Invasive methods of intracranial pressure monitoring including infusion tests

The gold standard of ICP monitoring, which was first introduced before 1951,12,27 still remains the measurement of intraventricular fluid pressure either directly or via a CSF reservoir, with the opportunity to exclude zero drift. Subdural fluid filled catheters are reasonably accurate below 30 mmHg. Risk of infection, epilepsy, and haemorrhage is less with subdural than with intraventricular catheters, but even the latter should be less than 5% overall. Catheter tip transducers are useful particularly for waveform analysis, whether placed intraventricularly, subdurally, or intracerebrally. Ventricular catheters permit the therapeutic drainage of CSF in cases of ventricular dilatation.

In more chronic conditions of ventricular dilatation, where ICP is not greatly raised, obstruction to CSF absorption may be confirmed by cSf infusion tests (ventricular or lumbar) taking care to adapt the technique to the site of any obstruction.28-30

The infusion study can be performed via the lumbar CSF space or via a pre-implanted ventricular access device. In both cases two needles are inserted (22G spinal needles for lumbar tests; 25G butterfly needles for ventricular studies). One needle is connected to a pressure transducer via a stiff saline-filled tube and the other to an infusion pump mounted on a purpose-built trolley containing a pressure amplifier and an IBM-compatible personal computer running software written in house. After 10 minutes of baseline measurement, the infusion of normal saline at a rate of 15 ml/min or 1 ml/min (if the baseline pressure was higher than 15 mmHg) starts and continues until a steady state ICP plateau is achieved (Figure 7.9). If the ICP increases to 40 mmHg, the infusion is interrupted. Following cessation of the saline infusion, ICP is recorded until it decreases to steady baseline levels. All compensatory parameters are calculated using computer-supported methods based on physiological models of the CSF circulation.30-33 Baseline ICP and RCSF characterise static conditions of CSF circulation. RCSF is calculated as the pressure increase during the infusion, divided by the infusion rate. A value below 13 mmHg/(ml/min) characterises normal CSF circulation.28 Above 18 mmHg/ (ml/min) the CSF circulation is clearly disturbed.34 Between 13 and 18 mmHg/(ml/min) there is a grey zone, when other

AMPn

ICPn ICPe -[mmHg]

Figure 7.9 Recording of ICP and pulse amplitude (AMP) during infusion study.

Constant rate infusion (1 ml/min) started 9 minutes after insertion of needles into Ommaya reservoir and finished 13 minutes later. ICP increased from 11 to 32 mmHg, indicating resistance to CSF outflow of 21 mmHg/(m/min)

ICPn ICPe -[mmHg]

Figure 7.9 Recording of ICP and pulse amplitude (AMP) during infusion study.

Constant rate infusion (1 ml/min) started 9 minutes after insertion of needles into Ommaya reservoir and finished 13 minutes later. ICP increased from 11 to 32 mmHg, indicating resistance to CSF outflow of 21 mmHg/(m/min)

compensatory parameters and clinical investigation should be considered to make a decision about shunting.33

The cerebrospinal elasticity coefficient (Ej) and pulse amplitude of ICP waveform (AMP) express the dynamic components of CSF pressure volume compensation.

E1 describes the compliance of the CSF compartment according to the formula:

Compliance of CSF space = Ci = 1/ {E: x (ICP-p0)}, where p0 is the unknown reference pressure level, representing hydrostatic difference between the site of ICP measurement and pressure indifferent point of cerebrospinal axis.35,36 Cerebrospinal compliance is inversely proportional to ICP, therefore comparison between different subjects can be made only at the same level of the difference: ICP - p0. The elastance coefficient E1 is independent of ICP, thus this coefficient is a much more convenient parameter when comparing individual patients. A low value of E1 (less 0 2 L/ml) is specific for a compliant system, whilst a high value indicates decreased pressure-volume compensatory reserve.

The pulse amplitude of ICP (AMP) increases proportionally when the mean ICP rises. The proportionality ratio (the AMP/P index) characterises both elastance of the cerebrospinal space and the transmission of arterial pulsations to the CSF compartment.30

Finally, the production of CSF fluid can be estimated using Davson's equation. However, the sagittal sinus pressure is unknown and cannot be easily measured without increasing the invasiveness of the whole procedure. Consequently, the Pss and CSF formation are estimated jointly using a non-linear model utilising the least square distance method during the computerised infusion test.33 It is important to mention that such an "estimate" of CSF production rate approximates CSF absorption, rather than the actual production rate. It is based upon the assumption that all circulating CSF is reabsorbed via the arachnoid granulations. In cases where significant CSF leakage into brain parenchyma occurs, CSF production may be grossly underestimated.

Twenty-four hour intracranial pressure monitoring in patients with so-called normal pressure hydrocephalus may reveal a high incidence of B waves during sleep which is a very helpful prognostic sign for the outcome following shunting (see also Figure 7.3i).29,36-38 Benign intracranial hypertension seldom requires more than CSF pressure monitoring through a lumbar catheter or needle for an hour.

