Cerebral perfusion pressure: management protocol and clinical results

1995 ◽  
Vol 83 (6) ◽  
pp. 949-962 ◽  
Author(s):  
Michael J. Rosner ◽  
Sheila D. Rosner ◽  
Alice H. Johnson
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebrospinal Fluid Drainage ◽  
Content Type ◽  
Vasopressor Support ◽  
Management Techniques ◽  
Gcs Score ◽  
Fine Print

✓ Early results using cerebral perfusion pressure (CPP) management techniques in persons with traumatic brain injury indicate that treatment directed at CPP is superior to traditional techniques focused on intracranial pressure (ICP) management. The authors have continued to refine management techniques directed at CPP maintenance. One hundred fifty-eight patients with Glasgow Coma Scale (GCS) scores of 7 or lower were managed using vascular volume expansion, cerebrospinal fluid drainage via ventriculostomy, systemic vasopressors (phenylephrine or norepinephrine), and mannitol to maintain a minimum CPP of at least 70 mm Hg. Detailed outcomes and follow-up data bases were maintained. Barbiturates, hyperventilation, and hypothermia were not used. Cerebral perfusion pressure averaged 83 ± 14 mm Hg; ICP averaged 27 ± 12 mm Hg; and mean systemic arterial blood pressure averaged 109 ± 14 mm Hg. Cerebrospinal fluid drainage averaged 100 ± 98 cc per day. Intake (6040 ± 4150 cc per day) was carefully titrated to output (5460 ± 4000 cc per day); mannitol averaged 188 ± 247 g per day. Approximately 40% of these patients required vasopressor support. Patients requiring vasopressor support had lower GCS scores than those not requiring vasopressors (4.7 ± 1.3 vs. 5.4 ± 1.2, respectively). Patients with vasopressor support required larger amounts of mannitol, and their admission ICP was 28.7 ± 20.7 versus 17.5 ± 8.6 mm Hg for the nonvasopressor group. Although the death rate in the former group was higher, the outcome quality of the survivors was the same (Glasgow Outcome Scale scores 4.3 ± 0.9 vs. 4.5 ± 0.7). Surgical mass lesion patients had outcomes equal to those of the closed head-injury group. Mortality ranged from 52% of patients with a GCS score of 3 to 12% of those with a GCS score of 7; overall mortality was 29% across GCS categories. Favorable outcomes ranged from 35% of patients with a GCS score of 3 to 75% of those with a GCS score of 7. Only 2% of the patients in the series remained vegetative and if patients survived, the likelihood of their having a favorable recovery was approximately 80%. These results are significantly better than other reported series across GCS categories in comparisons of death rates, survival versus dead or vegetative, or favorable versus nonfavorable outcome classifications (Mantel—Haenszel χ2, p < 0.001). Better management could have improved outcome in as many as 35% to 50% of the deaths.

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

2000 ◽  
Vol 92 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Niels Juul ◽  
Gabrielle F. Morris ◽  
Sharon B. Marshall ◽  
_ _ ◽  
Lawrence F. Marshall
Keyword(s):  
Head Injury ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Neurological Deterioration ◽  
Double Blind ◽  
Content Type ◽  
Fine Print

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.

Cerebrospinal fluid lactate and lactate/pyruvate ratios in hydrocephalus

1976 ◽  
Vol 44 (3) ◽  
pp. 337-341 ◽  
Author(s):  
James E. Raisis ◽  
Glenn W. Kindt ◽  
John E. McGillicuddy ◽  
Carole A. Miller
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Perfusion ◽  
Inverse Relationship ◽  
Redox State ◽  
Anaerobic Metabolism ◽  
Perfusion Pressure ◽  
Cerebral Metabolism ◽  
Content Type ◽  
Lactate And Pyruvate ◽  
Fine Print

✓ Cerebral metabolism in 21 hydrocephalic patients was studied. Preoperative and postoperative specimens of cerebrospinal fluid (CSF) were obtained and the cerebral perfusion pressure (CPP) was calculated in each instance. The specimens of CSF were analyzed for lactate and pyruvate and the lactate/pyruvate (L/P) ratio was calculated for each sample. The L/P ratio, which reflects the redox state of the cell, was used to determine the extent of anaerobic metabolism. An inverse relationship was noted between CPP and lactate as well as the L/P ratio. In general, the level of anaerobic metabolism was decreased after insertion of a shunt.

