The effect of resuscitative endovascular balloon occlusion of the aorta, partial aortic occlusion and aggressive blood transfusion on traumatic brain injury in a swine multiple injuries model

Michael Johnson, Timothy K. Williams, Sarah Ashley E. Ferencz, Anders J. Davidson, Rachel M. Russo, William T. O'Brien, Joseph M Galante, J. Kevin Grayson, Lucas P. Neff

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

BACKGROUND Despite clinical reports of poor outcomes, the degree to which resuscitative endovascular balloon occlusion of the aorta (REBOA) exacerbates traumatic brain injury (TBI) is not known. We hypothesized that combined effects of increased proximal mean arterial pressure (pMAP), carotid blood flow (Q carotid), and intracranial pressure (ICP) from REBOA would lead to TBI progression compared with partial aortic occlusion (PAO) or no intervention. METHODS Twenty-one swine underwent a standardized TBI via computer Controlled cortical impact followed by 25% total blood volume rapid hemorrhage. After 30 minutes of hypotension, animals were randomized to 60 minutes of continued hypotension (Control), REBOA, or PAO. REBOA and PAO animals were then weaned from occlusion. All animals were resuscitated with shed blood via a rapid blood infuser. Physiologic parameters were recorded continuously and brain computed tomography obtained at specified intervals. RESULTS There were no differences in baseline physiology or during the initial 30 minutes of hypotension. During the 60-minute intervention period, REBOA resulted in higher maximal pMAP (REBOA, 105.3 ± 8.8; PAO, 92.7 ± 9.2; Control, 48.9 ± 7.7; p = 0.02) and higher Q carotid (REBOA, 673.1 ± 57.9; PAO, 464.2 ± 53.0; Control, 170.3 ± 29.4; p < 0.01). Increases in ICP were greatest during blood resuscitation, with Control animals demonstrating the largest peak ICP (Control, 12.8 ± 1.2; REBOA, 5.1 ± 0.6; PAO, 9.4 ± 1.1; p < 0.01). There were no differences in the percentage of animals with hemorrhage progression on CT (Control, 14.3%; 95% confidence interval [CI], 3.6-57.9; REBOA, 28.6%; 95% CI, 3.7-71.0; and PAO, 28.6%; 95% CI, 3.7-71.0). CONCLUSION In an animal model of TBI and shock, REBOA increased Q carotid and pMAP, but did not exacerbate TBI progression. PAO resulted in physiology closer to baseline with smaller increases in ICP and pMAP. Rapid blood resuscitation, not REBOA, resulted in the largest increase in ICP after intervention, which occurred in Control animals. Continued studies of the cerebral hemodynamics of aortic occlusion and blood transfusion are required to determine optimal resuscitation strategies for multi-injured patients.

Original languageEnglish (US)
Pages (from-to)61-70
Number of pages10
JournalJournal of Trauma and Acute Care Surgery
Volume83
Issue number1
DOIs
StatePublished - Jul 1 2017

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Balloon Occlusion
Multiple Trauma
Blood Transfusion
Aorta
Swine
Intracranial Hypertension
Arterial Pressure
Resuscitation
Hypotension
Intracranial Pressure
Confidence Intervals
Traumatic Brain Injury
Hemorrhage
Blood Volume
Shock
Animal Models
Hemodynamics
Tomography

Keywords

  • endovascular
  • intra-aortic balloon
  • resuscitation
  • shock
  • Traumatic brain injury

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine

Cite this

The effect of resuscitative endovascular balloon occlusion of the aorta, partial aortic occlusion and aggressive blood transfusion on traumatic brain injury in a swine multiple injuries model. / Johnson, Michael; Williams, Timothy K.; Ferencz, Sarah Ashley E.; Davidson, Anders J.; Russo, Rachel M.; O'Brien, William T.; Galante, Joseph M; Grayson, J. Kevin; Neff, Lucas P.

In: Journal of Trauma and Acute Care Surgery, Vol. 83, No. 1, 01.07.2017, p. 61-70.

