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Neurosurgical Anesthesiology: Review Article

Monitoring Intracranial Pressure in Traumatic Brain Injury

Smith, Martin MBBS, FRCA

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doi: 10.1213/01.ane.0000297296.52006.8e
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The primary aim of the intensive care management of traumatic brain injury (TBI) is to prevent and treat secondary ischemic injury using a multifaceted neuroprotective strategy to maintain cerebral perfusion to meet the brain’s metabolic demands for oxygen and glucose. Because the brain is encased by the nonexpandable skull, an increase in intracranial pressure (ICP) may impede cerebral blood flow (CBF) and lead to cerebral ischemia. Increased ICP is an important cause of secondary brain injury, and its degree and duration is associated with outcome after TBI.1,2 ICP monitoring is the most widely used intracranial monitor because prevention and control of increased ICP and maintenance of cerebral perfusion pressure (CPP) are fundamental therapeutic goals after TBI.

This review will summarize the technical aspects of ICP monitoring and its role in the clinical management of TBI. Research applications will be discussed and controversies highlighted.


The principles of ICP were outlined by Professors Munroe and Kellie in the 1820s. In essence, they noted that, in adults, the brain is enclosed in a rigid case of bone and that the volume of its contents must remain constant if ICP is to remain constant. The intracranial compartment consists of brain approximately 83%, cerebrospinal fluid (CSF) approximately 11%, and blood approximately 6%. Under normal conditions there are two main components of ICP, CSF and vasogenic.3 The former is derived from the circulation of CSF and is responsible for baseline ICP. It may be deranged in pathologic states, causing an increase in ICP, because of resistance to CSF flow between intracerebral compartments secondary to brain swelling or expansion of intracranial mass lesions, or because CSF outflow is obstructed. The vasogenic component of ICP is associated with continuous, small fluctuations of cerebral blood volume (CBV). Vasogenic increases in ICP may be caused by hypercapnea, increase in cerebral metabolism, and cerebral hyperemia.

An increase in the volume of one of the components of the intracranial cavity (e.g., brain) requires a compensatory reduction in another (e.g., CSF) to maintain a constant pressure. Brain tissue is essentially incompressible, so any increase in ICP due to brain swelling initially results in extrusion of CSF and (mainly venous) blood from the intracranial cavity, a phenomenon known as “spatial compensation.” CSF plays the largest role in spatial compensation because it can be expelled from the intracranial cavity into the “reservoir” of the spinal theca.

The relationship between ICP and intracranial volume is described by the pressure-volume curve that comprises of three parts (Fig. 1). The first part of the curve is flat because compensatory reserves are adequate and ICP remains low despite increases in intracerebral volume (A-B in Fig. 1). When these compensatory mechanisms become exhausted, the pressure-volume curve turns rapidly upwards in an exponential fashion. Intracranial compliance is now critically reduced and a small increase in intracerebral volume causes a substantial increase in ICP (B-C in Fig. 1). At high levels of ICP, the curve plateaus as the capacity of cerebral arterioles to dilate in response to a reduction in CPP becomes exhausted. The high brain tissue pressure results in collapse of these dysfunctional vessels as cerebrovascular responses become terminally disrupted (C-D in Fig. 1).

Figure 1.
Figure 1.:
Intracranial pressure (ICP) volume curve. The curve has three parts: a flat part representing good compensatory reserve (A-B), an exponential part representing reduced compensatory reserve (B-C) and a final flat part representing terminal derangement of cerebrovascular responses at high ICP (C-D).

