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Acute clinical grading in pediatric severe traumatic brain injury and its association with subsequent intracranial pressure, cerebral perfusion pressure, and brain oxygenation

Anthony A. Figaji, Eugene Zwane, A. Graham Fieggen, Jonathan C. Peter, and Peter D. Leroux

continuously monitored ICP, CPP, PbtO 2 , and peripheral SaO 2 . In addition, all arterial blood gas samples were evaluated. Values considered abnormal were in keeping with recently published guidelines. 1 Intracranial Pressure The following ICP values were calculated and recorded for each patient as: mean ICP during the first 24 hours (mICP 24 ), mean ICP for the full duration of monitoring (mICP total ), number of episodes of ICP > 20 mm Hg, mean value for all ICP readings > 20 mm Hg (mICP > 20 mm Hg), and highest ICP (ICP peak ). Cerebral Perfusion Pressure

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What is the optimal threshold for cerebral perfusion pressure following traumatic brain injury?

Paul Vespa

Intensive care of the patient with traumatic brain injury centers on control of intracranial pressure and cerebral perfusion pressure (CPP). The optimal CPP by definition delivers an adequate supply of blood and oxygen to meet the metabolic demands of brain tissue. A great deal of controversy exists regarding the optimal CPP value, with disparate studies providing conflicting evidence for the use of supraphysiological CPP values. No study that accurately assesses the efficacy of normal CPP compared with elevated CPP has been performed, but several studies demonstrate that a CPP threshold exists on an individual basis for patients with TBI. The use of brain monitors of cerebral metabolism and oxygen supply may assist the clinician in the selection of the optimal CPP for an individual patient.

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What is the optimal cerebral perfusion pressure in children suffering from traumatic coma?

Iain R. Chambers and Fenella J. Kirkham

Head injury is a major cause of death and disability in children. Despite advances in resuscitation, emergency care, intensive care monitoring, and clinical practices, there are few data demonstrating the predictive value of certain physiological variables regarding outcome in this patient population. Mean arterial blood pressure (MABP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP = MABP − ICP) are routinely monitored in patients in many neurological intensive care units throughout the world, but there is little evidence indicating that advances in care have been matched with corresponding improvements in outcome.

Nonetheless, there is evidence that hypotension immediately following head injury is predictive of early death, and many patients with these features die with clinical signs of brain herniation caused by intracranial hypertension. Furthermore, available data indicate that a minimal and a mean CPP measured during intensive care are good predictors of outcome in survivors, but a target threshold to improve outcome has yet to be defined.

Some medical management strategies can have detrimental effects, and there is now a good case for undertaking a controlled trial of immediate or delayed craniectomy. Independent outcome in children following severe head injury is associated with higher levels of CPP. The ability to tolerate different levels of CPP may be related to age, and therefore any such surgical trial would need a carefully defined protocol so that the potential benefit of such a treatment is maximized.

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Assessment of critical thresholds for cerebral perfusion pressure by performing bedside monitoring of cerebral energy metabolism

Carl-Henrik Nordström

An intractable increase in intracranial pressure (ICP) leading to a progressive decrease in cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) is the dominating cause of death in patients with severe brain trauma. Arterial hypotension may further compromise CPP (and CBF) and significantly contributes to death. In addition, the injured brain is sensitive to raised CPP due to an increased permeability of the blood–brain barrier (BBB) to crystalloids and an impaired pressure autoregulation of the CBF. Given these circumstances, an increase in CPP will cause a net transport of water across the BBB and a further elevation in ICP. Accordingly, the assessment of the lower critical threshold for CPP is important for neurological intensive care. This level varies among different patients and different areas of the brain. In fact, the penumbral zones surrounding focal brain lesions appear to be the most sensitive. In the individual patient, preservation of normal cerebral energy metabolism within areas at risk during a decrease in CPP can be guaranteed by performing intracerebral microdialysis and bedside biochemical analyses.

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Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury

Niels Juul, Gabrielle F. Morris, Sharon B. Marshall, the Executive Committee of the International Selfotel Trial, and Lawrence F. Marshall

Object

Recently, a renewed emphasis has been placed on managing severe head injury by elevating cerebral perfusion pressure (CPP), which is defined as the mean arterial pressure minus the intracranial pressure (ICP). Some authors have suggested that CPP is more important in influencing outcome than is intracranial hypertension, a hypothesis that this study was designed to investigate.

Methods

The authors examined the relative contribution of these two parameters to outcome in a series of 427 patients prospectively studied in an international, multicenter, randomized, double-blind trial of the N-methyl-D-aspartate antagonist Selfotel. Mortality rates rose from 9.6% in 292 patients who had no clinically defined episodes of neurological deterioration to 56.5% in 117 patients who suffered one or more of these episodes; 18 patients were lost to follow up. Correspondingly, favorable outcome, defined as good or moderate on the Glasgow Outcome Scale at 6 months, fell from 67.8% in patients without neurological deterioration to 29.1% in those with neurological deterioration. In patients who had clinical evidence of neurological deterioration, the relative influence of ICP and CPP on outcome was assessed. The most powerful predictor of neurological worsening was the presence of intracranial hypertension (ICP >/= 20 mm Hg) either initially or during neurological deterioration. There was no correlation with the CPP as long as the CPP was greater than 60 mm Hg.

Conclusions

Treatment protocols for the management of severe head injury should emphasize the immediate reduction of raised ICP to less than 20 mm Hg if possible. A CPP greater than 60 mm Hg appears to have little influence on the outcome of patients with severe head injury.