Research output: Contribution to journalArticle

Johnson, Michael ; Williams, Timothy K. ; Ferencz, Sarah Ashley E. ; Davidson, Anders J. ; Russo, Rachel M. ; O'Brien, William T. ; Galante, Joseph M ; Grayson, J. Kevin ; Neff, Lucas P. / The effect of resuscitative endovascular balloon occlusion of the aorta, partial aortic occlusion and aggressive blood transfusion on traumatic brain injury in a swine multiple injuries model. In: Journal of Trauma and Acute Care Surgery. 2017 ; Vol. 83, No. 1. pp. 61-70.
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title = "The effect of resuscitative endovascular balloon occlusion of the aorta, partial aortic occlusion and aggressive blood transfusion on traumatic brain injury in a swine multiple injuries model",
abstract = "BACKGROUND Despite clinical reports of poor outcomes, the degree to which resuscitative endovascular balloon occlusion of the aorta (REBOA) exacerbates traumatic brain injury (TBI) is not known. We hypothesized that combined effects of increased proximal mean arterial pressure (pMAP), carotid blood flow (Q carotid), and intracranial pressure (ICP) from REBOA would lead to TBI progression compared with partial aortic occlusion (PAO) or no intervention. METHODS Twenty-one swine underwent a standardized TBI via computer Controlled cortical impact followed by 25{\%} total blood volume rapid hemorrhage. After 30 minutes of hypotension, animals were randomized to 60 minutes of continued hypotension (Control), REBOA, or PAO. REBOA and PAO animals were then weaned from occlusion. All animals were resuscitated with shed blood via a rapid blood infuser. Physiologic parameters were recorded continuously and brain computed tomography obtained at specified intervals. RESULTS There were no differences in baseline physiology or during the initial 30 minutes of hypotension. During the 60-minute intervention period, REBOA resulted in higher maximal pMAP (REBOA, 105.3 ± 8.8; PAO, 92.7 ± 9.2; Control, 48.9 ± 7.7; p = 0.02) and higher Q carotid (REBOA, 673.1 ± 57.9; PAO, 464.2 ± 53.0; Control, 170.3 ± 29.4; p < 0.01). Increases in ICP were greatest during blood resuscitation, with Control animals demonstrating the largest peak ICP (Control, 12.8 ± 1.2; REBOA, 5.1 ± 0.6; PAO, 9.4 ± 1.1; p < 0.01). There were no differences in the percentage of animals with hemorrhage progression on CT (Control, 14.3{\%}; 95{\%} confidence interval [CI], 3.6-57.9; REBOA, 28.6{\%}; 95{\%} CI, 3.7-71.0; and PAO, 28.6{\%}; 95{\%} CI, 3.7-71.0). CONCLUSION In an animal model of TBI and shock, REBOA increased Q carotid and pMAP, but did not exacerbate TBI progression. PAO resulted in physiology closer to baseline with smaller increases in ICP and pMAP. Rapid blood resuscitation, not REBOA, resulted in the largest increase in ICP after intervention, which occurred in Control animals. Continued studies of the cerebral hemodynamics of aortic occlusion and blood transfusion are required to determine optimal resuscitation strategies for multi-injured patients.",
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author = "Michael Johnson and Williams, {Timothy K.} and Ferencz, {Sarah Ashley E.} and Davidson, {Anders J.} and Russo, {Rachel M.} and O'Brien, {William T.} and Galante, {Joseph M} and Grayson, {J. Kevin} and Neff, {Lucas P.}",
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T1 - The effect of resuscitative endovascular balloon occlusion of the aorta, partial aortic occlusion and aggressive blood transfusion on traumatic brain injury in a swine multiple injuries model

AU - Johnson, Michael

AU - Williams, Timothy K.

AU - Ferencz, Sarah Ashley E.

AU - Davidson, Anders J.

AU - Russo, Rachel M.

AU - O'Brien, William T.

AU - Galante, Joseph M

AU - Grayson, J. Kevin

AU - Neff, Lucas P.