After TBI, increased ICP can be related to intracranial mass lesions, contusional injuries, vascular engorgement, and brain edema. Recent clinical studies have shown that brain edema, and not increased CBV as a result of vascular engorgement, is the major culprit responsible for brain swelling after TBI.4 Vasogenic brain edema, emanating from the blood vessels subsequent to blood-brain barrier compromise, has classically been considered the prevalent edema after TBI5,6 but recent magnetic resonance imaging studies have indicated that, in patients with significant brain swelling, cytoxic or cellular edema, occurring secondary to sustained intracellular water collection, predominates.5,7 Cytoxic edema is of decisive pathophysiologic importance, as it develops early and persists while blood-brain barrier integrity is gradually restored. These findings have implications for the treatment of TBI and suggest that cytotoxic and vasogenic brain edema are two entities that can be targeted simultaneously or independently, according to their temporal prevalence.5

When cerebral autoregulation is absent, an increase in arterial blood pressure (ABP) causes an increase in CBV and hence in ICP.3 An increase in CBV and ICP may also occur in response to changes in other systemic variables, such as arterial Paco2, temperature and intrathoracic or intraabdominal pressures, or because of intracranial events such as seizures. Intracranial hypertension may also occur because of acute or chronic disturbances of CSF drainage (hydrocephalus) and other, often diffuse, pathological processes, such as cerebral edema secondary to hepatic failure.


Normal ICP varies with age, body position, and clinical condition.8 The normal ICP is 7-15 mm Hg in a supine adult, 3-7 mm Hg in children, and 1.5-6 mm Hg in term infants. The definition of intracranial hypertension depends on the specific pathology and age, although ICP >15 mm Hg is generally considered to be abnormal. However, treatment is instituted at different levels depending on the pathology. For example, ICP >15 mm Hg warrants treatment in a patient with hydrocephalus,9 whereas after TBI, treatment is indicated when ICP exceeds 20 mm Hg.10 Thresholds vary in children and it has been recommended that treatment should be initiated during TBI management when ICP exceeds 15 mm Hg in infants, 18 mm Hg in children <8-yr-of-age and 20 mm Hg in older children and teenagers.11

ICP is not evenly distributed in pathologic states because CSF does not circulate freely and intracranial CSF volume may be low because of brain swelling. The assumption of one, uniform, ICP is therefore questionable and intraparenchymal pressure may not be indicative of “real” ICP, i.e., ventricular CSF pressure.12 In the injured brain, there may be intraparenchymal pressure gradients between the supra and infra-tentorial compartments13 and bilateral monitoring has revealed differential pressures across the midline in the presence of hematomas14 and also in the absence of space-occupying lesions.15

Increased ICP causes a critical reduction in CPP and CBF and may lead to secondary ischemic cerebral injury. A number of studies have shown that high ICP is strongly associated with poor outcome,16 particularly if the period of intracranial hypertension is prolonged.17 Increased ICP can also cause actual shift of brain substance resulting in structural damage to the brain and to herniation through the tentorial hiatus or foramen magnum. The latter results in pressure on the brainstem causing bradycardia and hypertension (the classic Cushing reflex) and, if untreated, respiratory depression and death.


ICP cannot be reliably estimated from any specific clinical feature or computed tomography (CT) finding and must actually be measured. Different methods of monitoring ICP have been described (Table 1) but two methods are commonly used in clinical practice: intraventricular catheters and intraparenchymal catheter-tip, microtransducer systems. Subarachnoid and epidural devices have much lower accuracy18,19 and are now rarely used. Measurement of lumbar CSF pressure does not provide a reliable estimate of ICP and may be dangerous in the presence of increased intracranial hypertension.20

