continuous monitoring of intracranial compliance after severe head injury: relation to data quality,...
TRANSCRIPT
ORIGINAL ARTICLE
Continuous monitoring of intracranial compliance after severe headinjury: relation to data quality, intracranial pressure and brain tissuePO2
K. L. KIENING, W. N. SCHOENING, J. F. STOVER & A. W. UNTERBERG
Department of Neurosurgery, Virchow Medical Centre, Charite, Humboldt-University at Berlin, Germany
AbstractThe objective of the present study was to test the new continuous intracranial compliance (cICC) device in terms of dataquality, relationship to intracranial pressure (ICP) and brain tissue oxygenation (PtiO2). A total of 10 adult patients with severetraumatic brain injury underwent computerized monitoring of arterial blood pressure, ICP, cerebral perfusion pressure, end-tidal CO2, cICC and PtiO2 providing a total of 1726 h of data. (1) The data quality assessed by calculating the ‘time of gooddata quality’ (TGDQ, %), i.e. the median duration of artefact-free time as a percentage of total monitoring time reached 98and 99% for ICP and PtiO2, while cICC measurements were free of artefacts in only 81%. (2) Individual regression analysisshowed broad scattered correlation between cICC and ICP ranging from low (r=0.05) to high (r=0.52) correlationcoefficients. (3) From 225 episodes of increased ICP (ICP 4 20 mmHg 4 10 min), only 37 were correctly predicted by apreceding decline in cICC to pathological values (5 0.5 ml/mmHg). (4) In all episodes of cerebral hypoxia (PtiO2
5 10 mmHg 4 10min), cICC was not pathologically altered. Based on the present results, we conclude that the currenthardware and software version of the cICC monitoring system is unsatisfactory concerning data quality, prediction ofincreased ICP and revelance of cerebral hypoxic episodes.
Key words: Cerebral oxygenation, multimodal cerebral monitoring, traumatic brain injury.
Introduction
Continuous measurement of intracranial pressure
(ICP) is a standard monitoring procedure in patients
suffering from severe traumatic brain injury (TBI).1
However, ICP monitoring alone does not always
predict any evolving structural and functional dete-
rioration related to progressive growth of contusions,
haematomas and oedema, due to compensatory
mechanisms related to shifting of cerebrospinal fluid
and general atrophy, especially in older patients,
making the extent of underlying pathology less
transparent. Assessing changes in ICP upon challen-
ging the intracranial compartment by adding fixed
amounts of volume are thought to unmask a
pathological relationship between pressure and vo-
lume, and to also predict forthcoming intracranial
hypertension when small increases in volume induce
a larger than normal increase in pressure under
conditions of exploited compensatory mechanisms
within the intracranial compartment, as for example,
in cases of space-occupying mass lesions. This
volume-pressure response of the intracranial com-
partment, referring to the ‘stiffness’ of the brain is
also known as the intracranial compliance (ICC).
Thus, continuous monitoring of ICC offers the
possibility to unmask an impending increase in ICP
before it actually occurs, thereby potentially prevent-
ing further impairment of the already damaged
brain.2
After mathematical analysis of the ICC and its
derived parameter ‘pressure volume index’ (PVI),3
intermittent measurements of intracranial compli-
ance parameters in patients with TBI have been
described depending upon manual injection or
withdrawal of defined fluid volumes into the cere-
brospinal fluid (CSF) compartment.4 Because this
technique is relatively cumbersome, prone to be
inaccurate, potentially dangerous in terms of in-
creased infection rate, time-consuming and only
provides discontinuous data, measurement of PVI
or ICC failed to advance to a routine clinical
monitoring parameter in the past. The recently
developed Aesculap1-Spiegelberg compliance sys-
Received for publication 7 January 2003. Accepted 19 May 2003.
Correspondence: Dr K. L. Kiening, Department of Neurosurgery, University Medical Center, Im Neuenheimer Feld 400, D-69120, Heidelberg, Germany.
