Vous êtes sur la page 1sur 13


Critical Care Management of Increased

Intracranial Pressure
Stephan A. Mayer, MD*²
and Ji Y. Chong, MD*

Mayer SA, Chong JY. Critical care management of increased Increased intracranial pressure (ICP) can result
intracranial pressure. J Intensive Care Med 2002;17:55±67.
from a number of insults to the brain, including
Increased intracranial pressure (ICP) is a pathologic state traumatic brain injury (TBI), stroke, encephalitis,
common to a variety of serious neurologic conditions, all of neoplasms, and abscesses (Table 1). The funda-
which are characterized by the addition of volume to the mental abnormality common to these diverse
intracranial vault. Hence all ICP therapies are directed toward
reducing intracranial volume. Elevated ICP can lead to brain
disease states is an increase in intracranial volume.
damage or death by two principle mechanisms: (1) global Accordingly, all treatments for elevated ICP work by
hypoxic-ischemic injury, which results from reduction of reducing intracranial volume. Prompt recognition
cerebral perfusion pressure (CPP) and cerebral blood ¯ow, and treatment of elevated ICP is essential because
and (2) mechanical compression, displacement, and herni- sustained elevated ICP can cause brain damage or
ation of brain tissue, which results from mass effect
associated with compartmentalized ICP gradients. In
be rapidly fatal.
unmonitored patients with acute neurologic deterioration,
head elevation (30 degrees), hyperventilation (pCO2 26±30
mmHg), and mannitol (1.0±1.5 g/kg) can lower ICP within Pathophysiology
minutes. Fluid-coupled ventricular catheters and intraparen-
chymal pressure transducers are the most accurate and
reliable devices for measuring ICP in the intensive care unit
Intracranial Compliance. The Monroe±Kellie
(ICU) setting. In a monitored patient, treatment of critical ICP doctrine dictates that the cranial vault is a ®xed
elevation (>20 mmHg) should proceed in the following steps: space that contains three compartments: blood,
(1) consideration of repeat computed tomography (CT) cerebrospinal ¯uid (CSF), and brain tissue. In the
scanning or consideration of de®nitive neurosurgical inter- average adult, the brain volume is 1400 ml, the
vention, (2) intravenous sedation to attain a quiet, motionless
state, (3) optimization of CPP to levels between 70 and 110
blood volume is 150 ml, and the CSF volume is 150
mmHg, (4) osmotherapy with mannitol or hypertonic saline, ml. CSF is produced by the choroid plexus in the
(5) hyperventilation (pCO2 26±30 mmHg), (6) high-dose ventricles at a rate of approximately 20 ml/hr, and
pentobarbital therapy, and (7) systemic cooling to attain drains into the venous system via the arachnoid villi
moderate hypothermia (32±33°C). Placement of an ICP and granulations [1]. This out¯ow is normally of low
monitor and use of a stepwise treatment algorithm are both
essential for managing ICP effectively in the ICU setting.
resistance; hence jugular venous pressure is the
chief determinant of ICP in healthy patients. Normal
ICP ranges from 50 to 200 mmH2O or 3±15 mmHg.
In routine intensive care unit (ICU) practice, the
goal of ICP management is to maintain levels below
20 mmHg.
In pathologic states characterized by increased
ICP (Table 1), additional volume is added to the
intracranial compartment. This can result from the
addition of an extrinsic mass lesion or from an
increase in the volume of CSF (hydrocephalus),
brain tissue (cytotoxic edema), or blood (vasogenic
edema). To maintain ICP within normal limits, these
From the Division of Critical Care Neurology, Departments of increases in intracranial volume are initially coun-
*Neurology and ²Neurosurgery, College of Physicians and terbalanced by volume reductions in the other
Surgeons, Columbia University, New York, NY.
compartments. CSF is displaced through the fora-
Received Jul 30, 2001, and in revised form Aug 24, 2001. Accepted men magnum into the paraspinal space, blood is
for publication Aug 28, 2001.
displaced from the intracranial to the extracranial
Address correspondence to Dr. Mayer, Neurological Institute,
710 West 168th St., Unit 39, New York, NY 10032, or e-mail: venous system, and the brain parenchyma is com-
sam14@columbia.edu. pressed. After these mechanisms are exhausted,

Copyright Ó 2002 Blackwell Science, Inc. 55

56 Journal of Intensive Care Medicine Vol 17 No 2 March/April 2002

Table 1. Conditions Associated with Increased ICP

Intracranial mass lesions

Subdural hematoma
Epidural hematoma
Brain tumor
Cerebral abscess
Intracerebral hemorrhage
Increased brain volume (cytotoxic edema)
Cerebral infarction
Global hypoxia-ischemia
Reye's syndrome
Acute hyponatremia
Increased blood and brain volume (vasogenic edema)
Hepatic encephalopathy
Traumatic brain injury Fig 1. Intracranial pressure-volume relationship. At
Meningitis point A, on the ¯at portion of the curve, the amplitude of
Encephalitis the arterial re¯ection in the ICP waveform is small (inset),
Hypertensive encephalopathy and the addition of volume leads to a small increase, in
Eclampsia pressure (A¢). At point B, on a steeper portion of the curve,
Subarachnoid hemorrhage the intracranial compartment is relatively noncompliant,
Dural sinus thrombosis the amplitude of the arterial re¯ection in the ICP wave-
Altitude-related cerebral edema form is large (inset), and addition of the same amount of
Increased CSF volume volume leads to a larger increase, in pressure (B¢). (Re-
Communicating hydrocephalus printed from Mayer SA. Management of increased intra-
Noncommunicating hydrocephalus cranial pressure. In: Wijdicks EFM, Diringer MN, Bolton
Choroid plexus papilloma CF, et al. Continuum: Critical Care. Minneapolis, MN:
American Academy of Neurology, 1997:47±61.)
intracranial compliance (DV/DP) falls sharply, and
even small increases in intracranial volume can lead
to dramatic elevations in ICP (Fig 1).
The relative state of intracranial compliance can
be assessed by inspection of the ICP waveform
(Fig 1, insets). ICP normally increases 2±3 mmHg
with each arterial pulse because of transient increa-
ses in cerebral blood volume (CBV). When intra-
cranial compliance is reduced, intracranial pulse
pressure can reach levels of 10±15 mmHg, which
re¯ects loss of the ability to accommodate even
small pulsatile increases in CBV. As intracranial
compliance falls, the morphology of the ICP
waveform also changes, in that the amplitude of
the second peak (the dicrotic wave) initially equals
and then exceeds the amplitude of the ®rst peak
(the percussion wave) (Fig 2).
Fig 2. ICP waveform in conditions of normal (top) and
abnormal (bottom) intracranial compliance. (Reprinted
Cerebral Perfusion Pressure. Cerebral perfu- from Chestnut RM, Marshall LF. Treatment of abnormal
sion pressure (CPP), de®ned as the mean arterial intracranial pressure. Neurosurg Clin N Am 1991;2:267±
pressure (MAP) minus ICP, is a critical determinant 284.)
of cerebral blood ¯ow (CBF) and plays an import-
ant role in ICP management. Normally CBF is subarachnoid hemorrhage, CBF may approximate a
``autoregulated'' at a constant level over a wide linear relationship with CPP, which creates a
range of CPPs (from 50 to 150 mmHg) (Fig 3). smaller range of optimal CPP (Fig 2). Reduction of
Pressure autoregulation of this type is mediated by CPP below the lower limit of autoregulation can
changes in arteriolar diameter and cerebrovascular lead to ischemia [2], whereas CPP elevation above
resistance. The autoregulatory curve is shifted to the the upper limit of autoregulation can be associated
left in children and shifted to the right in patients with hyperemia, exacerbation of vasogenic edema,
with chronic hypertension. In pathologic states and increased ICP [3]. Although the optimal CPP for
with impaired autoregulation, such as TBI and any particular patient may vary, as a rule of thumb
Mayer and Chong: Management of ICP 57

