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REVIEW ARTICLE
Year : 2018  |  Volume : 4  |  Issue : 2  |  Page : 63-67

Monitoring of Intracranial Pressure in Patients with Severe Traumatic Brain Injury: Review


1 Universidad Nacional Autonoma de Nicaragua, Managua, Nicaragua
2 University of Cartagena, Cartagena, Colombia
3 All India Institute of Medical Sciences, New Delhi, India
4 Neurosurgery Teaching Hospital, Baghdad, Iraq
5 Department of Neurology, State University of Campinas, Campinas, Sao Paulo, Brazil
6 Department of Neurosurgery, Cartagena Neurotrauma Research Group, University of Cartagena

Date of Web Publication28-Aug-2018

Correspondence Address:
Dr. Luis R Moscote-Salazar


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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mamcjms.mamcjms_1_18

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  Abstract 


Traumatic brain injury is a very heterogeneous entity that emerges over time. The neuromonitoring is critical for the prevention of secondary alterations, such as ischemia and hypoxia, which appear days after a primary injury. Neurosurgeons must understand that the phenomena are secondary to the primary lesion. Advances in multimodal neuromonitoring techniques have allowed evaluation of brain metabolism as well as other physiological parameters, including intracranial pressure, cerebral perfusion pressure, cerebral blood flow, brain temperature, blood pressure, and partial pressure of oxygen in brain tissue.

Keywords: Head trauma, hypoxia, ischemia, multimodal neuromonitoring, neurotrauma


How to cite this article:
Narvaez-Rojas AR, Mo-Carrascal J, Maraby J, Satyarthee GD, Hoz S, Joaquim AF, Moscote-Salazar LR. Monitoring of Intracranial Pressure in Patients with Severe Traumatic Brain Injury: Review. MAMC J Med Sci 2018;4:63-7

How to cite this URL:
Narvaez-Rojas AR, Mo-Carrascal J, Maraby J, Satyarthee GD, Hoz S, Joaquim AF, Moscote-Salazar LR. Monitoring of Intracranial Pressure in Patients with Severe Traumatic Brain Injury: Review. MAMC J Med Sci [serial online] 2018 [cited 2018 Sep 20];4:63-7. Available from: http://www.mamcjms.in/text.asp?2018/4/2/63/239992




  Introduction Top


Traumatic brain injury (TBI) has always been a public health problem. Severe brain traumatic injury is the leading cause of death worldwide, especially in children and in adults below the age of 45 years. In the context of severe head trauma, monitoring strategies have given the option of understanding the intracranial alterations due to the lesion. Monitoring of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is routinely used to guide the management of patients with severe brain trauma. The main parameter used to judge brain deterioration is the ICP. The neuromonitoring allows to recognize the deterioration of neurological function, to identify the presence of secondary brain injuries that can benefit from aimed therapeutic intervention, to know the pathophysiological changes that occur in a patient with brain injury and to obtain physiological data to individualize therapies, leading to appropriate evaluation and prognostication.[1],[2] A recent meta-analysis showed that the neurointensive management and assessment of ICP allow better functional results.[3],[4],[5],[6]

Patient assessment

Neurological examination complements the neuromonitoring. The application of sedative drugs alters the result of an objective neurological examination. The first thing to evaluate is the degree of alertness. The review should assess motor response, pupils, and response to painful stimuli. The depth of coma must be assessed by the Glasgow Coma Scale (GCS) or four Score (FOUR) score. Delirium should also be evaluated. Finally, a routine comprehensive evaluation of the patient includes neck stiffness, motor response, tendon reflexes, and plantar responses in addition to the cranial nerves. All patients with suspected intracranial hypertension must be strictly monitored for the presence of clinical signs of herniation. They then receive an immediate dose of mannitol (1 g/kg, Intravenous) and hyperventilation [arterial carbon dioxide tension (PaCO2) 25–30] and evaluated radiologically with computed tomography (CT) brain and by a neurosurgeon.

