Cerebral blood flow-metabolism coupling after traumatic brain injury (tbi) combined with hemorrhage

Matthew J. Fabian, John B. Schweitzer, Kenneth G Proctor

Research output: Contribution to journalArticle

Abstract

Introduction: Secondary insults, such as hemorrhagic hypotension, potentiate morbidity and mortality associated with TBI. There are few studies in large animals in which clinically-relevant treatment protocols can be applied. The purpose of this study was to define the changes in cerebral blood flow metabolism coupling for 72 hrs after fluid percussion injury (FPI) plus shock. Methods: Nine anesthetized mongrel swine were intubated, ventilated (FiO2=0.4, PEEP = 5, ETCO2=40), and instrumented in sterile conditions with arterial and pulmonary artery catheters. Through a midline craniotomy, a sagital sinus (SS) catheter was placed for monitoring intracranial pressure (ICP, mm Hg) glucose (Glu mM), lactate (Lac, mM) and O2 saturation. These values were compared to arterial (A) values to obtain A-SS gradients (A). After stabilization, FPI was delivered over the left parietal cortex. After l min, 40% of estimated blood volume was withdrawn through the arterial catheter. Cerebrovascular reactivity was tested with a 10 min challenge with FiCO2=0.1. After 1 hr shock, resuscitation consisted of shed blood plus supplemental crystalloid. Data were collected for 72 hr. Results: There were 6/9 survivors; all with histologie evidence of profound TBI. Cerebrovascular reactivity to CU2 was preserved but ICP change was potentiated. Time ICP CPP A-Glu A-SS A-Lact A-SS Glu A O2 sat A preinjury 3±1 9115 135±16 2512 1.1±0.1 5512 30"shock 0±13815115126 3018 3.910.1721460"shock 01035151031302317 5.210.77515120"resus 13128117 118121 1913 6.111.04814 180"resus 13139015 116120 2212 3.410.85114 240"resus 11129015 118119 2215 2.110.6 5212 72hrrecov 5118813 114111 2213 1.110.3 5913 Values are means! standard errors. "" p < .05 versus preinjury baseline. Conclusions: Global cerebral glucose supply/demand is maintained even with major changes in CPP, which is inconsistent with a global hypermetabolic state after TBI. However, these data provide no information on either blood or metabolism per se, but rather the coupling between the two.

Original languageEnglish
JournalCritical Care Medicine
Volume26
Issue number1 SUPPL.
StatePublished - Dec 1 1998
Externally publishedYes

Fingerprint

Cerebrovascular Circulation
Shock
Hemorrhage
Percussion
Catheters
Glucose
Parietal Lobe
Craniotomy
Wounds and Injuries
Intracranial Pressure
Clinical Protocols
Blood Volume
Resuscitation
Hypotension
Pulmonary Artery
Survivors
Lactic Acid
Swine
Morbidity
Mortality

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Cerebral blood flow-metabolism coupling after traumatic brain injury (tbi) combined with hemorrhage. / Fabian, Matthew J.; Schweitzer, John B.; Proctor, Kenneth G.

In: Critical Care Medicine, Vol. 26, No. 1 SUPPL., 01.12.1998.

Research output: Contribution to journalArticle

@article{a8a1177b74654ad1a14a08ae2096a264,
title = "Cerebral blood flow-metabolism coupling after traumatic brain injury (tbi) combined with hemorrhage",
abstract = "Introduction: Secondary insults, such as hemorrhagic hypotension, potentiate morbidity and mortality associated with TBI. There are few studies in large animals in which clinically-relevant treatment protocols can be applied. The purpose of this study was to define the changes in cerebral blood flow metabolism coupling for 72 hrs after fluid percussion injury (FPI) plus shock. Methods: Nine anesthetized mongrel swine were intubated, ventilated (FiO2=0.4, PEEP = 5, ETCO2=40), and instrumented in sterile conditions with arterial and pulmonary artery catheters. Through a midline craniotomy, a sagital sinus (SS) catheter was placed for monitoring intracranial pressure (ICP, mm Hg) glucose (Glu mM), lactate (Lac, mM) and O2 saturation. These values were compared to arterial (A) values to obtain A-SS gradients (A). After stabilization, FPI was delivered over the left parietal cortex. After l min, 40{\%} of estimated blood volume was withdrawn through the arterial catheter. Cerebrovascular reactivity was tested with a 10 min challenge with FiCO2=0.1. After 1 hr shock, resuscitation consisted of shed blood plus supplemental crystalloid. Data were collected for 72 hr. Results: There were 6/9 survivors; all with histologie evidence of profound TBI. Cerebrovascular reactivity to CU2 was preserved but ICP change was potentiated. Time ICP CPP A-Glu A-SS A-Lact A-SS Glu A O2 sat A preinjury 3±1 9115 135±16 2512 1.1±0.1 5512 30{"}shock 0±13815115126 3018 3.910.1721460{"}shock 01035151031302317 5.210.77515120{"}resus 13128117 118121 1913 6.111.04814 180{"}resus 13139015 116120 2212 3.410.85114 240{"}resus 11129015 118119 2215 2.110.6 5212 72hrrecov 5118813 114111 2213 1.110.3 5913 Values are means! standard errors. {"}{"} p < .05 versus preinjury baseline. Conclusions: Global cerebral glucose supply/demand is maintained even with major changes in CPP, which is inconsistent with a global hypermetabolic state after TBI. However, these data provide no information on either blood or metabolism per se, but rather the coupling between the two.",
author = "Fabian, {Matthew J.} and Schweitzer, {John B.} and Proctor, {Kenneth G}",
year = "1998",
month = "12",
day = "1",
language = "English",
volume = "26",
journal = "Critical Care Medicine",
issn = "0090-3493",
publisher = "Lippincott Williams and Wilkins",
number = "1 SUPPL.",

}

TY - JOUR

T1 - Cerebral blood flow-metabolism coupling after traumatic brain injury (tbi) combined with hemorrhage

AU - Fabian, Matthew J.

