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CPPMAP ICP=−
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
27
2.5.2.5 Ventilation
Hyperventilation (HV) causes blood and CSF alkalosis; this causes vasoconstriction
and, hence, reduces cerebral blood volume (CBV) and ICP.Sustained or prophylactic HV can be deleterious since it may cause cerebral ischemia. However, when
herniation is present, transient HV may be lifesaving. In select patients, for example, those with hyperemia and increased ICP, optimized HV can be useful. Jugular
bulb oximetry (SjvO2) or monitors of CBF or brain oxygen (PbtO2) should be used
to permit safer HV titration. For acute ICP management, HV should begin with a
PaCO2 goal of 34–36mmHg and be advanced to PaCO2 goal of 25–30mmHg if
there is no treatment response. In CENTER-TBI, the most commonly reported target for PaCO2 was 36–40 mmHg (4.8–5.3 kPa) in cases of controlled ICP
(<20mmHg, 69% of centers) and PaCO2 target of 30–35mmHg (4–4.7kPa) for
increased ICP (62%; 17).
2.5.2.6 CPP Augmentation
Prevention of secondary injury, for example, hypotension and hypoxia, avoidance
of systemic complications, and maintaining appropriate CPP, which is a surrogate
for CBF among others, are fundamental goals in management of acute brain injury
including TBI, SAH, and ICH.Cerebral perfusion pressure is dened as the difference between mean arterial pressure (MAP) and ICP (Eq.2.2). To calculate CPP
requires that arterial blood pressure and ICP be monitored. Ideally, the zero reference points should be the same, for example, the tragus as an external landmark.
This is important when the head of the bed is elevated since measuring ICP at the
level of the brain and BP at heart level can result in a CPP error of 15mmHg. This
error can be further exaggerated in tall patients. However, there is a variability in
both clinical practice and research reports in how MAP is measured to determine
CPP [109], prompting calls for adaptation of international standards for CPP
measurements.
Single-center observational cohorts show that time indices for CPP ≥70 and
<50 mmHg are associated with decreased and increased mortality, respectively
[110]. However, the ideal CPP to maintain in patients with acute brain injury (ABI)
remains debated. Early recommendations suggested a CPP >70mmHg was preferable in severe TBI.However, while the incidence of cerebral ischemia is decreased
using this threshold, an outcome benet is not observed because of increased pulmonary complications associated with uid and vasopressor use to maintain CPP
(94). In addition, normal CPP also does not always mean normal brain metabolism
(2.2)
28
P. Le Roux
[65, 66, 79]. The 3rd edition of the TBI guidelines suggested maintaining a CPP
between 50 and −70mmHg and avoiding active CPP elevation above 70 mmHg
with uids and vasopressors. Using minute-by-minute data in 259 adult patients,
Guiza etal. [111] recently observed that a “safe” zone between 60 and 70mmHg
could be identied for adults <65 years, provided CA was active and ICP was
≤25mmHg. Decient CA reduces the tolerability for low CPP and insults of CPP
<50mmHg were hardly tolerated, whereas ICP >25mmHg was associated with
poor outcome regardless of CPP.However, it should not be interpreted that CPP
management is not important during increased ICP.It is likely that the ICP reects
the severity of the patient’s condition, and hence, this drives the association with
poor outcome. In a survey from 66 neurotrauma sites in CENTER-TBI [17], the
most common CPP target was >60mmHg (60% of sites) and/or an individualized
target (38%). To support CPP, crystalloid uid loading (91%) was generally preferred over albumin (23%), and vasopressors (%) over inotropes (44%).
