The normal intracranial pressure (ICP) ranges within 7 to 15 mm Hg while in the vertical position, it does not exceed −15 mm Hg. Overnight sleep monitoring is considered the “gold standard” in conscious patients.
Typically, ICP lowering therapy initiates when ICP is greater than 20 to 25 mm Hg.
ICP-guided therapy has been the cornerstone in managing severe traumatic brain injury. Thus, ICP monitoring allows for the judicious use of interventions with a defined target point and thereby avoiding potentially harmful aggressive treatment.
Application of multimodal monitoring (MMM) in conjunction with adherence to Brain Trauma Foundation (BTF) guidelines during patient care bundle approaches have shown the positive outcomes as well as the minimized cost of acute care 1).
The need for a reliable, safe and reproducible technique to non-invasively assess ICP in the context of early screening and in the neurocritical care environment is obvious.
Even though since the end of the 19th century the spinal CSF pressure was used as indirect measure of intracranial pressure (ICP), the first reports of the use of continuous intracranial pressure monitoring via ventricular catheter were by Guillaume and Janny in 1951 2).
The first systematic use of a continuous ICP monitoring was historically made among patients with brain tumors 3). This monitoring was then tested and applied to other conditions, and further improvements in technology and technique 4) contributed to its worldwide diffusion.
Despite its widespread use, there is currently no class I evidence that ICP/CPP-guided therapy for any cerebral pathology improves outcomes; indeed some evidence suggests that it makes no difference, and some that it may worsen outcomes. Similarly, no class I evidence can currently advise the ideal CPP for any form of ABI. 'Optimal' CPP is likely patient-, time-, and pathology-specific. Further, CPP estimation requires correct referencing (at the level of the foramen of Monro as opposed to the level of the heart) for MAP measurement to avoid CPP over-estimation and adverse patient outcomes.
Evidence is emerging for the role of other monitors of cerebral well-being that enable the clinician to employ an individualized multimodality monitoring approach in patients with ABI.
While acknowledging difficulties in conducting robust prospective randomized studies in this area, such high-quality evidence for the utility of ICP/CPP-directed therapy in ABI is urgently required. So, too, is the wider adoption of multimodality neuromonitoring to guide optimal management of ICP and CPP, and a greater understanding of the underlying pathophysiology of the different forms of ABI and what exactly the different monitoring tools used actually represent 5).
Although the monitoring of intracranial pressure is widely recognized as standard care for patients with severe traumatic brain injury, its use in guiding therapy has incomplete acceptance, even in high-income countries 6) 7) 8).
In two randomized controlled trials (RCTs) and seven cohort studies involving 11,038 patients, ICP monitoring was not associated with a significant reduction in mortality (OR, 1.16; 95% CI, 0.87-1.54), with substantial heterogeneity (I(2) = 80%, P<0.00001), which was verified by the sensitivity analyses. No significant difference was found in the occurrence of unfavourable outcome (OR, 1.40; 95% CI, 0.99-1.98; I(2) = 4%, P = 0.35) and advese events (OR, 1.04; 95% CI, 0.64-1.70; I(2) = 78%, P = 0.03). However, we should be cautious to the result of adverse events because of the substantial heterogeneity in the comparison. Furthermore, longer ICU and hospital stay were the consistent tendency according to the pooled studies.
No benefit was found in patients with TBI who underwent ICP monitoring. Considering substantial clinical heterogeneity, further large sample size RCTs are needed to confirm the current findings 9).
In current clinical practice the intracranial pressure monitoring (ICP) is measured invasively using an intracranial (ventricular, parenchymal, subdural, or extradural) catheter connected to or integrated with a pressure transducer.
A prospective, observational study was conducted in 122 patients with TBI ≥13 years old with indications for monitoring who were being treated in neurosurgical intensive care units between January 2009 and December 2012. All enrolled patients required monitoring randomly using an external ventricular drain (EVD) or intraparenchymal fiberoptic monitor (IPM). Patients were placed into 2 groups depending on the type of monitoring device. Clinically relevant outcomes, refractory intracranial hypertension, survival rates, and device-related complications were compared between the 2 groups.
There was a significant between-group difference in the Glasgow Outcome Scale score 6 months after injury, which was the primary outcome. Refractory intracranial hypertension was diagnosed in 44 of 122 patients, and patients monitored using IPM had a higher percentage of refractory intracranial hypertension (51.7% vs. 21.0%, P < 0.001). The 1-month survival rate was 90.3% in the EVD group and 76.7% in the IPM group (log-rank test, P = 0.04), and patients managed with EVDs had a significantly higher 6-month postinjury survival rate compared with patients treated with IPMs (88.7% vs. 68.3%, log-rank test, P = 0.006). There was no statistically significant difference between the groups in device-related complications (P = 0.448).
Device selection for ICP monitoring provides prognostic discrimination, and use of EVDs may have a bigger advantage in controlling refractory intracranial hypertension. Based on our findings, we recommend routine placement of an EVD in patients with TBI, unless only parenchymal-type monitoring is available 12).
