Abstract
Despite recent research that has been equivocal, intracranial pressure (ICP) monitoring is invaluable in the management of neurocritical care patients, including head injury, poor grade subarachnoid hemorrhage, stroke, intracerebral hematoma, meningitis, acute liver failure, hydrocephalus, benign intracranial hypertension, etc. Monitoring of ICP requires an invasive transducer, and an intraventricular drain connected to an external pressure transducer is still considered to be the ‘‘gold standard’’ method.
However, some attempts have been made to measure ICP noninvasively, with promising results.
Information can be derived from ICP and its waveforms, including cerebral perfusion pressure, brain compensatory reserve, regulation of cerebral blood flow and volume, and content of vasogenic events. There are many possible conditions that can lead to elevated intracranial pressure, for acute, chronic, and both intracranial or extracranial causes. Since increased intracranial pressure is associated with increased morbidity and mortality, it should be promptly detected, and treatment must be immediately started with appropriate intensive care.
Keywords
Cerebral perfusion pressure, Intracranial pressure, Microtransducer, Neuromonitoring
Contents
Introduction 1
Pathophysiology 2
Invasive ICP 5
Noninvasive ICP 10
Invasive Readings and Interpretation 12
Effect of Anesthetics on Intracranial Pressure 15
Propofol 15
Barbiturates 18
Etomidate 18
Benzodiazepines 19
Opioids 19
Ketamine 19
Dexmedetomidine 20
Current Evidence, Applications, and Discussion 20
Suggested Readings 25
References 26
Introduction
Increased intracranial pressure (ICP) is an important cause of secondary brain injury, and it is associated with poor outcome. Several conditions are associated with intracranial hypertension (ICH), including extracranial (fever, increased abdominal and intrathoracic pressure, hypercarbia, hypoxia) and intracranial causes (cerebral edema, hematoma, contusion, cerebrospinal fluid (CSF) disturbance). In this setting, ICP monitoring is crucial in the management of neurocritical care patients, as clinical signs of ICH are tardive and poor predictors of elevated ICP.
Invasive monitoring through an intraventricular or intraparenchymal catheter is indicated in all severe traumatic brain injured (TBI) patients with positive brain computed tomography (CT) findings, or normal brain CT if the patient is older than 40 years or in the presence of systolic blood pressure below 90 mm Hg or in the case of abnormal flexion or extension in response to pain ; however, invasive techniques are associated with certain risks, including infections and hemorrhage ( Fig. 1.1 ).
Pathophysiology
Pathologic ICH is defined when ICP raises persistently above 20 mm Hg. The intracranial volume, consisting of brain parenchyma, blood, and CSF, is enveloped by the rigid skull bone. Under physiological conditions the total intracranial volume remains constant because of compensatory mechanisms, which operate to maintain a constant and adequate cerebral blood flow (CBF), and ICP. According to the Monro-Kellie doctrine, ICP is the result of the volume and compliance of each intracranial component (brain parenchyma, arterious blood, venous blood, CSF) within the intracranial compartment. The relationship between ICP variations and the volume of intracranial contents defines the compliance characteristics of the intracranial compartment. The intracranial compliance can be defined as the change in volume over the change in pressure (dV/dP).
In the presence of an intracranial mass (e.g., brain swelling, hydrocephalus, hematomas, or abscesses), compensatory mechanisms operate to maintain ICP and CBF constant by displacing CSF into the thecal sac and by compressing the cerebral venous compartment via venoconstriction and extracranial drainage.
The relationship between ICP and volume is not linear. Initially, pressure increases only slightly with increasing volume. There, compensatory mechanisms allow ICP to elevate only slightly with increase of volume. When these compensatory mechanisms have been exhausted or when autoregulation is impaired, small volume increases develop significant increases in pressure, leading to a dramatic rise in ICP ( Fig. 1.2 ).
