Traumatic brain injuries, as well as infectious diseases such as meningitis, can lead to brain swelling and dangerously high pressure in the brain.
If untreated, patients are at risk for brain damage, and in some cases elevated pressure can be fatal.
Current techniques for measuring pressure within the brain are so invasive that the measurement is only performed in the patients at highest risk.
However, that may soon change, now that a team of researchers from MIT and Boston Children’s Hospital has devised a much less invasive way to monitor intracranial pressure (ICP).
“Ultimately the goal is to have a monitor at the bedside in which we only use minimally invasive or noninvasive measurements and produce estimates of ICP in real time,” says Thomas Heldt, the W. M. Keck Career Development Professor in Biomedical Engineering in MIT’s Institute of Medical Engineering and Science, an associate professor of electrical and biomedical engineering, and a principal investigator in MIT’s Research Laboratory of Electronics.
In a study of patients ranging in age from 2 to 25 years, the researchers showed that their measurement is nearly as accurate as the current gold standard technique, which requires drilling a hole in the skull.
Heldt is the senior author of the paper, which appears in the Aug. 23 issue of the Journal of Neurosurgery: Pediatrics. MIT research scientist Andrea Fanelli is the study’s lead author.
Under normal conditions, ICP is between 5 and 15 millimeters of mercury (mmHg).
When the brain suffers a traumatic injury or swelling caused by inflammation, pressure can go above 20 mmHg, impeding blood flow into the brain.
This can lead to cell death from lack of oxygen, and in severe cases swelling pushes down on the brainstem – the area that controls breathing – and can cause the patient to lose consciousness or even stop breathing.
Measuring ICP currently requires drilling a hole in the skull and inserting a catheter into the ventricular space, which contains cerebrospinal fluid.
This invasive procedure is only done for patients in intensive care units who are at high risk of elevated ICP.
When a patient’s brain pressure becomes dangerously high, doctors can help relieve it by draining cerebrospinal fluid through a catheter inserted into the brain.
In very severe cases, they remove a piece of the skull so the brain has more room to expand, then replace it once the swelling goes down.
Heldt first began working on a less invasive way to monitor ICP more than 10 years ago, along with George Verghese, the Henry Ellis Warren Professor of Electrical Engineering at MIT, and then-graduate student Faisal Kashif.
The researchers published a paper in 2012 in which they developed a way to estimate ICP based on two measurements: arterial blood pressure, which is taken by inserting a catheter at the patient’s wrist, and the velocity of blood flow entering the brain, measured by holding an ultrasound probe to the patient’s temple.
For that initial study, the researchers developed a mathematical model of the relationship between blood pressure, cerebral blood flow velocity, and ICP.
They tested the model on data collected several years earlier from patients with traumatic brain injury at Cambridge University, with encouraging results.
In their new study, the researchers wanted to improve the algorithm that they were using to estimate ICP, and also to develop methods to collect their own data from pediatric patients.
They teamed up with Robert Tasker, director of the pediatric neurocritical care program at Boston Children’s Hospital and a co-author of the new paper, to identify patients for the study and help move the technology to the bedside.
The system was tested only on patients whose guardians approved the procedure.
Arterial blood pressure and ICP were already being measured as part of the patients’ routine monitoring, so the only additional element was the ultrasound measurement.
Fanelli also devised a way to automate the data analysis so that only data segments with the highest signal-to-noise ratio were used, making the estimates of ICP more accurate.
“We built a signal processing pipeline that was able to automatically detect the segments of data that we could trust versus the segments of data that were too noisy to be used for ICP estimation,” he says. “We wanted to have an automated approach that could be completely user-independent.”
The ICP estimates generated by this new technique were, on average, within about 1 mmHg of the measurements taken with the invasive method.
“From a clinical perspective, it was well within the limits that we would consider useful,” Tasker says.
In this study, the researchers focused on patients with severe injuries because those are the patients who already had an invasive ICP measurement being done.
However, a less invasive approach could allow ICP monitoring to be expanded to include patients with diseases such as meningitis and encephalitis, as well as malaria, which can all cause brain swelling.
“In the past, for these conditions, we would never consider ICP monitoring.
What the current research has opened up for us is the possibility that we can include these other patients and try to identify not only whether they’ve got raised ICP but some degree of magnitude to that,” Tasker says.
“These findings are very encouraging and may open the way for reliable, non-invasive neuro-critical care,” says Nino Stocchetti, a professor of anesthesia and intensive care medicine at Policlinico of Milan, Italy, who was not involved in the research.
“As the authors acknowledge, these results ‘indicate a promising route’ rather than being conclusive: additional work, refinements and more patients remain necessary.”
The researchers are now running two additional studies, at Beth Israel Deaconess Medical Center and Boston Medical Center, to test their system in a wider range of patients, including those who have suffered strokes.
In addition to helping doctors evaluate patients, the researchers hope that their technology could also help with research efforts to learn more about how elevated ICP affects the brain.
“There’s been a fundamental limitation of studying intracranial pressure and its relation to a variety of conditions, simply because we didn’t have an accurate and robust way to get at the measurement noninvasively,” Heldt says.
The researchers are also working on a way to measure arterial blood pressure without inserting a catheter, which would make the technology easier to deploy in any location.
“This estimate could be of greatest benefit in the pediatrician’s office, the ophthalmologist’s office, the ambulance, the emergency department, so you want to have a completely noninvasive arterial blood pressure measurement,” Heldt says. “We’re working to develop that.”