Recent research suggests that rather than a population-based target (CPP 50–70),
CPP should be individualized, that is, optimal patient-specic CPP (CCPopt). This
value, CPPopt, can vary between patients and over time in the same patient and may
range between 50 and 100mmHg. When patients are managed at or close to the
CPPopt, better outcomes are observed and levels both above and below the patient’s
optimal CPP level are associated with worse outcome [112, 113]. In particular,
patients maintained within 5mmHg of their optimal CPP do better, whereas patients
with larger discrepancy (>10mmHg) between real CPP and CPPopt more likely
have adverse outcomes. Whether using this to guide treatment makes a difference is
still to be elucidated at large because the quality of data is low [114].
2.5.2.7 Metabolic Suppression
The goal of metabolic therapy is to suppress cerebral metabolic rate of oxygen
(CMRO
). This in turn should decrease CBF, and because CBV is reduced, ICP
2
should decrease. In addition, vulnerable brain tissue may be preserved since CMRO2
is reduced in the face of decreased fuel delivery. CMRO2 may be reduced through
pharmacological means or temperature modulation. This generally is a Tier 3 strategy. However, in some circumstances, it may be used earlier—for example, induced
hypothermia for increased ICP in liver encephalopathy.
2.5.2.8 Pharmacologic Suppression
Agents such as barbiturates, benzodiazepines, or propofol may be administered to
induce coma (burst suppression). There is insufcient data to guide choice of these
agents. It should be remembered that barbiturates and propofol are myocardial
depressants and peripheral vasodilators, and invasive hemodynamic monitoring and
support often are needed when pharmacologic coma is induced. Barbiturates effectively treat increased ICP and are best indicated in patients who have adequate
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
29
cardiovascular function and intact CA.The most commonly used agent, pentobarbital, can be administered i.v. with a loading dose of 5mg/kg, followed by an infusion of 1–3mg/kg/h; a high-dose regimen may also be used with an i.v. bolus dose
of 10mg/kg over 30min followed by 5mg/kg/h infusion for 3h, followed by 1mg/
kg/h titrated to either burst suppression on continuous electroencephalogram monitoring or an ICP reduction. Whether barbiturate use improves outcome is unclear
since side effects such as immune suppression, hypotension (especially in volume
depleted patients), and decreased mucociliary clearance can mitigate any benet on ICP.
Another option for pharmacologic coma is propofol, which is given in an i.v.
loading dose of 2mg/kg, followed by a titrated infusion of up to 200mg/kg/min.
Propofol should be avoided in hypotensive or hypovolemic patients and prolonged
infusions or high doses have been associated with the development of a “propofol
infusion syndrome” of renal failure, hyperkalemia, myocardial failure, and metabolic acidosis, often resulting in death. The mechanism for this is not fully
understood.
2.5.2.9 Temperature Modulation
Mild-to-moderate hypothermia (32–34°C) can reduce ICP [115, 116]. Most singlecenter studies suggest that induced hypothermia is associated with better outcome.
However, this outcome benet is not observed in large randomized multicenter
studies in adults or children with severe TBI and may even be harmful in patients
with a lower injury severity [117, 118]. Furthermore, there is no role for prophylac-
tic hypothermia [119]. There also is a limited role in malignant cerebral infarction
[120]. In part, this lack of outcome benet may have to do with shivering that can
adversely affect brain metabolism [121] or the rate of posthypothermic rewarming,
which if too rapid can exacerbate neuronal injury [122]. Hence, when hypothermia
is used, rewarming should be considered if the patient’s ICP is stable and <20mmHg
for at least 48h, and implemented at a rate not faster than 0.1–0.25°C/h.
2.5.2.10 Decompressive Craniectomy
Decompressive craniectomy (DC), either unilateral or bifrontal, and when correctly
performed (i.e., of adequate size 12×15cm), is the most effective way to reduce
ICP, particularly when ICP is resistant to osmotic agents and medical management
[123, 124]. In addition, DCC has favorable effects on CPP and other aspects of brain
metabolism [123, 125–130]. Both intraabdominal and intrathoracic hypertension
can increase ICP or aggravate increased ICP.In select patients, decompressive laparotomy (DL), even if intraabdominal pressure is normal, can reduce elevated ICP
[131]. These procedures (DC and DL) often make care easier and eliminate the need
for other therapies that may have deleterious effects.
