Uncommon dyselectrolytemia complicating Guillain–Barré syndrome
A 41-year-old male presented with rapidly progressive symmetrical predominantly proximal quadriparesis of 4 days duration with tingling paresthesiae in limbs for 2 days. Productive cough for 2 days without fever occurred 1 week earlier. There was no history of alcohol consumption or exposure to drugs, bites, stings, and inoculations. He had no past history of similar symptoms, muscle aches, or thyroid dysfunction. There was no family history of neuromuscular diseases.\nHeart rate was 88 beats/minute and blood pressure was 130/80 mmHg without respiratory insufficiency. He was awake, alert with symmetrical proximal muscle weakness (shoulders 2/5, elbow and lower limbs 4/5, wrist and fingers 5/5 by Medical Research Council [MRC] grading). There was mild weakness in the intrinsic hand muscles. Sensations, cranial and neck muscles were normal; muscle stretch reflexes sluggish and plantars flexor.\nThe serum potassium was 2.6 mEq/L, magnesium 1.7 mg/dL with mild metabolic alkalosis. Serum creatinine kinase (CK) was normal. Quadriparesis remained unchanged despite correction of hypokalemia to 4.0 mEq/L over 12 hours at which time nerve conduction studies (NCS) revealed increased distal motor latencies, partial conduction block along with nonlength-dependent reduction of amplitudes []. Lumbar cerebrospinal fluid (CSF) revealed albuminocytological dissociation with 250 mg/dl protein and 20 cells/mm3 (lymphocytes 75%, polymorphs 25%).\nQuadriparesis progressed with appearance of asymmetric lower motor neuron facial weakness and on fourth hospital day he required mechanical ventilation. Plasmapheresis was initiated on the third hospital day with 10 L removed over the next 9 days. Serum potassium and magnesium levels declined despite oral and parenteral supplements. Although patient could be weaned from ventilator after 12 days with moderate improvement of quadriparesis, he continued to have persistent hypotension and bradycardia requiring vasopressor support. The serum cortisol, thyroid hormones, CK-MB, echocardiography, and abdominopelvic imaging by ultrasound and contrast enhanced computerized tomography were normal.\nRepeat nerve conductions before discharge revealed persistence of the abnormalities with increase in the latencies along with persistent dyselectrolytemia []. At discharge 42 days after admission, the muscle power was 4/5 and he walked with minimal assistance. He was discharged on potassium supplements, spiranolactone, and dietary modification for hypomagnesemia. During follow-up the weakness completely recovered by 4 months. At the last follow-up 30 months after discharge, patient has persistent hypomagnesemia (1.5 mg/dl) with hypocalciuria (90 mg/day; normal 100-300 mg/day). Nerve conductions revealed significant improvement of distal latencies, amplitudes, and conduction velocities at 18 months []. Serum magnesium and potassium levels in his siblings were normal.