CHAPTER 23 Intracranial Pressure Monitoring
Historical Perspective
The importance of intracranial pressure (ICP) was first recognized by Alexander Monro more than 200 years ago and is now referred to as the Monro-Kellie doctrine or the Monro-Kellie hypothesis.1 The Monroe-Kellie doctrine states that (1) the brain is housed in the nonexpandable skull, (2) brain parenchyma is fairly noncompressible, and (3) the volume of blood is relatively constant and outflow of venous blood is necessary for the inflow of arterial blood.1 Later, cerebrospinal fluid (CSF) was recognized as a component of brain volume in addition to brain parenchyma and blood and was incorporated into the doctrine. If there is a new intracranial mass lesion such as tumor or hematoma or an abnormal increase in the volume of any of the components, such as CSF (during hydrocephalus) or parenchyma (during brain edema), the volume of venous blood or CSF, or both, will decrease to accommodate. However, this compensatory reserve is limited, and any further increase in the volume of the pathologic lesion will lead to an increase in ICP because of the rigid, nonexpandable skull. An increase in ICP will then result in a decrease in perfusion pressure and cerebral blood flow and eventually cerebral herniation and death.1
For more than a century there has been clinical interest in measuring ICP. Early efforts to measure ICP were based on the observation that because the cranial and spinal CSF compartments communicate with each other, their pressure should be equal. Measurement of spinal CSF pressure through lumbar puncture should therefore reflect cranial CSF pressure, or ICP.1,2 However, it was soon recognized that measurement of opening pressure via lumbar puncture is associated with a risk for cerebral herniation in the presence of an intracranial mass lesion and that it may not reflect ICP if there is any obstruction to CSF flow between the cranial and spinal CSF compartments.
During the first half of the 20th century, several investigators had measured ventricular fluid pressure in a small number of patients.2 Its clinical use, however, was limited until the 1960s, at which time the pioneering neurosurgeon Nils Lundberg started to measure ICP with a ventricular catheter connected to an external strain gauge pressure transducer and a standard ink-writing potentiometer recorder.2 Drainage of CSF was also used to reduce ICP.2 This method of ICP monitoring and CSF drainage was used in more than 400 patients, many of whom had traumatic brain injury, and marked the beginning of the modern era in ICP monitoring.3
General Principles and Standard of Intracranial Pressure Monitoring Technology
Today, ICP monitoring is an integral part of neurocritical care. ICP monitoring has been used in the management of patients with traumatic brain injury, subarachnoid hemorrhage, intracranial tumor, intracranial hemorrhage, stroke, hydrocephalus, central nervous system infection, and fulminant hepatic failure.4
Since the 1960s, there has been a continuous effort to develop new technology for ICP monitoring. Nils Lundberg outlined the basic requirements for an ICP monitor, which still apply today: minimal trauma during placement, negligible risk for infection, no CSF leakage, easy to handle, reliable, and able to continue to function during various diagnostic and therapeutic procedures.3 The Association for the Advancement of Medical Instrumentation has developed the American National Standard for Intracranial Pressure Monitoring Devices, which specifies that an ICP monitoring device should have a pressure range between 0 and 100 mm Hg, accuracy of 2 mm Hg in the range of 0 to 20 mm Hg, and a maximal error of 10% in the range of 20 to 100 mm Hg.5 Throughout the years, many different ICP monitors have been developed, but only very few are in active clinical use today.
Current Intracranial Pressure Monitoring Technology
External Ventricular Drain
An external ventricular drain (EVD), or ventriculostomy drain, connected to an external strain gauge is currently the “gold standard” for measuring ICP.5 It remains the preferred method for monitoring ICP among U.S. neurosurgeons.6 An EVD can be placed at the bedside in the emergency department, intensive care unit (ICU), or the operating room, depending on local practice tradition. Most practitioners use anatomic landmarks (freehand technique) to insert the ventricular drain into the lateral ventricle with the tip in the foramen of Monro.6,7 The catheter can then be tunneled subcutaneously to minimize CSF leakage and infection.8 Ventricular fluid pressure, which represents ICP, is transmitted to an external strain gauge transducer via the fluid-filled EVD. The strain gauge transducer can be recalibrated without manipulation of the EVD. It can be connected to many standard ICU monitoring systems and allows ICP measurements to be displayed along with other physiologic data such as pulse, blood pressure, or central venous pressure.
Advantages of the EVD as an ICP monitoring device include its extensive history, low cost, and reliability.5,9 Most importantly, an EVD can also serve as a therapeutic device to remove CSF and lower ICP.2,5 In patients with subarachnoid or intraventricular hemorrhage, in which the elevated ICP is frequently due to hydrocephalus, an EVD is the most appropriate ICP monitoring device given its monitoring and therapeutic capabilities. However, an EVD has several weaknesses. Accurate placement of an EVD may be difficult with the freehand technique. In a recent survey of practicing neurosurgeons and residents, the success rate of cannulation of the ventricle was just 82%, even in the hands of practicing neurosurgeons.6 Currently, there is an EVD placement guide available that may increase the accuracy of placement of EVDs, although it is not widely used in the neurosurgical community.7 In some patients, it is simply not possible to place an EVD because of the small size of some ventricles or ventricular shift as a result of a mass lesion or severe edema.