Fig 3. Cerebral autoregulation curve. In the normal Fig 4. Pathologic ICP elevations. (A) Lundberg A (plat-
relationship (solid line), with CBF held constant across a eau) waves. (B) Lundberg B waves. (Reprinted from
wide range of CPP (50±150 mmHg). In disease states (e.g., Mayer SA. Management of increased intracranial pres-
vasospasm, ischemia, intracranial mass lesion), cerebral sure. In: Wijdicks EFM, Diringer MN, Bolton CF, et al.
blood ¯ow may become pressure passive (dotted line). Continuum: Critical Care. Minneapolis, MN: American
(Reprinted from Mayer SA. Management of increased Academy of Neurology, 1997:47±61.)
intracranial pressure. In: Wijdicks EFM, Diringer MN,
Bolton CF, et al. Continuum: Critical Care. Minneapolis,
MN: American Academy of Neurology, 1997:47±61.) process begins with a reduction in CPP, which
results from a drop in MAP or a surge in ICP [6]. To
CPP should be maintained above 70 mmHg to avert maintain CBF, the cerebral vasculature dilates and
ischemia, and below 110 mmHg to avoid break- CBV increases. This adds volume to the intracranial
through hyperperfusion. To accurately measure compartment, resulting in an increase in ICP and
CPP in the ICU, the pressure transducer used to further reduction of CPP. This initiates a vicious
measure MAP must be set at head level [4]. cycle in which cerebral vasodilation continues until
CBF also depends upon PaCO2 and PaO2 levels. it is maximal, at which point a ``plateau'' is reached
In general, the cerebral vessels are less responsive at a new level of increased CBV and ICP and
to changes in PaO2 than to those in PaCO2. decreased CPP and CBF. The plateau ends once
Arteriolar diameter and CBF progressively increase CBF is inadequate to maintain tissue oxygenation
as PaCO2 rises from 20 to 80 mmHg, whereas and ischemia develops. This results in a re¯ex
hypoxemia leads to vasodilation and increased CBF systemic pressor response mediated by a surge in
only when PaO2 falls below 50 mmHg [1]. systemic vascular resistance. MAP climbs and CPP is
restored (the termination spike), which allows the
Pathologic ICP Waves. Patients with reduced
intracranial compliance and elevated ICP may
develop pathologic ICP waves (Fig 4). Lundberg
A waves (plateau waves) are dangerous elevations
in ICP [5]. They occur suddenly, can reach levels of
50±100 mmHg, and can last from minutes to hours.
Plateau waves are characteristically associated with
``mirror'' reductions in CPP (Fig 5). When severe,
plateau waves are associated with reduced CPP and
CBF, leading to global hypoxic-ischemic damage.
Lundberg B waves are of lesser amplitude (5±20
mmHg) and of shorter duration (1±5 minutes) than
A waves. Although they are not directly harmful, B
waves are a useful marker of abnormal intracranial
Fig 5. Plateau waves followed by sustained ICP eleva-
compliance. Both of these waves characteristically
tion in a patient with traumatic brain injury. Early in the
end with a surge in systemic blood pressure and
course of the recording, plateau waves exceeding 90
ICP, known as a termination spike [5,6]. mmHg are associated with ``mirror'' reductions in CPP
A vasodilatory cascade model has been proposed below 50 mmHg. At the end of the recording, ICP remains
to explain the pathogenesis of pathologic ICP elevated between 40 and 60 mmHg, MAP falls below 75
waves [6,7]. According to this model, pathologic A mmHg, and CPP drops to 20 mmHg. At this point the
and B waves occur because CPP is inadequate. The patient became clinically brain dead.
58 Journal of Intensive Care Medicine Vol 17 No 2 March/April 2002

cerebral vessels to return to normal caliber, restor- lesions may have elevated ICP, brain tissue shifting,
ing CBV and ICP to normal levels. or both. Herniation is often rapidly fatal, but can be
reversed by reducing mass effect related to
compartmentalized ICP gradients with treatments
Signs of Increased ICP and Herniation such as mannitol, hypertonic saline, and hyperven-
The clinical manifestations of increased ICP are well
known, but are notoriously unreliable (Table 2). A
depressed level of consciousness and re¯ex hyper- ICP Monitoring
tension, the two most consistent signs, both re¯ect
the effects of globally reduced CBF. However, many Indications. Invasive monitoring of ICP is gener-
patients have multiple reasons for a depressed level ally indicated in patients who meet all three of the
of consciousness, and in some patients with signi®- following criteria:
cant shift and mass effect, ICP may be normal.
1. The patient is suspected to be at risk for elevated
Comatose patients with intracerebral hemorrhage
[8] and middle cerebral artery territory infarction [9],
2. The patient is comatose (Glasgow coma scale
for instance, may have ICP levels that vary from
score £ 8).
normal to highly elevated, and brain stem hernia-
3. The prognosis is such that aggressive ICU treat-
tion can occur in the absence of elevated ICP.
ment is indicated.
Cushing's triad (hypertension, bradycardia, and
irregular respiration), which was originally des- Suspicion of increased ICP is usually based on
cribed in response to elevated ICP, can also result clinical signs (Tables 2 and 3) and the results of a
from brain stem herniation. Because of the poor computed tomography (CT) scan showing signi®-
correlation between clinical signs and ICP, the only cant intracranial mass effect with midline shift or
way to properly diagnose increased ICP is to effacement of the basal cisterns. However, in
directly measure it. comatose patients with TBI, intracranial hyperten-
It is important to differentiate clinical signs of sion occurs in approximately 10% of patients with
increased ICP from signs of cerebral herniation normal CT scans; this risk is even higher in patients
(Table 3). Brain tissue displacement and herniation more than 40 years old, with motor posturing, or
occur when compartmentalized mass effect leads to with hypotension (systolic blood pressure < 90
ICP gradients [10,11]. Patients with intracranial mass mmHg) [12].
If a patient is awake and can follow commands, it
Table 2. Clinical Signs of Increased ICP is unlikely that ICP is dangerously elevated [13], and
Signs which are almost always present
the bene®ts of ventricular drainage or ICP monit-
Depressed level of consciousness oring probably do not outweigh the risks. Careful
(lethargy, stupor, oma) monitoring of mental status in an ICU will usually
Hypertension, with or without bradycardia suf®ce in these cases.
Symptoms and signs which are sometimes present
Headache Invasive ICP monitoring devices. Empiric ther-
Vomiting apy for increased ICP (i.e., standing doses of mann-
itol) without invasive monitoring is a distressingly
Sixth cranial nerve palsies
common practice. This approach is unsatisfactory

