Central Pontine Myelinolysis is often a feared complication of overly aggressive correction of hyponatremia. As a result, close monitoring and slow correction are desired in order to avoid too rapid increase in serum sodium. We describe a case in which an elderly gentleman, with a past medical history of CML and Polio, who was admitted to our hospital for generalized weakness, likely secondary to hyponatremia (120 mmol/L) caused by SIADH, was found to have Central Pontine Myelinolysis. Even though the patient was closely monitored by the Nephrology team with gentle correction of serum sodium via free water restriction, normal saline drip, fludrocortisone and salt tablet with daily sodium correction not exceeding 7 mmol/L, he inadvertently…show more content… Nine days before his admission to the hospital, he developed sudden onset of weakness and had extremely poor mobility that he required help to utilize the bathroom. He also required increasing assistance in ambulation. He stated that he quickly recovered and was well 2 days later. However, at a follow-up outpatient appointment with his primary care physician, his laboratory blood work showed that he had a serum sodium of 122 mmol/L. He was advised to go to the emergency room, but he declined. He was given a liter of normal saline instead. He returned to his primary care physician for blood work subsequently, and had a serum sodium of 120 mmol/L, and was sent to our emergency room for work-up of his hyponatremia. He was consequently admitted to the hospital. He was found to have hyponatremia (120 mmol/L with a baseline of 130-135 mmol/L according to the medical records from his primary care physician office). He had a past medical history of Chronic Myeloid Leukemia (CML), Polio, Rheumatoid Arthritis, Diabetes Type II and Coronary Artery Disease. He was in remission with his CML and was not being treated with…show more content… He was transferred to the ICU with a diagnosis of pneumonia. His chest x-ray revealed the finding of bilateral lower lung infiltrates, while a computed tomography angiography (CTA) showed no evidence of pulmonary embolism. The etiology of his pneumonia was mostly likely due to mucous plug that could not be cleared by the patient on his own. During his stay in the ICU, the patient continued to be on mechanical ventilation and had been treated with on DuoNeb and antibiotics (including doxycycline, vancomycin and ceftriaxone). Under the guidance of our Nephrology team, his fludrocortisone and salt tablet were slowly tapered off when the serum sodium reached around 140 mmol/L. He was maintained on normal saline, and his mean-arterial-blood pressure (MAP) was kept above 75 mmHg on average. During his stay in ICU, the patient was found to develop right-sided heart failure and oliguric AKI likely secondary to pre-renal hypo-perfusion with episodes of hypotension at night. A transtracheal echocardiogram was done on day 7 and day 13, which showed an ventricular ejection fraction of 60% and severe ventricular pressure and volume overload. In addition, the Creatinine reached 1.77 mg/dL on day 10 with an admission baseline of 0.70 mg/dL. D5W was started on day 8 along with furosemide diuresis to manage the CHF. His hyponatremia was corrected to a normal value of 140 mmol/L on day
