There are insufficient data to support a Level I recommendation for this topic.

Intracranial pressure (ICP) should be monitored in all salvageable patients with a severe traumatic brain injury (TBI; Glasgow Coma Scale [GCS] score of 3-8 after resuscitation) and an abnormal computed tomography (CT) scan. An abnormal CT scan of the head is one that reveals hematomas, contusions, swelling, herniation, or compressed basal cisterns.

ICP monitoring is indicated in patients with severe TBI with a normal CT scan if two or more of the following features are noted at admission: age over 40 years, unilateral or bilateral motor posturing, or systolic blood pressure (BP) < 90 mm Hg.

It is now clear that only part of the damage to the brain during TBI occurs at the moment of impact. Numerous secondary insults compound the initial damage in the ensuing hours and days. A large body of published data since the late 1970s reports that significant reductions in mortality and morbidity can be achieved in patients with severe TBI by using intensive managemenst protocols. These protocols emphasize early intubation, rapid transportation to an appropriate trauma care facility, prompt resuscitation, early CT scanning, and immediate evacuation of intracranial mass lesions, followed by meticulous management in an intensive care unit setting, which includes monitoring ICP.

The main objective of intensive monitoring is to maintain adequate cerebral perfusion and oxygenation and avoid secondary injury while the brain recovers. Cerebral perfusion is reduced and poorer outcomes are associated with systemic hypotension6 and intracranial hypertension (ICH). Cerebral perfusion pressure (CPP), an indirect measure of cerebral perfusion, incorporates mean arterial blood pressure (MAP) and ICP parameters. CPP values below 50 are associated with poor outcome (see CPP topic). The only way to reliably determine CPP and cerebral hypoperfusion is to continuously monitor ICP and blood pressure.

As with any invasive monitoring device, ICP monitoring has direct costs, uses medical personnel resources for insertion, maintenance, troubleshooting, and treatment, and has associated risks (see ICP Technology topic). These must be outweighed by the benefits or usefulness of ICP monitoring which can be captured in selecting patients that are at risk for ICH. This would also minimize the risks of prophylactic treatment of ICH in the absence of ICP monitoring.

There are three key questions addressing the utility of ICP monitoring in TBI patients:

1. Which patients are at risk for ICH?
2. Are ICP data useful?
3. Does ICP monitoring and treatment improve outcomes?

For this update, Medline was searched from 1996 through July of 2004 (see Appendix B for search strategy), and results were supplemented with literature recommended by peers or identified from reference lists. Of 36 potentially relevant studies, 12 were added to the existing table and used as evidence for this question (Evidence Tables I, II, and III).

The correlation between ICH and poor outcome in patients with severe TBI has been demonstrated in several studies. Comatose (GCS < 9) TBI patients constitute the group at highest risk for ICH. Admission CT scans are variable predictors of ICH in severe TBI patients as evidenced in the following studies:

In 1982, Narayan et al. reported a prospectively studied series of patients with severe TBI and found that, in comatose TBI patients with an abnormal CT scan, the incidence of ICH was 53-63%. In contrast, patients with a normal CT scan at admission had a relatively low incidence of ICH (13%). However, within the normal CT group, if patients demonstrated at least two of three adverse features (age over 40 years, unilateral or bilateral motor posturing, or systolic BP < 90 mm Hg), their risk of ICH was similar to that of patients with abnormal CT scans.

Others also have found a relatively low incidence of ICH in severe TBI patients with a normal CT scan. In 1986, Lobato et al. studied 46 patients with severe TBI who had completely normal CT scans during days 1-7 after injury. They reported "sustained elevation of the ICP was not seen in these patients, indicating that ICP monitoring may be omitted in cases with a normal scan." However, since one-third of the patients with a normal admission scan developed new pathology within the first few days of injury, the authors recommended a strategy for follow-up scanning. In 1990, in a prospective multicenter study of 753 severe TBI patients, Eisenberg et al. found that a patient whose admission CT scan does not show a mass lesion, midline shift, or abnormal cisterns has a 10-15% chance of developing ICH.

In 1998, Poca et al. correlated the Marshall CT classification of admission CT scans in severe TBI patients with incidence of ICH and found that three out of 94 patients had diffuse injury I (no visible intracranial pathology on CT). These patients had ICP less than 20 mm Hg; however, one patient had an evolution of the CT to diffuse injury II, demonstrating one out of three severe TBI patients with a normal admission CT evolved into new intracranial lesions.

In 2004, Miller et al. conducted a retrospective review of 82 patients with severe TBI without surgical mass lesions. They did not correlate CT characteristics of midline shift, basal cisterns, ventricular effacement, sulci compression, and gray/white matter contrast with initial ICP, although there was a correlation with later high ICP values.

Lee et al. (1998) studied the relationship of isolated diffuse axonal injury (DAI) to ICH in 36 out of 660 severe TBI patients. Patients were mildly hyperventilated and maximal hourly ICP values were recorded showing 90% of all the readings below 20 mm Hg. Ten patients had all ICP readings below 20 mm Hg, and the remainder had readings above 20 mm Hg, with four having readings above 40 mm Hg (which were associated with fever). Four patients died and discharge outcome was correlated with severity of DAI.

In summary, there is a markedly lower incidence of ICH in severe TBI patients with completely normal admission and follow up CT scans that do not have associated admission parameters. Abnormal CT scans are variable predictors of ICH except in CT scans showing severe intracranial pathology.