Table 3. Herniation Syndromes

Type Clinical hallmark Causes

Uncal (lateral transtentorial) Ipsilateral CN 3 palsy Temporal lobe mass lesion

Contralateral motor posturing
Central transtentorial Coma with progression from bilateral Diffuse cerebral edema
decorticate to decerbrate posturing
Rostral-caudal loss of brain stem re¯exes Acute hydrocephalus
Subfalcine Coma with asymmetric Convexity (frontal or parietal)
(contralateral > ipsilateral) motor posturing mass lesion
Cerebellar Sudden progression to coma with bilateral Cerebellar mass lesion
(upward or downward) motor posturing in a patient with cerebellar signs
Mayer and Chong: Management of ICP 59

because most ICP treatments are effective for a short INTRAPARENCHYMAL PRESSURE TRANSDUCERS. The pres-
time only, may lose their ef®cacy with prolonged sure transducer in these disposable devices is
use, and have side effects. Optimally therapy incorporated into the tip of a thin ®beroptic cable
should be given when ICP is high, and withheld (the Camino device) or within a strain-gauge
when it is normal. Only an invasive ICP monitor microsensor at the tip of a ¯exible catheter (the
makes this possible. The four main types of invasive Codman device). These catheters can be placed into
ICP monitors used in standard ICU practice are either the brain parenchyma or the ventricle via a
listed below, in general order of their accuracy and small burr hole and screw [16,17]. With intraparen-
reliability (Fig 6). chymal placement, the infection rate is exceedingly
low (approximately 1%) [18]. When combined with
INTRAVENTRICULAR CATHETERS. These devices directly a ventricular catheter, the system allows simulta-
connect the intracranial space to an external neous CSF drainage and continuous ICP measure-
pressure transducer via saline-®lled tubing. The ment. These devices only need to be calibrated
bedside pressure transducer must be positioned at once prior to insertion, and the accuracy of ICP
the level of the foramen of Monroe (external measurements is generally superior to those provi-
auditory meatus) to accurately re¯ect ICP. The ded by subarachnoid bolts or epidural transducers
catheter is usually connected to both a pressure [19]. A new version of the Codman monitor also
transducer and an external drainage system via a provides measurements of brain temperature. A
three-way stopcock. The system can then be set for third parenchymal monitor recently approved by
continuous ICP monitoring with intermittent CSF U.S. Food and Drug Administration (FDA) (the
drainage or continuous drainage with intermittent Spielberg device) features a small air-®lled balloon
ICP measurement. The major advantage to intra- at the tip of a ¯exible catheter; it has the advantage
ventricular catheters (IVCs) is that they allow of providing measurements of intracranial compli-
treatment of increased ICP via drainage of CSF. ance (calculated as a pressure/volume index) as
The main disadvantage is the high risk of infection well as ICP [20].
(ventriculitis or meningitis), which occurs in
10±20% of patients and increases dramatically after SUBARACHNOID BOLTS. This is another ¯uid-coupled
5 days [14]. Most neurointensivists administer system which connects the intracranial space to an
prophylactic antibiotics with gram-positive cover- external transducer at the bedside via saline-®lled
age, such as oxacillin 1±2 g every 6 hours, to tubing [21]. The subarachnoid bolt is actually a
minimize this risk. In a clinical trial of 228 IVC hollow screw that is inserted via a burr hole. The
patients, prolonged therapy with ampicillin sulbac- dura at the base of the bolt is perforated with a
tam in the ICU signi®cantly reduced the frequency spinal needle, allowing the subarachnoid CSF to ®ll
of CSF infection compared to patients given peri- the bolt. Pressure tubing is then connected to
operative treatment only (3% versus 11%) [15]. establish communication with a pressure monitor-
ing system. Although the infection risk is low, these
devices are prone to error, including underestima-
tion of ICP, screw displacement, and occlusion by
debris [22].

EPIDURAL TRANSDUCERS. These devices (the Gaeltec

device) are inserted deep into the inner table of the
skull and super®cial to the dura [23]. In most of these
devices, pressure is transduced by an optical sensor.
They have a low infection rate (approximately 1%)
[17], but are prone to malfunction, displacement,
and baseline drift that can exceed 5±10 mmHg after
more than a few days of use. Much of the inaccuracy
results from having the relatively inelastic dura
between the sensor tip and the subarachnoid space.
Fig 6. ICP monitoring devices. (A) Intraparenchymal
®beroptic probe or microsensor; (B) intraventricular
Noninvasive ICP Monitoring. At present there is
catheter; (C) epidural transducer; (D) subarachnoid bolt.
(Reprinted from Mayer SA. Management of increased no noninvasive method that can provide accurate
intracranial pressure. In: Wijdicks EFM, Diringer MN, continuous on-line measurement of ICP. However,
Bolton CF, et al. Continuum: Critical Care. Minneapolis, transcranial Doppler (TCD) ultrasonography,
MN: American Academy of Neurology, 1997:55.) which measures the velocity of blood ¯ow in the
60 Journal of Intensive Care Medicine Vol 17 No 2 March/April 2002

basal cerebral arteries, shows characteristic changes Table 4. Normal and Critical Values for SjvO2 and PbtO2
with increasing ICP [24]. As CPP falls, diastolic Monitors
velocity decreases and pulsatility increases, re¯ect- SjvO2 PbtO2
ing increased distal vascular resistance to ¯ow. (%) (mm Hg)
Though this ®nding is speci®c for severe intracra-
nial hypertension, TCD is not sensitive to mild to Normal valuea 62 37
Critical upper limit 80 NA
moderate ICP elevations. Lateralized asymmetries (indicates hyperemia)
in TCD pulsatility correlate with lesion volume in Critical lower limit 50 8
intracerebral hemorrhage, and are believed to (indicates ischemia)
re¯ect compartmentalized ICP gradients [25]. Prom- Average value in severe TBIa 73 ‹ 10 32 ‹ 19
ising new applications using ultrasound technology NA ˆ data not available.
to estimate ICP noninvasively have been described, Interpretation of critical values assumes normal FiO2 (£40%) and
but have not yet been validated in the clinical setting hematocrit.
Data from reference 34.
predominant concern, whereas SjvO2 is less in¯u-
Adjuncts to ICP Monitoring. Several new
enced by high FiO2 levels and hence may be a more
modalities have recently been introduced that can
reliable measure of relative hyperperfusion [34].
provide additional information regarding the ad-
equacy of cerebral perfusion and the extent of
CEREBRAL MICRODIALYSIS. This adjunctive monitoring
injury in patients undergoing ICP monitoring.
technique is labor intensive and has yet to gain
widespread acceptance. A probe is placed through
the skull and levels of different substances may be
measured using high-performance liquid chromato-
oring assesses the adequacy of global cerebral
graphy (HPLC). Lactate, glutamate, and more
oxygen delivery, whereas PbtO2 monitoring meas-
recently extracellular potassium have been meas-
ures regional oxygen tension. Both emerging
ured using this microdialysis. These levels correlate
technologies provide continuous information re-
with cerebral ischemia and poor outcome [35].
garding the adequacy of CPP and CBF at the tissue
level [29±31]. SjvO2 is measured with a 5-French MULTIMODAL MONITORING. Finally, a combination of
®beroptic oxygen saturation catheter placed retro- multiple monitoring techniques may soon be
grade in the internal jugular vein so that the tip is possible. Various prototypes are in development
positioned in the jugular bulb; PbtO2 is measured that can allow simultaneous monitoring of ICP,
with a miniaturized Clark electrode embedded in PbtO2, PbtCO2, pH, brain temperature, laser Dop-
the tip of a thin catheter inserted 3±4 cm into the pler ¯ow, and even microdialysis.
cerebral white matter (the Licox or Neurotrend
device). Both techniques can detect inadequate
CBF (i.e., ischemia), which may occur even in Management of Increased ICP
patients with relatively normal CPP [32], and
excessive CBF (i.e., hyperemia), which can aggra- General Care Issues. Proper management of all
vate ICP related to vasogenic edema and break- critically ill brain-injured patients begins with
through of autoregulation [33]. Accordingly these general care issues designed to optimize oxygen-
monitors can be used to optimize therapy: mannitol ation and cerebral blood ¯ow and to minimize
and vasopressor infusion reduce ICP and improve factors that can aggravate neuronal injury or trigger
cerebral oxygenation when SjvO2 or PbtO2 values ICP elevations. The following guidelines should be
fall below critical levels [30±32], whereas hyper- followed in all patients at risk for increased ICP:
ventilation reduces ICP and tissue oxygenation
when it is supranormal due to relative hyperperfu- PATIENT POSITIONING. As long as the patient is not
sion [31] (Table 4). The depth and duration of hypotensive (mean blood pressure < 60 mmHg),
ischemia detected by either device is highly corre- the head of the bed should be elevated to 30
lated with poor clinical outcome in patients with degrees and a straight head position should be
severe TBI [30,31]. Since neither monitor alone can maintained. Head elevation to 30 degrees reduces
detect all episodes of ischemia [34], selection of ICP by reducing jugular and cerebral venous
which type to use depends on the speci®c clinical pressure and enhancing venous out¯ow, without
circumstances at hand. PbtO2 monitoring is gener- signi®cantly lowering CPP, CBF, or cardiac output
ally easier to use, and is most desirable when [36,37]. Some have recommended a head ¯at
detection of ischemia in a speci®c brain region is the position to prevent any reductions of CPP that
Mayer and Chong: Management of ICP 61

