Energy expenditure and withdrawal of sedation in severe head-injured patients
OBJECTIVESTo determine the outcome of oxygen consumption (Vo2) and energy expenditure after cessation of sedation in severe head-injured patients and to assess its usefulness as a predictor of neurologic severity. DESIGNProspective, descriptive study. SETTINGNeurosurgical intensive care unit (ICU) i...
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| Veröffentlicht in: | Critical care medicine 1994-07, Vol.22 (7), p.1114-1119 |
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| creator | BRUDER, NICOLAS LASSEGUE, DESIRE PELISSIER, DANIEL GRAZIANI, NOEL FRANCOIS, GEORGES |
| description | OBJECTIVESTo determine the outcome of oxygen consumption (Vo2) and energy expenditure after cessation of sedation in severe head-injured patients and to assess its usefulness as a predictor of neurologic severity.
DESIGNProspective, descriptive study.
SETTINGNeurosurgical intensive care unit (ICU) in a university hospital.
PATIENTSFifteen severe head-injured patients with tracheostomies and who were mechanically ventilated and sedated at the time of the study.
INTERVENTIONSNone.
MEASUREMENTS AND MAIN RESULTSVo2 and energy expenditure were measured, using indirect calorimetry during and after discontinuation of sedation. After the measurement period, the patients were divided into two groups. Group 1 included patients who were completely weaned from sedation; group 2 included patients who had to be sedated again using predetermined criteria. In both groups, energy expenditure was close to basal energy expenditure during sedation, and increased to 150% of basal energy expenditure during the recovery period, with maximum hourly values 80% above basal energy expenditure. In group 1, Vo2 and energy expenditure changed from 284 ± 44 mL/min and 1833 ± 261 kcal/day during sedation to 390 ± 85 mL/min and 2512 ± 486 kcal/day for the period without sedation. During this period, there was a significant correlation between Vo2 and mean arterial pressure. For the recovery period, there was no difference in mean or maximum Vo2 between the two groups of patients. At 24 and 48 hrs after cessation of sedation, Vo2 and energy expenditure decreased to 30% above basal energy expenditure. These changes may be due to the recovery of muscular activity, weaning from mechanical ventilation, or an increase in the amount of circulating catecholamines.
CONCLUSIONIn severe head-injured patients, during the first 12 hrs after the discontinuation of sedation, the patients experienced a large increase in Vo2, energy expenditure, and mean arterial pressure. Although these changes have no prognostic value in our study, they have potential deleterious effects in head-injured patients. Methods that blunt these changes which have proven efficacious in anesthesia may be effective for intensive care patients. (Crit Care Med 1994; 22:1114–1119) |
| doi_str_mv | 10.1097/00003246-199407000-00011 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1097_00003246_199407000_00011</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>8026200</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3841-5e1df790bfb0e17065729bbea57bb23d0659ed7d261cf308e86d67b4ca775fa73</originalsourceid><addsrcrecordid>eNp1kTtPwzAUhS0EKqXwE5A8sAb8ShyPqCoPCcQCs2XHNzQldSI7JfTfY2jphiXrPs45Hj4jhCm5pkTJG5IOZ6LIqFKCyDRl6VJ6hKY052lgih-jKSGKZFwoforOYlwlh8gln6BJSVjBCJmi54WH8L7F8NWDd82wCYCNd3hshqULZjQt7mocwZmh6TxufOo_IZmWYFzW-FUKONwnFfwQz9FJbdoIF_s6Q293i9f5Q_b0cv84v33KKl4KmuVAXS0VsbUlQCUpcsmUtWByaS3jLi0UOOlYQauakxLKwhXSispImddG8hkqd-9WoYsxQK370KxN2GpK9A8g_QdIHwDpX0ApermL9hu7BncI7okk_Wqvm1iZtg7GV0082ARlRcFYsomdbezaAUL8aDcjBJ2otMNS__c9_BsX6n19</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Energy expenditure and withdrawal of sedation in severe head-injured patients</title><source>MEDLINE</source><source>Journals@Ovid Complete</source><creator>BRUDER, NICOLAS ; LASSEGUE, DESIRE ; PELISSIER, DANIEL ; GRAZIANI, NOEL ; FRANCOIS, GEORGES</creator><creatorcontrib>BRUDER, NICOLAS ; LASSEGUE, DESIRE ; PELISSIER, DANIEL ; GRAZIANI, NOEL ; FRANCOIS, GEORGES</creatorcontrib><description>OBJECTIVESTo determine the outcome of oxygen consumption (Vo2) and energy expenditure after cessation of sedation in severe head-injured patients and to assess its usefulness as a predictor of neurologic severity.
