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Evaluation and management of elevated intracranial pressure in adults Authors
Edward R Smith, MD
Sepideh Amin-Hanjani, MD
Section Editor
Michael J Aminoff, MD, DSc
Deputy Editor
Janet L Wilterdink, MD
Disclosures
All topics are updated as new evidence becomes available and our peer review process is
complete.
Literature review current through: Feb 2012. | This topic last updated: Feb 29, 2012.
INTRODUCTION — Elevated intracranial pressure (ICP) is a potentially devastating
complication of neurologic injury. Elevated ICP may complicate trauma, central nervous
system (CNS) tumors, hydrocephalus, hepatic encephalopathy, and impaired CNS venous
outflow (table 1) [1]. Successful management of patients with elevated ICP requires prompt
recognition, the judicious use of invasive monitoring, and therapy directed at both reducing
ICP and reversing its underlying cause.
The evaluation and management of adult patients with elevated ICP will be reviewed here.
Elevated intracranial pressure in children and specific causes and complications of elevated
ICP (eg, ischemic stroke, intracerebral hemorrhage, traumatic brain injury) are discussed
separately. (See "Elevated intracranial pressure in children" and "Management of acute
severe traumatic brain injury", section on 'Intracranial pressure' and "Initial assessment and
management of acute stroke" and "Spontaneous intracerebral hemorrhage: Prognosis and
treatment", section on 'Intracranial pressure control' and "Treatment of aneurysmal
subarachnoid hemorrhage", section on 'Management of complications'.)
PHYSIOLOGY — Intracranial pressure is normally ≤15 mmHg in adults, and pathologic
intracranial hypertension (ICH) is present at pressures ≥20 mmHg. ICP is normally lower in
children than adults, and may be subatmospheric in newborns [2]. Homeostatic
mechanisms stabilize ICP, with occasional transient elevations associated with physiologic
events, including sneezing, coughing, or Valsalva maneuvers.
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Intracranial components — In adults, the intracranial compartment is protected by the
skull, a rigid structure with a fixed internal volume of 1400 to 1700 mL. Under physiologic
conditions, the intracranial contents include (by volume) [3]:
Brain parenchyma — 80 percent
Cerebrospinal fluid — 10 percent
Blood — 10 percent
Pathologic structures, including mass lesions, abscesses, and hematomas also may be
present within the intracranial compartment. Since the overall volume of the cranial vault
cannot change, an increase in the volume of one component, or the presence of pathologic
components, necessitates the displacement of other structures, an increase in ICP, or both.
Thus, ICP is a function of the volume and compliance of each component of the intracranial
compartment, an interrelationship known as the Monro-Kellie doctrine [4,5].
The volume of brain parenchyma is relatively constant in adults, although it can be altered
by mass lesions or in the setting of cerebral edema (figure 1). The volumes of CSF and
blood in the intracranial space vary to a greater degree. Abnormal increases in the volume
of any component may lead to elevations in ICP.
CSF is produced by the choroid plexus and elsewhere in the central nervous system (CNS)
at a rate of approximately 20 mL/h (500 mL/day) [6]. CSF is normally resorbed via the
arachnoid granulations into the venous system. Problems with CSF regulation generally
result from impaired outflow caused by ventricular obstruction or venous congestion; the
latter can occur in patients with sagittal (or other) venous sinus thrombosis. Much less
frequently, CSF production can become pathologically increased; this may be seen in the
setting of choroid plexus papilloma. (See "Cerebrospinal fluid: Physiology and utility of an
examination in disease states".)
Cerebral blood flow (CBF) determines the volume of blood in the intracranial space. CBF
increases with hypercapnia and hypoxia. Other determinants of CBF are discussed below.
Autoregulation of CBF may be impaired in the setting of neurologic injury, and may result in
rapid and severe brain swelling, especially in children [7-9].
In summary, the major causes of increased intracranial pressure include:
Intracranial mass lesions (eg, tumor, hematoma)
Cerebral edema (such as in acute hypoxic ischemic encephalopathy, large cerebral
infarction, severe traumatic brain injury)
Increased cerebrospinal fluid (CSF) production, eg, choroid plexus papilloma
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Decreased CSF absorption, eg, arachnoid granulation adhesions after bacterial
meningitis
Obstructive hydrocephalus
Obstruction of venous outflow, eg, venous sinus thrombosis, jugular vein
compression, neck surgery
Idiopathic intracranial hypertension (pseudotumor cerebri)
Intracranial compliance — The interrelationship between changes in the volume of
intracranial contents and changes in ICP defines the compliance characteristics of the
intracranial compartment. Intracranial compliance can be modeled mathematically (as in
other physiologic and mechanical systems) as the change in volume over the change in
pressure (dV/dP).