Complications from EVD placement for ICP monitoring and CSF diversion include malposition, occlusion, hemorrhage, and infection. The malposition rate of EVDs ranges between 4% and 20%.10–13 Most of the misplaced EVDs did not have any significant clinical sequelae, but about 4% of these EVDs did require replacement.10,11,13 Occlusion by brain matter or blood clot occurs frequently, especially in patients with intraventricular or subarachnoid hemorrhage.10 Most of the occlusions can be resolved by flushing the EVD catheter.10 Hemorrhage secondary to placement of an EVD occurs infrequently. Hemorrhage rates ranging from 0% to 15% have been reported in the literature, with an average rate of 1.1%.5,11,13–15 Fortunately, most patients are asymptomatic from EVD-associated hemorrhage.11,15 Clinically significant hemorrhage requiring surgical evacuation occurs about 0.5% of the time, and results in intracerebral, subdural, and epidural hematoma.11,13,15 Coagulopathy is thought to be associated with an increase in the hemorrhage rate, and therapeutic anticoagulants and antiplatelet agents are also known to be associated with an increased risk for hemorrhage.16,17 In addition, laceration of a cortical artery can lead to traumatic pseudoaneurysm formation, and this complication has been reported with placement of ICP monitors.18
The most significant risk associated with an EVD is infection. Lozier and coworkers performed an extensive review of all the literature on infection associated with EVDs.19 The range of infection in all the series was 0% to 22%, with a cumulative incidence of 8.8%.19 More recent studies have found a similar rate of infection as well.20–22 Clinical characteristics that have been identified to be associated with increased EVD-associated infection include intraventricular hemorrhage, subarachnoid hemorrhage, craniotomy, CSF leakage, systemic infection, and depressed skull fracture.19,20 Technical factors that may contribute to CSF infection include the duration of catheterization and irrigation of the catheter.19 In 17 studies reviewed by Lozier and colleagues, 10 were found to have an association between the duration of catheterization and infection, whereas 7 did not find such association.19 Careful inspection of the raw data of the latter group showed that there was an increased risk for infection after day 10 in one study.19 More recent studies also show an increased risk for infection with a longer duration of catheterization.20,22,23 Most studies report that there are few infections during the first 5 days of drainage and monitoring with an EVD but that the infection rate increases significantly after 5 to 10 days of catheterization.13,24,25
Because of the relatively high rate of CSF infection in patients with EVDs, multiple interventions have been used in an attempt to minimize the infection rate. However, most studies are retrospective in nature and often do not have enough statistical power to detect small absolute differences in the incidence of infection.19 Such interventions are discussed in the following sections.
Venue of External Ventricular Drain Placement
Lozier and coworkers analyzed five studies that looked at whether there is a difference in infection rates in EVDs placed in the operating room, ICU, or emergency department.19 All but one of the studies revealed no significant difference in infection rate whether the EVD was placed in the operating room, ICU, or emergency department.19 Two more recent studies also did not find statistically significant differences in infection rate related to the venue of ventriculostomy drain insertion.22,23
Extended Tunneling
Subcutaneous tunneling of the EVD catheter was reported by Friedman and Vries in 1980 as a way to reduce the infection rate.8 Other investigators then extended the distance of tunneling to the upper part of the chest or abdomen and had an infection rate of 4%.26 Two recent studies reported conflicting results. Sandalcioglu and Stolke reported that there was a significant difference in infection rate (83% versus 17%) for catheters that were tunneled less than 5 cm subcutaneously versus catheters that were tunneled more than 5 cm, respectively.27 However, patient details were not available, and the infection rate of 83% in this study is significantly higher than most reported infection rates. Leung and coauthors, in contrast, did not find a significant difference in infection rate with long-tunneled EVDs.28 Most EVD insertion kits today contain a trocar for subcutaneous tunneling in excess of 5 cm.
Prophylactic Catheter Exchange
The observation that the infection rate rises with increased duration of drainage from an EVD prompted several investigators to advocate prophylactic catheter exchange.13,25 Several retrospective studies, however, showed that there was no benefit of prophylactic catheter exchange and that in fact there was a higher incidence of infection in the group in which catheters were routinely exchanged.19 This was also observed in one prospective, randomized trial comparing the infection rate in a group that underwent prophylactic catheter exchange versus a control group that did not undergo prophylactic catheter exchange.29
Prophylactic Antibiotic Use
Many studies have analyzed the use of prophylactic antibiotics for reduction of the infection rate of EVDs. Prophylactic antibiotics can be given periprocedurally only or administered during the entire duration that the catheter is in place. Studies in the 1970s suggested that prophylactic antibiotics did reduce the infection rate when compared with no antibiotics, but two studies conducted in the 1980s and one study in 2000 did not find any reduction in the EVD infection rate in patients who received periprocedural antibiotics versus patients who did not.19,30,31 Several other studies also compared prophylactic antibiotics given just periprocedurally versus during the entire duration when the EVD is in place. In a large retrospective study, Alleyne and colleagues did not find any significant difference in infection rates between the two groups.32 In a prospective, randomized controlled study, however, Poon and associates did find a reduction in CSF and systemic infection in the group that received prolonged antibiotic prophylaxis.33 It should be noted that infections that develop in patients who receive prolonged or broad-spectrum antibiotic prophylaxis, or both, for EVD placement are often caused by more virulent microorganisms such as Candida and gram-negative organisms.32–34 Currently, the “Guidelines for the Management of Severe Traumatic Brain Injury” does not recommend antibiotic prophylaxis for EVD placement/catheterization.35
Antibiotic-Impregnated Catheter
A recent development in EVD catheter technology is the antibiotic-impregnated catheter. An EVD catheter impregnated with rifampin is capable of releasing rifampin in a controlled-release manner. These EVD catheters have been shown to significantly reduce bacterial adhesion versus controls in vitro and in animal models.36 In one randomized controlled trial, Zabramski and coworkers showed that a catheter impregnated with minocycline and rifampin reduced the infection rate significantly from 9.4% to 1.3% when compared with the nonimpregnated catheter control group.37 Although antibiotic-impregnated catheters cost significantly more than nonimpregnated catheters, one also has to consider the overall expense and length of hospital stay for patients with EVD catheter–related infections.
