Continuing Education Activity

According to the Monro-Kellie theory, the cranial compartment is incompressible, and its contents (blood, cerebrospinal fluid, and brain tissue) are in an internal milieu of volume balance; thus, an increase in one must be offset by a reduction in the other components. Intracranial pressure–guided therapy has been the cornerstone in managing severe traumatic brain injury. Intracranial pressure (ICP) monitoring allows for the judicious use of interventions with a defined target point, thereby avoiding potentially harmful aggressive treatment.

Participants get an in-depth examination of ICP-guided therapy, emphasizing its role in managing severe traumatic brain injury. The course outlines current monitoring recommendations, covering invasive techniques like intraventricular catheters and noninvasive methods like transcranial Doppler ultrasound. Practical insights into judicious interventions with defined target points aim to prevent potentially harmful aggressive treatments. The activity also addresses the need for the collaborative efforts of an interprofessional team to minimize complications regarding the process and thereby safeguard patient safety.

Objectives:

• Identify the normal range of intracranial pressure and recognize the significance of deviations from this range in conscious patients.

• Differentiate between various modalities used for intracranial pressure monitoring, understanding their strengths, limitations, and appropriate applications in different clinical scenarios.

• Select appropriate interventions based on intracranial pressure readings and patient-specific factors, ensuring the judicious use of therapies to avoid aggressive and potentially harmful treatment.

• Coordinate care during intracranial pressure monitoring, ensuring seamless transitions between different care settings, and involving relevant team members to optimize patient outcomes and safety.

Introduction

The normal intracranial pressure (ICP) ranges from 7 to 15 mm Hg, while it does not exceed 15 mm Hg in the vertical position. Overnight sleep monitoring is considered the “gold standard” in conscious patients.[1] Typically, ICP lowering therapy initiates when pressure exceeds 20 to 25 mm Hg.[2] Refractory elevated ICP reduces cerebral perfusion pressure, accounting for cerebral ischemia and initiating herniation syndromes that eventually lead to death.[3][4]

Implementing multimodal monitoring with adherence to 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, thereby avoiding potentially harmful aggressive treatment. Brain Trauma Foundation guidelines during patient care bundle approaches have shown positive outcomes and the minimized cost of acute care.[5][6]

Anatomy and Physiology

Monro-Kellie Doctrine

According to the Monro-Kellie theory, the cranial compartment is incompressible, and its contents (blood, cerebrospinal fluid [CSF], and brain tissue) are in an internal milieu of volume balance; thus, an increase in one must be offset by a reduction in the other components. The Monro-Kellie hypothesis is based on a pressure-volume relationship that tries to keep the non-compressible aspect of the skull in a steady state.[7][8] CSF and cerebral blood volume are the primary buffers for extra volume increment.

Historical Perspective

Alexander Monro Secundus mentioned in his 1783 monograph that the brain tissue and blood volume remained constant and emphasized the necessity to egress blood equal to any foreign liquid injected inside the skull. George Kellie reinforced the assumption that the total amount of blood flowing within the skull remains constant. John Abercrombie was primarily responsible for propagating this doctrine across the medical world. However, they needed more information about the anatomy and physiology of the nervous system during that period to finish the hypothesis. They disregarded the CSF’s involvement, if not its mere existence, in ICP control. In his book On the Disorders of the Cerebral Circulation, Burrows disputed the concept of the skull as a perfect sphere and the invariability of blood volume. He claimed the CSF has a significant function in the control of ICP. He mentioned that cerebral blood volume could change, but only to the benefit or harm of the brain or CSF volumes.[9]

Harvey Cushing established this doctrine's clinical and physiological significance in the twentieth century by confirming Burrows’ findings of the CSF’s role in intracranial dynamics and the existence of 3 volumes that operate as compensators for volume depletion or insertion inside the skull.

Pierre Janny published his thesis on ICP monitoring, while Nils Lundberg presented it more than 60 years ago. Jean Guillaume and Pierre Janny used U-tube manometry to measure ICP in 1951. Heinrich Quincke monitored lumbar CSF pressure through a lumbar puncture in 1981. Nils Lundberg monitored CSF pressure using ventricular catheters through the frontal horn connecting to an externally placed transducer. ICP micro transducers were developed in the 1980s.