Tel: + 49 172 945 0989. Fax: + 49 622 158 80094. E-mail: [email protected]
British Journal of Neurosurgery, August 2003; 17(4): 311 – 318
ISSN 0268-8697 print/ISSN 1360-046X online/03/040311–08 # The Neurosurgical Foundation
DOI: 10.1080/02688690310001601199
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tem (ASCS) (Aesculap1, Tuttlingen, Germany),
however, allows quantitative computerized on-line
measurement of continuous intracranial compliance
(cICC) using a fully automated and ‘closed’ external
volume load, separated from the CSF drainage line.
This system has been shown to be feasible and safe in
both experimental,5 as well as clinical settings,
mainly in the field of hydrocephalus research,6 – 9
and is now commercially available. However, clinical
evaluation of cICC after severe TBI, in particular
concerning its data quality, diagnostic significance
and relationship to other established monitoring
techniques like ICP and brain tissue PO2 (PtiO2)
reflecting evolving cerebral oxidative impairment
during periods of reduced PtiO2, is still pending.
Consequently, in this clinical study using the cICC
device, we specifically investigated data quality, and
determined if changes in cICC correlate with
increases in ICP predict an impending increase in
ICP and reflect episodes of cerebral hypoxia.
Patients, material and methods
Demographic characteristics
From 1998 to 2002, a total of 13 patients with closed
severe TBI required extended intracranial compu-
terized monitoring of ICP, cICC and PtiO2 on the
neurosurgical intensive care unit (NICU) at the
Charite, Virchow Medical Centre. From these, three
patients had to be excluded from further analyses
because of short cICC monitoring time (1 – 2 h) due
to early indispensable decompressive surgery.
Hence, data of 10 adult, severely head-injured
patients with a postresuscitation Glasgow Coma
Scale (GCS) Score 5 9 could be analysed. Patients
predominantly presented with isolated severe TBI
and the intracranial pathology was graded according
to the Marshall CT-classification.10 All patients with
removed epidural haematomas (n=2) revealed
additional contusions. Only minor middle facial or
limb fractures were diagnosed resulting in a median
injury severity score (ISS)11 of 28 (range: 25 – 43). In
any case of cranial surgery to remove contusions
(n=3), acute subdural haematomas (n=2), contu-
sion and acute subdural haematoma (n=1) and
epidural haematomas (n=2), the skull flap was re-
fixed tightly and the dura was sutured ‘water tight’
after subdural procedures to ensure closed intracra-
nial compartment and thus guarantee valid cICC
measurements. In all patients, intubation, artificial
ventilation, administration of analgesics and seda-
tives had to be maintained longer than 12 days
(median: 19.5). Demographical information is sum-
marized in Table I.
Ethical permission
All demographic and monitoring data of patients
enrolled in the present study also contribute to an
ongoing European multi-centre study organized by
the ‘Neuro-Intensive Care Monitoring Research
Group’ (‘Brain-IT’; http://www.brainit.gla.ac.uk),7
designed to define the inherent variability of cICC
in severe TBI, subarachnoid haemorrhage, hydro-
cephalus and brain tumour. Permission for the study
presented here and contribution to the Brain-IT
database7 was granted by the local institutional ethics
committee at the Charite.
General management of patients
All patients were intubated and ventilated at the
accident site. GCS grading was performed either at
the accident site or in the emergency room, and the
extent of intracranial pathology was determined by
computerized tomography (CT). Space occupying
lesions were evacuated immediately in eight patients
(Table I). General intensive care management and
specifically the management of pathologically ele-
vated ICP strictly adhered to the ‘Guidelines for the
Management of Severe Traumatic Brain Injury’
brought forward by the Brain Trauma Foundation
of the American Association of Neurological Sur-
geons on behalf of the Joint Section on Neurotrauma
and Critical Care.1
TABLE I. Demographic data of the 10 investigated severely traumatic brain-injured patients
Patient
no.