Fiberoptic Intracranial Pressure Monitor
Fiberoptic devices for ICP monitoring in which the catheter tip measures the amount of light reflected off a pressure-sensitive diaphragm were developed in 1980s.38 The most widely studied fiberoptic device is the Camino fiberoptic ICP monitoring device (Integra Neuroscience, Plainsboro, NJ). The Camino fiberoptic ICP monitoring device can be placed in the subdural, intraparenchymal, and intraventricular space.
The intraparenchymal Camino ICP monitor has the most extensive clinical experience. The main strength of the intraparenchymal ICP monitor is ease of insertion. The most commonly used technique involves insertion of the monitor into the right frontal region, although it is possible to insert the probe into a region with pathology as well. However, it should be noted that compartmental pressure differentials had been observed in different regions of the brain, so the choice of where to insert the monitor is important.39,40 Because there is no need to cannulate the ventricular system, it is possible to insert the ICP monitor even in patients with severely compressed ventricles or those with a significant midline shift. Although this device has led to more widespread use of ICP monitoring in critically injured and ill patients, there are reports of some technical issues that should be kept in mind when using these devices.
A number of early studies demonstrated that there is a high correlation between ICP measured by the intraparenchymal Camino ICP device and ICP measured by an EVD, with a correlation coefficient (r) of greater than 0.9 in both studies.41 However, Schickner and Young found that the Camino overestimated ICP by an average of 9 mm Hg when compared with an EVD in 10 patients.42 Nevertheless, because of its ease of insertion and low complication rate, it has gained popularity since its introduction into the market. Many large clinical series involving the intraparenchymal Camino device have been published. In most clinical series it is the sole ICP monitoring device inserted, and overall clinical experience with the Camino as an ICP monitoring device has been positive.39–41,43,44 However, there have not been any large prospective or retrospective series that have compared the intraparenchymal fiberoptic device with an EVD as an ICP monitoring device in neurocritical care patients.
Complication rates associated with the Camino intraparenchymal device are comparatively low. In one large series of more than 1000 patients, the hemorrhage rate was just 2.5%, and the hemorrhages were all clinically silent.43 In the same series there was no clinical infection.43 In other series the hemorrhage rate has ranged from 0% to 5.1%.39–41,44,45 Surgical evacuation was required in one patient in all the series.45 The infection rate is also lower than that with an EVD. Although colonization of the catheter is frequent, meningitis occurred in just 3 patients in all the series.40,44,45
The most significant problem of the Camino fiberoptic device is zero drift. The device is first zeroed to atmospheric pressure (usually at room temperature) and then inserted into the brain parenchyma. Recalibration cannot be performed unless the transducer is removed from the patient, zeroed, and then reinserted. Zero drift then occurs over time, which will lead to an erroneous ICP reading. According to the manufacturer, the drift for the first 24 hours should be only 2 mm Hg and then should be 1 mm Hg for the first 5 days. However, clinical studies have shown that the daily drift is significantly larger than the manufacturer’s specification. Daily drift rates of 0.5 to 3.2 mm Hg have been reported, and the maximal drift reported in most studies is usually greater than 20 mm Hg (positive or negative).41,43–45 In most clinical series, recalibration was often needed, and this was often discovered when the clinical picture did not match the ICP reading or a negative ICP reading appeared on the monitor.43,45 However, there has been no report of erroneous ICP reading resulting in clinical mismanagement, such as missing an enlarging mass lesion.
