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Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury.

Bouzat P, Sala N, Payen JF, Oddo M - Ann Intensive Care (2013)

Bottom Line: Regulation of this interplay depends on the type of injury and may vary individually and over time.In this setting, patient management can be a challenging task, where standard ICP/CPP monitoring may become insufficient to prevent secondary brain injury.Looking beyond ICP and CPP, and applying a multimodal therapeutic approach for the optimization of CBF, oxygen delivery, and brain energy supply may eventually improve overall care of patients with head injury.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Intensive Care Medicine, CHUV-University Hospital, Rue du Bugnon 46, BH 08,623, CH-1011 Lausanne, Switzerland. mauro.oddo@chuv.ch.

ABSTRACT
Monitoring and management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is a standard of care after traumatic brain injury (TBI). However, the pathophysiology of so-called secondary brain injury, i.e., the cascade of potentially deleterious events that occur in the early phase following initial cerebral insult-after TBI, is complex, involving a subtle interplay between cerebral blood flow (CBF), oxygen delivery and utilization, and supply of main cerebral energy substrates (glucose) to the injured brain. Regulation of this interplay depends on the type of injury and may vary individually and over time. In this setting, patient management can be a challenging task, where standard ICP/CPP monitoring may become insufficient to prevent secondary brain injury. Growing clinical evidence demonstrates that so-called multimodal brain monitoring, including brain tissue oxygen (PbtO2), cerebral microdialysis and transcranial Doppler among others, might help to optimize CBF and the delivery of oxygen/energy substrate at the bedside, thereby improving the management of secondary brain injury. Looking beyond ICP and CPP, and applying a multimodal therapeutic approach for the optimization of CBF, oxygen delivery, and brain energy supply may eventually improve overall care of patients with head injury. This review summarizes some of the important pathophysiological determinants of secondary cerebral damage after TBI and discusses novel approaches to optimize CBF and provide adequate oxygen and energy supply to the injured brain using multimodal brain monitoring.

No MeSH data available.


Related in: MedlinePlus

PbtO2-guided management of CPP in individual patients. Example of a patient exhibiting a linear correlation between CPP and PbtO2, which suggests impaired cerebrovascular reactivity (elevated oxygen reactivity index, ORx, > 0.7). In this case, higher CPP thresholds (>80 mmHg) are required to prevent secondary ischemia (PbtO2 < 20 mmHg). This is an example of how PbtO2 monitoring may guide CPP management and the setting of “optimal” CPP at the bedside.
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Figure 3: PbtO2-guided management of CPP in individual patients. Example of a patient exhibiting a linear correlation between CPP and PbtO2, which suggests impaired cerebrovascular reactivity (elevated oxygen reactivity index, ORx, > 0.7). In this case, higher CPP thresholds (>80 mmHg) are required to prevent secondary ischemia (PbtO2 < 20 mmHg). This is an example of how PbtO2 monitoring may guide CPP management and the setting of “optimal” CPP at the bedside.

Mentions: CBF being an important determinant of PbtO2, it is possible to test at the bedside the individual response of PbtO2 to a vasopressor-induced increase of CPP/mean arterial pressure (MAP). This has originally been described as the oxygen reactivity index (ORx) and can be used to assess the state of cerebral autoregulation [45]. In practice, the PbtO2 response can be used to guide the management of CPP at the bedside. In pathological situations, the relationship between PbtO2 and CPP may become linear (Figure 3), hence manipulating CPP to maintain PbtO2 > 15–20 mmHg (PbtO2-directed strategy) might optimize CBF and avoid secondary ischemia [21,46]. Additional therapeutic interventions that may improve PbtO2 are described in section III.2 and Figure 4.


Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury.

Bouzat P, Sala N, Payen JF, Oddo M - Ann Intensive Care (2013)

PbtO2-guided management of CPP in individual patients. Example of a patient exhibiting a linear correlation between CPP and PbtO2, which suggests impaired cerebrovascular reactivity (elevated oxygen reactivity index, ORx, > 0.7). In this case, higher CPP thresholds (>80 mmHg) are required to prevent secondary ischemia (PbtO2 < 20 mmHg). This is an example of how PbtO2 monitoring may guide CPP management and the setting of “optimal” CPP at the bedside.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3716965&req=5

Figure 3: PbtO2-guided management of CPP in individual patients. Example of a patient exhibiting a linear correlation between CPP and PbtO2, which suggests impaired cerebrovascular reactivity (elevated oxygen reactivity index, ORx, > 0.7). In this case, higher CPP thresholds (>80 mmHg) are required to prevent secondary ischemia (PbtO2 < 20 mmHg). This is an example of how PbtO2 monitoring may guide CPP management and the setting of “optimal” CPP at the bedside.
Mentions: CBF being an important determinant of PbtO2, it is possible to test at the bedside the individual response of PbtO2 to a vasopressor-induced increase of CPP/mean arterial pressure (MAP). This has originally been described as the oxygen reactivity index (ORx) and can be used to assess the state of cerebral autoregulation [45]. In practice, the PbtO2 response can be used to guide the management of CPP at the bedside. In pathological situations, the relationship between PbtO2 and CPP may become linear (Figure 3), hence manipulating CPP to maintain PbtO2 > 15–20 mmHg (PbtO2-directed strategy) might optimize CBF and avoid secondary ischemia [21,46]. Additional therapeutic interventions that may improve PbtO2 are described in section III.2 and Figure 4.

Bottom Line: Regulation of this interplay depends on the type of injury and may vary individually and over time.In this setting, patient management can be a challenging task, where standard ICP/CPP monitoring may become insufficient to prevent secondary brain injury.Looking beyond ICP and CPP, and applying a multimodal therapeutic approach for the optimization of CBF, oxygen delivery, and brain energy supply may eventually improve overall care of patients with head injury.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Intensive Care Medicine, CHUV-University Hospital, Rue du Bugnon 46, BH 08,623, CH-1011 Lausanne, Switzerland. mauro.oddo@chuv.ch.

ABSTRACT
Monitoring and management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is a standard of care after traumatic brain injury (TBI). However, the pathophysiology of so-called secondary brain injury, i.e., the cascade of potentially deleterious events that occur in the early phase following initial cerebral insult-after TBI, is complex, involving a subtle interplay between cerebral blood flow (CBF), oxygen delivery and utilization, and supply of main cerebral energy substrates (glucose) to the injured brain. Regulation of this interplay depends on the type of injury and may vary individually and over time. In this setting, patient management can be a challenging task, where standard ICP/CPP monitoring may become insufficient to prevent secondary brain injury. Growing clinical evidence demonstrates that so-called multimodal brain monitoring, including brain tissue oxygen (PbtO2), cerebral microdialysis and transcranial Doppler among others, might help to optimize CBF and the delivery of oxygen/energy substrate at the bedside, thereby improving the management of secondary brain injury. Looking beyond ICP and CPP, and applying a multimodal therapeutic approach for the optimization of CBF, oxygen delivery, and brain energy supply may eventually improve overall care of patients with head injury. This review summarizes some of the important pathophysiological determinants of secondary cerebral damage after TBI and discusses novel approaches to optimize CBF and provide adequate oxygen and energy supply to the injured brain using multimodal brain monitoring.

No MeSH data available.


Related in: MedlinePlus