may occur with head elevation, which may be ¯ow, and have been shown to exacerbate hypoxic-
reasonable in selected cases [38]. However, head ischemic neuronal injury in experimental animals
elevation in excess of 45 degrees should generally [45]. As a general standard, acetaminophen and
be avoided because paradoxical increases in ICP cooling blankets should be given to all patients with
can occur in response to excessive CPP reduction sustained fevers in excess of 38.3°C (101.0°F), but
[39]. Sharp head angulation should also be avoided, evidence for their ef®cacy in neurologic patients is
as it may cause jugular venous compression, scant [46,47]. Endovascular cooling with the use of
increased venous backpressure, and increased ICP. closed-circuit water-circulating intravenous cathe-
ters is a promising new approach that is currently
FLUID MANAGEMENT. Only isotonic ¯uids, such as under development.
0.9% (normal) saline or lactated Ringer's solution, Recent studies suggest that indomethacin may be
should be used in patients at risk for elevated ICP. the ideal antipyretic to use in patients with
Cerebral edema is generally understood to result increased ICP. Indomethacin has been shown to
from the creation of ``idiogenic osmoles'' which decrease CBF and ICP in animal models and
draw water down an osmolar gradient into injured patients with TBI [48]. The mechanism of action is
brain tissue. Hypotonic ¯uids such as 5% dextrose not known, but may involve vasoconstriction of
or 0.45% (half-normal) saline should be strictly cerebral vessels and inhibition of prostaglandin
avoided because the free water contained in these synthesis [48].
¯uids can aggravate cerebral edema and increase
ICP [40]. Systemic hypo-osmolality (<280 mOsm/L) SEIZURE PROPHYLAXIS. Seizures can lead to profound
should be aggressively treated with mannitol or 3% elevations of CBF, CBV, and ICP, even in patients
hypertonic saline. The traditional practice of who are sedated or paralyzed [49]. This is secondary
restricting total ¯uid intake (dehydration therapy), to the increased cerebral metabolic demand that
with the goal of reducing the extracellular ¯uid occurs with seizures. Intravenous fosphenytoin
volume, has not been shown to signi®cantly impact (15±20 mg/kg loading dose, 3±5 mg/kg/day) is
brain water content or ICP. In fact, hypovolemia the preferred agent for seizure prophylaxis while in
may lead to inadequate CPP and a consequent the ICU.
increase in ICP [41].
Patients with elevated ICP should have a central STEROIDS. Dexamethasone and other steroids
venous line placed to monitor central venous should not be used as a standard treatment for ICP
pressure; this is particularly critical for patients because they are ineffective against cytotoxic
treated with mannitol or hypertonic saline. As a edema [50]. There is generally no role for steroids
general rule, a central venous pressure greater than in the treatment of mass effect related to cerebral
5 mmHg and equal to slightly positive daily net ¯uid infarction [51], intracerebral hemorrhage [52], or TBI
balance should be maintained by increasing the rate [53]. By contrast, vasogenic edema related to
of infusion of isotonic crystalloid, administering neoplasm or abscess is steroid responsive, and
0.9% saline or 5% albumin ¯uid boluses, or dexamethasone 4±20 mg every 6 hours can lead to
transfusing blood to maintain hematocrit at greater dramatic reductions in lesion volume [54].
than 24% [42].
Use of 1.5±3% hypertonic saline as a maintenance Emergent Treatment of Increased ICP in an
intravenous ¯uid for patients with cerebral edema is Unmonitored Patient. Emergency measures for
gaining popularity in the neurocritical care com- ICP control (Table 5) are appropriate for comatose
munity. Though support for this practice to date is patients who present acutely with clinical signs of
inconclusive, adequate clinical trials have yet to be increased ICP or herniation. These measures are
performed [43]. A small study of pediatric TBI
patients compared the use of 1.6% saline with
lactated Ringer's solution and found no differences Table 5. Emergency Measures for ICP Reduction
in ICP or CPP, though the hypertonic saline group
required fewer interventions to lower ICP [44]. Lack 1. Elevate head of bed 15±30 degrees.
2. Normal saline (0.9%) at 80±100 cc/hr
of uniform concentrations and poor de®nition of
(avoid hypotonic ¯uids).
dose-response relationships has limited the wide- 3. Intubate and hyperventilate (target pCO2 26±30
spread use of hypertonic saline to date. mmHg).
4. Mannitol 20% 1±1.5 g/kg via rapid intravenous
TEMPERATURE MANAGEMENT. Fevers should be trea- infusion.
ted aggressively. Temperature elevations increase 5. Foley catheter.
6. CT scan and urgent neurosurgical consultation.
ICP by increasing cerebral metabolism and blood
62 Journal of Intensive Care Medicine Vol 17 No 2 March/April 2002

designed to lower ICP as quickly and effectively as

possible in order to ``buy time'' before a de®nitive
neurosurgical procedure (craniotomy, ventriculos-
tomy, or placement of an ICP monitor) can be
performed. Aggressive hyperventilation and mann-
itol therapy are the cornerstones of this type of

