Background In severe hyperkalemia, neurologic symptoms are described more rarely than cardiac manifestations. We report a clinical case; present a systematic review of available literature on secondary hyperkalemic paralysis (SHP); and also discuss pathogenesis, clinical effects, and therapeutic options. Case Report A 75-year-old woman presented to the emergency department complaining of tetraparesis. Her serum potassium level was 11.4 mEq/L. Electrocardiogram (ECG) showed a pacemaker (PMK)-induced rhythm, with loss of atrial capture and wide QRS complexes. After emergency treatment to restore cell membrane potential threshold and lower serum potassium, neurologic and ECG signs completely disappeared. An acute myocardial infarction subsequently occurred, possibly linked to tachycardia induced by salbutamol therapy. We reviewed 99 articles (119 patients). Mean serum potassium was 8.8 mEq/L. In most cases, ECG showed the presence of tall T waves; loss of PMK atrial capture was documented in 5 patients. In 94 patients, flaccid paralysis was described and in 25, severe muscular weakness; in 65 patients, these findings were associated with other symptoms. Concurrent renal failure was often documented. The most frequent treatments were dialysis and infusion of insulin and glucose. Eighty-seven percent of patients had complete resolution of symptoms. Why Should an Emergency Physician Be Aware of This? Severe hyperkalemia is always a life-threatening medical emergency, as it can precipitate fatal dysrhythmias and paralysis. SHP should be considered in the differential diagnosis of neurologic signs and symptoms of uncertain etiology, especially in a subject with kidney failure or who is taking medications that may worsen renal function. The presence of a PMK does not necessarily impede hyperkalemic cardiac toxicity.