DESIGNProspective, descriptive study.
SETTINGNeurosurgical intensive care unit (ICU) in a university hospital.
PATIENTSFifteen severe head-injured patients with tracheostomies and who were mechanically ventilated and sedated at the time of the study.
INTERVENTIONSNone.
MEASUREMENTS AND MAIN RESULTSVo2 and energy expenditure were measured, using indirect calorimetry during and after discontinuation of sedation. After the measurement period, the patients were divided into two groups. Group 1 included patients who were completely weaned from sedation; group 2 included patients who had to be sedated again using predetermined criteria. In both groups, energy expenditure was close to basal energy expenditure during sedation, and increased to 150% of basal energy expenditure during the recovery period, with maximum hourly values 80% above basal energy expenditure. In group 1, Vo2 and energy expenditure changed from 284 ± 44 mL/min and 1833 ± 261 kcal/day during sedation to 390 ± 85 mL/min and 2512 ± 486 kcal/day for the period without sedation. During this period, there was a significant correlation between Vo2 and mean arterial pressure. For the recovery period, there was no difference in mean or maximum Vo2 between the two groups of patients. At 24 and 48 hrs after cessation of sedation, Vo2 and energy expenditure decreased to 30% above basal energy expenditure. These changes may be due to the recovery of muscular activity, weaning from mechanical ventilation, or an increase in the amount of circulating catecholamines.
CONCLUSIONIn severe head-injured patients, during the first 12 hrs after the discontinuation of sedation, the patients experienced a large increase in Vo2, energy expenditure, and mean arterial pressure. Although these changes have no prognostic value in our study, they have potential deleterious effects in head-injured patients. Methods that blunt these changes which have proven efficacious in anesthesia may be effective for intensive care patients. (Crit Care Med 1994; 22:1114–1119)</description><identifier>ISSN: 0090-3493</identifier><identifier>EISSN: 1530-0293</identifier><identifier>DOI: 10.1097/00003246-199407000-00011</identifier><identifier>PMID: 8026200</identifier><identifier>CODEN: CCMDC7</identifier><language>eng</language><publisher>Hagerstown, MD: Williams & Wilkins</publisher><subject>Acute Disease ; Adult ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Biological and medical sciences ; Blood Pressure ; Craniocerebral Trauma - epidemiology ; Craniocerebral Trauma - metabolism ; Craniocerebral Trauma - physiopathology ; Craniocerebral Trauma - therapy ; Emergency and intensive care: comas and nervous system diseases ; Energy Metabolism ; Fentanyl - administration & dosage ; Fentanyl - adverse effects ; Glasgow Coma Scale ; Humans ; Intensive care medicine ; Linear Models ; Medical sciences ; Midazolam - administration & dosage ; Midazolam - adverse effects ; Oxygen Consumption ; Prognosis ; Prospective Studies ; Substance Withdrawal Syndrome - epidemiology ; Substance Withdrawal Syndrome - metabolism ; Substance Withdrawal Syndrome - physiopathology ; Time Factors</subject><ispartof>Critical care medicine, 1994-07, Vol.22 (7), p.1114-1119</ispartof><rights>Williams & Wilkins 1994. All Rights Reserved.</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3841-5e1df790bfb0e17065729bbea57bb23d0659ed7d261cf308e86d67b4ca775fa73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4126622$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8026200$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BRUDER, NICOLAS</creatorcontrib><creatorcontrib>LASSEGUE, DESIRE</creatorcontrib><creatorcontrib>PELISSIER, DANIEL</creatorcontrib><creatorcontrib>GRAZIANI, NOEL</creatorcontrib><creatorcontrib>FRANCOIS, GEORGES</creatorcontrib><title>Energy expenditure and withdrawal of sedation in severe head-injured patients</title><title>Critical care medicine</title><addtitle>Crit Care Med</addtitle><description>OBJECTIVESTo determine the outcome of oxygen consumption (Vo2) and energy expenditure after cessation of sedation in severe head-injured patients and to assess its usefulness as a predictor of neurologic severity.
DESIGNProspective, descriptive study.
SETTINGNeurosurgical intensive care unit (ICU) in a university hospital.
PATIENTSFifteen severe head-injured patients with tracheostomies and who were mechanically ventilated and sedated at the time of the study.
INTERVENTIONSNone.