The Camino intraparenchymal device may be associated with mechanical problems. This was especially the case during the early study period because health care personnel were not familiar with the device and proper precaution in handling and securing the device was not taken. The fiberoptic cables are delicate and can be broken easily during transport or with patient movement. As many as 10% to 23% of the fiberoptic devices had a mechanical malfunction because of breakage of cable, dislocation of the probe, or other unknown factors.41 More recently, the rate of mechanical complication has been lower at about 5%.43
Currently, the Camino fiberoptic probe can also be inserted intraventricularly or in the subdural space. The intraventricular Camino bolt allows concurrent CSF drainage and ICP monitoring through the fiberoptic camino bolt. ICP measurement through the fiberoptic device placed intraventricularly correlates well with ICP measured through an external strain gauge, with 97% of the readings being within 5 mm Hg.46
Miniature Strain Gauge
A miniature strain gauge transducer has also been developed to monitor ICP, with the Codman MicroSensor ICP Transducer (Johnson & Johnson, New Brunswick, NJ) being the prototype. The Codman MicroSensor has a microchip pressure sensor at the tip of a flexible nylon cable that produces different electricity based on pressure.47 This MicroSensor can be placed in various compartments, including the ventricle, parenchyma, and subdural space. Gopinath and associates compared ICP measured by an intraventricularly placed MicroSensor with ICP measured by an EVD connected to an external strain gauge.47 There was excellent correlation between the two measurements, with a correlation coefficient of 0.97, and 90% of the readings were within 4 mm Hg of each other.47 Drift was minimal, with only 0.2 mm Hg of drift observed.47 For intraparenchymal ICP measurement, the miniature strain gauge appears to be less accurate. When ICP readings measured by an intraparenchymally placed sensor were compared with ICP from a ventriculostomy drain, Signorini and colleagues found that there was a constant offset between the two ICP readings that led to erroneous ICP readings from the MicroSensor.48 Similarly, Banister and coworkers found significant differences in ICP measurement from a parenchymal MicroSensor and a Camino ICP monitoring device.49 Moreover, several episodes of raised ICP with clinical significance were captured by the Camino ICP monitoring device but not by the MicroSensor in this particular study.49
A more recent study analyzed clinical use of the miniature strain gauge in 128 patients.50 The authors reported good clinical utility of the MicroSensor for ICP monitoring in neurocritical care patients, with no infection and no clinically significant hematomas noted (“several minor hematomas” were observed, however).50 Drift was just 0.9 mm Hg in this study.50 In 22 patients, a ventriculostomy was also performed, and ICP data from the two methods were compared.51 The authors reported good correlation of ICP measured by the two methods (r = 0.79), and a Bland and Altman plot revealed good concordance.50 Careful inspection of the raw data, however, revealed a mean difference of −1.2 mm Hg on the Bland and Altman plot, with a standard deviation of about 3 mm Hg. Inspection of the scatterplot data also revealed that a difference of more than 5 mm Hg was found frequently as well.
Two studies analyzed the MicroSensor placed in the subdural space. It was found that ICP measured by the MicroSensor placed in the subdural space had good correlation with pressure measured by a fluid-coupled transducer placed in the subdural space, as well as with pressure measured by a MicroSensor placed in the parenchyma.52 However, this was not compared with ICP measured by either ventriculostomy or other devices. In one series from Taiwan, the MicroSensor was used to monitor ICP in 120 patients with traumatic brain injury.53 There were no complications from monitor placement.53 Comparison of ICP measured by the subdurally placed MicroSensor with that measured by a ventriculostomy drain was done in 22 patients.53 The observed difference in pressure was −1 to −4 mm Hg, although no statistical analysis was performed in this case.53
Spiegelberg Parenchymal Transducer
The Spiegelberg Brain-Pressure Monitor uses an air pouch situated at the tip that is maintained at a constant volume. The pressure transducer is located in the ICP monitor, and recalibration to ambient pressure can be performed easily. Two studies evaluated the accuracy of ICP measurement of the Spiegelberg pressure sensor (intraparenchymal or subdural placement) versus ICP measured by ventriculostomy. Both studies revealed good correlation of ICP measured by the Spiegelberg pressure sensor with that measured by ventriculostomy.51,54 The initial clinical experience in 87 patients was positive, with no infection, one small hemorrhage, and a 3.4% mechanical complication rate.51
Emerging Technology
Compliance Monitor
A physiologic variable related to ICP is intracranial compliance. Compliance is defined as the change in volume per unit change in pressure. A low-compliance state means that a small change in volume will lead to a large change in pressure. A low-compliance state may therefore identify patients at risk for increasing ICP. The Spielberg Compliance Monitor uses the Spiegelberg Brain-Pressure Monitor as the sensor. To measure compliance, the monitor injects a small amount of air into the air balloon pouch and measures the pressure response to this change in volume. Calculation of compliance is then based on the changes in pressure during 200 cycles. The utility of compliance monitoring in the clinical setting is still unknown. Limited data suggest a significant inverse relationship between compliance and ICP in patients with traumatic brain injury and tumor.55 A less clear relationship exists for patients with hydrocephalus or subarachnoid hemorrhage.55 Abnormal compliance in traumatic brain-injured patients or those with thalamic hemorrhage has been shown to return to normal with surgical intervention based on a small number of patients.56,57 Currently, compliance monitoring is still at an experimental stage; preliminary data, however, suggest potential utility in the clinical setting.
Noninvasive Intracranial Pressure Monitoring
Since the 1960s there has been continuous effort to develop less invasive or noninvasive ICP monitors. Computed tomographic characteristics, clinical examination, and monitoring pressure in the epidural space have all been shown to be unreliable surrogates of ICP measurement.9,58 There have been numerous reports of promising technologies for measuring or deriving ICP noninvasively, although none is being used clinically on a large scale. Several techniques that have been studied more extensively are discussed in the following paragraphs.