Concept of intracranial hypertension

In 1820, Kelli Munroe first described the principles of the ICP. In patients with severe head trauma, the initial stages of brain injury are characterized by tissue damage, impaired cerebral metabolism, and blood flow. Physiologically in the brain, there are various mechanisms that dampen sudden changes in the intracranial contents caused by bruising or edema. Mechanisms such as the expulsion of cerebrospinal fluid leading to up to 7% displacement of venous content outside of the cranial vault. Maintains ICP as part of the brain compliance mechanism without increasing ICP. Secondary intracranial hypertension is the leading mechanism of death in patients with traumatic brain injury and contributes to secondary brain injury, if not properly handled. As previously mentioned, the doctrine of Monro–Kellie proposed that the rigid skull is occupied by three volumes: blood, brain, and spinal fluid, at least any additional volume, such as hematomas, cerebral edema, or hydrocephalus will result in increased ICP, when the compensatory shifts of the primary volumes have been exceeded. Therefore, any increase in volume of the elements of the intracranial content must also be offset by the decrease in other volumes. Nonetheless, the curve of compliance is not linear, so when compensatory mechanisms deplete, the intracranial compliance (ΔVolume/ΔPressure) failure of these ends abruptly, and thus, any small change in intracranial volume leads to significant elevations in ICP. The ability to store up to 150 mL of new intracranial volume without a significant increase in ICP occurs by shifting venous blood into the general circulation, and the outward movement of the cerebrospinal fluid is time and age-dependent. Older people tend to have more brain atrophy and, thus, rearrange greater amount of volume that slowly expands. Young people with acute processes counterpart become symptomatic more quickly to the same pathophysiological processes. Space-occupying lesions are discussed in further sections, and it will be assumed that these lesions were surgically evacuated. Abnormal cerebral autoregulation, blood flow, and cerebral edema persist as a cause of increased ICP.

ICP typically ranges from 7 to 15 mmHg supine in the adult, and intracranial hypertension is considered on values above 20 mm Hg. The ICP cannot be reliably estimated if not monitored. Thus, patients who meet the criteria will be subjected to invasive ICP monitoring via an intraventricular or intracerebral catheter. It has been shown in clinical studies that patients with head trauma and ICP above 20 mm Hg, particularly when they are refractory to treatment, have a worse prognosis and are more likely to have cerebral herniation syndromes.[4],[29] There is also a recent evidence that CPP below 60 to 70 mm Hg is associated with decreased brain oxygenation and altered metabolism and also worse prognosis.[4] The goal of neuromonitoring and neurotreatment is at least maintaining cerebral perfusion, oxygenation, and metabolism, limiting the progression of high ICP, desaturation phenomena, and edema, among others.

A simple way to indirectly estimate the global cerebral perfusion is by calculating the CPP which is equal to the mean arterial pressure minus ICP or cerebral venous pressure, but a normal perfusion pressure does not guarantee an optimal cerebral perfusion and oxygenation. This is where other strategies called multimodal neuromonitoring play an important role; these can be PtiO2 (tissue oxygen pressure), the SjVO2 (venous saturation jugular bulb), and evaluation of brain metabolites such as glucose, lactate, and so on. In relation to CPP, it has been considered that the change may influence the prognosis of patients with severe brain injury. TBI guidelines recommend that CPP should be maintained between 50 and 70 mm Hg back to a brain injury, with evidence of adverse prognostic, if cerebral perfusion pressure (PPC) is above or below the established range. Different indications have been established for the monitoring of intracranial pressure [Table 1].
Table 1: Indications for monitoring ICP

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Neuromonitoring techniques

Monitoring techniques in patients with TBI can be divided into three categories: ICP monitoring, blood flow monitoring, and biochemical substrates monitoring.[7],[8],[9],[10] The choice between the various forms of monitoring has become complex. The capacity monitoring of multiple, such as oxygenation and substrate concentration, as well as ICP parameters are becoming more common. As mentioned above, cerebral ischemia, hypoxia, and cell dysfunction are common after traumatic brain injury, inducing a reduced blood flow and the arrival of substrates occurring within minutes, which highlights the importance of early resuscitation.

