Neuromonitoring in the intensive care unit. I. Intracranial pressure and cerebral blood flow monitoring

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1 Intensive Care Med (2007) 33: DOI /s z REVIEW Anuj Bhatia Arun Kumar Gupta Neuromonitoring in the intensive care unit. I. Intracranial pressure and cerebral blood flow monitoring Received: 18 March 2007 Accepted: 22 March 2007 Published online: 24 May 2007 Springer-Verlag 2007 Part II of this article is available at: dx.doi.org/ /s A.Bhatia A.K.Gupta( ) Addenbrooke s Hospital, Department of Anaesthesia, Hills Road, CB2 2QQ Cambridge, UK akg01@globalnet.co.uk Tel.: Fax: A. K. Gupta Addenbrooke s Hospital, Neuroscience Critical Care Unit, Hills Road, CB2 2QQ Cambridge, UK Abstract Background: Monitoring the injured brain is an integral part of the management of severely brain injured patients in intensive care. Brain-specific monitoring techniques enable focused assessment of secondary insults to the brain and may help the intensivist in making appropriate interventions guided by the various monitoring techniques, thereby reducing secondary brain damage following acute brain injury. Discussion: This review explores methods of monitoring the injured brain in an intensive care unit, including measurement of intracranial pressure and analysis of its waveform, and techniques of cerebral blood flow assessment, including transcranial Doppler ultrasonography, laser Doppler and thermal diffusion flowmetry. Conclusions: Various modalities are available to monitor the intracranial pressure and assess cerebral blood flow in the injured brain in intensive care unit. Knowledge of advantages and limitations of the different techniques can improve outcome of patients with acute brain injury. Keywords Traumatic brain injury Intracranial pressure Ultrasonography, Doppler, transcranial Flowmetry, laser Doppler Thermal diffusion flowmetry Abbreviations ABP: arterial blood pressure AMP: amplitude of fundamental component of ICP waveform CBF: cerebral blood flow CBV: cerebral blood volume CO 2 : carbon dioxide CPP: cerebral perfusion pressure CSF: cerebrospinal fluid CT: computerised tomography DID: delayed ischaemic neurological deficit EDP: effective downstream pressure FV: flow velocity HDI: haemodynamic impairment ICP: intracranial pressure ICU: intensive care unit LDF: laser Doppler flowmetry MAP: mean arterial pressure MCA: middle cerebral artery MRI: magnetic resonance imaging ncpp: non-invasively determined cerebral perfusion pressure nicp: non-invasive ICP measurement PET: positron emission tomography PI: pulsatility index PRx: pressure reactivity index RI: resistance index RAP: correlation of amplitude and pressure of ICP waveform SAH: subarachnoid haemorrhage TBI: traumatic brain injury TCD: transcranial Doppler TD: thermal diffusion THRT: transient hyperaemic response test US: ultrasound ZFP: zero flow pressure

2 1264 Introduction Whilst there is little that neurointensive care can offer to prevent the brain damage sustained from the primary insult, the use of appropriate protocol-driven management can, however, minimise the effects of secondary insults on outcome [1]. Monitoring the injured brain is an integral part of the management of severely brain injured patients in intensive care and can be classified into general (systemic) and brain-specific methods. Although general systemic monitoring (e.g. invasive arterial blood pressure, end-tidal carbon dioxide, oxygen saturation of blood) is of vital importance in detecting gross global changes in physiology, brain-specific monitoring techniques enable more focused assessment of secondary insults to the brain and may help the intensivist in making appropriate interventions guided by the various monitoring techniques. An important adjunct to these techniques is the use of a variety of imaging modalities, which, as a result of significant advances over the last two decades, allow us to assess the brain with respect to structural abnormalities, blood flow and metabolism. The advantage of these techniques [computerised tomography (CT), magnetic resonance imaging (MRI), xenon-ct, positron emission tomography, single photon emission computerised emission tomography, magnetic resonance spectroscopy] is that they allow us to assess the interindividual heterogeneity by providing detailed information of different regions of the brain. However this information is not continuous and at present cannot be obtained at the bedside. This review focuses on brain-specific monitoring and will include aspects of intracranial pressure measurement and its interpretation, and methods to monitor cerebral blood flow. Intracranial pressure monitoring Intracranial pressure (ICP) is the pressure within the cranial vault relative to the ambient atmospheric pressure and is now regarded as a core monitoring parameter in the intensive care management of patients with acute brain injury. The ICP increases when compensatory mechanisms which control ICP, such as changes in cerebrospinal fluid (CSF) dynamics, cerebral blood flow (CBF) and cerebral blood volume (CBV), are