Table 1
Table 1:
Comparison of Intracranial Pressure (ICP) Monitoring Devices

The “gold standard” technique for ICP monitoring is a catheter inserted into the lateral ventricle, usually via a small right frontal burr hole. This can be connected to a standard pressure transducer via a fluid-filled catheter. The reference point for the transducer is the foramen of Munroe, although, in practical terms, the external auditory meatus is often used. Some ventricular catheters have a pressure transducer within their lumen and the ICP wave form is generally of better quality than traditional fluid-filled catheters connected to an external transducer. Ventricular catheters measure global ICP and have the additional advantages of allowing periodic external calibration, therapeutic drainage of CSF, and administration of drugs (e.g., antibiotics).20,21 However, placement of the catheter may be difficult if there is ventricular effacement or displacement due to brain swelling or intracranial mass lesions. The use of intraventricular catheters is complicated by infection in up to 11% of cases.22,23 This is a serious complication resulting in significant morbidity and mortality. The risk of infection increases after 5 days23 and this has been presumed to be related to retrograde colonization of the catheter. However, recent data suggest that CSF infection is also likely to be acquired during introduction of the catheter in a significant number of cases.24 Intraventricular catheters may become blocked, especially in the presence of subarachnoid blood or increased CSF protein. If the drainage holes at the tip of the ventricular catheter become partially blocked, resistance to CSF flow increases at the tip of the drain and a pressure gradient develops across the catheter. Catheters with an integral pressure transducer may then grossly underestimate ICP.25 Although the patency of catheters can often be restored by gentle flushing, repeated attempts significantly increase the risk of infection.23 Regular microbiological analysis of CSF samples to permit early diagnosis of ventriculitis is recommended by some, whereas others believe that routine sampling may actually predispose to higher infection rates because of the repeated opening of the closed drainage system. The use of antibiotic-impregnated catheters is associated with a lower infection rate,26 although catheters coated with hydrogel to impede bacterial adherence are not associated with reduced infection rates.27

Micotransducer-tipped ICP monitors can be sited in the brain parenchyma or subdural space, either through a skull bolt, a small burr hole or during a neurosurgical procedure. They are almost as accurate as ventricular catheters. Fiberoptic, strain gauge or pneumatic technologies are used to transduce pressure in modern microtransducer devices. The Camino ICP monitor (Integra Neuroscience, Plainsboro, NJ) uses a fiberoptic cable to direct light toward a miniature displaceable mirror at the catheter tip.28 Changes in ICP distort the mirror and the change in reflected light intensity is converted to a measured change in pressure. The Codman microsensor (Johnson and Johnson, Raynham, MA) incorporates two semiconductor strain gauges mounted on a thin diaphragm in titanium housing at the catheter tip. The diaphragm distorts in proportion to the applied pressure and a Wheastone bridge transduces changes in pressure to changes in resistance that are subsequently displayed as ICP.29 The Neurovent-P ICP monitor (Raumedic AG, Munchberg, Germany) is also based on an electronic chip strain gauge coated by a thin silicon membrane mounted at the distal tip of the catheter. The incorporation of the Wheastone bridge into the chip enhances the drift characteristics by reducing temperature sensitivity and the effects of nonpressure-related external strains.30 Neurovent catheters incorporating three monitoring variables (ICP, brain tissue oxygen partial pressure, and temperature) are now available, although clinical data with this device are limited.31 None of these devices allows in vivo pressure calibration and, after a preinsertion calibration during which they are zeroed relative to atmospheric pressure, their output is subject to the zero drift of the sensor. However, microtransducer systems perform well during in vitro testing, with drift as low as 0.6 ± 0.9 mm Hg after 5 days continuous use.32 Microtransducer systems are reliable and easy to use in the clinical setting, with recordings that are stable over time with minor zero drift.33 They have minimal infection and other complication rates34 but measured pressure may not be representative of true CSF pressure because of the intraparenchymal pressure gradients that may exist after TBI.35 More recently, a device incorporating pneumatic technology has been introduced. The Spiegelberg ICP monitor (Spiegelberg GmbH, Hamburg, Germany) uses a small air pouch balloon at the end of a catheter to sense changes in pressure.36 It can be used in parenchymal and intraventricular sites and zeroes automatically in vivo.