CBF is maintained relatively constant within a well-known range of mean arterial pressure (MAP) due to the modulation of cerebrovascular resistances. The relationship between ICP and MAP has been defined as the Pressure Reactivity index (PRx), considered the main marker of autoregulatory reserve. Low PRx values indicate a poor association between ICP and MAP and thus a good autoregulation capacity, whereas values approaching 1.0 indicate a strong positive association between the two parameters, thus a poor autoregulation ( Fig. 1.3 ).
Cerebral perfusion pressure (CPP), defined as the difference between MAP and ICP, is the driving force responsible for adequate brain perfusion and oxygenation. Following a significant ICP increase, CPP decreases, resulting in an inadequate brain tissue perfusion and oxygenation. The consequent ischemia will induce further cytotoxic edema resulting in even higher ICP.
In this perspective, an ICP increase is followed by an impairment of CBF, which is responsible for subsequent metabolic and functional alterations. On the other hand, a primary flow impairment or metabolic disfunction (such as hypoxia and hypoglycemia) with a consequent cytotoxic edema determines a very quick ICP increase.
Invasive ICP
External Ventricular Drainage
External ventricular drainage (EVD) is widely considered the gold standard for ICP monitoring ( Table 1.1 , Fig. 1.4 ).
| ICP method | Availability | Operator dependency | Suitable in emergency | Risk of infection/hemorrhage | Cost |
|---|---|---|---|---|---|
| EVD | Good | No | No | Yes | High |
| Intraparenchymal bolt | Good | No | No | Yes | High |
| Subdural probe | Good | No | No | Yes | High |
| Epidural probe | Good | No | No | Yes | High |
| Brain imaging | |||||
| Radiological findings CT | Good | No | Yes | No | Medium |
| Radiological findings MR | Medium | No | No | No | High |
| ONSD US | Good | Yes | Yes | No | Low |
| ONSD CT | Good | No | Yes | No | Low |
| Caption of transmitted ICP | |||||
| ONSD MR | Medium | No | No | No | High |
| TMD | Good | Yes | No | No | Low |
| Fundoscopy | Good | Yes | No | No | Low |
| Flow change detection | |||||
| TCD PI | Good | Yes | Yes | No | Low |
| TCD FVdICP | Good | Yes | Yes | No | Low |
| TCD CrCP | Good | Yes | Yes | No | Low |
| TCD black block | Good | Yes | Yes | No | Low |
| Ophthalmic artery | Low | Yes | Yes | No | Low |
| Monitoring of metabolism | |||||
| NIRS | Medium | Yes | No | No | Low |
| Assessment of neurophysiological function | |||||
| EEG | Low | Yes | No | No | Low |
| VEP | Low | Yes | No | No | Low |
| EOAEs | Low | Yes | No | No | Low |
| Time of flight | Low | NA | No | No | Low |
The EVD system is also useful to drain CSF for ICP control, further to manage acute hydrocephalus, intraventricular hemorrhage, and for direct intraventricular drug delivery. The main complications associated with EVD are malfunctioning due to malpositioning or obstruction, infections, and hemorrhage. Malpositionings occur with a rate of 1.5%–20% and can also damage crucial brain structures (internal capsule basal ganglia or thalamus, for example).
The risk of infection is higher with ventricular catheters than with parenchymal probes and may vary between 0 and 22% (averaging 10%) (revised in Ref. ). The coagulase-negative staphylococcus seems to be the most common infecting organism, responsible for nearly half of the cases, followed by Staphylococcus aureus (15%), and Klebsiella (6.6%). The risk of infection is significantly dependent on the time of permanence of the catheter (cut off over 5 days), the presence of cranial fracture with CSF leak or an extracranial infection site, and the insertion of more than one invasive ICP monitoring device. Catheter infection rate can be reduced by a strict adherence to a sterile practice during EVD positioning, generous subcutaneous catheter tunnelization, and by the minimization of catheter manipulation. Neither preventive catheter change nor antibiotics prophylaxis prior to EVD insertion seem to reduce the risk of EVD infections.
EVD positioning can further harbor risks of hemorrhagic complications, especially in patients with coagulopathy or low platelets (below 100,000). Postoperative CT positive for blood after EVD positioning was found in 41% in a consecutive series of 188 patients, though only in one out of four the hematoma was larger than 15 mL, and other authors found a cumulative rate of hemorrhagic complications ranging from 5.7% to 7%.
