypokalemic non-periodic paralysis associated with chronic alcoholism, diuretic use, anorexia/bulimia nervosa, renal tubular acidosis, primary hyperaldosteronism, and Gitelman syndrome. Patients with hypokalemic non-periodic paralysis require much higher doses of KCL to recover than those with hypokalemic periodic paralysis. In the setting of hypertension and hypokalemia, either diuretic induced or spontaneous, evaluation for primary hyperaldosteronism should be considered. In the setting of suppressed renin, hypokalemia and PAC > 20 ng/dL, confirmatory testing can be deferred.