There is a desire to develop less invasive methods of measuring ICP and methods using tympanic membrane displacement37 and ultrasound “time of flight” techniques38 have been described. Tympanic membrane displacement is a poor surrogate for invasive ICP measurements, but serial intra-patient measurements may be useful to determine temporal changes in ICP. More recently, transcranial Doppler ultrasonography has been used to provide a noninvasive estimate of ICP that may be clinically applicable,39 and CPP with an accuracy of ±10-15 mm Hg.40

Continuous digital recording of ICP is the most accurate method of data acquisition and display. ICP changes with time and averaging over at least 30 min should be used to calculate mean ICP and inform treatment decisions.9 Clinical records, particularly intensive care unit charts, often use single end-hour ICP recordings made by nurses and these correlate well with continuous recordings obtained during monitoring of brain injury.41 In a study of 115 patients with hydrocephalus, there was also a strong correlation between digital recordings of ICP and end-hour measurements, with a mean difference of 0.3 ± 1.26 mm Hg between the 2 methods.42 Computerized data collection allows display, interpretation and analysis of continuous ICP monitoring data as well as integration with other intracranial monitoring systems.43


Despite the widespread application of ICP monitoring, there are no data from randomized controlled trials that can clarify its role in acute coma.44 With the exception of monitoring after severe TBI, the indications for ICP monitoring are not well established and vary from center to center (Table 2). Case-mix adjusted mortality in comatose patients with intracranial hemorrhage is lower in those who receive ICP monitoring compared with those who do not45 and increased ICP is associated with poor prognosis after subarachoid hemorrhage.46 There is little evidence to support ICP monitoring in other neurological conditions, such as acute stroke, when there is no benefit over clinical monitoring alone.47 ICP monitoring after anoxic injury after cardiac arrest has little value in targeting treatment, although it may be useful in hepatic encephalopathy.

Table 2
Table 2:
Indications for Intracranial Pressure Monitoring


In 1982, Narayan et al.48 demonstrated in a prospective study of 133 patients that outcome prediction after TBI was increased when ICP monitoring was added to standard clinical observations. Subsequently, analysis of the National Traumatic Coma Data Bank showed that the proportion of hourly ICP recordings more than 20 mm Hg was the next most significant predictor of poor outcome after the usual clinical descriptors of age, admission motor score, and abnormal pupil respones.1,2

Despite the absence of Class 1 evidence demonstrating the benefit of ICP monitoring on outcome after TBI, there is a large body of clinical evidence supporting its use to guide therapeutic interventions, detect intracranial mass lesions early, and assess prognosis. ICP monitoring is recommended by consensus guidelines for head injury management10,49 and is accepted as a relatively low-risk, high-yield and value for money intervention.

The Brain Trauma Foundation recommends ICP monitoring in all patients with a severe TBI (Glasgow Coma Score 3-8) and either an abnormal CT scan or a normal scan and the presence of two or more of the following three risk factors at admission: age >40 yr; unilateral or bilateral motor posturing; a systolic a BP <90 mm Hg.49 There is around 60% chance of increased ICP in these patients.

Much information is available from ICP monitoring in addition to the measurement and display of absolute ICP. CPP is easily calculated as the difference between mean ABP (MAP) and ICP (CPP = MAP − ICP) and is a measure of the pressure gradient across the cerebral vascular bed. Pathologic ICP wave forms can be identified and analyzed. ICP monitoring can also be augmented by measurement of indices describing cerebrovascular pressure reactivity (CVR) and pressure-volume compensatory reserve.9,50

ICP changes in a limited number of patterns after TBI9:

  1. Low (<20 mm Hg) and stable ICP: This pattern is seen after uncomplicated head injury or during the early hours after severe TBI, before brain swelling evolves.
  2. High (>20 mm Hg) and stable ICP: This is the most common pattern seen after severe TBI.
  3. ICP waves: These reflect reduced intracranial compliance and are discussed in detail below.
  4. ICP changes related to changes in ABP: These occur in the presence of abolished cerebral autoregulatory responses when ICP changes directly with ABP.
  5. Refractory intracranial hypertension: In the absence of aggressive treatment strategies this may progress to herniation and death.