exhausted. Whilst routine ICP monitoring is widely accepted as a mandatory monitoring technique for management of patients with severe head injury and is a guideline suggested by the European Brain Injury Consortium [2], there is some debate over its efficacy in improving outcome from severe traumatic brain injury. A survey of Canadian neurosurgeons revealed that only 20.4% of the respondents had a high level of confidence in ICP monitoring [3], and a survey of neurointensive care units in the UK showing that only 75% of centres monitor ICP may reflect some of the drawbacks of ICP monitoring [4]. A recently published trial in survivors beyond 24 h following severe brain injury that compared ICP-targeted intensive care with management based on clinical observations and CT findings reported no improvement in outcome with ICP monitoring [5]. However, a review of neurocritical care and outcome from traumatic brain injury (TBI) suggested that ICP-/cerebral perfusion pressure (CPP)-guided therapy may benefit patients with severe head injury, including those presenting with raised ICP in the absence of a mass lesion and also patients requiring complex interventions [1]. Measurement of ICP ICP can be measured at different sites in the brain intraventricular and intraparenchymal measurements are more common, while extradural and subdural sensors are used occasionally. Intraventricular catheters are still thought of as the gold standard [6] as they allow direct measurement by insertion of a catheter into one of the lateral ventricles, which is connected to an external pressure transducer [7]. The advantages of these systems are that the clinician can check for zero drift and sensitivity of the measurement system in vivo. Access to the ventricular system also allows CSF drainage if the ICP rises. However, this interferes with ICP monitoring, and only one currently available catheter allows concomitant CSF drainage and ICP monitoring (Rehau, Switzerland). The drawbacks of such catheters include difficulty or failure of insertion in patients with advanced brain swelling, as the ventricles can be narrowed or effaced. An increase in risk of infection after a period of time is another potential problem, with reported rates of up to 10% [8] with modern ventricular micro-transducers even though these have excellent metrological properties [9]. There are now commercially available ventricular catheters with antibiotic-coated tips [Codman Bactiseal external ventricular drain catheter] that may reduce infection rates but more studies are required before their use in clinical practice can be supported. The intraparenchymal systems may be inserted through a support bolt or tunnelled subcutaneously from a burr hole. These have a micro-miniature strain gauge pressure sensor side-mounted at the tip (Codman) or a fibre-optic catheter (Camino, Innerspace). Change of pressure results in a change of resistance in the former and an alteration in reflection of the light beam in the latter. Intraparenchymal probes are a good alternative to ventricular catheters and have a low infection rate [10], but in one study a significant increase in colonisation at 5 days after insertion was reported [11]. The main problem with these catheters is a small drift of the zero line. Neither of these systems allows pressure calibration to be performed in vivo. After these systems are zeroed relative to atmospheric pressure during a pre-insertion calibration, their output

3 1265 is dependent on the zero drift of the sensor. Technical complications such as kinking of the cable and dislocation of the sensor have also been reported [12]. It should be remembered that these sensors reflect a local pressure value that may be misleading, as the ICP is not uniform within the skull, e.g. supratentorial measurements may not reflect infratentorial pressure. However, this is also a problem with intraventricular catheters. Subdural catheters are easily inserted following craniotomy but measurements are unreliable because when ICP is elevated, they are likely to underestimate the true ICP. These are also liable to blockage. Extradural probes have the advantage of avoiding penetration of the dura but are even more unreliable as the relationship between ICP and pressure in the extradural space is unclear. The Gaeltec ICP/B solid-state miniature ICP transducers are designed for use in the epidural space and are reusable, and the zero reference can be checked in vivo. However, measurement artefacts and decay in measurement quality with repeated use have limited the acceptance of this technology [13]. Despite these drawbacks, the subdural and epidural catheters are associated with a lower risk of infection, epilepsy and haemorrhage than ventricular catheters [14, 15]. The Spiegelberg ICP monitoring system is a fluidfilled catheter-transducer system that measures ICP using a catheter that has an air-pouch balloon situated at the tip. This device zeroes automatically in vivo and has shown lower zero drift than standard catheter-tip ICP devices [16]. This system can be used in epidural, subdural, intraparenchymal and