Pressure reactivity as a guide in the treatment of cerebral perfusion pressure in patients with brain trauma

2005 ◽  
Vol 102 (2) ◽  
pp. 311-317 ◽  
Author(s):  
Tim Howells ◽  
Kristin Elf ◽  
Patricia A. Jones ◽  
Elisabeth Ronne-Engström ◽  
Ian Piper ◽  
...  
Keyword(s):  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Regression Line ◽  
Brain Trauma ◽  
Treatment Protocols ◽  
Content Type ◽  
Arterial Blood ◽  
Pressure Reactivity ◽  
Fine Print

Object. The aim of this study was to compare the effects of two different treatment protocols on physiological characteristics and outcome in patients with brain trauma. One protocol was primarily oriented toward reducing intracranial pressure (ICP), and the other primarily on maintaining cerebral perfusion pressure (CPP). Methods. A series of 67 patients in Uppsala were treated according to a protocol aimed at keeping ICP less than 20 mm Hg and, as a secondary target, CPP at approximately 60 mm Hg. Another series of 64 patients in Edinburgh were treated according to a protocol aimed primarily at maintaining CPP greater than 70 mm Hg and, secondarily, ICP less than 25 mm Hg for the first 24 hours and 30 mm Hg subsequently. The ICP and CPP insults were assessed as the percentage of monitoring time that ICP was greater than or equal to 20 mm Hg and CPP less than 60 mm Hg, respectively. Pressure reactivity in each patient was assessed based on the slope of the regression line relating mean arterial blood pressure (MABP) to ICP. Outcome was analyzed at 6 months according to the Glasgow Outcome Scale (GOS). The prognostic value of secondary insults and pressure reactivity was determined using linear methods and a neural network. In patients treated according to the CPP-oriented protocol, even short durations of CPP insults were strong predictors of death. In patients treated according to the ICP-oriented protocol, even long durations of CPP insult—mostly in the range of 50 to 60 mm Hg—were significant predictors of favorable outcome (GOS Score 4 or 5). Among those who had undergone ICP-oriented treatment, pressure-passive patients (MABP/ICP slope ≥ 0.13) had a better outcome. Among those who had undergone CPP-oriented treatment, the more pressure-active (MABP/ICP slope < 0.13) patients had a better outcome. Conclusions. Based on data from this study, the authors concluded that ICP-oriented therapy should be used in patients whose slope of the MABP/ICP regression line is at least 0.13, that is, in pressure-passive patients. If the slope is less than 0.13, then hypertensive CPP therapy is likely to produce a better outcome.

Cerebral perfusion pressure, intracranial pressure, and head elevation

1986 ◽  
Vol 65 (5) ◽  
pp. 636-641 ◽  
Author(s):  
Michael J. Rosner ◽  
Irene B. Coley
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Pressure Waves ◽  
Content Type ◽  
Arterial Blood ◽  
Head Elevation ◽  
Adequate Hydration ◽  
Fine Print

✓ Previous investigations have suggested that intracranial pressure waves may be induced by reduction of cerebral perfusion pressure (CPP). Since pressure waves were noted to be more common in patients with their head elevated at a standard 20° to 30°, CPP was studied as a function of head position and its effect upon intracranial pressure (ICP). In 18 patients with varying degrees of intracranial hypertension, systemic arterial blood pressure (SABP) was monitored at the level of both the head and the heart. Intracranial pressure and central venous pressure were assessed at every 10° of head elevation from 0° to 50°. For every 10° of head elevation, the average ICP decreased by 1 mm Hg associated with a reduction of 2 to 3 mm Hg CPP. The CPP was not beneficially affected by any degree of head elevation. Maximal CPP (73 ± 3.4 mm Hg (mean ± standard error of the mean)) always occurred with the head in a horizontal position. Cerebrospinal fluid pressure waves occurred in four of the 18 patients studied as a function of reduced CPP caused by head elevation alone. Thus, elevation of the head of the bed was associated with the development of CPP decrements in all cases, and it precipitated pressure waves in some. In 15 of the 18 patients, CPP was maintained by spontaneous 10- to 20-mm Hg increases in SABP, and pressure waves did not occur if CPP was maintained at 70 to 75 mm Hg or above. It is concluded that 0° head elevation maximizes CPP and reduces the severity and frequency of pressure-wave occurrence. If the head of the bed is to be elevated, then adequate hydration and avoidance of pharmacological agents that reduce SABP or prevent its rise are required to maximize CPP.

