Literature DB >> 3399069

Central pontine myelinolysis in severely burned patients: relationship to serum hyperosmolality.

A C McKee1, M D Winkelman, B Q Banker.   

Abstract

The rapid correction or over-correction of hyponatremia is believed by many to be the crucial factor in the causation of central pontine myelinolysis (CPM). Over a 17-year period we found CPM in 10 (7%) of the 139 burn patients examined postmortem but in only 10 (0.28%) of the 3,528 patients in the general autopsy population (p less than 0.001). Each of the burn patients with CPM had suffered a prolonged, nonterminal episode of extreme serum hyperosmolality, whereas most burn patients without CPM had not suffered such an episode. The histologic age of the lesions correlated with the duration of time between the hyperosmolar episode and death. Hypernatremia, hyperglycemia, and azotemia, alone or combined, accounted for the hyperosmolality. No single electrolyte or metabolic derangement was essential, as in at least one burn patient with CPM the serum sodium, glucose, or blood urea nitrogen was normal during the hyperosmolar episode. Hyponatremia was not present in any burn patient with CPM. We conclude that severely burned patients, like alcoholics, are especially susceptible to CPM, and that in burn patients with CPM there is a striking association with serum hyperosmolality. The data also suggest that the rapid correction of hyponatremia exerts its effects by causing an osmotic shift and not because of any specific property of the sodium ion.

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Year:  1988        PMID: 3399069     DOI: 10.1212/wnl.38.8.1211

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


  24 in total

1.  Osmotic shifts, metabolic compromise, and the vulnerability of the pons.

Authors:  A C McKee
Journal:  West J Med       Date:  1992-11

2.  Diffuse demyelinating lesions of the brain after the rapid development of hypernatremia.

Authors:  W R Clark
Journal:  West J Med       Date:  1992-11

3.  Central pontine myelinolysis in a patient with AIDS.

Authors:  A H Holmes; M Esiri; C S Morris; A Edwards
Journal:  J Neurol Neurosurg Psychiatry       Date:  1992-07       Impact factor: 10.154

4.  Central pontine myelinolysis in a patient with hyperosmolar hyperglycemia and consistently normal serum sodium.

Authors:  Joseph D Burns; Steven C Kosa; Eelco F M Wijdicks
Journal:  Neurocrit Care       Date:  2009-06-30       Impact factor: 3.210

5.  Central pontine myelinolysis: historical and mechanistic considerations.

Authors:  Michael D Norenberg
Journal:  Metab Brain Dis       Date:  2010-02-25       Impact factor: 3.584

6.  Postoperative diabetes insipidus.

Authors: 
Journal:  BMJ       Date:  1989-02-18

7.  Central pontine myelinolysis and poorly controlled diabetes: MRI's hints for pathogenesis.

Authors:  Antonio Fasano; Francesco Cavallieri; Jessica Mandrioli; Annalisa Chiari; Paolo Nichelli
Journal:  Neurol Sci       Date:  2017-09-15       Impact factor: 3.307

8.  Decreased diffusion in central pontine myelinolysis.

Authors:  S C Cramer; K C Stegbauer; A Schneider; J Mukai; K R Maravilla
Journal:  AJNR Am J Neuroradiol       Date:  2001-09       Impact factor: 3.825

9.  Central pontine myelinolysis: a rare presentation secondary to hyperglycaemia.

Authors:  Monica Saini; Marlie Jane Mamauag; Rajinder Singh
Journal:  Singapore Med J       Date:  2015-04       Impact factor: 1.858

10.  Role of organic osmolytes in myelinolysis. A topographic study in rats after rapid correction of hyponatremia.

Authors:  Y H Lien
Journal:  J Clin Invest       Date:  1995-04       Impact factor: 14.808

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