Role of the Doctrine in Intracranial Hypertension

According to Monro and Kellie’s 1783 pressure-volume equations, when ICP rises, vascular blood and CSF are moved as part of a dynamic counterbalance to maintain normal pressure inside the inelastic skull, while brain tissue stays unaffected. Under pathological circumstances, if one of these compartments expands or a fourth one forms due to a mass-effect lesion such as a tumor or hematoma, one or more components must contract to prevent any subsequent rise in ICP. Since the parenchymal compartment cannot compensate for a rapid increase in ICP, cranial blood volume and CSF are responsible for this process. CSF is the primary buffer mechanism; this fluid migrates into the peri medullary subarachnoid area until displaced brain structures obstruct its flow. The vascular compartment’s capacity to correct for ICP is activated later and involves lowering the cerebral blood volume through jugular drainage.

Role of the Doctrine in Intracranial Hypotension

In individuals with intracranial hypotension, a decrease in CSF volume may result in a compensatory increase in brain or intracranial blood volume. Since the amount of brain tissue is typically considered constant, compensation would occur through increased blood volume, notably venous blood, because veins are more adaptable than arteries.[10] The Monro-Kellie theory may account for many magnetic resonance imaging anomalies seen in intracranial hypotension or CSF volume depletion, such as meningeal augmentation, subdural fluid collections, engorgement of cerebral venous sinuses, prominence of the spinal epidural venous plexus, and pituitary gland enlargement.[8] As a second consequence of CSF’s lack of buoyancy forces, brain tissue is forced downward, resulting in herniation. These effects are amplified by gravity while the patient is standing up, and they serve as a foundation for understanding both the clinical presentations of the condition as well as the imaging results.[11]

Interaction Between Cerebral Volume and ICP

Cerebral compliance is the volume required to produce a specific change in pressure. Thus, cerebral compliance may be defined as the cranial vault’s adaptive ability to increase volume.[12] The cerebral elastance, the pressure resulting from a known change in volume, is interpreted as the opposition to intracranial volume growth. The pressure-volume curve is divided into 3 phases.[12]

• Initial stage (phase 1): This stage is characterized by a high level of brain compliance and a low ICP. Despite the volume rise, there is no evidence of a subsequent increase in ICP. CSF and cerebral blood volume nullify the increase in volume.
• Transition stage (phase 2): This stage is characterized by poor brain compliance and a low ICP, although the latter gradually increases.
• Ascending stage (phase 3): This stage exhibits poor or non-existent compliance with elevated ICP, which is the beginning of decompensation. Compensatory processes become inactive, and tiny volume changes result in significant pressure increments.

Limitations of the Doctrine

• There is no mention of the role of CSF in the brain’s adaptive physiology.
• There is no mention of the effect of gravitation on the volume and pressure inside the skull.
• This is not applicable for children with open fontanels.

Indications

Brain Trauma Foundation Guidelines for Traumatic Brain Injury Management (Level II Recommendations)

 An ICP monitor is recommended in the following situations:

• Patients with Glasgow Coma Scale score of less than 8
• An abnormal computed tomogram (CT) scan of the head
• Two or more of the following are present: patient older than 40 years, unilateral or bilateral motor posturing, and systolic blood pressure less than 90 mm Hg.[13]

Other ICP Monitoring Recommendations (Level III Recommendations)

• Patients with an initial normal CT scan or with minor changes in CT images but later show features of neurologic worsening or progression on the repeat scan
• Evidence of brain swelling, eg, compressed or absent basal cisterns
• Patients with extensive bifrontal contusions independent of the neurological condition
• When sedation interruption to check neurological function is not justified, eg, respiratory failure from lung contusions and flail chest
• When the neurological examination is not reliable, eg, maxillofacial trauma or spinal cord injury
• A decompressive craniectomy is performed as a last resort for intracranial hypertension refractory to medical management
• Following craniotomy wherein there are relevant risk factors for the propagation of brain edema, eg, confounding hypoxia, hypotension, pupil abnormalities, midline shift greater than 5 mm [14]

Contraindications

Contraindications for placement of an invasive mode of ICP monitoring include:

• Concurrent use of anticoagulant drugs
• Bleeding disorders
• Scalp infection
• Brain abscess [15]