In 1965, Nils Lundberg et al. characterized ICP slow waves.51 “A” waves or “plateau” waves are steep increases in ICP from baseline to peaks of 50-80 mm Hg that persist for 5-20 min. These waves are always pathologic and may be associated with early signs of brain herniation, such as bradycardia and hypertension. They occur in patients with intact autoregulation and reduced intracranial compliance and represent reflex, phasic vasodilatation in response to reduced cerebral perfusion.52,53 The development of plateau waves leads to a vicious cycle, with reductions in CPP predisposing to the development of more plateau waves, further reductions in CPP and irreversible cerebral ischemia. “B” waves are rhythmic oscillations occurring at 0.5-2 waves/min with peak ICP increasing to around 20-30 mm Hg above baseline. They are related to changes in vascular tone, probably due to vasomotor instability when CPP is at the lower limit of pressure autoregulation. “C” waves are oscillations occurring with a frequency of 4-8/min and are of much smaller amplitude than B waves, peaking at 20 mm Hg. They occur synchronously with ABP, reflect changes in systemic vasomotor tone, and are of no pathologic significance.

Analysis of the ICP wave form in the time domain reveals three fundamental components: pulse wave form, respiratory wave form, and slow waves. The pulse wave form has several harmonic components, the fundamental of which has a frequency equal to the heart rate. The amplitude of this component (AMP) is used for the evaluation of various ICP-derived indices (see below). The respiratory wave form is related to the frequency of the respiratory cycle and occurs at 8-20 waves/min. Slow waves are generally less precisely defined than those described by Lundberg et al. and encompass all waves within the frequency limits of 0.05-0.0055 Hz (20 s to 3 min).

Several studies have shown that low power of slow waves may predict poor outcome after TBI.54 There is also a strong correlation between slow waves and fluctuations in the electroencephalogram,55 supporting the presence of a primary neuropacemaker in the brainstem responsible for fluctuations in CBF and generation of slow waves. Maintenance of ICP slow waves after TBI might therefore represent preservation of this pacemaker activity and of brainstem function.


The ICP response to slow spontaneous changes in ABP depends on the pressure-reactivity of cerebral vessels. This is a key component of pressure autoregulation and disturbed pressure reactivity implies disturbed pressure autoregulation. A pressure reactivity index (PRx) can be derived from continuous monitoring and analysis of slow waves in ABP and ICP.9,56 PRx is the linear correlation coefficient between ABP and ICP and its value ranges from −1 to +1. When the cerebrovascular bed is normally reactive, an increase in ABP leads to cerebral vasoconstriction within 5-15 s and a secondary reduction in CBV and ICP. Opposite effects occur when ABP is reduced. When CVR is impaired, changes in ABP are passively transmitted to CBV and ICP. PRx is determined by calculating the correlation coefficient of consecutive time-averaged data points of ICP and ABP recorded over a 4-min period.56 A negative value for PRx, when ABP is inversely correlated with ICP, indicates a normal CVR, and a positive value a nonreactive cerebral circulation. PRx correlates with standard measures of cerebral autoregulation based on transcranial Doppler ultrasonography56 and abnormal values are predictive of poor outcome after TBI.20 PRx can be monitored continuously and has been used to define individual CPP targets after TBI.57