In general, the rate of clinically significant hemorrhagic complications after EVD insertion is relatively low, even if still higher than with the use of the intraparenchymal probe, and they require surgical intervention only in a minority of cases.
Microtransducer Devices
An alternative to EVD for direct ICP assessment is represented by microtransducer devices, though these do not permit drainage of CSF to reduce ICP. They can be classified into fiber optic devices, pneumatic sensors, and strain gauge devices, and the probe can be positioned in the epidural, subdural, or intraparenchymal space ( Table 1.1 , Fig. 1.5 ).
Epidural and Subdural Devices
Epidural pressure monitoring devices have been shown to be safe and easy to use. Their accuracy compared to EVD for ICP monitoring is lower, with an overestimation in most cases. Such discrepancies are not related to the type of sensor used, but to the specific anatomical characteristics of the epidural intracranial space.
Similarly, subdural screws have shown to be associated with no nearby complication and seem easy to use. However, they are still considered unreliable for routine clinical practice, compared to EVD, and especially when ICP is below 20 mm Hg, they tend to underestimate ICP. Their accuracy in ICP detection overlapped with ventricular catheter ICP registrations only in 41%–58% of cases.
Intraparenchymal Microtransducers
Intraparenchymal microtransducers are the most widely used devices and demonstrated a good congruence with intraventricular measurements within accepted parameters.
The correlation coefficient between intraparenchymal and intraventricular ICP transducers was maximal in a small pilot study. Considering the good performance demonstrated by intraparenchymal devices, some authors supported their use for routine ICP monitoring, suggesting the use of the ventricular catheter just for the necessity of CSF drainage. Nevertheless, it has also been demonstrated that patients monitored with EVD have better outcomes at 6 months than patients monitored with an intraparenchymal device (51.7% vs. 21.0%, P < .001), as EVD allows direct treatment for increased ICP. In general, the choice of a proper device for ICP monitoring should take into account both the clinical and radiological considerations and perhaps also the neurosurgeon’s attitude.
Moreover, microtransducers have the disadvantage that after the placement of the probe, recalibration is not further possible, and the sensor can report imprecise ICP, whereas EVD can be recalibrated at any time. Complications associated with intraparenchymal ICP monitor are generally low. Infection rate is 1.6%, and postprocedural intracerebral blood is 15.6% of cases. Only 0.66% was clinically relevant, though nearly half of the patients showed in the postsurgical brain CT an edematous reaction surrounding the catheter.
Noninvasive ICP
Several authors attempted to find a noninvasive ICP method. According to the pathophysiological mechanism used to detect ICP increase, these methods can be divided into the following categories ( Table 1.1 ):
- •
brain imaging techniques, based on morphological changes associated with ICP increases (magnetic resonance (MR), CT, and optic nerve sheath diameter (ONSD) assessment)
- •
indirectly transmitted ICP caption (ONSD, fundoscopy, tympanic membrane displacement (TMD))
- •
flow change detection (transcranial Doppler (TCD), eyeball ophthalmic artery method)
- •
monitoring of metabolic alterations (near infrared spectroscopy (NIRS))
- •
neurophysiological registrations of functional activity (electroencephalography (EEG), including visual evoked potential (VEP), otoacoustic emissions, and time of flight (TOF) method)
Among these, ONSD for ICP detection based on CT, MR, and ultrasound has been studied by several authors. Many authors found a linear relationship between perioptic CSF pressure and ICP, and ONSD changes almost directly with ICP. ONSD is in continuity with the dura mater and the subarachnoidal interspace filled with CSF; therefore, CSF pressure variations change the volume of ONSD with fluctuations in the anterior, retrobulbar compartment. ONSD showed good sensitivity and specificity when compared to invasive ICP when measured on CT, MRI, and ultrasonography (US) ( Fig. 1.6 ). CT imaging has the advantage of being more available than MR and less operator dependent as compared to US. However, US ONSD is safe, quick, repeatable, and easily available.