Noninvasive ICP monitoring technology can be divided into several categories. In one category, the eye or the ear is used as a window into the cranium.59 A number of structures in the eye and the ear communicate with the CSF space and should therefore be influenced by ICP as well. The optic nerve is surrounded by subarachnoid space and a dural sheath, and the subarachnoid space will expand in the presence of increased ICP.60 Therefore, optic nerve sheath diameter (ONSD), which can be measured by ultrasound, should correlate with ICP.60 Although multiple studies have demonstrated a strong linear relationship between ONSD and ICP, the critical value of ONSD for detecting elevated ICP (ICP >20 mm Hg) is different in the various studies, thus limiting its potential use at this time.60,61 A similar principle is used by venous ophthalmodynamometry, which measures venous opening pressure (VOP), to calculate ICP.62 In one study of 21 patients, VOP correlated well with ICP.62 In 10 of 18 patients with ICP lower than 40 mm Hg, the calculated ICP from VOP was within 4 mm Hg of the measured ICP.62 The biggest drawback of venous ophthalmodynamometry is that it requires dilation of the pupil to perform the measurement and thus takes away one of the most critical neurological examination parameters in a comatose patient. In addition, both ONSD and VOP measurement can be performed only intermittently and therefore can be used just as a screening tool for ICP elevation rather than as a continuous monitor.
Cochlear fluid pressure is thought to be related to ICP and can be indirectly measured by tympanic membrane displacement.59 A number of studies have been performed to evaluate its utility as a surrogate for ICP, and the result has been mixed.59 Although there is a correlation between the two parameters, tympanic membrane displacement does not reliably predict ICP because of a wide predictive limit on linear regression.63
In another category, ICP measurement is based on the principle that increased ICP leads to changes in patterns of blood flow velocity in the intracranial arteries, which can be assessed by transcranial Doppler.64 ICP can then be derived with various mathematical models by using the blood flow velocity data.64,65 Several models have demonstrated the potential of these methods and shown that the derived ICP is within 6 mm Hg most of the time.64,65
Delay in visual evoked potentials has also been observed in patients with increased ICP.66 In the 1980s, the delay in visual evoked potentials was studied in pediatric patients with hydrocephalus and cerebral edema and found to have a significant correlation with ICP.67 Currently, one commercial ICP monitor (NIP-200 noninvasive ICP monitoring system, Chongqing HaiWeiKang Medical Instrument Company Chongqing City, China) is available in China that derives ICP measurement from this principle. In one study, Zhao and colleagues found that ICP measurements with this monitor correlated well with ICP obtained by lumbar puncture opening pressure or ICP measured in the epidural space.66 In another study, this monitor was used to monitor ICP and guide mannitol therapy in patients with intracerebral hemorrhage.68 Per report, this monitor had been used in more than 2000 patients by 2005.66
Pediatric Intracranial Pressure Monitoring
Only few studies are dedicated to the study of ICP monitoring in pediatric patients. In the “Guidelines for the Acute Medical Management of Severe Traumatic Brain Injury in Infants, Children, and Adolescents,” ICP monitoring is recommended only as an option for treating patients with severe traumatic brain injury (Glasgow Coma Scale score <8) because there is insufficient evidence to support it as a guideline.69 One study from the United Kingdom has shown that ICP monitoring was used 60% of the time in pediatric patients with severe traumatic brain injury, which is a very high rate in comparison to adults.70 However, it is noted by others that monitoring in infants younger than 1 year is very infrequent.71
Techniques of ICP monitoring vary from center to center and include EVDs, intraparenchymal ICP monitors, and subdural monitors.70,72,73 The complication rate of ICP monitoring in pediatric patients is probably comparable to that in adults. In one study, malposition of the EVD was noted 8.8% of the time.72 Hemorrhage was observed in 17.6% of patients, although clinically significantly hemorrhage requiring intervention was observed in just 1 patient (1.6%).72 Infection was observed in only 1 patient (1.6%).72 Although the hemorrhage rate and malposition rate were higher in this study than the cumulative adult rate, only 62 patients were studied in this report.72 For intraparenchymal monitors, the hemorrhage rate was 6.4% in one study and 10% in another study, and all of these hemorrhages were silent.72,74 There is no report on the correlation of ICP measured by ventriculostomy versus other devices in these studies.
, Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 5. Indications for intracranial pressure monitoring in pediatric patients with severe traumatic brain injury. Pediatr Crit Care Med. 2003;4:S19.
, Alleyne CHJr, Hassan M, Zabramski JM. The efficacy and cost of prophylactic and periprocedural antibiotics in patients with external ventricular drains. Neurosurgery. 2000;47:1124.
, Andrews PJ, Citerio G. Intracranial pressure. Part one: historical overview and basic concepts. Intensive Care Med. 2004;30:1730.
, Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. IV. Infection prophylaxis. J Neurotrauma. 2007;24(suppl 1):S26.
, Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma. 2007;24(suppl 1):S37.
, Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. VII. Intracranial pressure monitoring technology. J Neurotrauma. 2007;24(suppl 1):S45.
, Davis JW, Davis IC, Bennink LD, et al. Placement of intracranial pressure monitors: are “normal” coagulation parameters necessary? J Trauma. 2004;57:1173.
, Gelabert-Gonzalez M, Ginesta-Galan V, Sernamito-Garcia R, et al. The Camino intracranial pressure device in clinical practice. Assessment in 1000 cases. Acta Neurochir (Wien). 2006;148:435.
, Gopinath SP, Robertson CS, Contant CF, et al. Clinical evaluation of a miniature strain-gauge transducer for monitoring intracranial pressure. Neurosurgery. 1995;36:1137.