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

1998 ◽  
Vol 89 (6) ◽  
pp. 971-982 ◽  
Author(s):  
Paul Vespa ◽  
Mayumi Prins ◽  
Elizabeth Ronne-Engstrom ◽  
Michael Caron ◽  
Ehud Shalmon ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebral Microdialysis ◽  
Extracellular Glutamate ◽  
Content Type ◽  
The Mean ◽  
Fine Print

Object. To determine the extent and duration of change in extracellular glutamate levels after human traumatic brain injury (TBI), 17 severely brain injured adults underwent implantation of a cerebral microdialysis probe and systematic sampling was conducted for 1 to 9 days postinjury. Methods. A total of 772 hourly microdialysis samples were obtained in 17 patients (median Glasgow Coma Scale score 5 ± 2.5, mean age 39.4 ± 20.4 years). The mean (± standard deviation) glutamate levels in the dialysate were evaluated for 9 days, during which the mean peak concentration reached 25.4 ± 13.7 (µM on postinjury Day 3. In each patient transient elevations in glutamate were seen each day. However, these elevations were most commonly seen on Day 3. In all patients there was a mean of 4.5 ± 2.5 transient elevations in glutamate lasting a mean duration of 4.4 ± 4.9 hours. These increases were seen in conjunction with seizure activity. However, in many seizure-free patients the increase in extracellular glutamate occurred when cerebral perfusion pressure was less than 70 mm Hg (p < 0.001). Given the potential injury-induced uncoupling of cerebral blood flow and metabolism after TBI, these increases in extracellular glutamate may reflect a degree of enhanced cellular crisis, which in severe head injury in humans appears to last up to 9 days. Conclusions. Extracellular neurochemical measurements of excitatory amino acids may provide a marker for secondary insults that can compound human TBI.

The effect of cold-induced brain edema on cerebrospinal fluid formation rate

1980 ◽  
Vol 53 (5) ◽  
pp. 652-655 ◽  
Author(s):  
K. Gwan Go ◽  
Gerald M. Hochwald ◽  
Lenie Koster-Otte ◽  
Annie K. van Zanten ◽  
Mysore Gandhi
Keyword(s):  
Cerebrospinal Fluid ◽  
Brain Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Formation Rate ◽  
Content Type ◽  
Ventriculocisternal Perfusion ◽  
Fluid Formation ◽  
Csf Formation Rate ◽  
Fine Print

✓ The net contribution of vasogenic brain edema to cerebrospinal fluid (CSF) formation was studied by ventriculocisternal perfusion. Individual cats were perfused both before and 2 ½ hours after a severe cold-induced injury to the cerebral cortex, and the results were compared. Although the edema had occupied the larger part of the hemispheric white matter and bordered the lateral ventricle, a decrease rather than an increase in CSF formation rate was observed. This decrease was related to a decrease in the cerebral perfusion pressure by a regression equation that was not affected by the cold injury.

Use of indomethacin in brain-injured patients with cerebral perfusion pressure impairment: preliminary report

1995 ◽  
Vol 83 (4) ◽  
pp. 627-630 ◽  
Author(s):  
Alberto A. Biestro ◽  
Ricardo A. Alberti ◽  
Ana E. Soca ◽  
Mario Cancela ◽  
Corina B. Puppo ◽  
...  
Keyword(s):  
Cerebral Perfusion Pressure ◽  
Rectal Temperature ◽  
Standard Therapy ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Time Interval ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print ◽  
Indomethacin Treatment

✓ The effect of indomethacin, a cyclooxygenase inhibitor, was studied in the treatment of 10 patients with head injury and one patient with spontaneous subarachnoid hemorrhage, each of whom presented with high intracranial pressure (ICP) (34.4 ± 13.1 mm Hg) and cerebral perfusion pressure (CPP) impairment (67.0 ± 15.4 mm Hg), which did not improve with standard therapy using mannitol, hyperventilation, and barbiturates. The patients had Glasgow Coma Scale scores of 8 or less. Recordings were made of the patients' ICP and mean arterial blood pressure from the nurse's end-hour recording at the bedside, as well as of their CPP, rectal temperature, and standard therapy regimens. The authors assessed the effects of an indomethacin bolus (50 mg in 20 minutes) on ICP and CPP; an indomethacin infusion (21.5 ± 11 mg/hour over 30 ± 9 hours) on ICP, CPP, rectal temperature, and standard therapy regimens (matching the values before and during infusion in a similar time interval); and discontinuation of indomethacin treatment on ICP, CPP, and rectal temperature. The indomethacin bolus was very effective in lowering ICP (p < 0.0005) and improving CPP (p < 0.006). The indomethacin infusion decreased ICP (p < 0.02), but did not improve CPP and rectal temperature. The effects of standard therapy regimens before and during indomethacin infusion showed no significant changes, except in three patients in whom mannitol reestablished its action on ICP and CPP. Sudden discontinuation of indomethacin treatment was followed by significant ICP rebound. The authors suggest that indomethacin may be considered one of the frontline agents for raised ICP and CPP impairment.

