Osmotic demyelination syndrome following slow correction of hyponatremia: Possible role of hypokalemia
A 47-year-old non-alcoholic male presented to the ER with altered sensorium. One week earlier, he had been started on ofloxacin for a lower urinary infection, following which he developed oliguria and swelling of whole body. On examination, he had pedal edema, facial puffiness, and mild hypertension (146/92 mmHg). Urine examination revealed a protein 100 mg/dl, 18-20 WBC, and 2-4 RBC per HPF. Serum creatinine was 1.8 mg/dl, and a diagnosis of drug-induced interstitial nephritis was made. Furosemide (60 mg daily) was prescribed. A history of jaundice, diabetes, uremia, or trauma was denied.\nOn examination, the patient was an average-built man in grade 2-3 encephalopathy without any localizing neurological deficits. Rest of the general physical and systemic examination was normal. CBC was normal. Serum urea was 48 mg/dl (normal 10-38) and the creatinine 1.6 mg/dl (normal 0.6-1.2). Serum sodium was 94 mmol/l (normal 135-145), serum potassium 2.5 mmol/l (normal 3.5-5.3), and the chloride 105 mmol/l (normal 98-110). The serum osmolality was 238 mOsm/kg (normal 285-295) with a urine osmolality 292 mOsm/kg. Spot urinary sodium was <10 mmol/l (normal >20). ABG analysis and rest of serum biochemistry was normal. The patient was started on 3% NaCl till the sodium level reached 120, when 3% saline was replaced with 0.9 N saline. Correction was given at a rate not exceeding 8 mmol/l day, and serum sodium of 135 was achieved over a period of 8 days. Simultaneously, serum potassium levels were corrected with intravenous potassium chloride []. The patient's consciousness improved dramatically but only to deteriorate again after a period of 72 hours with steady deterioration over 24 hours till his speech became incomprehensible and he developed quadriparesis. Neurological examination revealed generalized spastic quadriparesis, mutism and inability to swallow, characteristic of a pseudobulbar state with spontaneous eye opening consistent with the diagnosis of locked-in-syndrome. MRI of the brain revealed symmetrical areas of altered signal intensity in the pons and basal ganglia, being hypointense on T1-weighted imaging [] and hyperintense on T2-weighted imaging [Figures and ]. The involved areas were also hyperintense on a fluid inversion recovery (FLAIR) images [], suggesting a diagnosis of pontine and extrapontine myelinolysis. The patient received supportive treatment for about a month when he succumbed to intercurrent sepsis.