, Holloway KL, Barnes T, Choi S, et al. Ventriculostomy infections: the effect of monitoring duration and catheter exchange in 584 patients. J Neurosurg. 1996;85:419.
, Hong WC, Tu YK, Chen YS, et al. Subdural intracranial pressure monitoring in severe head injury: clinical experience with the Codman MicroSensor. Surg Neurol. 2006;66(suppl 2):S8.
, Lundberg N. Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Acta Psychiatr Scand Suppl. 1960;36:1.
, Lundberg N, Troupp H, Lorin H. Continuous recording of the ventricular-fluid pressure in patients with severe acute traumatic brain injury. A preliminary report. J Neurosurg. 1965;22:581.
, Lozier AP, Sciacca RR, Romagnoli MF, et al. Ventriculostomy-related infections: a critical review of the literature. Neurosurgery. 2002;51:170.
, Poon WS, Ng S, Wai S. CSF antibiotic prophylaxis for neurosurgical patients with ventriculostomy: a randomised study. Acta Neurochir Suppl. 1998;71:146.
, Shapiro S, Bowman R, Callahan J, et al. The fiberoptic intraparenchymal cerebral pressure monitor in 244 patients. Surg Neurol. 1996;45:278.
, Signorini DF, Shad A, Piper IR, et al. A clinical evaluation of the Codman MicroSensor for intracranial pressure monitoring. Br J Neurosurg. 1998;12:223.
, Wiesmann M, Mayer TE. Intracranial bleeding rates associated with two methods of external ventricular drainage. J Clin Neurosci. 2001;8:126.
, Wong GK, Poon WS, Wai S, et al. Failure of regular external ventricular drain exchange to reduce cerebrospinal fluid infection: result of a randomised controlled trial. J Neurol Neurosurg Psychiatry. 2002;73:759.
, Yau Y, Piper I, Contant C, et al. Multi-centre assessment of the Spiegelberg compliance monitor: interim results. Acta Neurochir Suppl. 2002;81:167.
, Zabramski JM, Whiting D, Darouiche RO, et al. Efficacy of antimicrobial-impregnated external ventricular drain catheters: a prospective, randomized, controlled trial. J Neurosurg. 2003;98:725.
1 Andrews PJ, Citerio G. Intracranial pressure. Part one: historical overview and basic concepts. Intensive Care Med. 2004;30:1730.
2 Lundberg N. Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Acta Psychiatr Scand Suppl. 1960;36:1.
3 Lundberg N, Troupp H, Lorin H. Continuous recording of the ventricular-fluid pressure in patients with severe acute traumatic brain injury. A preliminary report. J Neurosurg. 1965;22:581.
4 Cremer OL. Does ICP monitoring make a difference in neurocritical care? Eur J Anaesthesiol Suppl. 2008;42:87.
5 Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. VII. Intracranial pressure monitoring technology. J Neurotrauma. 2007;24(suppl 1):S45.
6 O’Neill BR, Velez DA, Braxton EE, et al. A survey of ventriculostomy and intracranial pressure monitor placement practices. Surg Neurol. 2008;70:268.
7 O’Leary ST, Kole MK, Hoover DA, et al. Efficacy of the Ghajar Guide revisited: a prospective study. J Neurosurg. 2000;92:801.
8 Friedman WA, Vries JK. Percutaneous tunnel ventriculostomy. Summary of 100 procedures. J Neurosurg. 1980;53:662.
9 Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma. 2007;24(suppl 1):S37.
10 Bogdahn U, Lau W, Hassel W, et al. Continuous-pressure controlled, external ventricular drainage for treatment of acute hydrocephalus—evaluation of risk factors. Neurosurgery. 1992;31:898.
11 Kakarla UK, Kim LJ, Chang SW, et al. Safety and accuracy of bedside external ventricular drain placement. Neurosurgery. 2008;63:ONS162.
12 Khan SH, Kureshi IU, Mulgrew T, et al. Comparison of percutaneous ventriculostomies and intraparenchymal monitor: a retrospective evaluation of 156 patients. Acta Neurochir Suppl. 1998;71:50.
13 Paramore CG, Turner DA. Relative risks of ventriculostomy infection and morbidity. Acta Neurochir (Wien). 1994;127:79.
14 Guyot LL, Dowling C, Diaz FG, et al. Cerebral monitoring devices: analysis of complications. Acta Neurochir Suppl. 1998;71:47.
15 Wiesmann M, Mayer TE. Intracranial bleeding rates associated with two methods of external ventricular drainage. J Clin Neurosci. 2001;8:126.
16 Davis JW, Davis IC, Bennink LD, et al. Placement of intracranial pressure monitors: are “normal” coagulation parameters necessary? J Trauma. 2004;57:1173.
17 Ross IB, Dhillon GS. Ventriculostomy-related cerebral hemorrhages after endovascular aneurysm treatment. AJNR Am J Neuroradiol. 2003;24:1528.
18 Le H, Munshi I, Macdonald RL, et al. Traumatic aneurysm resulting from insertion of an intracranial pressure monitor. Case illustration. J Neurosurg. 2001;95:720.
19 Lozier AP, Sciacca RR, Romagnoli MF, et al. Ventriculostomy-related infections: a critical review of the literature. Neurosurgery. 2002;51:170.