AU - Schweitzer, John B.

AU - Proctor, Kenneth G

PY - 1998/12/1

Y1 - 1998/12/1

N2 - Introduction: Secondary insults, such as hemorrhagic hypotension, potentiate morbidity and mortality associated with TBI. There are few studies in large animals in which clinically-relevant treatment protocols can be applied. The purpose of this study was to define the changes in cerebral blood flow metabolism coupling for 72 hrs after fluid percussion injury (FPI) plus shock. Methods: Nine anesthetized mongrel swine were intubated, ventilated (FiO2=0.4, PEEP = 5, ETCO2=40), and instrumented in sterile conditions with arterial and pulmonary artery catheters. Through a midline craniotomy, a sagital sinus (SS) catheter was placed for monitoring intracranial pressure (ICP, mm Hg) glucose (Glu mM), lactate (Lac, mM) and O2 saturation. These values were compared to arterial (A) values to obtain A-SS gradients (A). After stabilization, FPI was delivered over the left parietal cortex. After l min, 40% of estimated blood volume was withdrawn through the arterial catheter. Cerebrovascular reactivity was tested with a 10 min challenge with FiCO2=0.1. After 1 hr shock, resuscitation consisted of shed blood plus supplemental crystalloid. Data were collected for 72 hr. Results: There were 6/9 survivors; all with histologie evidence of profound TBI. Cerebrovascular reactivity to CU2 was preserved but ICP change was potentiated. Time ICP CPP A-Glu A-SS A-Lact A-SS Glu A O2 sat A preinjury 3±1 9115 135±16 2512 1.1±0.1 5512 30"shock 0±13815115126 3018 3.910.1721460"shock 01035151031302317 5.210.77515120"resus 13128117 118121 1913 6.111.04814 180"resus 13139015 116120 2212 3.410.85114 240"resus 11129015 118119 2215 2.110.6 5212 72hrrecov 5118813 114111 2213 1.110.3 5913 Values are means! standard errors. "" p < .05 versus preinjury baseline. Conclusions: Global cerebral glucose supply/demand is maintained even with major changes in CPP, which is inconsistent with a global hypermetabolic state after TBI. However, these data provide no information on either blood or metabolism per se, but rather the coupling between the two.

AB - Introduction: Secondary insults, such as hemorrhagic hypotension, potentiate morbidity and mortality associated with TBI. There are few studies in large animals in which clinically-relevant treatment protocols can be applied. The purpose of this study was to define the changes in cerebral blood flow metabolism coupling for 72 hrs after fluid percussion injury (FPI) plus shock. Methods: Nine anesthetized mongrel swine were intubated, ventilated (FiO2=0.4, PEEP = 5, ETCO2=40), and instrumented in sterile conditions with arterial and pulmonary artery catheters. Through a midline craniotomy, a sagital sinus (SS) catheter was placed for monitoring intracranial pressure (ICP, mm Hg) glucose (Glu mM), lactate (Lac, mM) and O2 saturation. These values were compared to arterial (A) values to obtain A-SS gradients (A). After stabilization, FPI was delivered over the left parietal cortex. After l min, 40% of estimated blood volume was withdrawn through the arterial catheter. Cerebrovascular reactivity was tested with a 10 min challenge with FiCO2=0.1. After 1 hr shock, resuscitation consisted of shed blood plus supplemental crystalloid. Data were collected for 72 hr. Results: There were 6/9 survivors; all with histologie evidence of profound TBI. Cerebrovascular reactivity to CU2 was preserved but ICP change was potentiated. Time ICP CPP A-Glu A-SS A-Lact A-SS Glu A O2 sat A preinjury 3±1 9115 135±16 2512 1.1±0.1 5512 30"shock 0±13815115126 3018 3.910.1721460"shock 01035151031302317 5.210.77515120"resus 13128117 118121 1913 6.111.04814 180"resus 13139015 116120 2212 3.410.85114 240"resus 11129015 118119 2215 2.110.6 5212 72hrrecov 5118813 114111 2213 1.110.3 5913 Values are means! standard errors. "" p < .05 versus preinjury baseline. Conclusions: Global cerebral glucose supply/demand is maintained even with major changes in CPP, which is inconsistent with a global hypermetabolic state after TBI. However, these data provide no information on either blood or metabolism per se, but rather the coupling between the two.

UR - http://www.scopus.com/inward/record.url?scp=33750272841&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750272841&partnerID=8YFLogxK

M3 - Article

VL - 26

JO - Critical Care Medicine

JF - Critical Care Medicine

SN - 0090-3493

IS - 1 SUPPL.

ER -