intraventricular sites. Despite its obvious advantages, this system is still not used widely and requires further evaluation. ICP monitoring has several important applications, some of which are discussed below: Determination of CPP Management of acute brain injury is largely CPP directed. ICP is an important determinant of CPP [CPP = mean arterial pressure (MAP) ICP], which in turn affects CBF and CBV. The optimal level of CPP is still under some debate, with earlier studies recommending CPP > 70 mmhg [16] although many other centres maintain CPP between 60 and 70 mmhg and one centre permits CPP as low as 50 mmhg [17]. ICP correlation with outcome Experience from various centres with expertise in ICP monitoring and research into TBI confirms that mean ICP correlates with outcome with a threshold in the region of 25 mmhg. However no prospective study has been undertaken (and is unlikely) to prove this and Brain Trauma Foundation guidelines recommend ICP treatment should be initiated at an upper threshold of mmhg [18]. Waveform analysis Analysis of ICP waveforms can be used to obtain information about brain compliance. A computer program to correlate mean ICP and AMP has been developed [19]. The ICP waveform consists of three components, which overlap in the time domain but can be separated in the frequency domain. The pulse waveform has several harmonic components; the fundamental component has a frequency equal to the heart rate. The amplitude of this component (AMP) is very useful for the evaluation of various indices. The linear correlation coefficient RAP (R = symbol of correlation, A = amplitude, P = pressure) describes the relationship between pulse amplitude of ICP and mean ICP value over short periods of time (1 3 min). When RAP is positive, changes in AMP are in the same direction as changes in mean ICP. When RAP is negative, the change in AMP is reciprocal to those in mean ICP value. Lack of synchronisation between fast changes in amplitude and mean ICP is depicted by a RAP of 0. A potential application of this model is to predict outcome after severe head injury. This is possible because of the nature of relationship between mean ICP and AMP as the ICP increases, the linear correlation with AMP becomes distorted by an upper breakpoint which is associated with a decrease in RAP coefficient from +1 to negative values. A similar relationship between AMP and ICP is seen in patients with severe brain injury. A plot of RAP against ICP shows similar results RAP is positively correlated to ICP in patients with good outcomes, whereas the correlation decreases above ICP values of 20 mmhg and becomes negative above 50 mmhg in patients who die (Fig. 1) [20]. In the latter group of patients, the decrease in RAP from +1 to 0 or negative precedes the final decrease in ICP pulse amplitude and is a sign of impending brainstem herniation. Cerebrovascular pressure reactivity and derived indices Cerebrovascular pressure reactivity, which is the change in basal tone of smooth muscle in cerebral arterial walls in response to changes in transmural pressure, can be estimated from the ICP waveform by deriving the pressure reactivity index (PRx). PRx has been used to determine time responses to intracranial hypertension or changes in mean arterial blood pressure in brain-injured patients [21]. PRx is calculated as a linear correlation coefficient between averaged arterial blood pressure and ICP from a time window of 3 4 min. Good cerebrovascular reactivity is associated with negative PRx and a poor reactivity with a positive PRx value (Fig. 2). The PRx may be analysed as

4 1266 Fig. 1 Pulse amplitude of intracranial pressure (ICP) (AMP, fundamental harmonic component) increases with mean ICP until critical threshold is reached, above which it starts to decrease. The correlation coefficient between AMP and ICP (RAP) marks this threshold by decreasing from positive to negative values [20] Fig. 2 PRx index, calculated as linear correlation coefficient between averaged ABP and ICP. Good cerebrovascular reactivity is associated with negative PRx (a) and poor reactivity with positive PRx (b) [21]

5 1267 a time-dependent variable, responding to dynamic events such as ICP plateau waves or incidents of arterial hypoand hypertension. The validity of PRx for monitoring and quantifying cerebral vasomotor reactivity has been studied in patients with brain injury. A close link was found between cerebral blood flow and intracranial pressure in head-injured patients. This suggested that increases in arterial blood pressure and cerebral perfusion pressure may be useful for reducing intracranial pressure in selected braininjured patients, i.e. those with intact cerebral vasomotor reactivity [22]. There are drawbacks of monitoring ICP. It requires an invasive procedure and personnel to monitor as well as to react to changes. ICP monitoring is frequently performed by non-neurointensivists. A survey of intensive care units (ICU) in non-neurosurgical centres in the UK revealed that though more than half of all such ICUs were admitting patients with severe TBI, only 9% used