Stepwise Treatment Protocol for Elevated ICP

in a Monitored Patient. The primary goal of ICP
management in a monitored patient is to maintain
ICP below 20 mmHg and CPP above 70 mmHg.
Contemporary ICP management has changed in
recent years in two important aspects: CPP man- Fig. 7. The Columbia stepwise protocol for ICP
agement (in addition to ICP control) has become management.
increasingly emphasized, and the potential for
overzealous hyperventilation to cause excessive shorter duration of treatment than patients treated
vasoconstriction and aggravate ischemia has ad hoc [55].
become increasingly recognized. The stepwise
protocol presented here for managing ICP in a STEP 1: SURGICAL DECOMPRESSION OR CSF DRAIN-
monitored patient (Table 6) re¯ects these consid- AGE. The ®rst consideration in the face of an acute
erations. More than one step may be instituted increase in ICP should always be whether a
simultaneously, but only after all of the preceding de®nitive intervention, such as craniotomy or
steps have been addressed. Likewise, ICP therapy ventriculostomy, should be performed to remove
should be withdrawn in a similar stepwise fashion volume or decompress the skull. A repeat CT scan
(Fig 7). This algorithm should be initiated any time should be considered to rule out reaccumulation of
ICP remains greater than 20 mmHg for more than 10 an intracranial hemorrhage or worsening hydro-
minutes. cephalus. If a ventricular catheter is in place, the
Though we favor the protocol presented below system should be opened to drainage and 5±10 ml
because of its simplicity, other treatment algorithms of CSF removed.
may be equally effective. Use of a standardized, The option of some de®nitive surgical interven-
evidence-based protocol for ICP management al- tion should be continuously evaluated as additional
lows for ef®cient and well-coordinated treatment of steps to control ICP are added. Controlled lumbar
patients within an institution, and can improve CSF drainage (5±20 ml/hr) has been reported to
patient outcomes. In a retrospective study of reduce ICP and increase CPP in patients refractory
patients with TBI, patients treated with a standard- to medical therapy and ventricular drainage alone
ized algorithm of instituting and weaning ICP [56]. However, this intervention is feasible only if
therapies required fewer interventions and had a the basal cisterns are open on CT, and even in these
cases, transtentorial herniation remains a risk.
Decompressive hemicraniectomy is becoming in-
Table 6. Stepwise Treatment Protocol for Elevated ICPa
in a Monitored Patient creasingly used as an intervention of last resort for
patients who might otherwise require pentobarbital
1. Surgical decompression. Consider repeat CT or hypothermia. Wide cranial decompression can
scanning and de®nitive surgical intervention or de®nitively control ICP and reverse brain stem
ventricular drainage.
2. Sedation. Intravenous sedation to attain a
herniation, and has been reported to be effective for
motionless, quiet state. treating massive cerebral infarction [57], encephal-
3. CPP optimization. Pressor infusion if CPP is less than itis [58], head trauma [59], and intracerebral hemor-
70 mmHg, or reduction of blood pressure if CPP is rhage [60] in nonrandomized studies. Complica-
greater than 110 mmHg. tions of hemicraniectomy can include CSF leakage,
4. Osmotherapy. Mannitol 0.25±1.0 g/kg intravenously
(repeat every 1±6 hours as needed).
local wound infection or meningitis, intracranial
5. Hyperventilation. Target pCO2 levels of 26±30 mmHg. bleeding, and late hydrocephalus.
6. High-dose pentobarbital therapy. Load with 5±20
mg/kg, infuse 1±4 mg/kg/hr. STEP 2: SEDATION. Sedation is often overlooked as a
7. Hypothermia. Cool core body temperature to 32±33°C. key factor in ICP control. In patients with reduced
More than 20 mmHg for more than 10 minutes. intracranial compliance, ®ghting against physical
Refer to text for details. restraints or ``bucking'' the ventilator can increase
Mayer and Chong: Management of ICP 63

ICP by elevating intrathoracic and jugular venous ultrashort acting, it has favorable effects on ICP and
pressure. Arterial hypertension associated with seizure activity, and may have neuroprotective
agitation may further increase ICP if the patient is properties. In a study comparing propofol to
at the upper range of the autoregulatory curve. morphine in patients with severe TBI, patients
Before further measures are instituted, agitated treated with propofol had lower ICP values and
patients with increased ICP should be sedated to the more favorable long-term neurologic outcomes
point where they are quiet and motionless (Ramsey [64]. By contrast, paralysis with neuromuscular
level 5 or 6). A combination of a sedative-hypnotic blocking agents such as vecuronium, pancuronium,
and analgesic agent is usually most effective or cis-atracurium is rarely necessary, and places
(Table 7). The preferred regimen is the combina- patients at risk for prolonged paralysis due to
tion of an opioid, such as fentanyl (1±3 lg/kg/hr) or critical illness myopathy.
sufentanil (0.1±0.6 lg/kg/hr), to provide analgesia
and propofol (0.3±3 mg/kg/hr) for sedation. It is STEP 3: CPP OPTIMIZATION. If CPP is less than 70
important to use drugs that are short acting, such mmHg and ICP is greater than 20 mmHg, elevation
that the agent may be stopped for frequent neuro- of mean arterial blood pressure and CPP with a
logic assessments throughout the day. One study vasopressor such as dopamine or phenylephrine
showed that daily, scheduled interruption of seda- (Table 8) can lead to a re¯ex reduction of ICP, by
tion to examine patients not only reduced the eliminating cerebral vasodilation that occurs in
length of ventilator dependence and ICU length of response to inadequate perfusion (Fig 8). CPP
stay, but also decreased the need for other tests such optimization to levels well above 70 mmHg may
as brain imaging and lumbar punctures to evaluate be desirable in chronically hypertensive patients
alterations in mental status [61]. (whose autoregulatory curve is shifted to the right),
Neurocritical care patients, even when comatose, or in patients with low PbtO2 or SjvO2 levels or
can sense pain and require analgesia in addition to Lundberg A and B waves (since these ®ndings
sedation. Therefore careful use of a low-dose con- generally re¯ect insuf®cient CPP). The widely
tinuous infusion opioid in addition to propofol or accepted ``one size ®ts all'' approach to CPP
midazolam is recommended. Bolus injections of management (>70 mmHg) is in all likelihood an
opioids, however, should be used with caution in oversimpli®cation, and efforts should be made to
patients with elevated ICP. Bolus infusions of the optimize CPP whenever patients fail standard
sufentanil, fentanyl, and alfentanil can transiently therapy. One study that attempted to de®ne optimal
lower MAP and increase ICP due to autoregulatory CPP levels for severe TBI patients by analyzing
vasodilation of cerebral vessels [62]. This effect is receiver-operating curves found that a CPP of 55
seen primarily in patients with intact autoregulation, mmHg was the critical threshold for poor outcome
but can also occur in patients with abnormal auto- in adults [65]. It seems prudent to maintain CPP well
regulation [63]. Vasopressors may be used to avoid above this level in clinical practice, however, to
hypotension and possible re¯ex ICP elevation. provide an extra margin of safety. In an uncon-
Propofol may be the ideal sedative to use in trolled study of TBI patients with CPP main-
patients with elevated ICP; besides the fact that it is tained above 70 mmHg with phenylephrine and

Table 7. Selected Short-Acting Intravenous Sedatives for ICP Management

Agent Pharmacology Dosage Range

Sedative-analgesic agents
Morphine sulfate Opioid (sedative-hypnotic with analgesic 2±5 mg IVP every 1±4 hours
Fentanyl Opioid (short acting, 100 times more potent than 0.5±3.0 lg/kg/hr
Sufentanil Opioid (ultrashort acting) 0.1±0.6 lg/kg/hr
Sedative-hypnotic agents
Propofol Alkylphenol (ultrashort acting) 0.6±6 mg/kg/hr
Midazolam Benzodiazepine (short acting) 0.05±0.1 mg/kg/hr

Dosages are approximate and should be titrated to the patient's level of agitation and ICP. A combination of a sedative-analgesic and
sedative-hypnotic agent may be more effective than the use of a single agent.
64 Journal of Intensive Care Medicine Vol 17 No 2 March/April 2002

