Hyponatremia historical perspective: Difference between revisions
Feham Tariq (talk | contribs) |
Feham Tariq (talk | contribs) |
||
Line 73: | Line 73: | ||
* In 1952, Welt and colleagues presented patients with cerebral lesions (including trauma, tumor, and infection) and severe hyponatremia with clinical dehydration but no potassium retention. | * In 1952, Welt and colleagues presented patients with cerebral lesions (including trauma, tumor, and infection) and severe hyponatremia with clinical dehydration but no potassium retention. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} |
Revision as of 16:41, 21 May 2018
Hyponatremia Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Hyponatremia historical perspective On the Web |
American Roentgen Ray Society Images of Hyponatremia historical perspective |
Risk calculators and risk factors for Hyponatremia historical perspective |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Saeedeh Kowsarnia M.D.[2] Feham Tariq, MD [3]
Overview
In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the central nervous system and renal excretion of osmotically active solutes. In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesion. In 1950, Peters, Welt, and co-workers described few patients with encephalitis, hypertensive intracranial hemorrhage, and bulbar poliomyelitis who presented with severe dehydration and hypernatremia.
Historical Perspective
The historical perspective of hypernatremia is as follows:[1][2][3][4]
Discovery
- In 1858, Claude Bernard, French physiologist first proposed a direct relationship between the central nervous system and renal excretion of osmotically active solutes.
- In 1913, Jungmann and Meyer in Germany induced polyuria and increased urinary salt excretion in animals through medullary lesion.
- in 1950, Peters, Welt, and co-workers described few patients with encephalitis, hypertensive intracranial hemorrhage, and bulbar poliomyelitis who presented with severe dehydration and hyponatremia.
- In 1952, Welt and colleagues presented patients with cerebral lesions (including trauma, tumor, and infection) and severe hyponatremia with clinical dehydration but no potassium retention.
References
- ↑ J. Barcroft & H. Straub (1910). "The secretion of urine". The Journal of physiology. 41 (3–4): 145–167. PMID 16993045. Unknown parameter
|month=
ignored (help) - ↑ Czerny, A (1935). Ergebnisse der Inneren Medizin und Kinderheilkunde : Achtundvierzigster Band. Berlin, Heidelberg: Springer Berlin Heidelberg. ISBN 9783642906701.
- ↑ J. P. PETERS, L. G. WELT, E. A. H. SIMS, J. ORLOFF & J. NEEDHAM (1950). "A salt-wasting syndrome associated with cerebral disease". Transactions of the Association of American Physicians. 63: 57–64. PMID 14855556.
- ↑ L. G. WELT, D. W. SELDIN, W. P. NELSON, W. J. GERMAN & J. P. PETERS (1952). "Role of the central nervous system in metabolism of electrolytes and water". A.M.A. archives of internal medicine. 90 (3): 355–378. PMID 14952060. Unknown parameter
|month=
ignored (help)