There are various strategies to carry out monitoring of ICP, the gold standard being intra-ventricular monitoring of intracranial pressure by connecting this space to an external pressure transducer. Usually the catheter transducer and a drainage system with a stopcock are connected; this allows to measure ICP and ICP can be decreased by draining cerebrospinal fluid (CSF) in addition to joining the possibility of calibration in situ; it is possible to configure a system that continuously monitors ICP and possible intermittent CSF drainage or continuous intermittent CSF drainage along with measuring ICP. The risk of ventriculitis is increased if drainage catheter is in place beyond 5 days. Other systems for monitoring intraparenchymal ICP transducers are equipped at its tip with electronic sensors or fiber optics that can be easily placed by a neurosurgeon through a burr hole. These devices need to be calibrated prior to insertion, and its ability to measure the ICP is superior even to other devices such as subarachnoid screws or epidural transducers, which end up being less effective during the days after placement.

Subarachnoid bolts are fluid-coupled devices that connect intracranial space to external transducers. The insertion technique is neurosurgical through a burr hole; adjacent to the screw, core dura is pierced, so CSF fills the screw and is connected to the transducer the complications include risk of infection, occlusion detritus, and movement of the device.

Intracranial pressure monitoring

ICP above 20 mm Hg is associated with an increased mortality. Some intracranial situations are easy to detect and correct, such as the progression of brain contusions; other cases with diffuse cerebral edema corresponding to vasodilation or edema are not so easy to detect. Curve of volume–pressure has fluctuations known as “A” (steep rises in ICP to a plateau of ≥50 mm Hg and are sustained for 5–20 min before falling rapidly), “B” (rhythmic oscillations to 20–30 mmHg), and “C” (Traube–Hering waves originating in the arterial pressure), which describes changes in ICP, corresponds to volume increments having an exponential configuration, responding to all compensatory mechanisms such as the redistribution of cerebrospinal fluid of the supratentorial region toward the spinal sac; thus, ICP remains constant despite the increase in volume. When compensatory mechanisms are violated, ICP increases rapidly. ICP may not be reliable, if it is based on estimates of clinical examination or radiographic criteria only.

In patients suspected of having intracranial hypertension, intracranial monitoring is the gold standard for evaluation. In the traumatic brain injury, indications for monitoring include GCS less than 9, with an abnormal brain scan and patients with a lower score of 9 with a normal brain scan but over 40 years with hypotension or abnormal motor posturing. The Brain Trauma Foundation (BTF) recommends that ICP should be monitored in all recoverable patients with TBI with GCS 3 to 8, an abnormal CT, and after resuscitation (recommendation Level II). A couple of works carried out in Austria and the Netherlands reported that only 57% and 46%, respectively, of the candidates for monitoring ICP patients are being monitored; this apparently reveals that we are monitoring much less than what is required.

An intraventricular catheter attached to traditional fluids is the standard method and is inexpensive, but can undergo alterations or malfunction. The optical fiber (Integra Neurosciences, Plainsboro, New Jersey, USA) and transducing tip devices (Codman, Raynham, Massachusetts, USA) may be in the ventricle or in the brain parenchyma and be suitable for the measurement for several days but usually are more expensive, and we cannot recalibrate after locating. There is also a system that can monitor separate compartments allowing measurement of ICP and drainage of cerebrospinal fluid of this type, which is known Spielberg (Hamburg, Germany) transducer.

Chesnut et al. conducted a randomized multicenter trial of general acute care, which included a population over 13 years of age, with a total of 324 patients. Among the weaknesses of these studies is the lack of a control group, and they compared two strategies: one oriented for monitoring ICP and the other based on the evaluation of the clinical and imaging tests (TAC) management.[8] The study revealed similar results with both invasive and non-invasive monitoring of ICP. These results cannot afford to dismiss the utility of ICP for management of intracranial hypertension in patients when this strategy in other series has proved its usefulness. It should be mentioned that the study has important methodological defects in quality. It is worth mentioning again that monitoring ICP is the standard of care in many centers still having variability in the trend of use. In the Best Trip study population, patients with GCS less than 8 and subjected to strategies to reduce ICP below 20 mm Hg were not different from those managed with clinical and imaging parameters, but TBI is highly heterogeneous, where there are probably subgroups and where there are indeed differences suspect in relation to pathophysiological aspects where the biomechanical effect of primary and secondary lesion constitute determinant of the natural history of brain injury.