The relation between ICP and changes in intracerebral volume can be used to define an index of compensatory reserve (RAP). RAP is the relationship (R) between the AMP (A) and the mean ICP over 1-3 min (P).58 Values of this index also range from −1 to +1. In the first, flat, part of the ICP-volume curve there is lack of synchronization between AMP and ICP, representing good compensatory reserve. Here the RAP is zero and the ICP wave form amplitude is low. On the steep part of the curve, when compensatory reserves begin to fail, AMP varies directly with ICP and RAP is +1. ICP wave form amplitude now begins to increase as mean ICP increases, at first slowly and then more rapidly as compensatory reserves are exhausted. Finally, on the terminal part of the curve, RAP is <0. Now there is terminal derangement of the cerebral vasculature and a decrease in pulse pressure transmission from the arterial bed to the intracranial compartment resulting in low or absent ICP wave form amplitude. RAP can therefore be used to indicate a patient’s position on the pressure-volume curve and may be used to predict the response to treatment and the risk of clinical deterioration or herniation.50 RAP <0.5 in association with ICP >20 mm Hg is predictive of poor outcome after TBI.58

More recently, the Spiegelberg brain compliance monitor has been used to provide similar information. This method relies on the measurement of the ICP response to a known small increase in volume by inflating and deflating the air pouch at the end of the Spielberg ICP catheter. Although the device is still a research tool, it offers the possibility of early warning of critical decompensation and risk of herniation59 but its correlation with outcome has not been demonstrated.


Increased ICP correlates with higher risk of mortality and morbidity, but not all patients with intracranial hypertension have poor outcome.60 This is perhaps unsurprising because monitoring of ICP and CPP does not tell the whole story. It is impossible to know in an individual patient whether the targeted ICP or CPP is sufficient to allow the brain’s metabolic demands to be met at a particular moment. A recent study has demonstrated that brain resuscitation based on control of ICP and CPP alone does not prevent cerebral hypoxia in some patients after TBI.61 Measurement of ICP and CPP in association with monitors of the adequacy of cerebral perfusion, such as measurement of cerebral oxygenation (e.g., jugular venous oximetry, brain tissue oxygen partial pressure) and metabolic status (e.g., cerebral microdialysis), provide a more complete picture of the injured brain and its response to treatment. There is preliminary evidence to suggest that therapy directed to maintain brain tissue oxygenation as well as ICP/CPP is associated with reduced mortality after severe TBI.62 Multimodality intracranial monitoring is now widely used during neurointensive care to provide early warning of impending brain ischemia and guide targeted therapy to optimize cerebral perfusion and oxygenation.63

Despite its limitations, ICP monitoring remains central to the monitoring and management of severe TBI. Conventional approaches to management have concentrated on a reduction in ICP to prevent secondary cerebral ischemia. Treatment is usually initiated if ICP increases >20 mm Hg,10 although it is likely that the duration of intracranial hypertension and its response to treatment are also important prognostic indicators.64 Over the last decade, there has been a shift of emphasis from primary control of ICP to a multifaceted approach of maintenance of CPP and brain protection. High ICP and low CPP may result in cerebral ischemia and are strongly associated with fatal outcome.16 Induced hypertension using fluid resuscitation and vasopressors has been advocated to maintain CPP,65 but therapies to maintain high CPP are controversial. In one study, there was a fivefold increase in the occurrence of acute lung injury in a group of TBI patients managed with a CPP threshold of 70 mm Hg vs 50 mm Hg,66 suggesting that high CPP targets may only be achieved at the expense of significant complications. These might outweigh the potential benefits of this treatment strategy. Furthermore, if cerebral autoregulatory capacity is lost, an increase in CPP may result in hyperemia, increase in vasogenic edema and a secondary increase in ICP.67,68 It has recently been shown that excessive CPP is associated with a lower likelihood of favorable outcome after TBI.16 Debate remains about the optimal level of CPP,69 but the Brain Trauma Foundation has recently recommended that the CPP target after severe TBI should lie within the range of 50-70 mm Hg and that aggressive attempts to maintain CPP >70 mm Hg should be avoided because of the risk of acute lung injury.70 It is also now apparent that a CPP threshold (an “ideal” CPP) exists on an individual basis for patients with TBI.71 Patient and time-dependent differences in adequate and inadequate CPP are considerable and optimal CPP should be defined for each patient individually and frequently. Multimodality monitoring may assist the clinician in detecting optimal CPP and in balancing the risks and benefits of ICP and CPP-directed strategies.

