Central pontine myelinolysis (CPM) is often a feared complication of overly aggressive correction of hyponatremia (defined as < 135 mEq/L).1 Current guidelines1,2,3 dictate a slow correction of sodium, generally not exceeding 8-10 mEq/24 hrs to prevent CPM.1 CPM is a non-inflammatory demyelinating disease characterized by the loss of myelin in the base of the pons and carries a poor prognosis, often times resulting in death.
We present a case in which an elderly gentleman was admitted for generalized weakness, and was found to have moderate hyponatremia. Despite a gentle correction of serum sodium, with daily sodium correction not exceeding 7 mEq/L, he inadvertently developed CPM as revealed by MRI and neurological exam. This case report …show more content…
Among his many medical issues, he most notably has a history of chronic hyponatremia, chronic myeloid leukemia (CML) previously treated with Gleevec 300 mg twice daily for 9 years until 9 months ago - now in remission, polio, rheumatoid arthritis and diabetes type II.
Nine days prior to his admission, he developed sudden onset of generalized weakness, hindering his ability to ambulate and perform ADLs. He reported quickly recovering and felt well two days later (seven days before admission). Approximately a week after his initial complaint, his symptoms recurred which prompted him to go to an urgent care for evaluation. His laboratory blood work demonstrated a serum sodium of 122 mEq/L. He was highly advised to go to the emergency room at that time which he declined. Therefore, he was given a liter of normal saline at the center and was asked to return to his primary care physician for repeat blood work. One day prior to his hospital admission, he had a regular office appointment with his oncologist. Blood work was obtained and showed a serum sodium of 120 mEq/L, and he was immediately sent to the emergency room. Evaluation in the emergency room revealed profound hyponatremia with serum sodium of 120 mEq/L with a baseline of 130-135 mEq/L previously. His last measurement of serum sodium was 132 mEq/L, performed about one month before his admission. Per medical …show more content…
The use of Gleevec in high dosage has been known to be associated with SIADH4, an etiology for euvolemic, hypotonic hyponatremia. This may have contributed to the chronic hyponatremia in our patient. Our patient was also later found to have adrenal insufficiency based on the ACTH-stimulation test. Regardless of the etiology, chronic hyponatremia should be corrected with a specific limit and goal based on risk stratification (normal risk, low-to-moderate risk and high risk) of osmotic demyelination to avoid complications such as
We present a case in which an elderly gentleman was admitted for generalized weakness, and was found to have moderate hyponatremia. Despite a gentle correction of serum sodium, with daily sodium correction not exceeding 7 mEq/L, he inadvertently developed CPM as revealed by MRI and neurological exam. This case report …show more content…
Among his many medical issues, he most notably has a history of chronic hyponatremia, chronic myeloid leukemia (CML) previously treated with Gleevec 300 mg twice daily for 9 years until 9 months ago - now in remission, polio, rheumatoid arthritis and diabetes type II.
Nine days prior to his admission, he developed sudden onset of generalized weakness, hindering his ability to ambulate and perform ADLs. He reported quickly recovering and felt well two days later (seven days before admission). Approximately a week after his initial complaint, his symptoms recurred which prompted him to go to an urgent care for evaluation. His laboratory blood work demonstrated a serum sodium of 122 mEq/L. He was highly advised to go to the emergency room at that time which he declined. Therefore, he was given a liter of normal saline at the center and was asked to return to his primary care physician for repeat blood work. One day prior to his hospital admission, he had a regular office appointment with his oncologist. Blood work was obtained and showed a serum sodium of 120 mEq/L, and he was immediately sent to the emergency room. Evaluation in the emergency room revealed profound hyponatremia with serum sodium of 120 mEq/L with a baseline of 130-135 mEq/L previously. His last measurement of serum sodium was 132 mEq/L, performed about one month before his admission. Per medical …show more content…
The use of Gleevec in high dosage has been known to be associated with SIADH4, an etiology for euvolemic, hypotonic hyponatremia. This may have contributed to the chronic hyponatremia in our patient. Our patient was also later found to have adrenal insufficiency based on the ACTH-stimulation test. Regardless of the etiology, chronic hyponatremia should be corrected with a specific limit and goal based on risk stratification (normal risk, low-to-moderate risk and high risk) of osmotic demyelination to avoid complications such as