Equipment

Basic equipment sets should include the following:

• Nonsterile gloves, soap, brush, hand towel, razor, and a marker pen for parts preparation and marking of the site of placement of monitor devices 
• For the procedure, a face mask, sterile gown, gloves, an antiseptic solution, a drape, a local anesthetic agent, a 5-mL syringe, a number 11 or 15 surgical blade, and an ICP-monitoring kit
• Drill with a drill bit, a bolt, an ICP sensor, and a transducer per the methods utilized
• Suture material and a sterile dressing [15]

To monitor ICP, use intraventricular monitoring with a ventriculostomy, intraparenchymal strain gauge, or fiber-optic monitor. Therefore, it is essential to have the appropriate monitoring devices readily available. 

Personnel

Necessary personnel includes a composite healthcare team comprised of the following:

• A neurosurgeon
• A qualified assistant
• An attending nurse
• An anesthetist

Preparation

Before any medical procedure, the patient or their medical proxy should comprehensively explain the reason for the procedure and its potential risks. Additionally, obtain written consent. Strict adherence to aseptic guidelines is a cornerstone in preventing infection, and prophylactic antibiotics must be administered at the beginning of the procedure. A meticulous technique is vital in minimizing procedure-related complications.[15] The patient should be well sedated, assuring patency of their airway, and a local anesthetic should be administered at the allocated point of ventriculostomy or insertion of ICP monitoring devices.

Technique or Treatment

The placement of either a burr hole or a twist drill technique aids the insertion of the device. Kocher point is the choice for the ventriculostomy, which is 3 cm lateral of the midline and 1 cm anterior to the coronal suture. Other points of ventricular puncture include Keen, Dandy, and Frazier points. Once the hole in the skull is made, the monitor is placed into the lateral ventricle. 

Stringent analysis of the pressure and pulse amplitude of ICP waveforms is favored rather than its assessment from the height of the CSF column.[1]

The pulse component of the waveform shows the following 3 peaks:

1. P1 - percussion wave, due to arterial pulsation
2. P2 - tidal wave, represents brain compliance
3. P3 - dicrotic wave, owing to aortic valve closure

As brain compliance decreases, the waveform’s amplitude will increase, causing P2 to rise above P1 and P3. This will lead to a rounding of the waveform and the appearance of plateau waves, as well as Lundberg B and A waves.

Ventricular catheters represent a global ICP with minimal chances of drift and influence from pressure gradients between the parenchyma and ventricular system; this is the most reliable method of achieving maximum accuracy with minimal expense. There are added therapeutic benefits, including draining CSF and instilling medications such as antibiotics and thrombolytic agents.

Strain gauge- or fiber-optic-based systems inserted into the ventricles or brain parenchymas are more accurate than fluid-coupled or pneumatic devices. Parenchymal monitors are easier to insert in midline shift or malignant brain swelling cases, with no risks of blockage by hemorrhage or debris. However, they cannot be re-calibrated in vivo; they can only measure localized pressure and have drift issues in long-term usage. The current non-invasive techniques are not accurate enough to replace traditional invasive techniques.

Computed tomography and magnetic resonance images only provide a single-point snapshot picture. Pulsatility index from transcranial Doppler, tympanic membrane displacement (otoacoustic emissions), near-infrared spectroscopy, as well as optic nerve sheath diameter assessments have a study error margin of +/- 10 to 15 mm Hg with high inter-rater variability.

Complications

One assumption regarding ICP readings is that a single reading is inconclusive and that the pressure reflected in the mirror is representative of the overall pressure in the brain. However, this assumption is complicated by the pressure gradient present within the ventricular system and the interface between the brain’s parenchyma. Additionally, concerns arise regarding the accuracy, precision over time (drift), and in vivo calibration of various ICP measurement systems.[2][16]

When there is severe brain swelling with narrow ventricles, placing a catheter for monitoring ICP can be challenging. This can lead to further complications.