Table 8. Selected Short-Acting Vasoactive Drugs for ICP concerns also exist regarding the potential for
Management nitroprusside to directly dilate the cerebral vascu-
Agent Pharmacology Dosage Range lature and increase ICP. For these reasons, nitro-
prusside is best avoided in patients with elevated
Blood pressure reduction ICP, and should only be used if an ICP monitor is in
Labetolol a1 and b1 blocker 2±3 mg/min place. Experimental and clinical studies have dem-
Nicardipine Calcium channel 5±15 mg/hr onstrated that treatment of hypertension in patients
blocker with intracerebral hemorrhage does not exacerbate
perilesional ischemia [66] or cause re¯ex vasodila-
Blood pressure elevation
tion and increased ICP [67], as long as CPP remains
Dopamine a1 and b1 agonist 5±30 lg/kg/min within the normal range.
(at high doses)
Norepinephrine a1 and b1 agonist 0.03±0.6 lg/kg/min STEP 4: OSMOTHERAPY. If CPP is optimized, the patient
Phenylephrine a1 agonist 2±10 lg/kg/min is sedated, and ICP remains elevated, mannitol or
hypertonic saline should be given. Mannitol, an
osmotic diuretic, lowers ICP via its cerebral dehy-
norepinephrine, better outcomes were obtained drating effects. The effects of mannitol are biphasic.
than in previously reported patients with strictly Rapid infusion immediately creates an osmotic
ICP-based management [41]. gradient across the blood-brain barrier, which leads
If MAP and ICP are elevated in a sedated patient, to movement of water from brain parenchyma
treatment of arterial hypertension can sometimes to the intravascular compartment. The result is
lead to a parallel reduction of ICP. If CPP is greater decreased brain tissue volume, and hence reduced
than 110 mmHg and ICP is greater than 20 mmHg, ICP [68]. The secondary effect of mannitol results
hypertension should be carefully treated with a from its action as an osmotic diuretic. As mannitol is
short-acting agent (Table 7). However, extreme cleared by the kidneys, it leads to free water
caution should be used to avoid reduction of CPP clearance and increased serum osmolality. This
below 70 mmHg, which can trigger re¯ex cerebral leads to a more prolonged intracellular dehydrating
vasodilation and ICP elevation. Nitroprusside can effect as water ¯ows down the osmotic gradient
be particularly troublesome in this regard, and from the intracellular to the extracellular space.
The initial dose of mannitol 20% solution is 1±1.5
g/kg, followed every 1±6 hours with doses of 0.25±1
g/kg as needed. Repeated mannitol doses should
be given on the basis of ICP measurements rather
than as scheduled doses, unless the goal is to
establish and maintain a hyperosmolar state (300±
320 mOsm/L). The effect of a mannitol bolus on ICP
begins within 10±20 minutes, reaches its peak
between 20 and 60 minutes, and lasts for 4±6 hours,
but this may vary widely between patients. Adverse
effects of mannitol therapy include exacerbation of
congestive heart failure (due to the initial intravas-
cular volume expansion); volume contraction,
hypokalemia, and profound hyperosmolality (after
prolonged use); acute tubular necrosis (due to
excessive hyperosmolality); and ``rebound'' increa-
ses in ICP [69]. Patients treated repeatedly with
mannitol require frequent measurements of serum
electrolytes and osmolality, careful recording of
¯uid input and output, and central venous pressure
monitoring. Urinary volume losses should be
Fig 8. Demonstration of CPP augmentation resulting in
re¯ex ICP reduction. At approximately 9:30, the patient
replaced with normal (0.9%) saline to avoid volume
developed a plateau wave with ICP elevation from 20 to depletion.
40 mmHg, and CPP reduction from 100 to 70 mmHg. A Bolus infusion of 3%, 7.5%, 10%, or 24.3%
dopamine infusion was started at 9:45, with nearly im- hypertonic saline is gaining popularity as an
mediate normalization of ICP to 20 mmHg when CPP was alternative to bolus infusions of mannitol for ICP
restored to 100 mmHg. crises [43]. In an uncontrolled study of 3% saline/
Mayer and Chong: Management of ICP 65

acetate infusion (75±150 ml/hr) and intermittent causes hypotension, and usually requires the use of
boluses (250 ml) titrated to maintain serum sodium vasopressors to maintain CPP above 70 mmHg.
levels between 145 and 155 mEq/L, hypertonic Pentobarbital typically requires a loading dose of
saline lowered ICP related to TBI and brain tumors, 10±20 mg/kg, given in repeated 5 mg/kg boluses,
but not in patients with intracerebral hemorrhage or until a state of ¯accid coma with preserved pupillary
cerebral infarction [70]. Infusion of 2±5 ml/kg of reactivity is attained. Maintenance infusion is usu-
7.5% saline or 0.5±1.0 ml/kg of 23.4% saline over 30 ally about 1±4 mg/kg/hr. Continuous EEG monit-
minutes has also been shown to lower elevated ICP oring is helpful to avoid oversedation, since gener-
and augment CPP, with an effect that lasts several ally no further ICP reduction occurs once a burst-
hours [71,72]. A large head-to-head trial of mannitol suppression pattern is attained. If ICP is normalized
versus hypertonic saline is warranted. with pentobarbital, it is generally maintained for
24±48 hours. It can then be abruptly discontinued
STEP 5: HYPERVENTILATION. As a general rule, the goal because its highly lipophilic nature and long half-
of hyperventilation for ICP control should be to life (90 hours) result in a gradual reduction of blood
lower pCO2 to 30 mmHg, or to 25±30 mmHg in levels over several days.
extreme cases. The respiratory alkalosis caused by
hyperventilation lowers ICP by causing cerebral STEP 7: HYPOTHERMIA. Systemic hypothermia to lev-
vasoconstriction and reduced CBV [1]. The peak els of 32±33°C can lower ICP in some patients
effect of hyperventilation on ICP is generally refractory to pentobarbital [79±81]. This technique
reached within 30 minutes. Over the next 1±3 hours requires placement of cooling blankets under and
the effect gradually diminishes, as compensatory over the patient, iced gastric lavage, and pharma-
acid-base buffering mechanisms correct the alkalo- cologic paralysis with vecuronium or a similar
sis within the central nervous system [1]. In patients neuromuscular blocking agent to prevent shiver-
with elevated ICP due to hyperemia and increased ing. Prolonged hypothermia can be dangerous
CBV, however, the effect may be prolonged, and because of increased risk of infectious complica-
hyperventilation may be the treatment of choice tions, coagulopathy, and electrolyte derangements,
[73]. Hyperventilation should be tapered slowly among other hazards. Rewarming should always be
over 4±6 hours because abrupt cessation may lead done slowly, over at least a day, and passively,
to vasodilation and rebound increases in ICP. without active heating, to avoid rebound cerebral
Though it is postulated that prolonged severe edema or a systemic in¯ammatory response syn-
hyperventilation (pCO2 < 25 mmHg) can actually drome, which can be fatal.
exacerbate cerebral ischemia by causing profound In a small randomized controlled trial of severe
vasoconstriction, the deleterious effects of exces- TBI patients refractory to pentobarbital, mild-to-
sive hyperventilation may also include more labile moderate hypothermia (34°C) signi®cantly reduced
ICP. In a study of patients with TBI, prophylactic ICP, improved CPP, reduced CBF and cerebral
hyperventilation to a pCO2 of 25 mmHg resulted in metabolic rate (CMRO2), and reduced arteriojugu-
poorer outcome compared with normally ventila- lar venous oxygen differences [79]. Survival was
ted patients [74]. The authors hypothesized that 50% in hypothermia patients compared to 18% in
blood vessels may become hypersensitive to chan- the control group (p < 0.05). Later studies by the
ges in pCO2 after prolonged hyperventilation same group reported that hypothermia was most
because CSF buffering capacity is lost. In cases of effective for pentobarbital-refractory ICP elevations
pediatric head trauma, profound hypocarbia was between 20 and 40 mmHg [80], and that severe TBI
associated with decreased cerebral oxygen con- patients with low ICP do not bene®t from hypo-
sumption and ischemia [75]. SjvO2 monitoring is a thermia [81]. These reports, and the negative results
useful modality for ensuring that prolonged of a recent large National Institutes of Health (NIH)-
aggressive hyperventilation, if necessary, is not funded trial studying the effects of hypothermia as
critically reducing oxygen delivery to the brain. ®rst-line therapy for severe TBI [82], suggest that
hypothermia is not effective as a primary form of
STEP 6: PENTOBARBITAL THERAPY. High-dose barbitur- neuroprotection for severe TBI related to diffuse
ate therapy, given in doses equivalent general axonal injury.
anesthesia, can effectively lower ICP in most
patients refractory to the steps outlined above
[76,77]. The effect of pentobarbital is multifactorial, References
but most likely stems from a profound reduction of
cerebral metabolism, which is coupled to reduc- 1. Ropper AH, Rockoff MA. Physiology and clinical aspects of
tions of CBF and CBV [78]. Pentobarbital often raised intracranial pressure. In: Ropper AH, ed. Neurological
66 Journal of Intensive Care Medicine Vol 17 No 2 March/April 2002