30
P. Le Roux
In patients with stroke-related malignant hemispheric infarction, pooled analysis
of several RCTs show that DC decreases mortality and improves functional outcome [132, 133]. In these patients, however, surgery is usually performed without
knowledge of ICP since most of these patients do not receive an ICPM.Instead, the
decision is based on the clinical and imaging ndings. Questions remain about the
effects of DC on long-term outcome in TBI, in part because of methodological differences and patient heterogeneity [134, 135]. In addition there is variability about
the ICP cutoff for DC; in CENTER-TBI, 60% of sites use 25mmHg, 18% 30mmHg,
and 17% 20mmHg [136]. Consensus guidelines for DC (including primary—at the
time of initial craniotomy and secondary DC for increased ICP) in TBI were recently
published [28]. There does not appear to be a role for bifrontal DC in a patient with
diffuse injury particularly if performed to prevent increased ICP.The optimal candidate for secondary DC is a patient whose ICP elevation is likely the primary contributor to poor outcome and the primary injury is deemed compatible with
acceptable recovery and is receiving maximal medical management. Simple ICP
thresholds alone may be insufcient to make this decision. However, should also
consider clinical ndings, CT-scan results and data from other monitors if available.
The ICU-team should include a frank discussion with family members about
recovery-expectations and clinical outcome [137, 138]. Technical aspects of the
procedure, for example, size of bone ap, duraplasty, and postprocedure care
(including continued ICP monitoring) can also affect outcome [28, 124].
In general, if TBI patients survive to discharge after DC, most have a good functional outcome since improvement occurs with time [139]. When to replace the
bone ap or perform a cranioplasty, however, can further inuence outcome [140].
Indeed, several studies show cranial reconstruction can improve CBF and aid in
recovery [141, 142]. There has been limited study on this issue. A recent retrospective single-center analysis over a 10-year period suggests that cranioplasty performed between 15 and 30days after initial DC may reduce infection and seizures,
whereas waiting >90days may decrease the risk of hydrocephalus but increase the
seizure risk [143].
2.6 ICP Management andOutcome
Multiple, large cohort studies demonstrate that increased ICP is independently associated with mortality after TBI.The relationship with functional outcome is less
clear. The risk of death is proportionally greater the higher the ICP, a longer duration of increased ICP and when increased ICP is refractory to treatment [1–5, 26,
29, 68, 71, 73, 144]. Although less studied, several clinical series demonstrate that
elevated ICP and poor outcome are associated with SAH and ICH, although this
outcome may depend more on disease severity [5, 145–148]. A variety of dynamic
characteristics of the ICP signal that are associated with outcome have also been
identied, for example, the duration of increased ICP episodes [149], the area under
the ICP curve [71], the ICP variability [150], and the CPP/ICP ratio [151].
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
31
However, whether treating increased ICP makes a difference to outcome remains
poorly dened. There are several reasons for this, including confounding by indication, methodological issues, and patient and management heterogeneity. In addition, it would be unethical to perform a trial where some patients with elevated ICP
were treated and others were not, given the relationship between increased ICP and
mortality. Hence, no RCT has addressed (or will address) the inuence of ICP management. Attempts have been made to answer the question using analyses of trauma
or TBI registries, quality assurance studies, guideline adherence, within- or acrossinstitution protocol studies, and meta-analysis of clinical series. There are limitations to many of these studies; for example, they examine the use of an ICPM rather
than the ICP treatment per se but in general the vast majority of studies demonstrate
a signicant outcome benet to guideline adherence, and specically, ICPM use
and to ICP treatment [152–163]. For example, one of the largest studies comparing
ICP-monitored patients to those without included 10,628 patients with severe TBI
in the ACS TQIP [154]. Although ICPMs were only used in 17.6% of patients, its
use was associated with a signicant decrease in mortality. Studies that use propensity scores, which is a form of “retrospective randomization,” show that the use of
an ICPM is associated with an 8% reduction in risk-adjusted mortality [164]. There
are rare case series or administrative databases that nd a similar or no outcome
benet with ICPM use [165, 166].
