Reversible electrophysiological abnormalities in hypokalemic paralysis: Case report of two cases
A 20-year-old girl with no significant past medical illness presented with flaccid are flexic quadriparesis of 2 day duration. She had bulbar and respiratory involvement in form of dysphagia and her single breath count was nine. She also had cranial nerve involvement in form of bilateral facial weakness, neck flexor weakness, and dysphagia. The power in all muscle groups was 1/5. There was no sensory loss, bladder disturbance, or higher function disturbance. She was evaluated for electrolyte abnormalities (suspecting a possible diagnosis of hypokalemic paralysis). The electrocardiography (ECG) showed U waves. Arterial blood gas analysis showed normal pH, normal partial pressures of oxygen and carbon dioxide, and normal bicarbonate levels. Simultaneously, she underwent NC study. The NC study showed significant reduction in CMAP amplitudes of all motor nerves. The distal latencies and conduction velocities were normal in the motor nerves. However, the F-waves were non recordable in all the tested motor nerves. SNAP were also normal. Based on the electrophysiological findings, an alternate diagnosis of acute motor axonal neuropathy (AMAN) form of Guillain-Barre syndrome (GBS) was also considered. In the meantime serum potassium report was available and was 1.9 mmol/L. With administration of potassium (160 meq intravenous over 24 h followed by 60 meq per day in three divided doses orally in form of potassium chloride) patient showed dramatic clinical improvement. Based on this, the original diagnosis of hypokalemic paralysis with quadriparesis with cranial nerve and respiratory involvement was confirmed. NC studies were repeated 24 h after the initial study, by which time patient's motor power was back to normal and serum potassium was 2.9 mmol/L. Repeat NC was found to be normal. The secondary causes of hypokalemia including thyrotoxicosis, renal tubular acidosis, gastrointestinal loss were ruled out (FT3-3.20 pg/mL, FT4-1.10 ng/dL, TSH − 3.80 uIU/mL, arterial pH − 7.45). The short and long duration exercise test to document channelopathy as cause of hypokalemia was planned, but patient did not give consent for the same. As no definite secondary cause of hypokalemia could be found, the patient was not put on any prophylactic therapy. The patient was advised against heavy manual labour and avoiding heavy carbohydrate meals.