20 Bota DP, Lefranc F, Vilallobos HR, et al. Ventriculostomy-related infections in critically ill patients: a 6-year experience. J Neurosurg. 2005;103:468.
21 Korinek AM, Reina M, Boch AL, et al. Prevention of external ventricular drain–related ventriculitis. Acta Neurochir (Wien). 2005;147:39.
22 Park P, Garton HJ, Kocan MJ, et al. Risk of infection with prolonged ventricular catheterization. Neurosurgery. 2004;55:594.
23 Arabi Y, Memish ZA, Balkhy HH, et al. Ventriculostomy-associated infections: incidence and risk factors. Am J Infect Control. 2005;33:137.
24 Holloway KL, Barnes T, Choi S, et al. Ventriculostomy infections: the effect of monitoring duration and catheter exchange in 584 patients. J Neurosurg. 1996;85:419.
25 Mayhall CG, Archer NH, Lamb VA, et al. Ventriculostomy-related infections. A prospective epidemiologic study. N Engl J Med. 1984;310:553.
26 Khanna RK, Rosenblum ML, Rock JP, et al. Prolonged external ventricular drainage with percutaneous long-tunnel ventriculostomies. J Neurosurg. 1995;83:791.
27 Sandalcioglu IE, Stolke D. Failure of regular external ventricular drain exchange to reduce CSF infection. J Neurol Neurosurg Psychiatry. 2003;74:1598.
28 Leung GK, Ng KB, Taw BB, et al. Extended subcutaneous tunnelling technique for external ventricular drainage. Br J Neurosurg. 2007;21:359.
29 Wong GK, Poon WS, Wai S, et al. Failure of regular external ventricular drain exchange to reduce cerebrospinal fluid infection: result of a randomised controlled trial. J Neurol Neurosurg Psychiatry. 2002;73:759.
30 Aucoin PJ, Kotilainen HR, Gantz NM, et al. Intracranial pressure monitors. Epidemiologic study of risk factors and infections. Am J Med. 1986;80:369.
31 Rebuck JA, Murry KR, Rhoney DH, et al. Infection related to intracranial pressure monitors in adults: analysis of risk factors and antibiotic prophylaxis. J Neurol Neurosurg Psychiatry. 2000;69:381.
32 Alleyne CHJr, Hassan M, Zabramski JM. The efficacy and cost of prophylactic and periprocedural antibiotics in patients with external ventricular drains. Neurosurgery. 2000;47:1124.
33 Poon WS, Ng S, Wai S. CSF antibiotic prophylaxis for neurosurgical patients with ventriculostomy: a randomised study. Acta Neurochir Suppl. 1998;71:146.
34 May AK, Fleming SB, Carpenter RO, et al. Influence of broad-spectrum antibiotic prophylaxis on intracranial pressure monitor infections and subsequent infectious complications in head-injured patients. Surg Infect (Larchmt). 2006;7:409.
35 Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. IV. Infection prophylaxis. J Neurotrauma. 2007;24(suppl 1):S26.
36 Hampl J, Schierholz J, Jansen B, et al. In vitro and in vivo efficacy of a rifampin-loaded silicone catheter for the prevention of CSF shunt infections. Acta Neurochir (Wien). 1995;133:147.
37 Zabramski JM, Whiting D, Darouiche RO, et al. Efficacy of antimicrobial-impregnated external ventricular drain catheters: a prospective, randomized, controlled trial. J Neurosurg. 2003;98:725.
38 Ostrup RC, Luerssen TG, Marshall LF, et al. Continuous monitoring of intracranial pressure with a miniaturized fiberoptic device. J Neurosurg. 1987;67:206.
39 Gambardella G, d’Avella D, Tomasello F. Monitoring of brain tissue pressure with a fiberoptic device. Neurosurgery. 1992;31:918.
40 Poca MA, Sahuquillo J, Arribas M, et al. Fiberoptic intraparenchymal brain pressure monitoring with the Camino V420 monitor: reflections on our experience in 163 severely head-injured patients. J Neurotrauma. 2002;19:439.
41 Shapiro S, Bowman R, Callahan J, et al. The fiberoptic intraparenchymal cerebral pressure monitor in 244 patients. Surg Neurol. 1996;45:278.
42 Schickner DJ, Young RF. Intracranial pressure monitoring: fiberoptic monitor compared with the ventricular catheter. Surg Neurol. 1992;37:251.
43 Gelabert-Gonzalez M, Ginesta-Galan V, Sernamito-Garcia R, et al. The Camino intracranial pressure device in clinical practice. Assessment in 1000 cases. Acta Neurochir (Wien). 2006;148:435.
44 Martinez-Manas RM, Santamarta D, de Campos JM, et al. Camino intracranial pressure monitor: prospective study of accuracy and complications. J Neurol Neurosurg Psychiatry. 2000;69:82.
45 Munch E, Weigel R, Schmiedek P, et al. The Camino intracranial pressure device in clinical practice: reliability, handling characteristics and complications. Acta Neurochir (Wien). 1998;140:1113.
46 Chambers KR, Kane PJ, Choksey MS, et al. An evaluation of the Camino ventricular bolt system in clinical practice. Neurosurgery. 1993;33:866.
47 Gopinath SP, Robertson CS, Contant CF, et al. Clinical evaluation of a miniature strain-gauge transducer for monitoring intracranial pressure. Neurosurgery. 1995;36:1137.
