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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

Cerebral microdialysis-guided management of glycemic control in individual patients. Example of a patient showing a linear relationship between blood and brain glucose, measured by cerebral microdialysis (CMD) glucose. Because of low CMD glucose <1 mmol/L, infusion of a 10% glucose solution was administered and was associated with a parallel increase of both arterial blood and CMD glucose. This illustrates the potential value of CMD for the management of blood glucose control in patients with severe brain injuries, aiming to prevent secondary systemic insults (brain glucopenia in this case).
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Figure 5: Cerebral microdialysis-guided management of glycemic control in individual patients. Example of a patient showing a linear relationship between blood and brain glucose, measured by cerebral microdialysis (CMD) glucose. Because of low CMD glucose <1 mmol/L, infusion of a 10% glucose solution was administered and was associated with a parallel increase of both arterial blood and CMD glucose. This illustrates the potential value of CMD for the management of blood glucose control in patients with severe brain injuries, aiming to prevent secondary systemic insults (brain glucopenia in this case).

Mentions: Cerebral microdialysis has greatly contributed to better manage glucose control in TBI patients at high risk for secondary brain injury [62,63]. Glucose is the main energy source for the human brain. Therefore adequate glucose supply is crucial to maintain brain function. Supply of glucose is provided by selective transporters (GLUT) that allow glucose diffusion across the blood brain barrier to brain cells. Glucose supply to the brain is highly dependent on the availability of glucose from the systemic circulation (Figure 5) [64]. Therefore, so-called “intensive” blood glucose control with the use of insulin therapy may reduce brain glucose availability and potentially increase energy dysfunction or aggravate metabolic distress [63,65-67]. Moderate (≈8-10 mmol/L) vs. intensive (≈4.5-6 mmol/L) glucose control does not confer any benefit on TBI outcome [68]. Using CMD, systemic glucose concentration can be targeted to CMD glucose, to avoid neuroglucopenia (CMD <1 mmol/L). In some patients, this can occur already at blood glucose levels <8 mmol/l, and therefore systemic glucose must be adapted to avoid low brain glucose, by keeping blood glucose at 8–10 mmol/L, if necessary by giving slow infusion of 10% i.v. glucose. It is important to realize however that reduced brain glucose can be due to other reasons, including ischemia/energy crisis, elevated ICP/low CPP; in these circumstances, these causes must be treated first. Given these findings, when CMD is available precise blood glucose levels should be targeted to CMD glucose to avoid levels <1 mmol/L. Otherwise, moderate blood glucose control (≈8-10 mmol/L) is recommended for the management of patients with severe brain injury.


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)

Cerebral microdialysis-guided management of glycemic control in individual patients. Example of a patient showing a linear relationship between blood and brain glucose, measured by cerebral microdialysis (CMD) glucose. Because of low CMD glucose <1 mmol/L, infusion of a 10% glucose solution was administered and was associated with a parallel increase of both arterial blood and CMD glucose. This illustrates the potential value of CMD for the management of blood glucose control in patients with severe brain injuries, aiming to prevent secondary systemic insults (brain glucopenia in this case).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Cerebral microdialysis-guided management of glycemic control in individual patients. Example of a patient showing a linear relationship between blood and brain glucose, measured by cerebral microdialysis (CMD) glucose. Because of low CMD glucose <1 mmol/L, infusion of a 10% glucose solution was administered and was associated with a parallel increase of both arterial blood and CMD glucose. This illustrates the potential value of CMD for the management of blood glucose control in patients with severe brain injuries, aiming to prevent secondary systemic insults (brain glucopenia in this case).
Mentions: Cerebral microdialysis has greatly contributed to better manage glucose control in TBI patients at high risk for secondary brain injury [62,63]. Glucose is the main energy source for the human brain. Therefore adequate glucose supply is crucial to maintain brain function. Supply of glucose is provided by selective transporters (GLUT) that allow glucose diffusion across the blood brain barrier to brain cells. Glucose supply to the brain is highly dependent on the availability of glucose from the systemic circulation (Figure 5) [64]. Therefore, so-called “intensive” blood glucose control with the use of insulin therapy may reduce brain glucose availability and potentially increase energy dysfunction or aggravate metabolic distress [63,65-67]. Moderate (≈8-10 mmol/L) vs. intensive (≈4.5-6 mmol/L) glucose control does not confer any benefit on TBI outcome [68]. Using CMD, systemic glucose concentration can be targeted to CMD glucose, to avoid neuroglucopenia (CMD <1 mmol/L). In some patients, this can occur already at blood glucose levels <8 mmol/l, and therefore systemic glucose must be adapted to avoid low brain glucose, by keeping blood glucose at 8–10 mmol/L, if necessary by giving slow infusion of 10% i.v. glucose. It is important to realize however that reduced brain glucose can be due to other reasons, including ischemia/energy crisis, elevated ICP/low CPP; in these circumstances, these causes must be treated first. Given these findings, when CMD is available precise blood glucose levels should be targeted to CMD glucose to avoid levels <1 mmol/L. Otherwise, moderate blood glucose control (≈8-10 mmol/L) is recommended for the management of patients with severe brain injury.

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