ICP data can be used to predict outcome and worsening intracranial pathology, calculate and manage CPP, allow therapeutic CSF drainage with ventricular ICP monitoring and restrict potentially deleterious ICP reduction therapies. ICP is a robust predictor of outcome from TBI and threshold values for treatment are recommended based on this evidence (see ICP Threshold topic).

ICP monitoring can be the first indicator of worsening intracranial pathology and surgical mass lesions. Servadei et al. (2002) studied 110 consecutive patients with traumatic subarachnoid hemorrhage, of which 31 had severe TBI and ICP monitoring. ICP monitoring was the first indicator of evolving lesions in 20% of the severe TBI group, four out of five of whom received an operation.

CPP management cannot be done without measuring ICP and MABP. CPP levels are used for therapeutic intervention that targets both MABP and ICP (see CPP topic).

Prophylactic treatment of ICP without ICP monitoring is not without risk. Prolonged hyperventilation worsens outcome and significantly reduces cerebral blood flow based on jugular venous oxygen saturation monitoring. Prophylactic paralysis increases pneumonia and ICU stay. Barbiturates have a significant risk of hypotension and prophylactic administration is not recommended. Mannitol has a variable ICP response in both extent of ICP decrease and duration.

In summary, ICP data are useful for prognosis and in guiding therapy.

A randomized trial of ICP monitoring with and without treatment is unlikely to be carried out. Similarly, a trial for treating or not treating systemic hypotension is not likely. Both hypotension and raised ICP are the leading causes of death in severe TBI, and are treated if either is suspected, regardless of whether ICP or blood pressure is monitored. The question remains, does ICH reflect an irreversible, evolving pathology sustained at the time of injury? The question can be answered partially by examining the outcome of those patients that respond to therapies that lower ICP.

Eisenberg et al. (1988) reported in a multi-center study of the use of pentobarbital to treat patients with ICP elevations refractory to all other therapy.8 In their study, patients whose ICP could be controlled had a much better outcome than those in whom it could not be controlled.

Saul and Ducker32 prospectively studied 127 severe TBI patients who were treated with mannitol and CSF drainage for an ICP 20-25 mm Hg, and were compared to a similar group of 106 patients treated at a lower ICP of 15 mm Hg. They found a significant reduction in mortality in the lower ICP threshold treatment group.

Howells et al. found that patients who respond to CPP treatment which incorporated ICP had better outcomes. They studied 64 patients treated according to a CPP directed protocol (CPP > 70 and ICP < 25 mm Hg). Patients with intact pressure autoregulation who responded to the CPP protocol by decreasing ICP had a significantly better outcome compared to those patients who responded by increasing ICP (pressure passive autoregulation). It may be that patients with intact pressure autoregulation would have tolerated high ICP and low CPP without a change in outcome, but determining this would have required a "do not treat" arm of the study.

Decompressive craniectomy for ICH is associated with better outcomes in those patients that have a decrease in ICP. Aarabi et al. studied 50 consecutive severe TBI patients, 40 of whom had intractable ICH and underwent decompressive craniectomy, leading to a significantly lowered ICP from a mean of 24 to 14 mm Hg. For the 30-day survivors of the original sample (n = 39), good outcome (Glasgow Outcome Scale score [GOS] of 4 or 5) occurred in 51.3%. Similar results were reported by Timofeev et al. in 49 severe TBI patients with ICH that underwent decompressive craniectomy.

Does ICP monitoring per se make a difference in outcome? Cremer et al. reported a retrospective analysis of severe TBI patients managed at two different trauma centers who differed in the use of ICP monitoring. One center with 122 patients that did not monitor ICP but used ICP lowering treatment (82% sedatives and paralytics, 25% mannitol, 22% hyperventilation and 2% ventricular drainage) was compared to another with 211 patients that used ICP monitoring in 67% of severe TBI patients and treated ICP significantly more except for hyperventilation and ventricular drainage which was equally used in both centers. There was no difference in mortality or 12-month GOS. However, differences between the groups in the sample render the findings minimally useful. More than twice the patients in the ICP monitoring center had hypotension on admission compared to the center that did not monitor ICP, which also had a significant number of patients transferred from other hospitals.

Protocols that incorporate ICP monitoring and other advanced monitoring have demonstrated improved outcomes when compared to earlier time periods without a protocol. In addition the frequency of ICP monitoring in trauma centers has been reported to be associated with improved outcomes.

In summary, patients who do not have ICH or who respond to ICP-lowering therapies have a lower mortality than those who have intractable ICH. There are no data on patients with untreated ICH compared to treated ICH and little data on the outcome of patients that respond to ICP lowering therapies.

There is evidence to support the use of ICP monitoring in severe TBI patients at risk for ICH. ICP cannot be reliably predicted by CT scan alone. ICP data are useful in predicting outcome and guiding therapy, and there is an improvement in outcomes in those patients who respond to ICP lowering therapies. The limited data on improvement in outcome in those patients that respond to ICP lowering treatment warrants ICP monitoring to treat this group of patients. Not monitoring ICP while treating for elevated ICP can be deleterious and result in a poor outcome.

A randomized clinical trial (RCT) of ICP monitoring, with and without treatment, would be extremely useful in establishing the value of ICH treatment, but it is unlikely considering that most TBI experts consider ICP or CPP parameters to be the primary basis for ICU management decisions in the care of the severe TBI patient. Further studies on sequential normal CT scans in severe TBI patients and the incidence of ICH and evolving lesions would be useful to identify a group that may not require ICP monitoring and treatment.