You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 113 No. 6, JUNE 1964 TABLE OF CONTENTS
  Archives
  •  Online Features
  ARTICLES
 This Article
 •References
 •Full text PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (56)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Acute Encephalopathy Occurring During Hemodialysis

The Reverse Urea Effect

HART deC. PETERSON, MD; AUGUST G. SWANSON, MD

Arch Intern Med. 1964;113(6):877-880.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Although hemodialysis is generally safe and effective in treating acute renal failure, symptoms of headache, agitation, and confusion occasionally develop.1 We have recently observed three patients who developed a severe encephalopathy during hemodialysis. In all three cases neurological deterioration coincided with rapid reduction of blood urea, and we postulate that the blood-brain barrier prevented a parallel and equally rapid reduction of brain urea. This produced an osmotic differential between brain and blood causing movement of water into brain with resultant water intoxication and brain swelling.

Report of Cases

CASE 1.

—A 14-year-old boy (UWH 151-157) with a three-year history of chronic renal failure was referred to the University of Washington Hospital for hemodialysis.

On admission he appeared chronically ill. Funduscopic examination revealed arteriovenous nicking, tortuous vessels, and arteriolar narrowing. He had a rachitic rosary, and his heart was enlarged to percussion. His blood pressure was 150/110 mm Hg, and . . . [Full Text PDF of this Article]


Author Affiliations

SEATTLE

Special Fellow, US Public Health Service BT-836, present address: Department of Neurology, New York Hospital, 525 E 68th St, New York (Dr. Peterson); Associate Professor of Neurology and Pediatrics, Cornell University Medical College, New York (Dr. Swanson).

From the Division of Neurology, University of Washington School of Medicine.


Footnotes

Received for publication Nov 14, 1963; accepted Dec 20.

Read before the annual meeting of the American Academy of Neurology, Minneapolis, April 26, 1963.



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1964 American Medical Association. All Rights Reserved.