Meta-analysis of studies published since 2007 that include 25,229 patients shows
improved survival in patients who receive an ICP monitor [167]. Overall compliance with ICP and CPP goals remains variable and <50% adult patients eligible for
ICP monitoring actually receive an ICP monitor [154, 156, 163, 168]. This allows
comparativeness effectiveness research. For example, Cnossen etal. [169] examined care of 503 moderate or severe TBI in ve level I trauma centers in the
Netherlands. Treatment was associated with patient characteristics and varied
widely among centers, even after case-mix correction. Outcome was more favorable
in patients treated in aggressive centers than those treated in nonaggressive centers
(dened on the frequency of ICP monitoring). The inference of these various studies
is that adherence to guidelines on ICP- and CPP-directed therapies appears to be
associated with decreased mortality, although it remains unclear if this association
is causal. In addition, the studies do not conrm that ICP treatment (or what aspect
of treatment) is benecial per se but rather that the use of an ICPM helps.
The Benchmark Evidence from South American Trials: Treatment of Intracranial
Pressure (BEST TRIP) trial was a recent RCT that attempted to answer how ICP
monitor use may affect care in a resource-limited environment [170]. Patients
(>13years old) in general ICUs in Bolivia and Ecuador were randomized to management strategies for severe TBI, one of which was triggered by an ICP monitor.
Outcome was similar in the two groups, which is to be expected since there is no
control group. Care was more efcient in the ICPM group but the vast majority of
patients did not develop increased ICP.Many have (mis) interpreted this trial to suggest that there is no need to treat ICP.This is far from the truth and, despite its title,
BEST TRIPS is not a trial of ICP care per se and not even a trial of ICP monitoring.
Indeed, a recent consensus meeting on the trial indicated that for those who
32
currently monitor ICP, there is no reason to change practice and that the trial lacks
external validity and raises more research questions rather than answers any clinical
questions [56]. In particular, it is important to dene what constitutes intracranial
hypertension and whether ICP as a numeric threshold is simply a marker for underlying pathophysiologic processes or an independent target. From a clinical standpoint, ICP monitoring should be used as part of a multimodal approach to the patient
and viewed as an additional tool available to the clinician to manage patients
with TBI.
P. Le Roux
2.7 Are Other Monitors Necessary toFully Understand ICP
andIts Management?
ICP and CPP treatment remain central and critical to care of acute brain injury
(ABI). However, converging evidence from several different lines of research suggests that care based on only ICP and CPP thresholds may be an oversimplication
of a complex problem [65–70, 73, 79, 88, 171–173]. The implication of this is that
additional measures of ICP, for example, ICP waveform analysis, RAP, PRx, or CO2
reactivity or use of other monitors, that is, MMM, can augment ICP care. In addition, autoregulation is known to play an important protective role in tolerating episodes of raised ICP (Klein) and when impaired is associated with poor outcome.
However, cerebrovascular reactivity remains relatively independent of intracranial
hypertension therapeutic intensity, suggesting that current therapies do not adequately modulate impaired autoregulation [174].
2.7.1 Other Measures ofICP
Based on the Monro-Kellie doctrine, the cranial compartment can accommodate
between 50 and 150mL of additional volume before ICP increases. This compensatory reserve or compliance is age dependent, and is not linear. In turn, it is inuenced by CA.Knowing where a patient is on the curve at a given time provides
important information about the risk of a rapid ICP increase (and so a change in
CBF) or herniation.