Age
(years) Sex GCS ISS CT classification*
Days of incubation,
analgesia & sedation
Days in
NICU
1 48 m 3 25 Evac. mass lesion 12 18
2 35 m 6 34 Diffuse injury III 16 24
3 54 m 7 43 Evac. mass lesion 15 19
4 75 m 3 25 Diffuse injury IV 19 19
5 29 m 3 43 Evac. mass lesion 20 22
6 57 m 8 27 Evac. mass lesion 30 31
7 61 m 3 25 Evac. mass lesion 24 24
8 22 m 3 29 Evac. mass lesion 21 20
9 67 f 3 38 Evac. mass lesion 25 34
10 49 m 3 25 Evac. mass lesion 18 18
Median 51.5 — 3 28 — 19.5 21
*According to reference 10.
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Multimodal cerebral monitoring
Mean arterial blood pressure (MAP) recorded
from a radial arterial catheter levelled to the
external acoustic canal (EAC), ICP, cerebral
perfusion pressure (CPP), end-tidal CO2
(ETCO2), cICC and PtiO2 were recorded simul-
taneously using a multimodal computerized cere-
bral monitoring system (LabVIEW1, National
Instruments, Austin, TX) programmed to digitize
parameter signals with a frequency of 1/min.12 In
addition, all daily activities interfering with data
acquisition, e.g. manipulations by the healthcare
professionals, were documented on a spread sheet
enabling off-line artefact detection at later time
points.
Aesculap-Spiegelberg compliance system: systemdescription, measurement technique, and catheterplacement
Briefly, the ASCS system consists of a two- part
monitoring system for ICP and compliance measure-
ment and a double lumen intraventricular catheter
(probe no. SND 13.1.13 XL13; outside diameter:
3 mm).
The ASCS double lumen intraventricular cathe-
ter was positioned via a conventional frontal burr
hole into the lateral ventricle of the non- or lesser-
injured hemisphere, respectively. Correct catheter
location was assured by CT scan. To challenge the
intracranial volume, one catheter lumen prefilled
with 0.1 ml air, automatically delivers an addi-
tional 0.1 ml of air to the pouch surrounding the
catheter tip. The air is injected over 2.5 s, held for
1 s and withdrawn over 2.5 s, resulting in ICP
changes detected via the second lumen, i.e. the
CSF drainage lumen, using a conventional fluid-
coupled pressure transducer levelled to the EAC.
These signals are then sampled and mathemati-
cally processed with a 200-data point moving
average analysis in the ASCS monitor, thus
calculating the intracranial compliance by a mod-
ification of the formula: ICC (ml/mmHg)=DV(ml)/DP (mmHg). Sufficient fluid-coupled ICP
measurement, as well as CSF drainage are assured
by an interfacing ASCS-operated clamp, allowing
automatic opening and closing of the CSF
drainage line. Every minute, the clamp opens for
10 seconds. During this time, no fluid- coupled
ICP data acquisition is possible and ICP is
‘frozen’ to the last measured value. Thus, eight
cICC data points are generated per minute.
Because 200 cICC measurements are necessary
to determine an adequate cICC value, stable cICC
data can only be expected as early as 24 min upon
initiating the monitoring period. In addition, the
fluid-coupled ICP measurement is imperative to
determine cICC, whereas regular ICP values are
detected via the air pouch.
Measurement of brain tissue PO2
Cerebral white matter PtiO2 was monitored with a
flexible polarographic ‘Clark-type’ microcatheter
(Licox1, Integra Neuroscience, Plainsboro, NJ) with
a diameter of 0.8 mm, a stirring artefact 5 4%, a
response time T90%/358C of 70 s, a sensitivity drift
+ 1% per day and a measured tissue surface area of
about 13 mm2. This probe was inserted via a
separate small burr hole close to the ASCS catheter
with an insertion depth of 34 mm below the dura
level. Brain tissue PO2 values are continuously
averaged over a 500-ms period and adjusted to the
actual body core temperature by the Licox1 com-
puter. The Licox1 system has been extensively and
successfully evaluated under clinical conditions for
data quality, measurement reliability, and detection
of cerebral hypoxic episodes.13 – 16
Off-line data review, artefact elimination and dataanalysis
Artefact detection was performed by a software
replay module (LabVIEW1, National Instruments,
Austin, TX) automatically seeking for data outside
a preset range, which also allows detection of
obvious technical errors as, e.g. cable disconnec-
tion.12 For example, for cICC, the preset range
was 0 – 4 ml/mmHg to exclude inadequately low
(5 0 ml/mmHg) and high values (4 4 ml/mmHg).