Considerable effort continues into the detailed analysis of the ICP trace to determine whether it is possible to reveal the mechanism of raised ICP and whether autoregulatory reserve remains intact. The pulsatile waveform of ICP hypothetically includes information about both transmission of the arterial pulse pressure through the arterial walls and the compliance of the brain. This information is not always clear and demands specific computer analysis and critical interpretation, thereby restricting its use to only a few centres.

It has been proposed9 that congestion or vascular brain swelling may be present when the ratio of the amplitudes of the pulse and respiratory components of the ICP trace exceeds two, when there is an increase in the high frequency centroid,39 or when there is a high amplitude transfer function for the harmonics from arterial pressure to ICP. Such a transfer function is calculated from the Fourier transform of the digitised signal.40 Continuous multimodality monitoring is required to draw any

ICPD 36 [mmHg] 32

28 24 20

[mmHg2]

SIOWD

waves

Respiratory^ waves a

Time [min] Pulse wave

sra 1

4th harmonic

Frequency [Hz]

Figure 7.10 Example of ICP recording showing pulse, respiratory, and "slow waves" overlapped in time-domain (upper panel) and separated in frequency domain (lower panel)

safe conclusions, however, and should include some measure of cerebral blood flow (for example, transcranial Doppler sonography) and indirect measures of cerebral metabolism (for example, EEG, jugular venous oxygen saturation). Indices of imminent decompensation would be very helpful but volume pressure responses,41 pressure volume indices, or definition of the contribution of CSF outflow resistance to intracranial pressure5 are not suitable for routine clinical use.

Using computer analysis the ICP waveform can be interpreted far more precisely. Basic breakdown to pulse wave, respiratory wave, and slow waves (of a period from 20 seconds to 3 minutes) can be done using frequency analysis (Figure 7.10).

A few complex indices describing cerebrospinal dynamics have been introduced. Although they are not in standard use, more advanced readers may benefit from this methodology.

Pressure-volume compensatory reserve index (RAP)

The RAP index (correlation coefficient [R] between AMP amplitude [A] and mean pressure [P]) was derived by linear correlation between 40 consecutive, time-averaged data points of AMP and ICP acquired over 6.4 seconds. This index indicates the degree of correlation between AMP and mean ICP over short periods of time (~ 4 minutes). Its clinical significance has been discussed before.9 Theoretically, the RAP coefficient indicates the relationship between ICP and changes in volume of the intracerebral space, known as the "pressure-volume curve".2,20,30 An RAP coefficient close to 0 indicates lack of synchronisation between changes in AMP and mean ICP. This denotes a good pressure-volume compensatory reserve at low ICP (Figure 7.1b). When RAP rises to +1, AMP varies directly with ICP and this indicates that the "working point" of the intracranial space shifts to the right towards the steep part of the pressure-volume curve. Here compensatory reserve is low, therefore any further rise in volume may produce a rapid increase in ICP. Following head injury and subsequent brain swelling RAP is usually close to +1. With further increase in ICP, AMP decreases and RAP values fall below zero. This occurs when the cerebral autoregulatory capacity is exhausted and the pressure-volume curve bends to the right as the capacity of cerebral arterioles to dilate in response to a cerebral perfusion pressure decrement is exhausted, and they tend to passively collapse. This indicates terminal cerebrovascular derangement with a decrease in pulse pressure transmission from the arterial bed to the intracranial compartment (Figure 7.11).

Cerebrovascular pressure-reactivity index (PRx)

A second ICP-derived index is the pressure-reactivity index (PRx), which incorporates the philosophy of assessing cerebrovascular pressure reactivity by observing the response of ICP to spontaneous changes in arterial blood pressure (ABP).10 Using computational methods similar to calculation of the RAP index, PRx is determined by calculating the correlation coefficient between 40 consecutive, time-averaged data points of ICP and ABP. A positive PRx signifies a positive gradient of the regression line between the slow components of ABP and ICP, which we hypothesise to be associated with a passive behaviour of a non-reactive vascular bed. A negative value of PRx reflects a normally reactive vascular bed, as ABP waves provoke inversely correlated waves in ICP (Figure 7.12). This index correlates well with indices of autoregulation based on transcranial Doppler ultrasonography.42,43 Furthermore,

AMPD

RAP 02

AMPD

Time [hours]

Figure 7.11 Example of the relationship between pulse wave amplitude (AMP) and mean intracranial pressure (ICP) recorded during a 46 hour period, during which terminal intracranial hypertension developed.

Time [hours]

Figure 7.11 Example of the relationship between pulse wave amplitude (AMP) and mean intracranial pressure (ICP) recorded during a 46 hour period, during which terminal intracranial hypertension developed.

Pulse amplitude increased first proportionally to the change in ICP but started to decrease when ICP increased above 80 mmHg. The regression plot between AMP and ICP (bottom panel) indicated a biphasic relationship of positive and negative slopes. The correlation coefficient between AMP and ICP (RAP) was positive before 32 hours but negative after that, indicating terminal cerebrovascular deterioration abnormal values of both PRx and RAP, respectively indicative of poor autoregulation or deranged cerebrospinal compensatory reserve, have been demonstrated to be predictive of a poor outcome following head injury (Figure 7.13).44,45

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