There has never been a randomized, controlled trial demonstrating outcome benefit in patients in whom treatment is guided by ICP monitoring. As a consequence, there is considerable variability in the use of monitoring and treatment modalities among institutions.72,73 In a study from the United States, ICP monitors were placed in only 58% of patients who fulfilled established criteria for monitoring, and therapies to reduce increased ICP were routinely applied in those patients with no monitoring.72 In a European survey,73 ICP monitoring was performed in only 37% of appropriate patients and, although ICP monitoring was almost universal in a Canadian study of severe TBI, only 20% of neurosurgeons believed that outcome was affected by ICP monitoring.74

The differences in the approach to ICP monitoring and management after TBI are likely to reflect the conflicting evidence available to clinicians. In one study, an “aggressive” management protocol, including the placement of ICP monitors, was associated with decreased risk of mortality (hazard ratio, 0.43; 95% confidence interval, 0.27-0.66) and shorter length of hospital stay, although there was no difference in functional status in survivors at discharge.72 Another study demonstrated that adherence to a protocol for TBI management based on the Brain Trauma Foundation guidelines is associated with a nonsignificant reduction in mortality and a significant improvement in functional outcome in survivors.75 Invasive monitoring of systemic and cerebral variables to guide treatment decisions results in increased resource usage, but the significant improvement in outcome justifies the increased cost of the treatment episode.76 However, one study has challenged some of these established findings. Cremer et al. conducted an observational study to investigate the effect of ICP/CPP targeted therapy on outcome and therapy intensity in 333 patients with severe TBI.77 This study compared patients managed in two centers. Admission to each center was determined only by the geographical location in which the original trauma occurred, and patient characteristics were well balanced between the two centers. In center A, ICP was not monitored but supportive intensive care was provided to maintain MAP >90 mm Hg. Other therapeutic interventions were directed by clinical observations and CT findings. In center B, ICP was monitored and treatment provided to maintain ICP <20 mm Hg and CPP >70 mm Hg. In-hospital mortality was similar in both centers (34% vs 33%, P = 0.87) and the odds ratio for a more favorable outcome after ICP/CPP-targeted therapy was 0.95 (95% confidence interval, 0.62-1.44). Intensity of treatment, measured by use of sedatives, vasopressors, mannitol and barbiturates, was higher in center B and the median time on mechanical ventilation was also greater in center B (12 days vs 5 days, P < 0.001). In summary, this study demonstrated that intensive care directed by ICP monitoring resulted in increased levels of therapy intensity and prolonged mechanical ventilation compared to clinically guided therapy, without evidence for improved outcome after severe head injury.

The conflicting data on monitoring and management of ICP have reignited the debate about the need for a prospective, randomized, controlled trial of ICP monitoring and ICP/CPP-targeted treatment. Evidence suggesting that targeting brain tissue oxygenation in addition to ICP/CPP might bring additional outcome benefits62 suggests that any such trial should be extended to include other aspects of multimodal monitoring. The time is perhaps right for interested groups to reconsider the possibility of conducting an outcome trial to compare ICP/CPP-targeted treatment versus diagnosis and targeted therapy based on multimodality monitoring versus supportive intensive care without monitoring after TBI. However, the practicality and ethical acceptability of such a trial will, no doubt, be the subject of continued debate.


ICP is a complex variable. It provides information about ICP and CPP, cerebral compensatory mechanisms and mechanisms contributing to CBF regulation. Continuous measurement of ICP and analysis of ICP wave forms offers insights into pathophysiology and prognosis. ICP monitoring has become an established component of brain monitoring after TBI and is used to guide treatment. Despite the introduction of new monitoring technologies measuring a multitude of intracranial variables, ICP remains robust, only moderately invasive and widely applicable after TBI.


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