MEASUREMENTS AND MAIN RESULTSVo2 and energy expenditure were measured, using indirect calorimetry during and after discontinuation of sedation. After the measurement period, the patients were divided into two groups. Group 1 included patients who were completely weaned from sedation; group 2 included patients who had to be sedated again using predetermined criteria. In both groups, energy expenditure was close to basal energy expenditure during sedation, and increased to 150% of basal energy expenditure during the recovery period, with maximum hourly values 80% above basal energy expenditure. In group 1, Vo2 and energy expenditure changed from 284 ± 44 mL/min and 1833 ± 261 kcal/day during sedation to 390 ± 85 mL/min and 2512 ± 486 kcal/day for the period without sedation. During this period, there was a significant correlation between Vo2 and mean arterial pressure. For the recovery period, there was no difference in mean or maximum Vo2 between the two groups of patients. At 24 and 48 hrs after cessation of sedation, Vo2 and energy expenditure decreased to 30% above basal energy expenditure. These changes may be due to the recovery of muscular activity, weaning from mechanical ventilation, or an increase in the amount of circulating catecholamines.
CONCLUSIONIn severe head-injured patients, during the first 12 hrs after the discontinuation of sedation, the patients experienced a large increase in Vo2, energy expenditure, and mean arterial pressure. Although these changes have no prognostic value in our study, they have potential deleterious effects in head-injured patients. Methods that blunt these changes which have proven efficacious in anesthesia may be effective for intensive care patients. (Crit Care Med 1994; 22:1114–1119)</description><subject>Acute Disease</subject><subject>Adult</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Craniocerebral Trauma - epidemiology</subject><subject>Craniocerebral Trauma - metabolism</subject><subject>Craniocerebral Trauma - physiopathology</subject><subject>Craniocerebral Trauma - therapy</subject><subject>Emergency and intensive care: comas and nervous system diseases</subject><subject>Energy Metabolism</subject><subject>Fentanyl - administration & dosage</subject><subject>Fentanyl - adverse effects</subject><subject>Glasgow Coma Scale</subject><subject>Humans</subject><subject>Intensive care medicine</subject><subject>Linear Models</subject><subject>Medical sciences</subject><subject>Midazolam - administration & dosage</subject><subject>Midazolam - adverse effects</subject><subject>Oxygen Consumption</subject><subject>Prognosis</subject><subject>Prospective Studies</subject><subject>Substance Withdrawal Syndrome - epidemiology</subject><subject>Substance Withdrawal Syndrome - metabolism</subject><subject>Substance Withdrawal Syndrome - physiopathology</subject><subject>Time Factors</subject><issn>0090-3493</issn><issn>1530-0293</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kTtPwzAUhS0EKqXwE5A8sAb8ShyPqCoPCcQCs2XHNzQldSI7JfTfY2jphiXrPs45Hj4jhCm5pkTJG5IOZ6LIqFKCyDRl6VJ6hKY052lgih-jKSGKZFwoforOYlwlh8gln6BJSVjBCJmi54WH8L7F8NWDd82wCYCNd3hshqULZjQt7mocwZmh6TxufOo_IZmWYFzW-FUKONwnFfwQz9FJbdoIF_s6Q293i9f5Q_b0cv84v33KKl4KmuVAXS0VsbUlQCUpcsmUtWByaS3jLi0UOOlYQauakxLKwhXSispImddG8hkqd-9WoYsxQK370KxN2GpK9A8g_QdIHwDpX0ApermL9hu7BncI7okk_Wqvm1iZtg7GV0082ARlRcFYsomdbezaAUL8aDcjBJ2otMNS__c9_BsX6n19</recordid><startdate>199407</startdate><enddate>199407</enddate><creator>BRUDER, NICOLAS</creator><creator>LASSEGUE, DESIRE</creator><creator>PELISSIER, DANIEL</creator><creator>GRAZIANI, NOEL</creator><creator>FRANCOIS, GEORGES</creator><general>Williams & Wilkins</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>199407</creationdate><title>Energy expenditure and withdrawal of sedation in severe head-injured patients</title><author>BRUDER, NICOLAS ; LASSEGUE, DESIRE ; PELISSIER, DANIEL ; GRAZIANI, NOEL ; FRANCOIS, GEORGES</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3841-5e1df790bfb0e17065729bbea57bb23d0659ed7d261cf308e86d67b4ca775fa73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Acute Disease</topic><topic>Adult</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Craniocerebral Trauma - epidemiology</topic><topic>Craniocerebral Trauma - metabolism</topic><topic>Craniocerebral Trauma - physiopathology</topic><topic>Craniocerebral Trauma - therapy</topic><topic>Emergency and intensive care: comas and nervous system diseases</topic><topic>Energy Metabolism</topic><topic>Fentanyl - administration & dosage</topic><topic>Fentanyl - adverse effects</topic><topic>Glasgow Coma Scale</topic><topic>Humans</topic><topic>Intensive care medicine</topic><topic>Linear Models</topic><topic>Medical sciences</topic><topic>Midazolam - administration & dosage</topic><topic>Midazolam - adverse effects</topic><topic>Oxygen Consumption</topic><topic>Prognosis</topic><topic>Prospective Studies</topic><topic>Substance Withdrawal Syndrome - epidemiology</topic><topic>Substance Withdrawal Syndrome - metabolism</topic><topic>Substance Withdrawal Syndrome - physiopathology</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BRUDER, NICOLAS</creatorcontrib><creatorcontrib>LASSEGUE, DESIRE</creatorcontrib><creatorcontrib>PELISSIER, DANIEL</creatorcontrib><creatorcontrib>GRAZIANI, NOEL</creatorcontrib><creatorcontrib>FRANCOIS, GEORGES</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Critical care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BRUDER, NICOLAS</au><au>LASSEGUE, DESIRE</au><au>PELISSIER, DANIEL</au><au>GRAZIANI, NOEL</au><au>FRANCOIS, GEORGES</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Energy expenditure and withdrawal of sedation in severe head-injured patients</atitle><jtitle>Critical care medicine</jtitle><addtitle>Crit Care Med</addtitle><date>1994-07</date><risdate>1994</risdate><volume>22</volume><issue>7</issue><spage>1114</spage><epage>1119</epage><pages>1114-1119</pages><issn>0090-3493</issn><eissn>1530-0293</eissn><coden>CCMDC7</coden><abstract>OBJECTIVESTo determine the outcome of oxygen consumption (Vo2) and energy expenditure after cessation of sedation in severe head-injured patients and to assess its usefulness as a predictor of neurologic severity.
DESIGNProspective, descriptive study.
SETTINGNeurosurgical intensive care unit (ICU) in a university hospital.
PATIENTSFifteen severe head-injured patients with tracheostomies and who were mechanically ventilated and sedated at the time of the study.
INTERVENTIONSNone.
MEASUREMENTS AND MAIN RESULTSVo2 and energy expenditure were measured, using indirect calorimetry during and after discontinuation of sedation. After the measurement period, the patients were divided into two groups. Group 1 included patients who were completely weaned from sedation; group 2 included patients who had to be sedated again using predetermined criteria. In both groups, energy expenditure was close to basal energy expenditure during sedation, and increased to 150% of basal energy expenditure during the recovery period, with maximum hourly values 80% above basal energy expenditure. In group 1, Vo2 and energy expenditure changed from 284 ± 44 mL/min and 1833 ± 261 kcal/day during sedation to 390 ± 85 mL/min and 2512 ± 486 kcal/day for the period without sedation. During this period, there was a significant correlation between Vo2 and mean arterial pressure. For the recovery period, there was no difference in mean or maximum Vo2 between the two groups of patients. At 24 and 48 hrs after cessation of sedation, Vo2 and energy expenditure decreased to 30% above basal energy expenditure. These changes may be due to the recovery of muscular activity, weaning from mechanical ventilation, or an increase in the amount of circulating catecholamines.
CONCLUSIONIn severe head-injured patients, during the first 12 hrs after the discontinuation of sedation, the patients experienced a large increase in Vo2, energy expenditure, and mean arterial pressure. Although these changes have no prognostic value in our study, they have potential deleterious effects in head-injured patients. Methods that blunt these changes which have proven efficacious in anesthesia may be effective for intensive care patients. (Crit Care Med 1994; 22:1114–1119)</abstract><cop>Hagerstown, MD</cop><pub>Williams & Wilkins</pub><pmid>8026200</pmid><doi>10.1097/00003246-199407000-00011</doi><tpages>6</tpages></addata></record> |
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| ispartof | Critical care medicine, 1994-07, Vol.22 (7), p.1114-1119 |
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| source | MEDLINE; Journals@Ovid Complete |
| subjects | Acute Disease Adult Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Biological and medical sciences Blood Pressure Craniocerebral Trauma - epidemiology Craniocerebral Trauma - metabolism Craniocerebral Trauma - physiopathology Craniocerebral Trauma - therapy Emergency and intensive care: comas and nervous system diseases Energy Metabolism Fentanyl - administration & dosage Fentanyl - adverse effects Glasgow Coma Scale Humans Intensive care medicine Linear Models Medical sciences Midazolam - administration & dosage Midazolam - adverse effects Oxygen Consumption Prognosis Prospective Studies Substance Withdrawal Syndrome - epidemiology Substance Withdrawal Syndrome - metabolism Substance Withdrawal Syndrome - physiopathology Time Factors |
| title | Energy expenditure and withdrawal of sedation in severe head-injured patients |
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