| IMAGES IN ACADEMIC MEDICINE |
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| Year : 2016 | Volume
: 2
| Issue : 2 | Page : 249-252 |
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Central pontine myelinolysis: Insight into pathogenesis, in the absence of hyponatremia
Mark William Fegley1, Amitoj Singh2, Santo Longo3, Shree Gopal Sharma4, Sudip Nanda2
1 Department of Family Medicine, St. Luke's University Health Network, Bethlehem, Pennsylvania, USA
2 Department of Internal Medicine, St. Luke's University Health Network, Bethlehem, Pennsylvania, USA
3 Department of Pathology, St. Luke's University Health Network, Bethlehem, Pennsylvania, USA
4 Department of Pathology, University of Arkansas, Fayetteville, Arkansas, USA
Correspondence Address:
Sudip Nanda
Department of Internal Medicine, St. Luke's University Hospital Network, 801 Ostrum Street, Bethlehem, Pennsylvania 18015
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2455-5568.196871
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Central pontine myelinolysis (CPM) is a well-recognized iatrogenic complication of rapid correction of chronic hyponatremia. Dehydration of the brain and shrinkage of the oligodendrocyte cause separation of the myelin sheath from the axons. This damage can cause the full clinical spectrum of CPM. We report a patient with pseudohyponatremia, diabetes with hyperglycemia, hepatitis C-induced liver cirrhosis, malnutrition, and hypokalemia who developed CPM. The patient had not used insulin for 3 days during which he became hyperglycemic. After reinstitution of his insulin treatment, he developed clinical signs and radiological evidence of CPM. We review the cerebral adaptive mechanisms for the prevention of cellular shrinkage and CPM. This will help identify patient population who are at an increased risk of developing CPM in the absence of hyponatremia.
The following core competencies are addressed in this article: Patient care, medical knowledge. |
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