Compliance and waveform analysis can be examined through the pressure volume index. However, this requires injection of uid through an EVD.Instead, ICP
waveform analysis provides important information about the state of compliance
[175]. With every systole there is a certain pulsatile increase in the cerebral blood
volume that leads to a corresponding ICP increase. This increase or dP/dV is proportional to the elastance (inverse of compliance of the cranial compartment at that
point in time). In a noncompliant brain, the waveform changes and P2 (the rebound)
of the wave becomes greater than P1 (the percussion or arterial wavelet). In recent
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
33
years, studies have examined the pressure-volume compensatory reserve index
(RAP), which is dened as the correlation coefcient between the amplitude and
mean pressure of the ICP.A RAP coefcient close to zero indicates little correlation
between the ICP pulse amplitude and the mean ICP and reects a good compensatory reserve. In contrast, a RAP coefcient that approximates one indicates that the
pulse amplitude of the ICP varies directly with mean ICP, that is, the pressure volume curve has shifted to the right and that compensatory reserve has been exhausted
[176]. ICP waveform analysis, therefore, has great promise as a tool to aid clinical
evaluation and targeted ICP care. However, specialized software and high-frequency
data collection systems are needed to effectively use these methods. In the ICU,
there are qualitative estimates of compliance, for example, how does ICP respond or
vary during stimulation and what is the therapeutic index, that is, what and how
much treatment is need to control ICP?
2.7.1.1 Pressure Reactivity Index (PRx)
With recent data processing advances and computerized bedside monitoring, the
relationship between ICP and MAP or pressure reactivity index (PRx) can be measured. PRx has the advantage that it can be measured continuously in any patient
with a parenchymal ICPM, an arterial pressure line, and the appropriate analysis
software. This provides a real-time analysis of CA.In the normal brain, increases in
MAP result in cerebral vasoconstriction within 5–15s, with an associated reduction
in CBV and ICP, that is, an inverse correlation between MAP and ICP, indicated by
a negative value for PRx. This represents a reactive vascular bed and intact CA.If
cerebrovascular reactivity is impaired, CBV and ICP increase passively with blood
pressure (BP), with opposite changes when BP is reduced. Hence, an increasingly
positive PRx value (close to +1) indicates impaired cerebral pressure reactivity. This
model works best when the cranium is intact since following DC changes in CBF
and CBV will not necessarily lead to changes in ICP since the cranial compliance is
altered [177]. PRx has been most studied in TBI where several studies demonstrate
that impaired PRx is associated with poor outcome [112, 113, 178]. In nontraumatic
pathologies, the mean ow index (Mx), derived from Transcranial Doppler (TCD),
that measures the correlation between mean middle cerebral artery blood ow
velocity and CPP (or MAP) may be a better measure.
Importantly PRx can be used to guide therapy and enhance prognostic decisions.
First, choosing a CPP target can be speculative in individual patients but using PRx,
patient-specic CPP, and ICP thresholds can be identied. These patient-specic
thresholds show a more robust relationship with outcome than population-based
targets [73, 112, 113, 178, 179]. Second, PRx can be used to estimate optimal CPP
(CPPopt); the more time a patient is at their individual CPPopt, the more likely
outcome will be favorable since it reduces the risks of excessively high or low
CPP.However, there is potential to over interpret CPPopt targets when the values of
pressure reactivity indices are close to zero. Finally, knowledge about PRx can help
decide whether to use ICP- or CPP-based therapy with a CPP-targeted approach
34
P. Le Roux
being preferable when pressure reactivity is intact, while an ICP-oriented strategy is
better in pressure passive patients (MAP/ICP regression line at least 0.13; Howells).
However, further research is required to examine this concept that intuitively makes
sense and that of personalization of ICP monitoring (i.e., waveform analysis, pulse
amplitude, pressure reactivity, and longitudinal trajectories) to develop individualized targeted care.
