Intracranial pressure monitoring

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.

Refractory elevated ICP reduces cerebral perfusion pressure (CPP), thereby accounting for cerebral ischemia and initiating brain herniation syndromes that eventually lead to death.

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.

see Noninvasive intracranial pressure monitoring.

Intracranial pressure monitoring in children.

see Intracranial pressure monitoring indications.

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⁾.

see Idiopathic normal pressure hydrocephalus intracranial pressure monitoring.

Intracranial pressure monitor placement.

D/C monitor when ICP is normal × 48–72 hrs after withdrawal of ICP therapy. Caution: IC-HTN may have delayed onset (often starts on day 2–3, and day 9–11 is a common second peak, especially in peds). see delayed deterioration. Avoid a false sense of security imparted by a normal early ICP.

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 ¹⁰⁾.

Intracranial pressure monitoring case series.