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Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury

Niels Juul, Gabrielle F. Morris, Sharon B. Marshall, The Executive Committee of the International Selfotel Trial, and Lawrence F. Marshall

Object

Recently, a renewed emphasis has been placed on managing severe head injury by elevating cerebral perfusion pressure (CPP), which is defined as the mean arterial pressure minus the intracranial pressure (ICP). Some authors have suggested that CPP is more important in influencing outcome than is intracranial hypertension, a hypothesis that this study was designed to investigate.

Methods

The authors examined the relative contribution of these two parameters to outcome in a series of 427 patients prospectively studied in an international, multicenter, randomized, double-blind trial of the N-methyl-D-aspartate antagonist Selfotel. Mortality rates rose from 9.6% in 292 patients who had no clinically defined episodes of neurological deterioration to 56.4% in 117 patients who suffered one or more of these episodes; 18 patients were lost to follow up. Correspondingly, favorable outcome, defined as good or moderate on the Glasgow Outcome Scale at 6 months, fell from 67.8% in patients without neurological deterioration to 29.1% in those with neurological deterioration. In patients who had clinical evidence of neurological deterioration, the relative influence of ICP and CPP on outcome was assessed. The most powerful predictor of neurological worsening was the presence of intracranial hypertension (ICP ≥ 20 mm Hg) either initially or during neurological deterioration. There was no correlation with the CPP as long as the CPP was greater than 60 mm Hg.

Conclusions

Treatment protocols for the management of severe head injury should emphasize the immediate reduction of raised ICP to less than 20 mm Hg if possible. A CPP greater than 60 mm Hg appears to have little influence on the outcome of patients with severe head injury.

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Is there an upper limit of intracranial pressure in patients with severe head injury if cerebral perfusion pressure is maintained?

Jeffrey S. Young, Osbert Blow, Florence Turrentine, Jeffrey A. Claridge, and Andrew Schulman

Authors of recent studies have championed the importance of maintaining cerebral perfusion pressure (CPP) to prevent secondary brain injury following traumatic head injury. Data from these studies have provided little information regarding outcome following severe head injury in patients with an intracranial pressure (ICP) greater than 40 mm Hg, however, in July 1997 the authors instituted a protocol for the management of severe head injury in patients with a Glasgow Coma Scale score lower than 9. The protocol was focused on resuscitation from acidosis, maintenance of a CPP greater than 60 mm Hg through whatever means necessary as well as elevation of the head of the bed, mannitol infusion, and ventriculostomy with cerebrospinal fluid drainage for control of ICP. Since the institution of this protocol, nine patients had a sustained ICP greater than 40 mm Hg for 2 or more hours, and five of these had an ICP greater than 75 mm Hg on insertion of the ICP monitor and later experienced herniation and expired within 24 hours. Because of the severe nature of the injuries demonstrated on computerized tomography scans and their physical examinations, these patients were not aggressively treated under this protocol. The authors vigorously attempted to maintain a CPP greater than 60 mm Hg with intensive fluid resuscitation and the administration of pressor agents in the four remaining patients who had developed an ICP higher than 40 mm Hg after placement of the ICP monitor. Two patients had an episodic ICP greater than 40 mm Hg for more than 36 hours, the third patient had an episodic ICP greater than of 50 mm Hg for more than 36 hours, and the fourth patient had an episodic ICP greater than 50 mm Hg for more than 48 hours. On discharge, all four patients were able to perform normal activities of daily living with minimal assistance and experience ongoing improvement.

Data from this preliminary study indicate that intense, aggressive management of CPP can lead to good neurological outcomes despite extremely high ICP. Aggressive CPP therapy should be performed and maintained even though apparently lethal ICP levels may be present. Further study is needed to support these encouraging results.

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Cerebral pressure autoregulation and optimal cerebral perfusion pressure during neurocritical care of children with traumatic brain injury

Fartein Velle, Anders Lewén, Timothy Howells, Anders Hånell, Pelle Nilsson, and Per Enblad

insults to achieve the best possible long-term outcome. 5 The optimal threshold targets for intracranial pressure (ICP) and cerebral perfusion pressure (CPP) are not completely elucidated in children. 6 It is of outmost importance to gain further knowledge concerning the pathophysiology of TBI in children to optimize NIC and to develop individualized management. Instead of using fixed targets for CPP, cerebrovascular pressure reactivity–directed targets for CPP could be beneficial in NIC 7 – 10 but have so far been studied to a lesser extent in children. 11 – 16

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Novel index for predicting mortality during the first 24 hours after traumatic brain injury

Hakseung Kim, Hack-Jin Lee, Young-Tak Kim, Yunsik Son, Peter Smielewski, Marek Czosnyka, and Dong-Joo Kim

L owered cerebral blood flow (CBF) is an immediate consequence of traumatic brain injury (TBI). 35 The subsequent secondary ischemic insult in the brain is a well-known phenomenon; hence, maintaining an adequate level of CBF is considered to be one of the primary objectives during the management of TBI. 6 Normally, the cerebral circulation maintains a relatively constant CBF, despite the fluctuations in cerebral perfusion pressure (CPP), through an intrinsic, homeostatic mechanism known as cerebral autoregulation. 25 However, this mechanism often fails in

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ICP, CPP, and PRx in traumatic brain injury and aneurysmal subarachnoid hemorrhage: association of insult intensity and duration with clinical outcome

Teodor Svedung Wettervik, Anders Hånell, Timothy Howells, Elisabeth Ronne Engström, Anders Lewén, and Per Enblad

T raumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (aSAH) are two types of acute brain injury with high rates of mortality and neurological sequelae. 1 , 2 Both severe TBI and aSAH patients are at high risk of developing secondary brain injury. Neurointensive care (NIC) in these patients aims to prevent, monitor, detect, and treat secondary insults to avoid secondary brain injury. 3 The traditional main NIC variables are intracranial pressure (ICP) and cerebral perfusion pressure (CPP), and recently pressure reactivity index (PRx) is