PY - 2017/7/1

Y1 - 2017/7/1

N2 - BACKGROUND Despite clinical reports of poor outcomes, the degree to which resuscitative endovascular balloon occlusion of the aorta (REBOA) exacerbates traumatic brain injury (TBI) is not known. We hypothesized that combined effects of increased proximal mean arterial pressure (pMAP), carotid blood flow (Q carotid), and intracranial pressure (ICP) from REBOA would lead to TBI progression compared with partial aortic occlusion (PAO) or no intervention. METHODS Twenty-one swine underwent a standardized TBI via computer Controlled cortical impact followed by 25% total blood volume rapid hemorrhage. After 30 minutes of hypotension, animals were randomized to 60 minutes of continued hypotension (Control), REBOA, or PAO. REBOA and PAO animals were then weaned from occlusion. All animals were resuscitated with shed blood via a rapid blood infuser. Physiologic parameters were recorded continuously and brain computed tomography obtained at specified intervals. RESULTS There were no differences in baseline physiology or during the initial 30 minutes of hypotension. During the 60-minute intervention period, REBOA resulted in higher maximal pMAP (REBOA, 105.3 ± 8.8; PAO, 92.7 ± 9.2; Control, 48.9 ± 7.7; p = 0.02) and higher Q carotid (REBOA, 673.1 ± 57.9; PAO, 464.2 ± 53.0; Control, 170.3 ± 29.4; p < 0.01). Increases in ICP were greatest during blood resuscitation, with Control animals demonstrating the largest peak ICP (Control, 12.8 ± 1.2; REBOA, 5.1 ± 0.6; PAO, 9.4 ± 1.1; p < 0.01). There were no differences in the percentage of animals with hemorrhage progression on CT (Control, 14.3%; 95% confidence interval [CI], 3.6-57.9; REBOA, 28.6%; 95% CI, 3.7-71.0; and PAO, 28.6%; 95% CI, 3.7-71.0). CONCLUSION In an animal model of TBI and shock, REBOA increased Q carotid and pMAP, but did not exacerbate TBI progression. PAO resulted in physiology closer to baseline with smaller increases in ICP and pMAP. Rapid blood resuscitation, not REBOA, resulted in the largest increase in ICP after intervention, which occurred in Control animals. Continued studies of the cerebral hemodynamics of aortic occlusion and blood transfusion are required to determine optimal resuscitation strategies for multi-injured patients.

AB - BACKGROUND Despite clinical reports of poor outcomes, the degree to which resuscitative endovascular balloon occlusion of the aorta (REBOA) exacerbates traumatic brain injury (TBI) is not known. We hypothesized that combined effects of increased proximal mean arterial pressure (pMAP), carotid blood flow (Q carotid), and intracranial pressure (ICP) from REBOA would lead to TBI progression compared with partial aortic occlusion (PAO) or no intervention. METHODS Twenty-one swine underwent a standardized TBI via computer Controlled cortical impact followed by 25% total blood volume rapid hemorrhage. After 30 minutes of hypotension, animals were randomized to 60 minutes of continued hypotension (Control), REBOA, or PAO. REBOA and PAO animals were then weaned from occlusion. All animals were resuscitated with shed blood via a rapid blood infuser. Physiologic parameters were recorded continuously and brain computed tomography obtained at specified intervals. RESULTS There were no differences in baseline physiology or during the initial 30 minutes of hypotension. During the 60-minute intervention period, REBOA resulted in higher maximal pMAP (REBOA, 105.3 ± 8.8; PAO, 92.7 ± 9.2; Control, 48.9 ± 7.7; p = 0.02) and higher Q carotid (REBOA, 673.1 ± 57.9; PAO, 464.2 ± 53.0; Control, 170.3 ± 29.4; p < 0.01). Increases in ICP were greatest during blood resuscitation, with Control animals demonstrating the largest peak ICP (Control, 12.8 ± 1.2; REBOA, 5.1 ± 0.6; PAO, 9.4 ± 1.1; p < 0.01). There were no differences in the percentage of animals with hemorrhage progression on CT (Control, 14.3%; 95% confidence interval [CI], 3.6-57.9; REBOA, 28.6%; 95% CI, 3.7-71.0; and PAO, 28.6%; 95% CI, 3.7-71.0). CONCLUSION In an animal model of TBI and shock, REBOA increased Q carotid and pMAP, but did not exacerbate TBI progression. PAO resulted in physiology closer to baseline with smaller increases in ICP and pMAP. Rapid blood resuscitation, not REBOA, resulted in the largest increase in ICP after intervention, which occurred in Control animals. Continued studies of the cerebral hemodynamics of aortic occlusion and blood transfusion are required to determine optimal resuscitation strategies for multi-injured patients.

KW - endovascular

KW - intra-aortic balloon

KW - resuscitation

KW - shock

KW - Traumatic brain injury

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