and neurosurgical intensive care, 3rd ed. Philadelphia: Lip- 24. Hassler W, Steinmetz H, Gawlowski J. Transcranial Doppler
pincott-Raven, 1993:11±28 ultrasonography in raised intracranial pressure and in intra-
2. Jennet WB, Harper AM, Meller JD, et al. Relationship be- cranial circulatory arrest. J Neurosurg 1988;68:745±751
tween cerebral blood ¯ow and cerebral perfusion pressure. 25. Mayer SA, Thomas CE, Diamond BE. Asymmetry of intra-
Br J Surg 1970;57:390±397 cranial hemodynamics as an indicator of mass effect in acute
3. Shinnoj E, Strangaard S. Pathogenesis of hypertensive en- intracerebral hemorrhage: a transcranial Doppler study.
cephalopathy. Lancet 1973;1:461±462 Stroke 1996;27:1788±1792
4. Nates JL, Niggemeyer LE, Anderson MB, et al. Cerebral per- 26. Schmidt B, KlingelhoÈfer J, Schwarze JJ, et al. Noninvasive
fusion pressure monitoring alert! [letter]. Crit Care Med prediction of intracranial pressure curves using transcranial
1997;25:895±896 Doppler ultrasonography and blood pressure curves. Stroke
5. Lundberg N. Continuous recording and control of ventricular 1997;28:2465±2472
¯uid pressure in neurosurgical practice. Acta Psychiatr Scand 27. Pranevicius O, Bertasius K, Pranevicius K, et al. Non-inva-
Suppl 1960;149:1±19 sive dynamic assessment of the elasticity of intracranial
6. Rosner MJ, Becker DP. Origin and evolution of plateau structures. Acta Neurol Scand 1992;86:512±516
waves: experimental observations and a theoretical model. 28. Czosnyka M, Smielewski P, Piechnik S, et al. Critical closing
J Neurosurg 1984;60:312±324 pressure in cerebrovascular circulation. J Neurol Neurosurg
7. Czosnyka M, Smielewski P, Piechnik S, et al. Hemodynamic Psychiatry 1999;66:606±611
characterization of intracranial pressure plateau waves in 29. Robertson C, Gopinath S, Goodman JC et al. SjvO2 monit-
head-injured patients. J Neurosurg 1999;91:11±19. oring in head-injured patients. J Neurotrauma 1995;12:891±
8. Ropper AH, King RB. Intracranial pressure monitoring in 896
comatose patients with cerebral hemorrhage. Arch Neurol 30. van den Brink WA, van Santbrink H, Steyerberg EW, et al.
1984;41:725 Brain oxygen tension in severe head injury. Neurosurgery
9. Frank J. Large hemispheric infarction, deterioration and in- 2000;46:868±878
tracranial pressure. Neurology 1995;45:1286±1290 31. Cruz J. The ®rst decade of continuous monitoring of jugular
10. Wol¯a CE, Luerssen TG, Bowman RM, et al. Brain tissue bulb oxyhemoglobin saturation: management strategies and
pressure gradients by expanding frontal epidural mass clinical outcome. Crit Care Med 1998;26:344±351
lesion. J Neurosurg 1996;84:642±647 32. Cruz J. Continuous monitoring of cerebral oxygenation in
11. Sahuquillo J, Poca M-A, Arribas M, et al. Intrahemispheric acute brain injury: injection of mannitol during hyperventi-
supratentorial intracranial pressure gradients in head-injured lation. J Neurosurg 1990;73:725±730
patients: Are they clinically important? J Neurosurg 33. Cormio M, Valadka AB, Robertson CS. Elevated jugular ve-
1999;90:16±26 nous oxygen saturation after severe head injury. J Neurosurg
12. Narayan RK, Kishore PR, Becker DP, et al. Intracranial 1999;90:9±15
pressure: To monitor or not to monitor? A review of our 34. Gopinath SP, Valadka AB, Uzura M, et al. Comparison of
experience with severe head injury. J Neurosurg jugular venous oxygen saturation and brain tissue PO2 as
1982;56:650±659 monitors of cerebral ischemia after head injury. Crit Care Med
13. Papo I, Janny P, Caruselli G, et al. Intracranial pressure time 1999;27:2337±2345
course in primary intracerebral hemorrhage. Neurosurgery 35. Hutchinson P, Hutchinson D, Barr RH et al. A new cranial
1979;4:504±511 access device for cerebral monitoring. Br J Neurosurg
14. Mayhall CG, Archer NH, Lamb VA, et al. Ventriculostomy 2000;14:46±48
related infections: a prospective epidemiologic study. N Engl 36. Durward QJ, Amacher AL, DelMaestro RF, et al. Cerebral
J Med 1984;310:553±559 and cardiovascular responses to head elevation in patients
15. Poon WS, Ng S, Wai S. CSF antibiotic prophylaxis for neu- with intracranial hypertension. J Neurosurg 1983;59:938±
rosurgical patients with ventriculostomy: a randomised 944
study. Acta Neurochir Suppl 1998;71:146±148 37. Feldman Z, Kanter MJ, Robertson CS, et al. Effect of head
16. Ostrup RC, Luerssen TG, Marshall LF, et al. Continuous elevation on intracranial pressure, cerebral perfusion pres-
monitoring of intracranial pressure with a miniaturized sure, and cerebral blood ¯ow in head-injured patients. J
®beroptic device. J Neurosurg 1987;67:206±209 Neurosurg 1992;76:207±211
17. Gopinath SP, Robertson CS, Contant CF, et al. Clinical eval- 38. Rosner MJ, Coley IB. Cerebral perfusion pressure, intra-
uation of a miniature strain-gauge transducer for monitoring cranial pressure, and head elevation. J Neurosurg
intracranial pressure. Neurosurgery 1995;36:1137±1140 1986;65:636±641
18. Levin A. The use of a ®beroptic intracranial pressure monitor 39. Moraine J, Berre J, Melot C. Is cerebral perfusion pressure a
in clinical practice. Neurosurgery 1977;1:266±271 major determinant of cerebral blood ¯ow during head ele-
19. Sundbarg G, Nordstrom CH, Messeter K, et al. A com- vation in comatose patients with severe intracranial lesions? J
parison of intraparenchymatous and intraventricular pres- Neurosurg 2000;92:606±614
sure recording in clinical practice. J Neurosurg 40. Mayer SA. Fluid management in subarachnoid hemorrhage.
1987;67:841±845 Neurologist 1995;1:71±85.
20. Yau Y-H, Piper IR, Clutton RE, et al. Experimental evaluation 41. Rosner MJ, Rosner SD, Johnson AH. Cerebral perfusion
of the Spielberger intracranial pressure and intracranial pressure: management protocol and clinical results. J Neu-
compliance monitor. Technical note. J Neurosurg rosurg 1995;83:949±962
2000;93:1072±1077 42. Herbert PC, Wells G, Blajchman MA, et al. A multicenter,
21. Vries JK, Becker DP, Yang HF. A subarachnoid screw for randomized, controlled clinical trial of transfusion require-
monitoring intracranial pressure. J Neurosurg 1973;39:416± ments in critical care. N Engl J Med 1999;340:409±417
419 43. Qureshi AI, Suarez JI. Use of hypertonic saline solutions in
22. Miller JD, Bobo H, Kapp JP. Inaccurate pressure readings treatment of cerebral edema and intracranial hypertension.
from subarachnoid bolts. Neurosurgery 1986;19:253±255 Crit Care Med 2000;28:3301±3313
23. Ream AK, Silverberg GD, Corbin SD, et al. Epidural meas- 44. Simma B, Burger R, Falk M, et al. A prospective, randomized
urement of intracranial pressure. Neurosurgery 1979;5:36±43 and controlled study of ¯uid management in children with
Mayer and Chong: Management of ICP 67