ICP monitoring as a routine [23]. This has significant implications, especially as there is a lack of class I evidence about the efficacy of ICP monitoring in reducing morbidity and mortality. It is possible that uptake of ICP monitoring may increase if a non-invasive technique can be used. There is currently keen interest in development of non-invasive methods of ICP monitoring which include the use of transcranial Doppler ultrasonography [24]. An example of this is a procedure for continuously simulated ICP derived from simultaneously recorded curves of ABP and flow velocity (FV) in the middle cerebral artery (MCA) that has been validated in patients with TBI [25]. This approach involves a dynamic systems analysis technique and enables modelling of physiological systems in which the inner structure is too complex to be described mathematically. The validity of this model was confirmed during infusion studies in patients with hydrocephalus [26]. Use of such non-invasive ICP (nicp) measurement techniques may make ICP monitoring accessible to a wider range of ICUs. generally derived from the MCA as it is easy to insonate, carries a large proportion of supratentorial blood and its location allows easy fixation of the probe (to keep the angle of insonation constant) for prolonged monitoring. The transtemporal window through the thin bone above the zygomatic arch is commonly used to insonate the proximal segment (M1) of the MCA. In each patient, the same insonation window should be used throughout the entire study period. As the volume of blood flowing through a vessel depends on the velocity of the moving cells and the diameter of the vessel concerned, then for a given blood flow, the velocity will increase with decreases in vessel diameter. Figure 3 shows a diagrammatic representation of a typical TCD waveform from the MCA. Mean FV (FV mean )is the weighted mean velocity that takes into account the different velocities of the formed elements in the blood vessel insonated and is normally around 55 ± 12 cm s 1.This represents the most physiological correlate with the actual CBF. The time-mean FV refers to the mean value of FV max and is determined from the area under the spectral curve. The shape of the envelope (maximal shift) of the Doppler spectrum from peak systolic flow to enddiastolic flow with each cardiac cycle is known as the waveform pulsatility. The FV waveform is determined by the ABP waveform, the viscoelastic properties of the cerebral vascular bed and blood rheology. In the absence of vessel stenosis or vasospasm, changes in ABP or blood rheology, the pulsatility reflects distal cerebrovascular resistance. This resistance is usually quantified by the pulsatility index (PI or Gosling index): PI = (FV systolic FV diastolic )/FV mean. Normal PI ranges from 0.6 to 1.1 with no significant side-to-side or cerebral interarterial differences and shows better correlation with Assessment of blood flow Transcranial Doppler ultrasonography Transcranial Doppler ultrasonography (TCD) is an extremely useful method for non-invasively monitoring cerebral haemodynamics, by measuring red cell FV in real time using the Doppler shift principle. Ultrasound (US) waves are generated using a 2-MHz pulsed Doppler instrument. In order to penetrate the skull, the same transducer is used both for transmitting and receiving wave energy at regular intervals. The moving blood acts as a reflector, first receiving the transmitted wave from the transducer and then reflecting it back. FV is calculated using the formula for Doppler shift. Changes in FV correlate with changes in CBF only if the angle of insonation and the diameter of the insonated vessel remain constant [27]. Data are Fig. 3 Method of determining systolic (V s ), diastolic (V d )andtimeaveraged mean flow velocity (V mean ) from the spectral outline. FV is flow velocity and PI is pulsatility index [PI =(V s V d )/V mean ]. (Reproduced with permission from Greenwich Medical Media. In: Gupta AK, Summors A, Notes in Neuroanaesthesia and Critical Care, 2001)

6 1268 CPP than ICP. Another index that can be used to quantify vessel resistance is the resistance index (RI or Pourcelot index): RI = (FV systolic FV diastolic )/FV systolic. Applications of TCD There are many advantages of using TCD. It is noninvasive, relatively inexpensive and provides real-time information with high temporal resolution. Some of the clinical applications of TCD include the following: Assessment of cerebral autoregulation and vasoreactivity TCD is used in assessment of cerebral autoregulation and vasoreactivity to carbon dioxide (CO 2 ) as loss of these mechanisms in patients with brain injury may indicate a poor prognosis. Autoregulation can be tested by response of the TCD trace to vasopressor infusion (static autoregulation) or thigh tourniquet deflation (dynamic autoregulation). Autoregulation may also be tested at the bedside using the transient hyperaemic response test (THRT) [28], which assesses the hyperaemic response in the TCD waveform following 5 9 s of digital carotid artery compression. Lam et al. found that following