Pressure-volume index as a function of cerebral perfusion pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 369-376 ◽  
Author(s):  
W. John Gray ◽  
Michael J. Rosner
Keyword(s):  
Body Temperature ◽  
Linear Relationship ◽  
Cerebral Perfusion Pressure ◽  
Adenosine Triphosphate ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Volume Index ◽  
Content Type ◽  
Adult Cats ◽  
Fine Print

✓ The pressure-volume index (PVI) was measured as a function of cerebral perfusion pressure (CPP) in 12 adult cats. Anesthesia was induced with methohexital in six animals and with pentobarbital in six animals; all were maintained on an N2O:O2 (70%:30%) mixture. The CPP was either increased in 10-torr increments using norepinephrine or decreased by a combination of adenosine triphosphate and hemorrhage in subgroups. Three estimations of PVI were made at each level of CPP. The PaCO2, body temperature, and hematocrit were controlled at normal levels throughout. In both groups there was a linear relationship between PVI and CPP with increasing CPP being reflected by a rise in PVI. This relationship was more marked in the methohexital group: PVI = 0.37 ml + 0.0005 mm Hg CPP in the pentobarbital group, and PVI = 0.14 ml + 0.0019 mm Hg CPP in the methohexital group. These results indicate that the PVI is not independent of CPP but is a function of CPP and is profoundly influenced by anesthesia.

Effect of cerebral perfusion pressure on contusion volume following impact injury

1999 ◽  
Vol 90 (3) ◽  
pp. 520-526 ◽  
Author(s):  
Stefan-Nikolaus Kroppenstedt ◽  
Michael Kern ◽  
Ulrich-Wilhelm Thomale ◽  
Gerd-Helge Schneider ◽  
Wolfgang Reinhardt Lanksch ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Experimental Conditions ◽  
Content Type ◽  
Arterial Blood ◽  
Controlled Cortical Impact Injury ◽  
Impact Injury ◽  
Fine Print

Object. Although it is generally acknowledged that a sufficient cerebral perfusion pressure (CPP) is necessary for treatment of severe head injury, the optimum CPP is still a subject of debate. The purpose of this study was to investigate the effect of various levels of blood pressure and, thereby, CPP on posttraumatic contusion volume.Methods. The left hemispheres of 60 rats were subjected to controlled cortical impact injury (CCII). In one group of animals the mean arterial blood pressure (MABP) was lowered for 30 minutes to 80, 70, 60, 50, or 40 mm Hg 4 hours after contusion by using hypobaric hypotension. In another group of animals the MABP was elevated for 3 hours to 120 or 140 mm Hg 4 hours after contusion by administering dopamine. The MABP was not changed in respective control groups. Intracranial pressure (ICP) was monitored with an ICP microsensor. The rats were killed 28 hours after trauma occurred and contusion volume was assessed using hematoxylin and eosin—stained coronal slices. No significant change in contusion volume was caused by a decrease in MABP from 94 to 80 mm Hg (ICP 12 ± 1 mm Hg), but a reduction of MABP to 70 mm Hg (ICP 9 ± 1 mm Hg) significantly increased the contusion volume (p < 0.05). A further reduction of MABP led to an even more enlarged contusion volume. Although an elevation of MABP to 120 mm Hg (ICP 16 ± 2 mm Hg) did not significantly affect contusion volume, there was a significant increase in the contusion volume at 140 mm Hg MABP (p < 0.05; ICP 18 ± 1 mm Hg).Conclusions. Under these experimental conditions, CPP should be kept within 70 to 105 mm Hg to minimize posttraumatic contusion volume. A CPP of 60 mm Hg and lower as well as a CPP of 120 mm Hg and higher should be considered detrimental.

Pressure-volume index as a function of cerebral perfusion pressure

1987 ◽  
Vol 67 (3) ◽  
pp. 377-380 ◽  
Author(s):  
W. John Gray ◽  
Michael J. Rosner
Keyword(s):  
Blood Flow ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Complex Function ◽  
Volume Index ◽  
Content Type ◽  
Adult Cats ◽  
Hydrogen Clearance ◽  
Fine Print

✓ The pressure-volume index (PVI) was measured in six adult cats while cerebral perfusion pressure (CPP) was reduced from normal levels to below the autoregulatory range by a continuous infusion of adenosine triphosphate. Anesthesia was induced with methohexital and maintained with an N2O:O2 (70%:30%) mixture. Body temperature, hematocrit, and PaCO2 were held constant throughout each experiment. Cerebral blood flow (CBF) was measured by the hydrogen clearance method. At CPP levels over 50 mm Hg, CBF remained relatively constant despite changes in CPP. Within this range, the PVI varied directly with CPP (PVI = 0.24 ml + 0.0013 mm Hg CPP). Below the autoregulatory range, CBF fell progressively with further decreases in CPP; in this range, PVI was found to increase as CPP fell (PVI = 0.84 ml − 0.0071 mm Hg CPP). These results indicate that the PVI is a complex function of CPP, varying directly with CPP within the autoregulatory range and indirectly with CPP below the autoregulatory range.

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