48 Signorini DF, Shad A, Piper IR, et al. A clinical evaluation of the Codman MicroSensor for intracranial pressure monitoring. Br J Neurosurg. 1998;12:223.
49 Banister K, Chambers IR, Siddique MS, et al. Intracranial pressure and clinical status: assessment of two intracranial pressure transducers. Physiol Meas. 2000;21:473.
50 Koskinen LO, Olivecrona M. Clinical experience with the intraparenchymal intracranial pressure monitoring Codman MicroSensor system. Neurosurgery. 2005;56:693.
51 Lang JM, Beck J, Zimmermann M, et al. Clinical evaluation of intraparenchymal Spiegelberg pressure sensor. Neurosurgery. 2003;52:1455.
52 Gray WP, Palmer JD, Gill J, et al. A clinical study of parenchymal and subdural miniature strain-gauge transducers for monitoring intracranial pressure. Neurosurgery. 1996;39:927.
53 Hong WC, Tu YK, Chen YS, et al. Subdural intracranial pressure monitoring in severe head injury: clinical experience with the Codman MicroSensor. Surg Neurol. 2006;66(suppl 2):S8.
54 Chambers IR, Siddique MS, Banister K, et al. Clinical comparison of the Spiegelberg parenchymal transducer and ventricular fluid pressure. J Neurol Neurosurg Psychiatry. 2001;71:383.
55 Yau Y, Piper I, Contant C, et al. Multi-centre assessment of the Spiegelberg compliance monitor: interim results. Acta Neurochir Suppl. 2002;81:167.
56 Abdullah J, Zamzuri I, Awang S, et al. Preliminary report on Spiegelberg pre and post-operative monitoring of severe head-injured patients who received decompressive craniectomy. Acta Neurochir Suppl. 2005;95:311.
57 Ng SC, Poon WS, Chan MT. Cerebral haemodynamic assessment in patients with thalamic haemorrhage: a pilot study with continuous compliance monitoring. Acta Neurochir Suppl. 2005;95:299.
58 Poca MA, Sahuquillo J, Topczewski T, et al. Is intracranial pressure monitoring in the epidural space reliable? Fact and fiction. J Neurosurg. 2007;106:548.
59 Raksin PB, Alperin N, Sivaramakrishnan A, et al. Noninvasive intracranial compliance and pressure based on dynamic magnetic resonance imaging of blood flow and cerebrospinal fluid flow: review of principles, implementation, and other noninvasive approaches. Neurosurg Focus. 2003;14(4):e4.
60 Geeraerts T, Launey Y, Martin L, et al. Ultrasonography of the optic nerve sheath may be useful for detecting raised intracranial pressure after severe brain injury. Intensive Care Med. 2007;33:1704.
61 Kimberly HH, Shah S, Marill K, et al. Correlation of optic nerve sheath diameter with direct measurement of intracranial pressure. Acad Emerg Med. 2008;15:201.
62 Firsching R, Schutze M, Motschmann M, et al. Venous ophthalmodynamometry: a noninvasive method for assessment of intracranial pressure. J Neurosurg. 2000;93:33.
63 Shimbles S, Dodd C, Banister K, et al. Clinical comparison of tympanic membrane displacement with invasive ICP measurements. Acta Neurochir Suppl. 2005;95:197.
64 Schmidt B, Czosnyka M, Klingelhofer J. Clinical applications of a non-invasive ICP monitoring method. Eur J Ultrasound. 2002;16:37.
65 Ragauskas A, Daubaris G, Dziugys A, et al. Innovative non-invasive method for absolute intracranial pressure measurement without calibration. Acta Neurochir Suppl. 2005;95:357.
66 Zhao YL, Zhou JY, Zhu GH. Clinical experience with the noninvasive ICP monitoring system. Acta Neurochir Suppl. 2005;95:351.
67 York D, Legan M, Benner S, et al. Further studies with a noninvasive method of intracranial pressure estimation. Neurosurgery. 1984;14:456.
68 Tan G, Zhou J, Yuan D, et al. Formula for use of mannitol in patients with intracerebral haemorrhage and high intracranial pressure. Clin Drug Investig. 2008;28:81.
69 Adelson PD, Bratton SL, Carney NA, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter 5. Indications for intracranial pressure monitoring in pediatric patients with severe traumatic brain injury. Pediatr Crit Care Med. 2003;4:S19.
70 Morris KP, Forsyth RJ, Parslow RC, et al. Intracranial pressure complicating severe traumatic brain injury in children: monitoring and management. Intensive Care Med. 2006;32:1606.
71 Keenan HT, Nocera M, Bratton SL. Frequency of intracranial pressure monitoring in infants and young toddlers with traumatic brain injury. Pediatr Crit Care Med. 2005;6:537.
72 Anderson RC, Kan P, Klimo P, et al. Complications of intracranial pressure monitoring in children with head trauma. J Neurosurg. 2004;101:53.
73 Wiegand C, Richards P. Measurement of intracranial pressure in children: a critical review of current methods. Dev Med Child Neurol. 2007;49:935.
74 Blaha M, Lazar D, Winn RH, et al. Hemorrhagic complications of intracranial pressure monitors in children. Pediatr Neurosurg. 2003;39:27.
