ICP Monitoring in Traumatic Brain Injury

ICP Monitoring in Traumatic Brain Injury

Blog written by Dr Jose Chacko

Timely recognition of intracranial hypertension is a crucial component of neurocritical care. In patients who are sedated and mechanically ventilated, sole dependence on the clinical features of raised intracranial pressure (ICP) including pupillary dilatation may lead to inordinate delays in the performance of critical interventions. Hence, continuous, direct measurement of ICP is often performed combined with clinical evaluation and brain imaging to identify deterioration in the neurological status. Non-invasive techniques including ultrasonographic evaluation using the optic nerve sheath diameter and pulsatility index on transcranial doppler may be useful tools; however, their reliability has not been fully established.

Methods of ICP measurement 

Until a few decades ago, ICP measurement was performed solely through intraventricular catheters. Such catheters also offer the option of CSF drainage to reduce ICP as appropriate. Drainage of CSF may be advantageous in patients with hydrocephalus. However, in patients with severe traumatic brain injury (TBI), elevated ICP occurs due to complex pathophysiology including hemorrhagic mass lesions, and focal or generalized cerebral edema, often associated with perturbations in the cerebral vasomotor reactivity. CSF drainage alone is usually ineffective to protect the brain under these circumstances.

Currently, intraparenchymal monitoring of ICP is commonly performed using a strain gauge (Codman microsensor) or a fiber optic monitor (Camino® Intracranial Pressure Monitor). Parenchymal monitors are easier to insert, particularly in patients with cerebral edema and midline shift wherein insertion of external ventricular drains (EVD) may be technically difficult. Furthermore, unlike EVDs, parenchymal monitors are easier to use and devoid of complications related to catheter blockage.

Other noninvasive methods of ICP monitoring include – Transcranial Doppler, Optic Nerve sheath diameter measurement, tympanic membrane displacement and papilloedema noticed with fundoscopy.

The pathophysiology of raised ICP 

Following severe TBI, the ICP may be an important indicator of adverse outcomes, with a six-fold increase in the risk of death when it exceeds 40 mm Hg.¹ However, the relationship between ICP and long-term functional outcomes may be less robust.² The ICP-based management of severe TBI is based on a cerebral perfusion pressure (CPP) target with the goal of avoiding macrovascular dysfunction and cerebral ischemia. The adequacy of cerebral perfusion using a target CPP is based on preserved cerebral autoregulatory mechanisms. However, autoregulatory limits may be variably deranged in the presence of TBI. Furthermore, low CPP and inadequate perfusion may not be the sole propagators of secondary brain injury. Although perfusion may remain reasonably intact, diffusion barriers may occur, leading to the inability of brain tissue to increase oxygen extraction in the face of reduced perfusion.³ Such mechanisms of injury are not easily recognized and may trigger or exacerbate brain injury even with preserved perfusion pressures and blood flows.⁴ Potential benefits of a therapeutic strategy based on a CPP target of 70 mm Hg may be offset by an increase in the incidence of cardiorespiratory complications, including acute respiratory distress syndrome.⁵ Hence, newer guidelines recommend a lower CPP target between 60–70 mm Hg.⁶

The guidelines of the Brain Trauma Foundation recommend therapeutic intervention if the ICP rises above a threshold level of 22 mm Hg.⁶ This cut-off is largely based on physiological considerations based on the Munroe-Kelly doctrine. However, setting a rigid numerical threshold may be too simplistic and fallacious, as neuronal dysfunction may well occur even with an ICP below a threshold level, as suggested by an increase in the lactate/pyruvate ratio.⁷

ICP monitoring and outcomes: what is the evidence?

