Central pontine myelinolysis secondary to hypokalaemic nephrogenic diabetes insipidus.

Hdl Handle:
http://hdl.handle.net/10147/127199
Title:
Central pontine myelinolysis secondary to hypokalaemic nephrogenic diabetes insipidus.
Authors:
Davenport, C; Liew, A; Vic Lau, P; Smith, D; Thompson, C J; Kearns, G; Agha, A
Affiliation:
Academic Department of Endocrinology, Beaumont Hospital, Dublin, Ireland.
Citation:
Central pontine myelinolysis secondary to hypokalaemic nephrogenic diabetes insipidus. 2010, 47 (Pt 1):86-9 Ann. Clin. Biochem.
Journal:
Annals of clinical biochemistry
Issue Date:
Jan-2010
URI:
http://hdl.handle.net/10147/127199
DOI:
10.1258/acb.2009.009094
PubMed ID:
19940203
Abstract:
Central pontine myelinolysis (CPM) has been described in alcoholic patients and in the aftermath of rapid correction of chronic hyponatraemia. We describe a case of CPM occurring secondary to nephrogenic diabetes insipidus (DI), which developed as a consequence of severe hypokalaemia. A 63-year-old man with alcohol dependence was admitted to hospital with severe pulmonary sepsis and type 1 respiratory failure. On admission, he had euvolaemic hyponatraemia of 127 mmol/L, consistent with a syndrome of inappropriate antidiuretic hormone secondary to his pneumonia. Following admission, his plasma potassium dropped from 3.2 to a nadir of 2.3 mmol/L. Mineralocorticoid excess, ectopic adrenocorticotrophic hormone production and other causes of hypokalaemia were excluded. The hypokalaemia provoked significant hypotonic polyuria and a slow rise in plasma sodium to 161 mmol/L over several days. Plasma glucose, calcium and creatinine were normal. The polyuria did not respond to desmopressin, and subsequent correction of his polyuria and hypernatraemia after normalization of plasma potassium confirmed the diagnosis of nephrogenic DI due to hypokalaemia. The patient remained obtunded, and the clinical suspicion of osmotic demyelination was confirmed on magnetic resonance imaging. The patient remained comatose and passed away 10 days later. This is the first reported case of nephrogenic DI resulting in the development of CPM, despite a relatively slow rise in plasma sodium of less than 12 mmol/L/24 h. Coexisting alcohol abuse, hypoxaemia and hypokalaemia may have contributed significantly to the development of CPM in this patient.
Item Type:
Article
Language:
en
MeSH:
Alcoholism; Diabetes Insipidus, Nephrogenic; Humans; Hypokalemia; Male; Middle Aged; Myelinolysis, Central Pontine
ISSN:
1758-1001

Full metadata record

DC FieldValue Language
dc.contributor.authorDavenport, Cen
dc.contributor.authorLiew, Aen
dc.contributor.authorVic Lau, Pen
dc.contributor.authorSmith, Den
dc.contributor.authorThompson, C Jen
dc.contributor.authorKearns, Gen
dc.contributor.authorAgha, Aen
dc.date.accessioned2011-04-05T14:26:26Z-
dc.date.available2011-04-05T14:26:26Z-
dc.date.issued2010-01-
dc.identifier.citationCentral pontine myelinolysis secondary to hypokalaemic nephrogenic diabetes insipidus. 2010, 47 (Pt 1):86-9 Ann. Clin. Biochem.en
dc.identifier.issn1758-1001-
dc.identifier.pmid19940203-
dc.identifier.doi10.1258/acb.2009.009094-
dc.identifier.urihttp://hdl.handle.net/10147/127199-
dc.description.abstractCentral pontine myelinolysis (CPM) has been described in alcoholic patients and in the aftermath of rapid correction of chronic hyponatraemia. We describe a case of CPM occurring secondary to nephrogenic diabetes insipidus (DI), which developed as a consequence of severe hypokalaemia. A 63-year-old man with alcohol dependence was admitted to hospital with severe pulmonary sepsis and type 1 respiratory failure. On admission, he had euvolaemic hyponatraemia of 127 mmol/L, consistent with a syndrome of inappropriate antidiuretic hormone secondary to his pneumonia. Following admission, his plasma potassium dropped from 3.2 to a nadir of 2.3 mmol/L. Mineralocorticoid excess, ectopic adrenocorticotrophic hormone production and other causes of hypokalaemia were excluded. The hypokalaemia provoked significant hypotonic polyuria and a slow rise in plasma sodium to 161 mmol/L over several days. Plasma glucose, calcium and creatinine were normal. The polyuria did not respond to desmopressin, and subsequent correction of his polyuria and hypernatraemia after normalization of plasma potassium confirmed the diagnosis of nephrogenic DI due to hypokalaemia. The patient remained obtunded, and the clinical suspicion of osmotic demyelination was confirmed on magnetic resonance imaging. The patient remained comatose and passed away 10 days later. This is the first reported case of nephrogenic DI resulting in the development of CPM, despite a relatively slow rise in plasma sodium of less than 12 mmol/L/24 h. Coexisting alcohol abuse, hypoxaemia and hypokalaemia may have contributed significantly to the development of CPM in this patient.-
dc.language.isoenen
dc.subject.meshAlcoholism-
dc.subject.meshDiabetes Insipidus, Nephrogenic-
dc.subject.meshHumans-
dc.subject.meshHypokalemia-
dc.subject.meshMale-
dc.subject.meshMiddle Aged-
dc.subject.meshMyelinolysis, Central Pontine-
dc.titleCentral pontine myelinolysis secondary to hypokalaemic nephrogenic diabetes insipidus.en
dc.typeArticleen
dc.contributor.departmentAcademic Department of Endocrinology, Beaumont Hospital, Dublin, Ireland.en
dc.identifier.journalAnnals of clinical biochemistryen
dc.description.provinceLeinster-

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