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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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Effect of reduced cerebral perfusion pressure on cerebral blood flow following inhibition of nitric oxide synthesis

Ingunn R. Rise and Ole J. Kirkeby

number of studies that have been published on the subject, there is considerable controversy regarding the role of this agent in cerebrovascular regulation. The combination of high intracranial pressure and hypotension is common in many patients in neurosurgical wards, and maintenance of autoregulation is crucial for these patients. Cerebral vasomotor responses to changes in cerebral perfusion pressure (CPP) serve protective functions. Loss of vasomotor reactivity leads to a poor outcome in patients who receive neurosurgical intensive care 20, 32 because the

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How low can you go? Intracranial pressure, cerebral perfusion pressure, and respiratory obstruction in children with complex craniosynostosis

Richard Hayward and Sonia Gonsalez

Object. Elevated intracranial pressure (ICP) is a well-recognized complication affecting children suffering from complex forms of craniosynostosis. The effects of ICP, including those on vision, and the underlying mechanisms involved remain uncertain. The aim of this study was to examine the relationships among ICP, cerebral perfusion pressure (CPP), and the episodic alterations in respiratory obstruction that are common in children with craniosynostosis.

Methods. Eleven children with complex craniosynostosis underwent monitoring overnight, including simultaneous recording of subdural ICP, arterial blood pressure (ABP), and a variety of respiratory parameters. Sleep status was also analyzed. Mean values were calculated for all variables, including ICP, CPP, and ABP, during both quiet and active sleep.

Mean ICP during quiet sleep was elevated in five patients, borderline in three, and normal in three children. During active sleep, plateaus of high mean ICP were observed in all patients. Marked decreases in CPP were demonstrated during active sleep with absolute values as low as 14 mm Hg. During quiet sleep, the mean baseline CPP was 53.3 mm Hg (range 34–70 mm Hg). During active sleep, CPP fell to a mean of 32.6 mm Hg (range 23–52 mm Hg). All patients experienced obstructive breathing problems, including 10 with obstructive sleep apnea, the effects of which demonstrated a temporal relationship to the alterations in sleep status, ICP, and CPP. Elevations of ABP appeared modest and remained within the normal limits for age.

Conclusions. The findings of this study indicate that ICP, CPP, and respiratory obstruction interact in a vicious cycle, an observation that helps explain the pattern of plateau waves of elevated ICP characteristic among children with complex forms of craniosynostosis. The data gathered in this series revealed levels of CPP considerably lower than those described previously in clinical reports. Such reductions in CPP most likely contribute to the neurological, cognitive, and ophthalmological morbidity from which these children suffer frequently; therefore, the results of this study have important implications for the management of children with complex forms of craniosynostosis as well as for our understanding of the control of cerebral blood flow in general.

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Focal brain oxygen, blood flow, and intracranial pressure measurements in relation to optimal cerebral perfusion pressure

Adam I. Pelah, Marek Czosnyka, Sarah Menacho, Enyinna Nwachuku, and Gregory W. J. Hawryluk

derive the cerebral perfusion pressure (CPP) and autoregulatory status. Also, the ICP waveform can inform intracranial compliance. 18 In 2002 Steiner et al. first described an ICP-derived metric known as the optimal CPP (CPP opt ). 19 CPP opt is the value of CPP at which cerebral autoregulation is most active and the pressure reactivity index (PRx) 20 is most negative. Some investigators have pursued the possibility that a TBI treatment paradigm targeting CPP opt may improve outcomes. 21 , 22 Although some studies including the recently completed COGiTATE (CPPopt

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Portable head CT scan and its effect on intracranial pressure, cerebral perfusion pressure, and brain oxygen

Clinical article

Kaitlin Peace, Eileen Maloney-Wilensky, Suzanne Frangos, Marianne Hujcs, Joshua Levine, W. Andrew Kofke, Wei Yang, and Peter D. Le Roux

techniques (FiO 2 challenge and follow-up CT scan). Physiological Measurements The following parameters were continuously monitored before and after pHCT in each patient: 1) heart rate using 5- or 12-lead electrocardiogram, 2) mean arterial blood pressure (MABP) by radial artery catheter, 3) SaO 2 by pulse oximetry, 4) ICP, 5) brain temperature, and 6) local PbtO 2 . Cerebral perfusion pressure was calculated from the measured parameters (CPP = MABP − ICP). Physiological parameters were recorded continuously using a bedside monitor (Component Monitoring System M

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Cerebral Perfusion Pressure and Clinical Outcome

Neurosurgical Forum: Letters to the Editor To The Editor Julio Cruz , M.D., Ph.D. The Comprehensive International Center for Neuroemergencies São Paulo, Brazil 158 159 This letter is in regard to a recently published paper (Juul N, Morris GF, Marshall SB, et al: Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury. J Neurosurg 92: 1–6, January, 2000). The authors found in a large series of brain injured patients that intracranial hypertension is the most devastating event

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Cerebral Perfusion Pressure or Intracranial Pressure?

Neurosurgical Forum: Letters To The Editor To The Editor Jeffrey S. Young , M.D. University of Virginia Health Sciences Center Charlottesville, Virginia 191 192 The controversy over cerebral perfusion pressure (CPP)—directed as opposed to intracranial pressure (ICP)—directed critical care management of the head-injured patient has increased over the last several years. Each center that cares for a large number of patients with severe head injuries has had to examine its own practice strategies in an attempt to integrate CPP management into its management

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Cerebral Perfusion Pressure and Contusion Volume

Neurosurgical Forum: Letters to the Editor To The Editor Julio Cruz , M.D., Ph.D. The Comprehensive International Center for Neuroemergencies São Paulo, Brazil 161 162 This letter is in regard to a recently published paper (Kroppenstedt SN, Kern M, Thomale UW, et al: Effect of cerebral perfusion pressure on contusion volume following impact injury. J Neurosurg 90: 520–526, March, 1999). The authors reported their experience with an animal model of brain trauma that does not verify much of what has been found in severe acute brain trauma in humans. Hypobaric

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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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Increase in extracellular glutamate caused by reduced cerebral perfusion pressure and seizures after human traumatic brain injury: a microdialysis study

Paul Vespa, Mayumi Prins, Elizabeth Ronne-Engstrom, Michael Caron, Ehud Shalmon, David A. Hovda, Neil A. Martin, and Donald P. Becker

increased glucose utilization that follows brain injury is accompanied by a concurrent reduction of CBF that creates a state of vulnerability to secondary insults. 32, 36 This mismatch between glucose utilization and reduction in CBF occurs at a time when extracellular glutamate is elevated. 4, 36 In human brain injury a similar reduction in CBF to near-ischemic levels occurs during this period. 8, 31, 38 Decreases in cerebral perfusion pressure (CPP) to less than 60 mm Hg and jugular venous oximetry below 55% are recognized clinical events that may occur during this