A Japanese database analysis studied 1091 patients with TBI. The level of consciousness according to the Glasgow Coma Scale (GCS), pupillary abnormalities, CT findings, treatment modalities employed, and outcomes were compared between patients who underwent ICP monitoring and those who did not. More frequent use of hyperventilation, osmotic diuretics, sedative agents, temperature management, and surgical intervention was observed among patients who underwent ICP monitoring compared to those who did not. Although hospital mortality was significantly lower among patients who underwent ICP monitoring, there was no difference in favorable neurological outcomes.⁸

Lele et al. performed a secondary analysis of a prospective cohort study of 200 patients from a level 1 trauma center in India. Patients with severe TBI (GCS <8) and ventilated for at least 48 h were evaluated. ICP-guided treatment was followed in 126 (63%) patients. A propensity-based analysis was carried out with inverse probability weighting to compare patients who underwent ICP monitoring with those who did not. In-hospital mortality was lower among patients who underwent ICP monitoring (adjusted relative risk: 0.50, 95% CI: 0.29–0.87). However, there was no significant improvement in neurological outcomes assessed by the Glasgow Outcome Score at hospital discharge, and 3, 6, and 12 months of follow-up. The presence of intraventricular hemorrhage and cerebral edema was associated with poor outcomes. In the subgroup of patients without intraventricular hemorrhage or cerebral edema, ICP-guided therapy resulted in improved outcomes.⁹

A study of ICP monitoring from The American College of Surgeons Trauma Quality Improvement Program database evaluated patients with isolated severe TBI who fulfilled the criteria for ICP monitoring. Among 4880 patients included, ICP monitoring was performed in only 529 (10.8%) patients. Patients with and without ICP monitoring were compared regarding demographic characteristics, comorbidities, mechanism of injury, the Abbreviated Injury Scale (AIS), vital signs, and findings on the brain CT scan. On step-wise logistic regression analysis, ICP monitoring was found to be an independent predictor of in-hospital mortality, the requirement for mechanical ventilation, longer ICU stay, systemic complications, and lower functional independence at discharge. This study revealed poor compliance with the BTF recommendations for ICP monitoring; outcomes were also unfavorable among patients who underwent ICP-guided treatment.¹⁰

The BEST:TRIP trial randomized 324 patients with severe TBI and a GCS of 3–8, treated in ICUs from 6 sites in Bolivia and Ecuador.¹¹ In the ICP group, standard treatment modalities were employed to maintain an ICP of less than 20 mm Hg for a median of 3.6 days. The control group was managed according to a protocol based on clinical and CT findings including osmotic agents, mild hyperventilation if appropriate, and ventricular drainage as required. The use of high-dose barbiturates and decompressive craniectomy were employed in patients with worsening of neurological status, persistent cerebral edema, and clinical features suggestive of intracranial hypertension. Hypertonic saline therapy and hyperventilation were more often used in the control group, while high-dose barbiturate therapy use was more in the ICP group. The use of mannitol, CSF drainage, craniotomy for evacuation of mass lesions, and decompressive craniectomy was similar between groups.

The primary outcome was a composite of 21 parameters including duration of survival, impairment of conscious level, and the neuropsychological status, assessed within 6 months of commencement of the study. This composite outcome, assessed as an average percentile, was not different between groups (median 56 vs. 53, p=0.49). Among the secondary outcomes, the Glasgow Outcome Scale Extended  (GOS-E) score at 6 months (ICP vs. control: 44% vs. 39%), 14-day (21% vs. 30%) and 6-month mortality (39% vs. 40%) were also not different between the two groups.

The study was limited by the use of a composite primary outcome of 21 different parameters, and questionable generalizability as it was conducted in relatively resource-limited settings in South America. The results may not be extrapolatable to healthcare settings where ICP-guided therapy is routinely followed.

A recent observational cohort study included 2395 patients with TBI, intracranial or subarachnoid hemorrhage from 146 ICUs in 42 countries.¹² These patients had altered levels of sensorium with absent eye-opening and no response to verbal commands. Among this cohort, 1332 patients underwent ICP monitoring, while 1063 did not. Patients who underwent ICP monitoring received more intense treatment as indicated by a higher therapeutic intensity level (TIL) score. In-hospital mortality (28% vs 42%, p <0.0001) and 6-month mortality (34% vs. 49%, p <0.0001) were significantly lower in patients who underwent ICP monitoring compared to those who did not. Furthermore, unfavorable neurological outcomes at 6 months, defined as a score of <5 on the Glasgow Outcome Scale Extended (GOSE) was significantly less in patients who had ICP monitoring (60% vs. 65%, p <0.039). On propensity score weighting, ICP monitoring was associated with a significantly lower 6-month mortality among patients with at least one non-reactive pupil. However, no significant difference in mortality was observed in patients with bilateral non-reactive pupils. These findings were confirmed on sensitivity analysis after exclusion of patients with GCS of 3 and bilateral non-reactive pupils, and those who died with 48 h.