Thereafter, data were re-evaluated considering the
notes on the spreadsheet to assure complete
removal of remaining artefacts. Thus, all manip-
ulations (e.g. calibration, flushing, other necessary
patient manipulations, etc.) were removed from the
dataset.
. For data quality analysis, total monitoring
time, as well as artefact-free time of MAP, ICP,
CPP, ETCO2, PtiO2 and cICC was deter-
mined in individual patients. Thereon, the
‘time of good data quality’ could be calculated
using the equation: TGDQ (%)= artefact free
time (min)6 100%/Total monitoring time
(min).
. To achieve closest correlation of cICC to ICP,
individual polynomial non-linear regression
analysis was performed.
. The time-dependent relationship between
cICC and ICP allowed to specify the potency
of cICC in predicting an impending increase in
ICP, by defining ‘pathological episodes’ for
ICP (ICP 4 20 mmHg 4 10 min) and cICC
(cICC 5 0.5 ml/mmHg 4 10 min). Subse-
quently, these episodes were sorted according
to distinct patterns depending on the time
course of their occurrence. For this we coined
the terms ‘type I pattern’ (pathological ICP
followed by pathological cICC episode), ‘type
II pattern’ (pathological cICC followed by
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pathological ICP episode), ‘type III pattern’
(pathological ICP without related pathological
cICC episode) and ‘type IV pattern’ (patholo-
gical cICC episode without related pathologi-
cal ICP episode).
. To determine the changes of cICC during
cerebral hypoxia, ‘cerebral hypoxic episodes’
(CHE) were defined as a PtiO2 5 10 mmHg
4 10 min.14,15 Possible causes for these CHE
were further analysed by individual linear
regressions of PtiO2 and cICC, as well as
MAP, ICP, CPP and ETCO2.
Statistical analysis
All results are given as medians. SigmaPlot 2001
7.01 for Windows (SPSS ScienceTM, Chicago, IL)
was used for regression analyses (regression line,
confidence interval, correlation coefficient).
Results
Data quality analysis
The sum of artefact free total monitoring time of
all patients was 103,568 min (1726 h=72 days).
After removing the artefacts, all investigated para-
meters showed a sufficient median TGDQ (97 –
99%) with the exception of cICC (Table II). The
overall median cICC was only 81%, with a broad
range extending from 28.5 to 94.6% in the
individual patients (Table II). A typical original
recording demonstrates a frequently observed
source of artefacts in cICC measurement (‘drift
phenomenon’; Fig. 1), revealing one major reason
for the low TGDQ in cICC. Overall, TGDQ was
reduced due to device instability in 86% (cICC
4 4 ml/mmHg) of the acquired data and in 14%
due to failure in measuring cICC related to
collapsed ventricles (10%) or engorged CSF
drainage line (4%).
Correlation of cICC and ICP
By plotting cICC against ICP, individual regression
analysis followed a non-linear inverse second order
equation and revealed a broad scattered correlation
coefficient (r), ranging from 0.05 to 0.52. Five
patients showed no correlations at all (patients nos
2 – 6; rrange = 0.05 – 0.10), while four revealed med-
ium correlations (patients nos 1, 7, 8, 10;
rrange = 0.27 – 0.36) and one demonstrated a good
correlation (patient no. 9) with r=0.52 (Fig. 2). In
Fig. 2, the cICC revealed the highest variability
within ICP values 4 10 mmHg (n=3379; range:
0.40 – 3.74 ml/mmHg), which started to decrease
with increasing ICP values (ICP 4 10 – 20 mmHg:
n=9731; range: 0.34 – 2.22 ml/mmHg; ICP 4 20 –
30 mmHg: n=2715; range: 0.34 – 0.97 ml/mmHg)
reaching the smallest variability at ICP values
4 30 mmHg (n=125, range: 0.36 – 0.62 ml/
mmHg).