Journal information: Journal of Neurosurgery: Pediatrics
Provided by Massachusetts Institute of Technology
The concept of monitoring the intracranial pressure (ICP) as an indicator of dysfunc-tional intracranial compliance can be thought to be a practical approach to a historical doctrine proposed by Monroe and Kellie centuries ago[1–3].
Simplistically, Monroe and Kellie likened ICP to a mild positive pressure created by the brain, cerebral blood volume and cerebrospinal fluid (CSF) in a semi-rigid skull box.
These components normally compensate for changes in each other, however, when this compensatory reserve is exhausted, potentially catastrophic neurological sequelae of intracranial hypertension occurs.
Such perturbations of intracranial compliance occur in a variety of brain insult pathologies such as traumatic brain injury (TBI), intracranial space occupying lesions (ICSOL), intracranial heamorrhage (ICH) and subarachnoid haemorrhage (SAH).
Hence, monitoring of intracranial pressure assumes importance in the aforementioned diverse neurologically injured population as an indication for commencement of ICP control measures as well as in risk stratification, prognosti-cation and assessing response to therapy.
ICP monitoring as a novel modality was introduced to the medical fraternity by Guillaume and Janny in 1951.
However, the credit of popularizing ICP monitoring goes to Lundberg and his colleagues who systematized and established the protocol for its use in 1960.
ICP monitoring was more of a research tool for the ensuing three decades till its use in neurointensive care became an established practice following recommendations for its use in brain trauma foundation guidelines which were first published in 1995 and subsequently modified in 2016[6–9].
The aim of this review is to establish the pathophysiological basis of ICP moni-toring, the physicality of such monitoring, the various brain injury states where it is used as well as a look at the armamentarium of modalities now available to have an idea about intracranial compliance.
We also take a look at the evidence for the usefulness of such monitoring in clinical practice in terms of influencing outcome and sequelae in brain injured patients.
ICP – THE CURVE AND SOME IMPORTANT VALUES
As is evident from the already discussed Monroe-Kellie doctrine, there is an existing volume of reserve in the brain which is around 60-80 mL in young persons and approximately 100-140 mL in geriatric population.
This surprising paradox in intracranial compliance can be explained by ongoing cerebral atrophy with age.
The volume pressure curve denoting the relationship between ICP and intracranial volume is depicted in the Figure Figure1.
The normal values of ICP are elucidated in the Table Table1.
Normal values of intracranial pressure monitoring
|Age group||ICP value in mm of Hg|
|Adults (supine)||5 – 15|
|Children||3 – 7|
|Infants||1.5 – 6|
When pathological conditions cause an increase in intracranial volume, the initial intracranial volume expansion till 30 mL is well compensated by CSF and venous blood movement out of the cranial vault.
The compressibility of the constituents which are expanding determines the final intracranial compliance.
For example, blood and CSF excess in the brain (intracranial haemorrhage and hydrocephalous) results in a steep curve owing to their incompressible nature.
The volume pressure relationship is much more gradual when compressible brain parenchyma is involved (tumours and ICSOLs).
ICP WAVEFORM: PHYSIOLOGICAL BASIS AND PATHOLOGICAL VARIATIONS
The intracranial pressure waveform is pulsatile in nature and correlates with respira-tory and cardiac cycle (Figure (Figure2)).
The amplitude of the respiratory waves varies between 2 to 10 mmHg.
The wave mirrors changes in intrathoracic pressure with respiration and increases in ICP obliterate the variation in amplitude. The cardiac component of the ICP wave correlates with pressure dynamics and its amplitude varies between 1 to 4 mm of Hg (Figure (Figure2).
The different waves in the vascular ICP waveform are depicted in Figure Figure3.
P1 wave (Percussion wave) reflects the arterial pulses of the carotid plexus into the CSF.
P2 wave (Tidal wave) is thought to represent ICP proper as a correlate of the arterial pulses reflected off the brain parenchyma.
The P3 wave (Dicrotic notch) reflects aortic valve closure.
Attempts have been made by Hammar et al to use the morphology of the ICP pulse wave as a surrogate marker of intracranial elastance.
They decided that the systolic part of the vascular ICP waveform reflects arterial activity while the caudal descending segment denotes the pressure in SVC.
Hence when the ICP increases the caudal part of the ICP waveform (the P2 component) assumes the shape of an arterial pulse and when there is CVP elevation, the waveform approximate a venous pulse.
When the ICP is elevated, the vascular (cardiac) waveform amplitude increases while the respiratory waveform amplitude decreases.
Other phenomena which are visible in dysfunctional intracranial compliance include occurrence of P waves as well as elevation of P2 and rounding off of the waveform (Figure (Figure4)).
The occurrence of these phenomena are useful in clinical practice in that these alert the neurophysician to initiate ICP control measures on an urgent basis.
It is pertinent to note here that increased ICP can produce characteristic waveform variously classified by Lundberg into A, B and C waves.
Lundberg A waves are the ones which denote highest rise in ICP (50-100 mmHg). They are generally indicative of high degree of cerebral ischemia and impending brain herniation and persist for 5 to 10 min (Figure (Figure5).
Lunenburg B waves occur for a lesser period of time (1 to 2 min), the ICP elevation or not as much, 20 to 30 mm Hg, and are rhythmic in nature. They indicate evolving cerebral injury causing a gradual increase in ICP (Figure (Figure5)[13,14].
Lundberg C waves correlate with blood pressure fluctuations brought about by baroreceptors and chemoreceptor reflex mechanisms and have no clinical significance.