an aneurysmal subarachnoid haemorrhage, patients with an initial impairment of the response to THRT were more likely to develop delayed ischaemic neurological deficits (DIDs) than patients with a normal response [29]. In a study using induced oscillations in the ABP (by controlling ventilation) and calculating the phase shifts between FV (measured using TCD) and ABP, cerebral autoregulation was found to be impaired preceding the onset of clinical vasospasm [30]. Detection of vasospasm following subarachnoid haemorrhage TCD is often used in the clinical setting to determine presence of vasospasm. The primary effect of a decrease in vessel lumen diameter is an increase in flow resistance, and this results in an increase in FV. An MCA FV mean above 120 cm s 1 is regarded as being significant [31] and may indicate either hyperaemia or vasospasm. Although it is generally regarded that vasospasm is likely if the ratio of MCA FV to extracranial ICA FV (Lindegaard ratio) is greater than 3 [32] and hyperaemia is present if MCA FV > 120 cm s 1 with a Lindegaard ratio less than 3, the distinction is not well defined, especially when commonly used TCD indices for diagnosis of vasospasm are compared with cerebral perfusion findings using PET. PET scans of patients following subarachnoid haemorrhage (SAH) who developed DIDs showed a wide range of cerebral perfusion disturbances, with TCD indices failing to indicate these changes [33]. Thus detection of vasospasm on TCD may not be associated with delayed cerebral ischaemia and vice versa. Care must therefore be taken when interpreting TCD data, and these should be matched with clinical findings, and other investigations such as xenon-ct flow measurements may help to improve prediction of vasospasm and hence avoid repeated angiography [34]. However, when compared with angiography for the MCA, TCD has been shown to give high levels of specificity and positive predictive value for vasospasm. Ratsep et al. found that vasospasm detected by TCD is associated with haemodynamic impairment (HDI, defined as blood flow velocity values consistent with vasospasm in conjunction with impaired THRT); thus, detection of HDI could identify patients at risk for ischaemic complications [35]. Role of TCD in management of traumatic brain injury Following traumatic brain injury, TCD monitoring can be used to observe changes in FV, waveform pulsatility and for testing cerebral vascular reserve. The autoregulatory threshold or breakpoint (the CPP at which autoregulation fails), which provides a target CPP value for treatment, can also be determined by continuously recording the FV from the MCA. At very low levels of CPP, as in brain death, the microcirculation collapses. The net blood flow diminishes, and the TCD pattern either shows low flow or reversed flow during diastole. Non-invasive determination of CPP There is currently much interest in the use of TCD for noninvasive determination of CPP (ncpp). This involves estimation of CPP from parameters derived from MCA FV and the ABP [24]. Schmidt et al. found that absolute difference between real CPP (i.e. MAP ICP) and ncpp (i.e. determined using TCD) was less than 13 mmhg in the majority of measurements for a range of CPPs between 60 and 100 mmhg. Such a difference may have significant implications in patients with raised ICP (and possibly lower CPP). The absolute value of side-to-side (i.e. interhemispheric) difference in ncpp was significantly greater when CT evidence of brain swelling was present and was also correlated with mean ICP [36]. This technique needs to be evaluated in further randomised trials focusing on its accuracy, cost-effectiveness and validity before it can be recommended for routine use. Measurement of zero flow pressure A recent development is the use of TCD to measure zero flow pressure (ZFP), i.e. the pressure at which CBF ceases,

7 1269 which gives an estimate of the effective downstream pressure (EDP) of the cerebral circulation (Fig. 4). EDP, rather than ICP, is believed to determine the effective CPP in the absence of intracranial hypertension. FV in the MCA is measured by TCD. EDP is derived from the ZFP as extrapolated by regression analysis of instantaneous ABP/MCA FV relationships. Buhre et al. reported that extrapolation of ZFP enables detection of elevated ICP in patients with severe head injury [37]. Thees et al. studied the correlation between critical closing pressure determined using TCD and ICP measured invasively. They found that using ICP to determine CPP might overestimate the effective CPP, i.e. the difference between MAP and CCP [38]. Further evaluation is needed before this non-invasive technique of measuring CPP can be accepted as a standard. Confirmation of brain death TCD has been suggested as a highly specific and sensitive test for confirmation of brain death. It can be a useful method to confirm brain death in patients in whom traditional brain death criteria cannot be used because of possible residual effects of sedative drugs [39]. The transtemporal approach is commonly used but the transorbital approach has also been