cICC and prediction of impending increase in ICP
The data analysis revealed 41 type I episodes
(median duration: 40 min; range: 10 – 418 min;
Fig. 3), 37 type II episodes (median duration:
93 min; range: 18 – 1451 min), 147 type III episodes
(median duration: 20 min; range: 10 – 181 min), and
118 type IV episodes (median duration: 38 min;
range: 10 – 1070 min; s; Table III). Therefore, from
a total of 225 episodes of increased ICP (types I, II
and III episodes), only 37 were detected by a
preceding low cICC (type II episodes). In contrast,
prolonged pathological cICC was present in 118
episodes, which were not associated with high ICP
values (type IV episodes; Table III).
cICC during cerebral hypoxic episodes
In five patients, 10 cerebral hypoxic episodes (CHE)
were found with a median duration of 41.5 min
TABLE II. Total monitoring time (TMT), artefact free time [minutes & %] and median TGDQ (%) in monitored parameters
TMT
MAP ICP CPP ETC02 cICC PtiO2
Patient no. (min) (min) (%) (min) (%) (min) (%) (min) (%) (min) (%) (min) (%)
1 8123 8059 99.2 8054 99.1 7996 98.4 8029 98.4 7062 86.9 6472* 99.8*
2 5854 5827 99.5 4966 84.8 4944 84.4 —{ —{ 3843 65.6 5842 99.8
3 3173 3119 98.3 3127 98.6 3085 97.2 3095 97.5 1718 54.1 3147 99.2
4 9943 9641 97.0 9428 94.8 9314 93.8 9660 97.1 7650 76.9 9531 95.8
5 13,756 13,583 98.7 13,622 99.0 13,479 98.0 13,647 99.2 12,965 94.2 13,200 96.0
6 7253 7172 98.9 7212 99.4 7134 98.4 7218 99.5 2064 28.5 7177 98.9
7 7468 7378 98.4 7299 97.7 7268 97.3 7113 96.7 6338 84.9 7124 95.4
8 15,361 15,122 98.9 15,252 99.3 15,042 98.0 15,224 99.1 11,473 74.7 15,270 99.4
9 23,316 22,477 96.4 22,198 95.2 21,430 91.9 23,297 99.9 21,727 93.2 22,917 98.3
10 9321 9053 97.1 9033 96.9 8819 94.6 9315 99.9 9037 94.6 9020 96.8
TGDQ [%] — — 99 — 98 — 97 — 99 — 81 — 99
*PtiO2 measurement of patient no. 1 started 1635 min later than the other parameters.
{No ETCO2 data stored.
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(range: 12 – 144 min; Table IV). Individual regres-
sion analyses revealed, significant linear second order
correlations in patient nos 6 and 10, for MAP, ICP
and CPP to PtiO2 (Table IV, Fig. 4). No significant
coherence were observed in regressions for cICC and
ETCO2 to PtiO2. During all CHE, cICC never
dropped below the threshold of 0.5 ml/mmHg.
Discussion
New devices for intensive care monitoring have to
undergo meticulous testing particularly in regard to
their data quality in comparison with already
established parameters and their validity before
diagnostic and therapeutic consequences can be
drawn at the bedside. In this context, invasive brain
tissue PO2 monitoring has been repeatedly shown to
fulfil these criteria.14 – 18 This far, the validity of the
ASCS device in relation to the ‘gold standard’ of
compliance measurement (conventional manual
volume-pressure technique) has been validated
experimentally in sheep5 and clinically in hydro-
cephalic patients.6 Furthermore, cICC is presently
under intense clinical investigation by advanced off-
line analyses in a multi- centre approach.7,9 Based on
these two studies, pathological cICC threshold in
FIG. 1. Typical original recording (patient no. 6) revealing changes in ICP (solid line), PtiO2 (dotted line) and cICC (long dashed line). From
75 to 100 min, cICC showed a ‘drift phenomenon’ with a sudden deterioration to elevated cICC values (4 10 ml/mmHg), while ICP and
PtiO2 were reliably recorded, illustrating one major source of cICC artefacts accounting for the low median TGDQ of 81%.
n
FIG. 2. Non-linear regression analysis of ICP v. cICC in patient no. 9 follows an inverse second order regression equation. The high cICC
variability at lower ICP values declined with increasing ICP, but reached an acceptable range only at ICP values4 30 mmHg (0.36 – 0.62 ml/
mmHg).
