Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Object: The purpose of this study was to evaluate the extent and timing of impairment of cerebral pressure autoregulation after severe head injury.
Methods: In a prospective study of 122 patients with severe head trauma (median Glasgow Coma Scale Score 6), dynamic tests of pressure autoregulation were performed every 12 hours during the first 5 days postinjury and daily during the next 5 days. The autoregulatory index ([ARI] normal value 5 +/- 1.1) was calculated for each test. The changes in the ARI over time were examined and compared with other physiological variables. The ARI averaged 2.8 +/- 1.9 during the first 12 hours postinjury, and continued to decrease to a nadir of 1.7 +/- 1.1 at 36 to 48 hours postinjury. At this nadir, in 87% of the patients the value was less than 2.8. This continued deterioration in the ARI during the first 36 to 48 hours postinjury occurred despite an increase in cerebral blood flow ([CBF], p < 0.05) and in middle cerebral artery blood flow velocity ([BFV], p < 0.001), and could not be explained by changes in cerebral perfusion pressure, end-tidal CO2, or cerebral metabolic rate of O2. A marked decrease in cerebrovascular resistance ([CVR], p < 0.001) accompanied this deterioration in the ARI. Patients with a relatively higher BFV on Day 1 had a lower CVR (p < 0.05) and more impaired pressure autoregulation than those with a lower BFV.
Conclusions: The inability of cerebral vessels to regulate CBF normally may play a role in the vulnerability of the injured brain to secondary ischemic insults. These studies indicate that this vulnerability continues and even increases beyond the first 24 hours postinjury. Local factors affecting cerebrovascular tone may be responsible for these findings.
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Source |
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http://dx.doi.org/10.3171/jns.2002.97.5.1054 | DOI Listing |
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