Multimodal Monitoring in Head
Injured Patients Management of CPP:
Detection and Treatment of
optimal CPP
Jürgen Meixensberger
Department of Neurosurgery
CPP = index of input pressure determining CBF and perfusion
1. Why?
2. Critical Border ?
3. Time Course ?
4. Individual
optimized CPP ?
5. Therapy
Effect of
reduced CBF
ml/100g/min
Ischemia
Edema, Lactate
Penumbra
Loss of electric
activity
Loss of Na/K
Pump, ATP
Infarction
Cell death
Risk to secondary ischemic brain damage
 Traumatic brain injury
diffuse
focal, multiple
 Subarachnoid
Hemorrhage
Vasospasm
 Ischemic Stroke
Penumbra
Guideline German Society of Neurosurgery
Traumatic Brain Injury in Adults
CPP
„Adequate cerebral perfusion pressure is necessary to
provide a sufficient cerebral blood flow.
The question, whether to treat increased ICP or
maintainance of CPP as first treatment goal, is still
controversial in the literature.“
AWMF – Leitlinien – Register Nr. 008/001
Cerebral Perfusion Pressure CPP
Definition
Cerebral Perfusion Pressure* is a surrogate of
cerebral blood flow CBF.
CBF = CPP (MAP – ICP*)/CVR
* Referenced to the Foramen of Monroi
CPP and Cerebral Oxygenation
Induced Hypertension
Jaeger M, Acta Neurochir 2005
Valadka A, Acta Neurochir 2002
Menzel M, J Neurosurg Anesthesiol 1999
Doppenberg E, Surg Neurol 1998
Meixensberger J, JNNP 2003
Individual increasing of CPP guided
by PtiO2 >10 mmHg decreased
significantly amount of hypoxic
episodes after TBI.
1. Why?
2. Critical Border ?
3. Time Course ?
4. Individual
optimized CPP ?
5. Causes
6. Therapy
CPP=70 mmHg
CPP=90 mmHg
Coles JP, Brain 2004
 The optimal CPP in patients suffering from TBI is unclear.
 Recommendations:
From CPP>50, > 60 mmHg to CPP>90 mmHg
 Reduced as well as high CPP influenced Outcome in a
negative manner.
Robertson et al. Crit Care Med 1999, Contant et al. J Neurosurg 2001 (n=189)
Balestreri et al. Neurocrit Care 2006 (n=429)
Outcome - Function of ICP and CPP
Balestreri et al
Neurocritical Care 2006
N = 429
Optimal CPP
Brain Trauma Foundation, J Neurotrauma 2003,2007
CPP < 70 mmHg
CPP > 60 mmHg
Avoid CPP < 50 mmHg
Intact Autoregulation:
CPP > 70 mmHg
Robertson C, Crit Care Med 1999Robertson et al.,
Contant et al. J Neurosurg 2001 (n=189)
Balestreri et al. Neurocrit Care 2006 (n=429)
EBIC, Acta Neurochir 1997
CPP 60–70 mmHg
Meixensberger J, Acta Neurochir 1993
Optimized CPP - Therapy
CPP (mmHg)
ptiO2 < 10 mmHg
*
50
68 %
60
42 %
70
20 %
80
8%
TBI N = 30
* Episode > 10 min
3. Time Course ?
4. Individual
optimized CPP ?
5. Causes
6. Therapy
%
%
10 mmHg
pptitiOO22 << 10
mmHg
1
F
R
E
Q
U
E
N
C
Y
Relative Frequenz
1. Why?
2. Critical Border ?
Day1 1-2
Tag
-2
Day33-5
Tag
-5
Day66-8
Tag
-8
0.8
0.6
0.4
0.2
0
> 40
> 50
> 60
> 70
> 80
CPP
CPP(mmHg)
mmHg
> 90
> 100
1. Why?
2. Critical Border ?
3. Time Course ?
4. Individual
optimized CPP ?
5. Causes
Effect of
reduced CBF
ml/100g/min
Ischemia
Edema, Lactate
Penumbra
Loss of electric
activity
Loss of Na/K
Pump, ATP
6. Therapy
Infarction
Cell death
 Concept individual optimized CPP (CPPopt)
Steiner et al. Crit Care Med 2002 (n=114)
 Based on continous monitoring of cerebrovascular
pressure reactivity index PRX
 PRx = moving correlation coefficient MAP / ICP
Czosnyka et al. Neurosurgery 1997
PRx
Individual optimized CPP
CPPopt
CPP
Steiner et al. Crit Care Med 2002
PRx
Individual optimized CPP
+ PtiO2
CPPopt
CPP
Steiner et al. Crit Care Med 2002
 TBI
n=33
 Continous Monitoring (ICM-plus Software)
MAP
ICP
[Codman]
CPP
PtiO2 [Licox]
 PRx = moving correlationcoefficient MAP / ICP
Czosnyka et al. Neurosurgey 1997
 Data analysis
CPP vs. PRx
CPP vs. PtiO2
CPP-class of 5 mmHg
Results:
 CPPopt
n=28/33
 CPPopt
n=7
60-65 mmHg
n=1
65-70 mmHg
n=8
70-75 mmHg
n=1
75-80 mmHg
n=6
80-85 mmHg
n=3
85-90 mmHg
n=2
90-95 mmHg
PRx
(85 %)
CPP
PRx
CPPopt
CPP
PtiO2 PRx
CPPopt
CPP
PRx
CPPopt
CPP
PtiO2 PRx
CPPopt
CPP
PtiO2 PRx
n=28
CPPopt
CPP
Jaeger et al Crit Care Med 2010
Therapeutic Options: CPP > 60, < 70 mmHg *
 Induced hypervolemia with cristalloids
Cave: heart insufficience
 No body/head – elevation 0°
 Inotropica – infusion
Cave: acute coronary syndrome, arrhythmia
 Diuretics – Reduction of centralvenous pressure
 Ventilation - „best PEEP“ - concept
* Option; Prognostic value only given by case reports;
Management of CPP after TBI
Recommendations:
Avoid CPP < 50 mmHg – to minimize edema
formation
CPP > 70 – 80 mmHg – can improve perfusion if
autoregulation is intact
Class II evidence CPP of 60 mmHg – sufficient CBF
and cerebral perfusion in most cases
Ancillary monitoring is helpful to target CPP
Management of CPP after TBI
Recommendations:
Need for more data
 Individualized optimal CPP
based on hemodynamic monitoring/
pressure autoregulation indices
 Randomized outcome studies
Thank You for Your Attention !