It has been documented in the literature on the role of combined strategies for handling ICP (sedation, hyperosmolar therapy, and drainage of cerebrospinal fluid).[11] Several studies have shown that the sustained increase in ICP above 20 mm Hg is associated with poor prognosis. Jian et al. reported that mortality rate was 14% in patients with ICP of less than 20 mm Hg, but 34% with ICP above 30 mm Hg within 48 h. The BTF (USA) recommends reducing the ICP with a threshold of 20 mm Hg (recommendation Level II). Currently, the treatment of patients with suspected intracranial hypertension is based on a staggering of clinical and pharmacological measures, which may culminate surgical treatment. The non-use of ICP monitoring can be considered a fully empirical treatment.[12],[13],[14],[15],[16],[17],[18],[19],[20]

Why should we monitor the ICP?

Operability

Neurosurgeons may find it difficult to base their decision for surgery purely on clinical criteria or imagine. Persistently raised ICP becomes the pillar for timely decision for surgical intervention.[21],[22],[23],[24],[25]

Outcome

It is known that sustained intracranial hypertension is an element of poor prognosis in patients with neurotrauma and neurocritical, and this element is useful to take subsequent decisions and give the information to relatives.

Anticipating injuries

Timely intervention to a possible progression of cerebral edema or the appearance of new intracranial lesions is useful; even from the appearance of small increases in ICP, neurospecialists can establish measures to stop the development of deleterious conditions.

Avoid unnecessary therapies

The assessment of ICP by trained personnel as an indicator is useful for not implementing treatments based on empiricism (aggressive fluid therapy, prolonged hyperventilation, etc.).

Quality and patient safety

Measuring the ICP lets us know if uses of other strategies are being effective during patient management, for example, optimization of sedation and paralysis.

ICP monitoring and ecology

Monitoring ICP is not a treatment; it is only one of several strategies for early diagnosis, therefore it does not reduce mortality by itself. Other factors such as training of medical and paramedical staff, deep knowledge of pathophysiology, available resources also contribute indirectly to the outcome. The study of Bolivia and Ecuador would hardly be approved by an ethics committee in a developed country. The implementation of future studies whose methodology includes the assessment of the relationship between human factors and processes of care, analysis of health systems, and so on will help to learn about various aspects of the neurotraumatic disease.[35],[37]


  Conclusions Top


Therapeutic interventions in severe TBI are influenced by both local and systemic disorders. Monitoring ICP must remain a cornerstone in the field of neurotrauma in the management of intracranial hypertension until the emergence of new evidence. It is important to finally note that details of care and specific resources should be available within the spectrum of care of a trauma system monitoring ICP is only a part of the multimodal neuromonitoring, which has been associated with better prognosis when compared only with patients undergoing ICP monitoring.[15]

About 80% of patients with severe TBI worldwide are managed in regions/environments of low and middle income. These areas are characterized not only by a population with an increased risk of TBI but also for the lack of basic prevention programs and inadequate supply of prehospital care after an advanced surgical procedure.

Improvements in quality of care for patients with severe TBI have resulted in a reduction of mortality and have been tried out in high-income areas due to improvements in the care system and not just in one intervention.[25] One aspect to consider is that if ICP is routinely monitored in severe TBI, it would mean that patients have received correct neuromanagement, but if we monitor, we will encourage the correct and safe practices for our patients.[4],[6],[26],[27],[28],[29],[30],[31],[32],[33],[34] In conclusion, patients at risk of developing intracranial hypertension should have ICP monitoring for proper management.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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