The recent Brain Trauma Foundation guidelines have given Level II B recommendation for the routine use of ICP monitoring in severe TBI.

Summary 

• Aiming for rigid cut-off levels of ICP may not be appropriate as micro and macrovascular dysfunction and impaired glucose utilization may occur even with normal ICP levels
• ICP-guided management may benefit patients who sustain a severe brain injury, especially in clinical settings that are accustomed to ICP-based management
• Monitoring systems alone cannot be expected to alter outcomes; it is the therapeutic strategy that evolves based on the information generated that may impact outcomes
• A comprehensive, individualized approach combining clinical findings, imaging, and, in selected patients, ICP monitoring may be the optimal strategy
• Advanced monitoring including brain tissue oxygen tension, cerebral microdialysis,  and transcranial doppler may be tools of the future that may enable optimized delivery of oxygen and energy substrates to the injured brain

References

1.         Treggiari MM, Schutz N, Yanez ND, Romand J-A. Role of intracranial pressure values and patterns in predicting outcome in traumatic brain injury: a systematic review. Neurocrit Care. 2007;6(2):104-112. doi:10.1007/s12028-007-0012-1

2.         Badri S, Chen J, Barber J, et al. Mortality and long-term functional outcome associated with intracranial pressure after traumatic brain injury. Intensive Care Med. 2012;38(11):1800-1809. doi:10.1007/s00134-012-2655-4

3.         Menon DK, Coles JP, Gupta AK, et al. Diffusion limited oxygen delivery following head injury. Crit Care Med. 2004;32(6):1384-1390. doi:10.1097/01.ccm.0000127777.16609.08

4.         Le Roux P. Intracranial pressure after the BEST TRIP trial: a call for more monitoring. Current Opinion in Critical Care. 2014;20(2):141-147. doi:10.1097/MCC.0000000000000078

5.         Robertson CS, Valadka AB, Hannay HJ, et al. Prevention of secondary ischemic insults after severe head injury. Crit Care Med. 1999;27(10):2086-2095. doi:10.1097/00003246-199910000-00002

6.         Carney N, Totten AM, O’Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6-15. doi:10.1227/NEU.0000000000001432

7.         Vespa PM, O’Phelan K, McArthur D, et al. Pericontusional brain tissue exhibits persistent elevation of lactate/pyruvate ratio independent of cerebral perfusion pressure. Crit Care Med. 2007;35(4):1153-1160. doi:10.1097/01.CCM.0000259466.66310.4F

8.         Suehiro E, Fujiyama Y, Koizumi H, Suzuki M. Directions for Use of Intracranial Pressure Monitoring in the Treatment of Severe Traumatic Brain Injury Using Data from The Japan Neurotrauma Data Bank. J Neurotrauma. 2017;34(14):2230-2234. doi:10.1089/neu.2016.4948

9.         Lele A, Kannan N, Vavilala MS, et al. Patients Who Benefit from Intracranial Pressure Monitoring without Cerebrospinal Fluid Drainage After Severe Traumatic Brain Injury. Neurosurgery. 2019;85(2):231-239. doi:10.1093/neuros/nyy247

10.       Piccinini A, Lewis M, Benjamin E, Aiolfi A, Inaba K, Demetriades D. Intracranial pressure monitoring in severe traumatic brain injuries: a closer look at level 1 trauma centers in the United States. Injury. 2017;48(9):1944-1950. doi:10.1016/j.injury.2017.04.033

11.       Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367(26):2471-2481. doi:10.1056/NEJMoa1207363

12.       Robba C, Graziano F, Rebora P, et al. Intracranial pressure monitoring in patients with acute brain injury in the intensive care unit (SYNAPSE-ICU): an international, prospective observational cohort study. The Lancet Neurology. 2021;20(7):548-558. doi:10.1016/S1474-4422(21)00138-1