Complications of Ventricular Catheter-Based ICP Monitoring

• Intracranial and tract hemorrhage - 10%
• Infection (ventriculitis) - 20%
• Technical failure (failure to tap ventricle or misplacement) - 5%
• Over-drainage can lead to aneurysmal rebleed and complicate the upward transtentorial herniation in cases of hydrocephalus.
• Kinks and blockages by air, blood, and debris are frequent, leading to poor or false ICP recordings.
• There can be localized elevations of ICP due to compartmentalization from mass lesions.[14]

Clinical Significance

ICP Monitoring Methods 

• Fluid-based system (ventricular catheter) - The Foramen of Monro is mainly used as a reference for zero leveling. Frequent zeroing is imperative. There are inherent risks for misplacement, hemorrhages, and infections. ICP source signals are also prone to inaccuracies owing to air bubbles, debris, movements, and kinks.
• Implantable ICP sensors
• Parenchymal - The readings are based on zero drift of the sensor following pre-insertion zeroing against atmospheric pressure. Possible limitations include placement-dependent readings, drifts in zero reference values, bleeds, and infections.
• Subdural - applied in conjunction with craniotomy
• Epidural - has low sensitivity [12]

Types of ICP Monitoring Systems

• Fiber-optic (Integra)
• Strain-gauge (Codman)
• Raumedic (Neurovent P)
• Pneumatic (Spiegelberg)[12]

Monitoring Variables 

• Cerebral perfusion pressure is the most widely followed surveillance model.
• A correlation coefficient (R) between amplitude and pressure (RAP) index with a value >0.6 is indicative of impaired pressure-volume reserve.
• Pressure reactivity index (PRx)[12]

Monitoring Indices 

• The most studied ICP waveform parameter is the ICP mean wave amplitude with a value <4 mm Hg considered normal.
• The intracranial arterial amplitude correlation index is the correlation between ICP and arterial blood pressure wave amplitudes.[12]

ICP Waveform 

• This consists of the following domain components:
• Respiratory waveforms
• Pulse pressure waveforms
• P1 (percussion wave) - arterial pulsation from the choroid plexus
• P2 (tidal wave) - a proxy for intracranial compliance
• P3 (dicrotic wave)
• Vasogenic waveforms (eg, Lundberg A and B waves) - associated with fluctuations in cerebral blood volume
• Mayer waves (analogously termed C-waves) - sympathetic nervous activity involved in regulating BP [17][18]

Quality Assessment 

American National Standards Institute and the Association for the Advancement of Medical Instrumentation recommend a reading difference between invasive and noninvasive monitoring systems by only:

• 2 mm Hg at ICP of 0 to 20 mm Hg 
• Less than 10% at ICP of 20 to 100 mm Hg [12]

ICP is not a single number or threshold, but a result of various brain processes interconnected through multiple spectrums, such as compliance, hemodynamic strain, and metabolic dysfunction.[14]

The stair step-type linear algorithmic protocol for managing ICP has significant flaws. This protocol assumes the patterns and consequences of ICP increase are similar, with the only difference being how they respond or resist them—but this is primarily based on empirical evidence. Therefore, a tiered system approach has been formulated for managing refractory ICP by implementing an “individualized ICP threshold” aided by waveform analysis through the RAP or pressure-volume index (PVI).[1] The RAP index is the correlation coefficient between mean pressure and ICP mean pulse amplitude, AMP.

When the RAP value is higher, it means there is less compliance. As the ICP increases, the RAP gradually drops below 0, which indicates the autoregulatory capacity has been exhausted. This results in a right shift on the pressure-volume curve. If the cerebral perfusion pressure continues to increase, it can lead to the paradoxical passive collapse of the arterioles.[1]

PVI, or the apparent volume implementing a 10-fold ICP increase, is 25 to 30 mL. ICP waveform analysis also reveals a gradual increase in the amplitude of P2, becoming greater than P1.[14] Similarly, pathological Lundberg waves also appear. 

Among various armamentariums to calculate autoregulation, such as brain tissue oxygen, near-infrared spectroscopy, thermal dilution regional cerebral blood flow, and microdialysis, brain tissue oxygen tension has the most significant evidence base for signifying the same.[19]

Benchmark Evidence From South American Trials

The Treatment of Intracranial Pressure trial concluded that ICP-based management showed no significant favorable outcome compared to serial computed tomography scans and clinical examination guidance management.[20] There were various limitations of the study, the foremost being a lack of specific recommendations regarding diagnosis, inclusion criteria, and governing patterns of interventions. There was also methodological heterogeneity and bias relating to missing data.[4] There were also concerns regarding the generalized validity of the results, which also provoked doubts regarding the ethical standards of the study.[21] The ICP-reducing therapy has deleterious effects, such as prolonged hyperventilation, reduced cerebral blood flow, and possible propagation of cerebral ischemia. Similarly, fluids and vasopressors for maintaining cerebral perfusion pressure greater than or equal to 70 mm Hg carry the risk of acute lung injury.

