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ORIGINAL ARTICLE Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO 2 K. L. KIENING, W. N. SCHOENING, J. F. STOVER & A. W. UNTERBERG Department of Neurosurgery, Virchow Medical Centre, Charite ´, Humboldt-University at Berlin, Germany Abstract The objective of the present study was to test the new continuous intracranial compliance (cICC) device in terms of data quality, relationship to intracranial pressure (ICP) and brain tissue oxygenation (PtiO 2 ). A total of 10 adult patients with severe traumatic brain injury underwent computerized monitoring of arterial blood pressure, ICP, cerebral perfusion pressure, end- tidal CO 2 , cICC and PtiO 2 providing a total of 1726 h of data. (1) The data quality assessed by calculating the ‘time of good data quality’ (TGDQ, %), i.e. the median duration of artefact-free time as a percentage of total monitoring time reached 98 and 99% for ICP and PtiO 2 , while cICC measurements were free of artefacts in only 81%. (2) Individual regression analysis showed broad scattered correlation between cICC and ICP ranging from low (r = 0.05) to high (r = 0.52) correlation coefficients. (3) From 225 episodes of increased ICP (ICP 4 20 mmHg 4 10 min), only 37 were correctly predicted by a preceding decline in cICC to pathological values ( 5 0.5 ml/mmHg). (4) In all episodes of cerebral hypoxia (PtiO 2 5 10 mmHg 4 10min), cICC was not pathologically altered. Based on the present results, we conclude that the current hardware and software version of the cICC monitoring system is unsatisfactory concerning data quality, prediction of increased 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 Aesculap 1 -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 Br J Neurosurg Downloaded from informahealthcare.com by Universite De Sherbrooke on 11/07/14 For personal use only.

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Page 1: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO               2

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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Page 2: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO               2

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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Page 3: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO               2

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

Continuous monitoring of intracranial compliance 313

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Page 4: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO               2

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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Page 5: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO               2

(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).

Continuous monitoring of intracranial compliance 315

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Page 6: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO               2

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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Page 7: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO               2

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).

Continuous monitoring of intracranial compliance 317

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Page 8: Continuous monitoring of intracranial compliance after severe head injury: relation to data quality, intracranial pressure and brain tissue PO               2

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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