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TBI, subarachnoid haemorrhage and brain tumours
was defined as 4 0.5 ml/mmHg,7,9 while in hydro-
cephalic patients a higher value is probably appro-
priate (median cICCICP20 – 30 mmHg= 0.80+ 0.26
ml/mmHg).7 In detail, the median cICC associated
with an increased ICP (4 20 mmHg) was 0.51 ml/
mmHg (range: 0.29 – 0.73 ml/mmHg) in the severe
TBI population (n=19).9 Hence, we adopted the
threshold of 0.5 ml/mmHg for our analyses.
In comparison with all other monitored para-
meters (MAP, ICP, CPP, ETCO2, PtiO2), cICC was
clearly identified in our study to have the least
FIG. 3. Individual example (patient no. 4) of a ‘type I pattern’ (pathological ICP phase followed by pathological cICC episode): ICP (solid
line) remained elevated as of 21 min (horizontal arrow) followed by a delayed decrease (17 min) in cICC (dotted line) below the pathological
threshold of 0.5 ml/mmHg (vertical arrow).
TABLE III. Frequency of ‘type I – IV episodes’*
Patient no. Type I episodes (n) Type II episodes (n) Type III episodes (n) Type IV episodes (n)
1 8 4 40 4
2 5 7 5 8
3 0 0 10 1
4 1 7 9 32
5 11 9 21 24
6 0 1 14 1
7 0 0 0 14
8 4 0 36 1
9 10 5 12 16
10 2 4 0 17
S 41 37 147 118
*For definitions of type I-IV episodes see text.
TABLE IV. Characteristics of cerebral hypoxic episodes
Patient
Median
MAP
Median
ICP
Median
CPP
Median
ETC02
Median
PtiO2
Median
cICC
no. n (mmHg) (mmHg) (mmHg) (mmHg) (mmHg) (mmHg) PtiO2 correlated to
5 2 94.9 20.1 75.3 25.7 9.3 0.60 —
6 4 100.1 23.5 73.8 31.1 7.9 1.32 MAPr=0.51, ICPr=0.43,
CPPr=0.57
8 1 87.0 11.0 76.0 31.0 9.0 1.00 —
9 1 87.0 15.0 72.0 24.0 9.0 0.57 —
10 2 92.0 13.0 80.0 29.0 8.1 0.55 MAPr=0.63, ICPr=0.60,
CPPr=0.62
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satisfactory data quality (Table II). From all mon-
itoring devices used in severe TBI, only jugular
venous oximetry presents with a lower TGDQ
(*60%) than cICC,15,19 possibly attributable to
the described ‘drift phenomenon’ (Fig. 1), obstruc-
tion of the fluid column (e.g. by clotting or co-
aptation of the ependymal lining as the ventricle
collapses due to CSF draining or increased brain
swelling) occurring frequently after severe TBI. The
wide individual range in TGDQ, extending from
28.5 to 94.6% (Table II) emphasizes the poor
reliability of the cICC monitoring, especially if
intracranial resistance increases as in the case of
evolving brain oedema formation. As revealed by the
representative patient no. 6, the highest individual
median ICP (23.5 mmHg; Table IV) was associated
with the lowest TGDQ in cICC (28.5%; Table II).
This lack of information is most unfortunate in a
critical situation where valid cICC monitoring could
add substantial information to specifically guide the
therapy. The occurrence of at least four consecutive
software errors during the study period underlines
the premature technical condition of the ASCS.