In a retrospective observational study, manual chart abstraction was used to obtain time-indexed ICP values during a period of 2 years from patients diagnosed with severe traumatic brain injury who had received simultaneous EVD and IPM placement.
When all time points were compared, the correlation between EVD and IPM was strong (r = 0.6955). However, when limiting the ICP values to be <20 or <25 in either the EVD or the IPM, the correlation was noted to be weaker (r = 0.3576 and r = 0.4232, respectively).
There is inadequate evidence to support that intraparenchymal ICP values can be treated in a similar manner to ICP values obtained from an EVD 13).
The predictive quality of intracranial pressure (ICP) monitoring has for many years been a matter of debate. We correlate ICP data comparing MRI data with the outcome after severe traumatic brain injury to evaluate their prognostic potency.
This study compares the results of ICP monitoring, MRI, coma duration and outcome according to Glasgow Outcome Scale obtained in 32 patients having suffered severe TBI. Level of significance was set to p≤0.05 in statistical tests.
The MRI results were closely correlated with coma duration and Glasgow Outcome Scale, but the ICP measurements were not. With the exception of severe, bipontine lesions, there is no other region of the brain in which increased evidence of traumatogenic lesions emerges as the intracranial pressure rises. Just bipontine lesions that proof to be infaust correlate with elevated ICP values.
ICP monitoring does not allow individual prognostic conclusions to be made. Implantation of an intracranial pressure sensor alone for making a prognostic estimate is not advisable. The use of intracranial pressure measurements in the retrospective appraisal of disease progress is highly problematic. However, MRI diagnostic in patients with severe TBI improves prognostic potency of clinical parameters 15).
248 patients with mean age of 34.6 ± 16.6 years among whom there were 216 (87.1%) men and 32 (12.9%) women. Eighty five (34.2%) patients had favorable outcome and 163 (65.8%) had unfavorable. Khalili et al found that those with favorable outcome had significantly lower age (p=0.004), higher GCS on admission (p<0.001), lower Rotterdam score (p=0.035), less episodes of intracranial hypertension (p<0.001) and lower max recorded ICP (p=0.041). These factors remained statistically significant after elimination of confounders by multivariate logistic regression model.
Age, on admission GCS, Rotterdam score, intracranial hypertension and max recorded ICP are important determinants of outcome in patients with severe TBI. ICP monitoring assisted us in targeted therapy and management of patients with severe TBI 16).
ICP monitors were inserted into 287 patients (59.5%). After propensity score matching, ICP monitoring significantly decreased 6-month mortality. ICP monitoring also had a greater impact on the most severely injured patients on the basis of head computed tomography data (Marshall computed tomography classification IV) and on patients with the lowest level of consciousness (GCS scores 3-5). After propensity score matching, monitoring remained nonassociated with a 6-month favorable outcome for the overall sample. However, monitoring had a significant impact on the 6-month favorable outcomes of patients with the lowest level of consciousness (GCS scores 3-5).
ICP monitor placement was associated with a significant decrease in 6-month mortality after adjustment for the baseline risk profile and the monitoring propensity of patients with diffuse severe TBI, especially those with GCS scores of 3 to 5 or of Marshall computed tomography classification IV 17).
During 1977-1978, 127 patients with severe head injury were admitted and underwent intracranial pressure monitoring. All patients had Glasgow Coma Scale (GCS) scores of 7 or less. All received identical initial treatment according to a standardized protocol. The patients' average age was 29 years; 60% had multiple trauma, and 35% needed emergency intracranial operations. Treatment for elevations of ICP was begun when ICP rose to 20 to 25 mm Hg, and included mannitol therapy and drainage of cerebrospinal fluid (CSF) when possible. Forty-three patients (34%) had ICP greater than or equal to 25 mm Hg; of these, 36 (84%) died. The mortality rate of the entire group was 46%. During 1979-1980, 106 patients with severe head injury were admitted and underwent ICP monitoring. Their average ager was 29 years; 51% had multiple trauma, and 31% underwent emergency intracranial surgery. All patients received the same standardized protocol as the previous series, with the exception of the treatment of ICP. In this present series: if ICP was 15 mm Hg or less (normal ICP), patients were continued on hyperventilation, steroids, and intensive care; if ICP was 16 to 24 mm Hg, mannitol was administered and CSF was drained; if ICP was 25 mm Hg or greater, the patients were randomized into a controlled barbiturate therapy study. Twenty-six patients (25%) had ICP's of 25 mm Hg or greater, compared to 34% in the previous series (p less than 0.05), and 18 of these 26 patients (69%) died. The overall mortality for this current series was 28% compared to 46% in the previous series (p less than 0.0005). This study reconfirms the high mortality rate if ICP is 25 mm Hg or greater; however, the data also document that early aggressive treatment based on ICP monitoring significantly lessens the incidence of ICP of 25 mm Hg or greater and reduces the overall mortality rate of severe head injury 18).