severe head injury; lactated Ringer's solution versus hyper- 65. Chambers I, Treadwell R, Mendelow AD. Determination of
tonic saline. Crit Care Med 1998;26:1265±1270 threshold levels of cerebral perfusion pressure and intra-
45. Busto R, Dietrich WD, Globus MY, et al. Small differences in cranial pressure in severe head injury by using receiver-
intraischemic brain temperature critically determine the ex- operating characteristic curves: an observational study in
tent of ischemic injury. J Cereb Blood Flow Metab 291 patients. J Neurosurg 2001;94:412±416
1987;7:129±138 66. Powers WJ, Zazulia AR, Videen TO, et al. Autoregulation of
46. O'Donnell J, Axelrod P, Fisher C, et al. Use and effectiveness cerebral blood ¯ow surrounding acute (6±22 hours) intra-
of hypothermia blankets for febrile patients in the intensive cerebral hemorrhage. Neurology 2001;57:18±24
care unit. Clin Infect Dis 1996;24:1208±1213 67. Qureshi AI, Wilson DA, Hanley DF, et al. Pharmacologic
47. Mayer SA, Commichau C, Scarmeas N, et al. Clinical trial of reduction of mean arterial pressure does not adversely affect
an air-circulating cooling blanket for fever control in critic- regional cerebral blood ¯ow and intracranial pressure in
ally-ill neurologic patients. Neurology 2001;56:292±298 experimental intracerebral hemorrhage. Crit Care Med
48. Slavik R, Rhoney D. Indomethacin: a review of its cerebral 1999;27:965±971
blood ¯ow effects and potential use for controlling intra- 68. Messeter K, Nordstrom CH, Sundbarg G, et al. Cerebral
cranial pressure in traumatic brain injury patients. Neurol Res hemodynamics in patients with acute severe head injury.
1999;21:491±499 J Neurosurg 1986;64:231±237
49. Lassen NA. Control of the cerebral circulation in health and 69. Kaufmann AM, Cardoso ER. Aggravation of vasogenic
disease. Circ Res 1974;34:749±760 cerebral edema by multiple dose mannitol. J Neurosurg
50. Fishman RA. Brain edema. N Engl J Med 1975;293:706±711 1993;44:584±589
51. Anderson DC, Cranford RE. Corticosteroids in ischemic 70. Qureshi A, Suarez J, Bhardwaj A, et al. Use of hypertonic
stroke. Stroke 1979;10:68±71 (3%) saline/acetate infusion in the treatment of cerebral
52. Pourgvarin H, Bhoopat TW, Viriyavejakul A, et al. Effects of edema: effect on intracranial pressure and lateral displace-
dexamethasone in primary supratentorial intracerebral ment of the brain. Crit Care Med 1998;26:440±446
hemorrhage. N Engl J Med 1987;316:1229±1233 71. Suarez J, Qureshi A, Bhardwaj A, et al. Treatment of re-
53. Cooper PR, Moody S, Clark WK, et al. Dexamethasone and fractory intracranial hypertension with 23.4% saline. Crit
severe head injury: a prospective double-blind trial. J Neu- Care Med 1998;26:1118±1122
rosurg 1979;51:307±331 72. Hartl R, Ghajar J, Hochleuthner, et al. Hypertonic/hyper-
54. Galich JM, French LA. Use of dexamethasone in the treatment oncotic saline reliably reduces ICP in severely head-injured
of cerebral edema resulting from brain tumors and brain patients with intracranial hypertension. Acta Neurochir
surgery. Am Pract 1961;12:169±174 Suppl 1997;70:126±129
55. McKinley B, Parmley C, Tonneson A. Standardized man- 73. Obrist W, Lang®tt T, Jaggi JL, et al. Cerebral blood ¯ow and
agement of intracranial pressure: a preliminary clinical trial. J metabolism in comatose patients with acute head injury. J
Trauma 1999;46:271±279 Neurosurg 1984;61:241±253
56. MuÈnch EC, Bauhuf C, Horn P, et al. Therapy of malignant 74. Muizelaar JP, Marmarou A, Ward JD, et al. Adverse effects of
intracranial hypertension by controlled lumbar cerebro- prolonged hyperventilation in patients with severe head
spinal ¯uid drainage. Crit Care Med 2001;29:976±981 injury: a randomized clinical trial. J Neurosurg 1991;75:731±
57. Schwab S, Steiner T, Aschoff A, et al. Early hemicraniectomy 739
in patients with complete middle cerebral artery infarction. 75. Skippen P, Seear M, Poskitt K, et al. Effect of hyperventila-
Stroke 1998;29:1888±1893 tion on regional cerebral blood ¯ow in head-injured chil-
58. Schwab S, Junger E, Spranger M, et al. Craniectomy: an dren. Crit Care Med 1997;25:1402±1409
aggressive treatment approach in severe encephalitis. 76. Rea GL, Rockswold GL. Barbiturate therapy in uncon-
Neurology 1997;48:412±417 trolled intracranial hypertension. Neurosurgery 1983;12:
59. Guerra WK, Gaab MR, Dietz H, et al. Surgical decompres- 401±404
sion for traumatic brain swelling: indications and results. J 77. Eisenberg HM, Frankowski RF, Contant CF, et al. High-dose
Neurosurg 1999;90:187±196 barbiturate control of elevated intracranial pressure in
60. Mayer SA, Connolly ES, Bates J, et al. Decompressive hemi- patients with severe head injury. J Neurosurg 1988;69:15±23
craniectomy for massive cerebral hemorrhage [abstract]. 78. Cormio M, Gopinath S, Valadka A, et al. Cerebral hemo-
Stroke 2001;32:357 dynamic effects of pentobarbital coma in head-injured
61. Kress JP, Pohlman AS, O'Connor MF, et al. Daily inter- patients. J Neurotrauma 1999;16:927±936
ruption of sedative infusions in critically ill patients 79. Shiozaki T, Sugimoto H, Taneda M, et al. Effect of mild
undergoing mechanical ventilation. N Engl J Med 2000; hypothermia on uncontrollable intracranial hypertension
342:1471±1477 after severe head injury. J Neurosurg 1993;79:363±368
62. Albanese J, Viviand X, Potie F, et al. Sufentanil, fentanyl, and 80. Shiozaki T, Sugimoto H, Taneda M, et al. Selection of
alfentanil in head trauma patients: a study on cerebral severely head injured patients for mild hypothermia therapy.
hemodynamics. Crit Care Med 1999;27:407±411 J Neurosurg 1998;89:206±211
63. de Nadal M, Ausina A, et al. Effects on intracranial pressure of 81. Shiozaki T, Kato A, Taneda M, et al. Little bene®t from
fentanyl in severe head injured patients. Neurochirurgia mild hypothermia therapy for severely head injured
1998;71(suppl):10±12 patients with low intracranial pressure. J Neurosurg 1999;
64. Kelly D, Goodale D, Williams J, et al. Propofol in the treat- 91:185±191
ment of moderate and severe head injury: a randomized, 82. Clifton GL, Miller ER, Choi SC, et al. Lack of effect of induc-
prospective double-blinded pilot trial. J Neurosurg tion of hypothermia after acute brain injury. N Engl J Med
1999;90:1042±1051 2001;344:556±563