Thus, improvements are necessary concerning soft-
ware quality and ICP measurement technology (e.g.
change from fluid-coupled to, for example, strain
gauge systems to avoid misreadings due to collapsed
ventricles and catheter obstruction). The vastly
scattered cICC data (0.34 – 0.97 ml/mmHg) within
an ICP range of 4 20 – 30 mmHg (Fig. 2) and the
low detection rate of an impending ICP rise of only
16% (37 out of 225 episodes; Table III) further
substantiate the low impact of valid cICC measure-
ments on episodes of markedly elevated ICP. In
addition, the actual value of cICC in neuromonitor-
ing after TBI turns questionable, since no major
disturbances in cICC were noted when CPP was
significantly reduced as ICP reached 30 mmHg in
the four observed cerebral hypoxic episodes of
patient no. 6 (Table IV, Fig. 4).
A crucial point in cICC monitoring is the time
delay of cICC assessment attributed to the system
integrated 200-data point moving average analyses.
Thus, ongoing acute intracranial deterioration can
only be detected with a temporal delay. In addition,
cICC reacts ‘asynchronous’ to ICP and cICC data
are perturbed for as long as 24 min in case of
occurring artefacts. As a consequence, and as
reported in patients with subarachnoid haemorrhage
and brain tumours,9 pathological cICC was not
associated with an ICP 4 20 mmHg in all patients.
At least in some individuals, cICC correlated grossly
with ICP (range of correlation coefficients in patients
nos 1, 7, 8, 9, 10: 0.27 – 0.52 ml/mmHg; Fig. 2).
In contrast to the promising studies of cICC in
hydrocephalic patients7 – 9 presenting with large
ventricles, more chronic and slower changes in ICP
with more stable and progressive adaptive processes,
cICC monitoring following TBI is complicated by
certain disease-related problems, e.g. the heteroge-
neity in cranial injury patterns, the difficult puncture
of the mostly small ventricles, and the squeezed
ventricles due to progressive swelling. One possible
approach to solve at least some of these problems is
the development of an intraparenchymal cICC
device that is currently underway.5 – 20
FIG. 4. Regression analyses (data taken from four cerebral hypoxic
episodes of patient no. 6) revealed high linear second order
correlations between MAP, ICP, CPP and PtiO2. Upper and lower
lines indicate 95% confidence interval. PtiO2 values 5 7 mmHg
coincided with low CPP values 570 mmHg. Pathological PtiO2
values (510 mmHg) also occurred despite sufficient CPP values,
reflecting the critical intracranial impairment in face of increased
ICP (up to 30 mmHg).
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For a final evaluation of cICC in severe TBI, we
have to keep in mind that the present data are
derived from a small cohort (n=10), although ample
sampling time is provided (72 days). In addition, the
threshold of 0.5 ml/mmHg used to assess pathologi-
cal cICC values in TBI originates from still
preliminary results.9 At present, it cannot be ruled
out that the duration of cICC below a given
threshold may be more important than an absolute
cICC threshold.9 Moreover, interim analyses of the
Brain-IT dataset9 point to the possibility that,
overall, a decreased compliance of less than 0.6 ml/
mmHg is of pathological importance. However, a
definitive threshold will not be known until the
required number of patients have been recruited.
However, without the implementation of extended
immediate accessible statistical features, such ana-
lyses in cICC currently have to be performed off-line
and, therefore, are not suitable for the bedside
situation.
Conclusions
Continuous monitoring of intracranial compliance
using the Aesculap1-Spiegelberg compliance system
in patients with severe TBI is currently unsatisfactory
in regard to data quality and relation to ICP. At
present, the obtained data do not convincingly
predict increases in ICP following TBI. Further-
more, they provide no relevant information with
reference to the cause of cerebral hypoxic episodes.
Ultimately, the utility of this technology in this
patient group will depend upon the completion and
validation of a number of technical developments
including an intraparenchymal cICC probe20 and
improved time-series analyses9 of the raw data to
potentially improve both prediction of increased ICP
and the time of good quality data.
Acknowledgements
This work was supported by a grant of the
‘Kuratorium ZNS’ (project no. 99011) and the
‘Humboldt-University at Berlin’.
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