Hyperkalemia: A rare cause of acute flaccid quadriparesis
A 73-year-old diabetic, hypertensive and hypothyroid female presented with the complaints of rapidly progressive ascending paraparesis, progressing to AFQ in about 10 h. She woke up with bilateral lower limb weakness with gradual inability to move upper limbs and had developed difficulty in breathing by the time she presented to the hospital. She was on glimipride, metformin, thyroxine, atenolol, ramipril and spironolactone. There was no other significant history.\nOn admission, she was conscious and oriented. Her pulse rate, blood pressure, respiratory rate and temperature were 72/min, 124/60 mmHg, 20/min and 98°F, respectively. Her oxygen saturation was 93% on room air. Neurological evaluation revealed normal pupils, symmetrical normal bulk and hypotonia in all limbs. Upper limbs had proximal and distal power of 4/5. In lower limbs, proximal and distal power was 2/5 with no sensory deficit. Deep tendon reflexes were absent. Bilaterally the plantar reflexes were mute. There were no lateralizing signs and the cranial nerves were normal. Other systemic examination was unremarkable. A clinical diagnosis of acute inflammatory demyelinating polyneuropathy was made. Arterial blood gas mixed primary metabolic and the respiratory acidosis and initial serum potassium level was 9.1 mmol/L. Other laboratory tests were normal. Electrocardiograph [] showed tall T wave in anterior and lateral leads.\nRaised potassium levels raised the possibility of hyperkalemia induced AFQ. Urgent antihyperkalemic measures in the form of calcium gluconate, insulin dextrose solution, furosemide, beta-2 agonist nebulization and calcium polystyrene sulfonate (K-bind) with sorbitol, were instituted. Patient required non-invasive ventilation (NIV) support for type-2 respiratory failure. Hemodialysis was not required as she had a good urine output and serum potassium levels showed steady decline. Serial declining level of K+: 9.1, 8.6, 7.1, 6.1, 4.4 was accompanied by improving power and resulted in weaning of ventilatory support within 48 h.\nA nerve conduction velocity (NCV) study on day 1 was suggestive of demyelination. Subsequent NCV on day 4 was normal. She was shifted to the ward on day 4 by which time her biochemical parameters were normal. Electrocardiography on day 2 [] showed normal T wave in anterior and lateral leads.