successfully employed [40]. The limitations of using TCD are that it requires a certain degree of technical expertise, is operator dependent, and the skull thickness, which varies with age, gender and race, may cause problems with transmission of ultrasound. In fact, 10% of normal subjects cannot be assessed due to lack of an adequate temporal window. The incidence of failure can be reduced by increasing the power and perhaps by use of 1 MHz probes [41]. In addition, TCD monitoring focuses on the major cerebral arteries but flow characteristics in the cerebral microcirculation may be quite different to those in the major arteries. Despite these limitations, TCD holds promise of further applications for real-time indirect assessment of CBF, non-invasive ICP and CPP. Laser Doppler flowmetry Laser Doppler flowmetry (LDF) allows continuous realtime measurements of local microcirculatory blood flow (red cell flux) with good dynamic resolution. Doppler shift of reflected monochromatic laser light induced by movement of red blood cells within the microcirculation is measured. The magnitude and frequency distribution of the wavelength changes are directly related to the number and velocity of red blood cells but unrelated to the direction of their movement. A mm diameter fibreoptic laser probe is placed in contact with or within brain tissue and conducts scattered light back to a photodetector within the flowmeter sensor. The signal is processed to give a continuous voltage fluctuation versus time which is linearly proportional to the real blood flow [42]. The probe can be positioned in proximity to an area of intracranial injury to monitor pathologic variations of microvascular blood flow. LDF is considered an excellent technique for instantaneous, continuous and real-time measurements of regional CBF and for assessment of relative regional CBF changes. LDF has a quick response to fluctuations in tissue perfusion and is relatively inexpensive. The relationship between LDF and CPP has been found to change with time, and this can indicate an improvement or deterioration in autoregulation [43]. The main drawbacks of this technique are that it is not a quantitative measure of CBF and measures CBF in a small brain volume (1 2 mm 3 ). It is invasive and prone to artefacts produced by patient movement or probe displacement, which limits its clinical applicability. However, it is a useful measure of local microcirculatory changes in combination with other monitoring techniques and has been used to assess autoregulation, CO 2 reactivity and responses to therapeutic interventions [44] and to detect ischaemic insults [45, 46]. Thermal diffusion flowmetry Fig. 4 Direct assessment of cerebral zero flow pressure. In a patient with severe intracranial hypertension, no flow was observed in the middle cerebral artery during diastole. The epidurally measured ICP was 48 mmhg. (Reproduced with permission from [37]) Thermal conductivity of cerebral cortical tissues varies proportionally with CBF, and measurement of thermal diffusion (TD) at the cortical surface can be used for CBF determination [47]. A monitor that measures TD

8 1270 flowmetry consists of two small metal plates, which are thermistors, one of which is heated. Insertion of a TD probe on the surface of the brain at a cortical region of interest allows CBF to be calculated from the temperature difference between the plates. An intraparenchymal TD probe has also been evaluated and the results are encouraging [48]. Although the changes in CBF are relative, the probes may be calibrated against absolute methods such as xenon-133 or xenon-ct measurement of CBF to give absolute values that assess blood flow changes in a small volume of brain (± mm 3 ). Placement of the sensor over large surface vessels should be avoided. Similar sensors have been used to guide therapy for patients with severe brain injury and intracerebral haematomas [49, 50]. Animal studies by Vajkoczy et al. revealed that TD microprobes provide continuous real-time assessment of intraparenchymal regional blood flow that was comparable with measurement by xenon-enhanced CT [51]. TD flowmetry was characterised by more favourable diagnostic reliability and was reported to be more sensitive than TCD ultrasonography in assessing patients with reversible vasospasm following intra-arterial injection of papaverine in patients with SAH [52]. TD flowmetry has the potential for bedside monitoring of cerebral perfusion at the tissue level, but it is invasive and more clinical trials are needed to validate its use. The intraparenchymal probes have excellent temporal resolution and it is possible that in the future a large part of a single vascular territory may be monitored with single or multiple probes. This review has explored methods of assessing and measuring intracranial pressure and cerebral blood flow in the injured brain in the intensive care unit. Appropriate use and knowledge of benefits and limitations of these techniques can improve the outcome of patients with acute brain injury. References 1. 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