Limitations of Invasive ICP Monitoring

• Proper identification of a pulsatile single ICP waveform is the primary limiting variable. A visual inspection of a snapshot of processed signals or fluid-level fluctuations interprets this waveform.
• This approach relies heavily on advanced technology. However, several factors can hinder its success, including ICP source signals, quality control, and variations in reference pressure. Additionally, there are risks associated with electrostatic discharge and errors in baseline pressure.
• It is still uncertain whether the ICP value of the cerebral hemisphere opposite to the external ventricular drain (EVD) placement, the infratentorial ICP value from the EVD placed in an infratentorial location, and the ICP readings of the craniospinal compartment are accurate.
• ICP is affected by body postures and brain compliance and shows diurnal variations.[12]

The current ICP monitor measures static ICP (mean ICP) as the average of the ICP peaks over a short time window, not pulsatile ICP.[12][17] Real-time ICP monitoring devoid of artifacts and processed via a robust machine learning algorithm is the ultimate goal.[18] The “holy grail” in neurosurgery is a noninvasive intracranial pressure technique capable of real-time monitoring.[17] 

The data mining approach to the ICP signal is comprised of:

• The data processing layer for filtering and cleaning signals
• The information layer for extracting information
• The application layer for modeling and mapping information has recently been introduced [18]

Noninvasive Methods of ICP Monitoring

• Physical examination - Pupillary asymmetry, motor posturing, and Glasgow Com Scale ≤8 have shown a positive correlation with increased ICP.
• Neuroimaging - A loss of a gray-white interface, effacement of basal cisterns, ventricle compression, midline shift, and herniation are salient features of increased ICP.
• Brain elastance metric - This has been developed and depends on the ventricles’ size and cerebrospinal fluid’s volume. However, limitations in availability and economic factors are currently restricting its use.
• Optic nerve sheath diameter assessment - This is measured at a depth of 3 mm from the posterior pole of the globe. This assessment is a promising bedside tool due to its easy applicability, accessibility, and reproducibility. However, it is operator-dependent, and the specificity declines when acute fluctuations in ICP occur.
• Transcranial Doppler (TCD) - This bedside procedure assesses cerebral blood flow velocity via cerebral circulation and pulsatility index. Other indices associated with TCD include cerebral blood flow velocity waveform, middle cerebral artery flow velocity, radial artery blood pressure, and 2D ophthalmic artery Doppler ultrasonography. However, TCD requires training, is operator-dependent, does not provide continuous monitoring, and does not apply to 10% to 15% of the patients due to a lack of a cranial window.
• Otic methods - These depend on the patency of the cochlear aqueduct and mirror changes in otoacoustic emission reflective of varied ICP. This studies tympanic membrane response to a stapedial reflex (stapedial excursions) via distortion-product otoacoustic emissions and acoustoelasticity.
• Acoustic methods - These are dependent upon head-generated sounds following the application of ultrasonic time of flight.
• Near-infrared spectroscopy - This confers metabolic changes and alterations in cerebral oxygenation due to changes in ICP.
• Electroencephalogram (EEG) - This looks at EEG burst duration, power spectral analysis, entropy, and bispectral index. There is a good correlation between ICP elevation and a shift in N2 latency of the visual evoked response.
• A neurological pupillary index and a pupillometer can be used to measure the pupillary light reflex.
• Skull elasticity - This is measured via a noninvasive strain sensor.
• Venous ophthalmodynamometry - This measures the central retinal vein pressure.
• Anterior fontanelle pressure monitoring - This is used in infants.
• Telemetric and miniature sensors, like Neurovent-P-tel and Sensor Reservoir, have issues with biocompatibility, reliability of power sources, efficient telemetry, reference pressure drift, bleeds, and infections.
• Biodegradable pressure sensors are also being explored.[12][17]