2.7.1.2 Multimodality Monitoring
Cerebral microdialysis (CMD) studies show that cell energy dysfunction can occur
before ICP or CPP changes and independently from ICP or CPP [66, 67, 79, 172,
180–182]. This implies that additional monitors are necessary to better understand
what is happening in a patient and essential to targeted and mechanistic therapy,
including that for increased ICP [69, 70]. Alternatively, predictive models based on
machine learning (articial intelligence) from continuous time series of ICP and
other data may provide accurate predictions of physiologic crises and so allow earlier application of targeted interventions [183, 184]. There are a variety of monitors
now available, for example, CBF, continuous EEG, brain oxygen, microdialysis,
autoregulation, near-infrared spectroscopy, among others, that allow real-time bedside assessment. There is no one monitor that is “better” than the other and no single
technique can be expected to provide complete information about the brain’s health
and, hence, a combination of monitors is needed. This approach, often called multimodality monitoring (MMM), has evolved in recent years along with the growth of
bioinformatics. In reality, it is practiced all the time, that is, we combine data from
the clinical exam, CT scan, and laboratory analysis. Several lines of evidence indicate that MMM can optimize care of brain-injured patients [184–187]. Indeed, in a
recent phase II trial, goal-directed therapy guided by brain oxygen, ICP, and CPP
monitoring appears to be superior to standard ICP- and CPP-guided therapy [88]. A
phase III trial to examine this question is now underway. In short, ICP is best managed with more than just an ICP monitor.
2.8 Conclusion
The management of neurocritical care patients and specically those with acute
brain injury, for example, TBI, SAH, or ICH, to name a few, can be immensely
complicated. Management of ICP is a cornerstone of this care. How best to manage
ICP can be augmented with additional monitors and use of bioinformatics to better
understand the mechanisms behind changes in ICP and to enhance targeted care
with a physiologically integrative approach [183, 188]. To further help patient care,
several guidelines about when and how to use different monitors and management
YES I. Second Tier Treatment
EMERGENCY DEPARTMENT (ED)
2 Neuro-ICU: Monitoring andManagement ofIntracranial Pressure. APractical Review
35
algorithms based on expert consensus are available for TBI and non-TBI pathologies [10–15, 20, 25, 28, 35, 74, 75]. In summary, it is important not to think of ICP
(its numeric value) as the target but rather as an indicator of the existence of an
underlying pathophysiological process that needs treatment, that is, the key question is not what to do if ICP is increased but why is it increased. Hence, in managing
ICP, it is important not to get caught up in simply treating numbers but rather to
integrate information from multiple sources to target individualized care.
Algorithm
PATIENT ADMISSION
ABCD
Level of consciousness (GCS)
Bilateral pupillary reactivity
Hemodynamic stability?
Oxigenation?
CONSIDER
Basic TBI Therapy
ADMISSION
Non-Contrast Brain CT scan
CONSIDER
CONTINUE: CONSIDER
Basic Therapy
REPEAT (48 h)
Brain CT-Scan
SWELLING ? YES
NO
CONSIDER
Awaking
CONSIDER
Taper ICP Therapy SWELLING ?
NO YES
II. Mild Hyperventilation (Option)
INTENSIVE CARE UNIT (ICU)
Clinical Status of Patient
DIAGNOSIS
CRITICAL ILL PATIENT
ACUTE BRAIN INJURY
BRAIN CT-SCAN
SWELLING?
I. Add basic ICP Therapy
(PaCO2 30–35 mmHg)
III. Hyperosmolar Therapy
(Scheduled Dosing)
CONTINUE
Basic ICP Therapy
CONSIDER
I. 5th Day Brain CT Scan
REPEAT (48 h)
Brain CT-Scan
SWELLING ?
NO YES
ESCALATE
ICP THERAPY
I. Neuroworsening Protocol
II. Second Tier Treatment
NO
CONSIDER
ABCD airway-breathing-circulation-disability, CT computed tomography, ICP intracranial
pressure
36
P. Le Roux
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