Enhancing Healthcare Team Outcomes

Mandatory patient safety checklists must be implemented by the healthcare team involved in the process to ensure better clinical outcomes and prioritize patient safety by minimizing complications. The following guidelines have to be adhered to:

• There is a valid treatment order sheet. 
• All reportable limits are specified.
• The external ventricular drain (EVD) point is at a prescribed level, with the transducer leveled to the tragus of the ear.
• The EVD column is oscillating.
• There is monitoring for normal ICP waveforms.
• The ICP waveform is pulsatile on the monitor.
• Avoid any soaking at the wound site or junctions within the monitor set.
• A judicious assessment of drained cerebral spinal fluid volume must be done.
• There must be a stringent evaluation of the patient’s neurological status consistently.
• There must be coordination of care between the members of the healthcare team. 
• FCLinicians must provide family education and support.

Monitoring intracranial pressure requires a team effort involving various healthcare professionals such as doctors, nurse practitioners, physician assistants, and specialized nurses. By collaborating across disciplines, the interprofessional team can achieve the best possible results for the patient. The nurse monitors intracranial pressure and promptly communicates any changes to the medical team. Additionally, they assist the medical team by conducting regular neurological and hemodynamic evaluations. When working harmoniously, healthcare professionals can significantly improve patient outcomes in those undergoing intracranial pressure monitoring.

Role of Invasive ICP Monitoring in Trauma

The use of ICP monitoring and ICP management is highly variable across the globe.[22] Significant better neurological outcomes and minimized 6-month mortality in patients with at least 1 non-reactive pupil (hazard ratio [HR] of 0.35) have been observed.[22] Patients with ICP monitoring are also more likely to survive (overall survival, 1.54; the number needed to treat, 10).[23] The only randomized controlled trial of ICP monitoring, which studied 324 patients in Bolivia and Ecuador, found no differences in outcomes among patients with and without ICP monitoring.[24]

Role of Invasive ICP Monitoring in Spontaneous Intracerebral Hemorrhage 

Invasive ICP monitoring in spontaneous intracerebral hemorrhage has reduced mortality but did not improve functional outcomes at 6 months (HR, 0.49).[25]

Nursing, Allied Health, and Interprofessional Team Interventions

The advantage of the ventricular monitoring device is the facility for egress of CSF in cases of a sustained rise in ICP (greater than or equal to 20 mm Hg for 5 minutes or longer). Still, the disadvantage is that simultaneous monitoring, as well as CSF drainage, is not possible. The amount of CSF to be drained can be guided as per the recommended target ICP (commonly set as 10 mm Hg) or can be aided with visual guidance in improving the ICP waveform analysis obtained from the concurrent application of intraparenchymal monitors or through clinical neurological examination.[26] Care always needs to be taken to prevent paradoxical upward transtentorial herniation due to jealous drainage of CSF.

Surgical decompression is the usual recommendation; there is a refractory rise in ICP and clinical deterioration despite the stepwise escalation in the management tiers aimed to counteract the same, such as sedation, neuromuscular blockade, mild hyperventilation, hyperosmolar therapies, and barbiturate coma.[26]

The ICP monitoring devices are removed once the ICP is normalized with sustained or improved clinical neurology (motor score at least 5) for at least 48 to 72 hours without any interventions. In cases of ventricular devices, the EVD can undergo clamping, or, ideally, a gradual increment in its height (training of the EVD) is attained to watch for any clinical deterioration in the patient for at least 48 hours. 

Strict aseptic precautions and care also need to be implemented during its removal. The head end should be lowered to prevent pneumocephalus and pneumoventricle risk. The catheter tip can be sent for bacteriological analysis in cases of persisting fever with features of meningitis. The wound is closed in layers to minimize the CSF leak and infection risk. The patient should be strictly monitored for any signs of clinical deterioration for at least 24 hours, with all preparations made for emergency placement of a new EVD or ICP monitor device.

Nursing, Allied Health, and Interprofessional Team Monitoring

Interprofessional Team Monitoring Should Include

• Hourly CSF drainage
• Ensure CSF oscillation inside the tubes
• Confer no soakage of the wound
• Ensure the correct height of EVD
• Zeroing of the EVD height at the level of the foramen of Monro or tragus of the ear
• Stringent neurological monitoring of the patient
• Monitor hourly ICP