The compliance relationship is nonlinear, and compliance decreases as the combined volume
of the intracranial contents increases. Initially, compensatory mechanisms allow volume to
increase with minimal elevation in ICP. These mechanisms include:
Displacement of CSF into the thecal sac
Decrease in the volume of the cerebral venous blood via venoconstriction and
extracranial drainage
However, when these compensatory mechanisms have been exhausted, significant
increases in pressure develop with small increases in volume, leading to abnormally
elevated ICP (figure 2).
Thus, the magnitude of the change in volume of an individual structure determines its effect
on ICP. In addition, the rate of change in the volume of the intracranial contents influences
ICP. Changes that occur slowly produce less of an effect than those that are rapid. This can
be recognized clinically in some patients who present with large meningiomas and minimally
elevated or normal ICP. Conversely, other patients may experience symptomatic elevations
in ICP from small hematomas that develop acutely.
Cerebral blood flow — Following a significant increase in ICP, brain injury can result from
brainstem compression and/or a reduction in cerebral blood flow (CBF). CBF is a function of
the pressure drop across the cerebral circulation divided by the cerebrovascular resistance,
as predicted by Ohm's law [10]:
CBF = (CAP - JVP) ÷ CVR
where CAP is carotid arterial pressure, JVP is jugular venous pressure, and CVR is
cerebrovascular resistance.
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Cerebral perfusion pressure (CPP) is a clinical surrogate for the adequacy of cerebral
perfusion. CPP is defined as mean arterial pressure (MAP) minus ICP.
CPP = MAP - ICP
Autoregulation — CBF is normally maintained at a relatively constant level by
cerebrovascular autoregulation of CVR over a wide range of CPP (50 to 100 mmHg) (figure
3) [11,12]. However, autoregulation of CVR can become dysfunctional in certain pathologic
states, most notably stroke or trauma. In this setting, the brain becomes exquisitely
sensitive to even minor changes in CPP [11-13].
Another important consideration is that the set-point of autoregulation is also changed in
patients with chronic hypertension. With mild to moderate elevations in blood pressure, the
initial response is arterial and arteriolar vasoconstriction. This autoregulatory process both
maintains tissue perfusion at a relatively constant level and prevents the increase in
pressure from being transmitted to the smaller, more distal vessels [11]. As a result, acute
reductions in blood pressure, even if the final value remains within the normal range, can
produce ischemic symptoms in patients with chronic hypertension (figure 3) [11].
Cerebral perfusion pressure — Conditions associated with elevated ICP, including mass
lesions and hydrocephalus, can be associated with a reduction in CPP. This can result in
devastating focal or global ischemia. On the other hand, excessive elevation of CPP can lead
to hypertensive encephalopathy and cerebral edema due to the eventual breakdown of
autoregulation, particularly if the CPP is >120 mmHg [11,14,15]. A higher level of CPP is
tolerated in patients with chronic hypertension because the autoregulatory curve has shifted
to the right (figure 3) [11,15]. (See "Malignant hypertension and hypertensive
encephalopathy in adults", section on 'Mechanisms of vascular injury'.)
Ultimately, global or local reductions in CBF are responsible for the clinical manifestations of
elevated ICP. These manifestations can be further divided into generalized responses to
elevated ICP and herniation syndromes.
CLINICAL MANIFESTATIONS — Global symptoms of elevated ICP include headache,
which is probably mediated via the pain fibers of cranial nerve (CN) V in the dura and blood
vessels, depressed global consciousness due to either the local effect of mass lesions or
pressure on the midbrain reticular formation, and vomiting.
Signs include CN VI palsies, papilledema secondary to impaired axonal transport and
congestion (picture 1), spontaneous periorbital bruising [16] and a triad of bradycardia,
respiratory depression, and hypertension (Cushing's triad, sometimes called Cushing's reflex
or Cushing's response) [3]. While the mechanism of Cushing's triad remains controversial,
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many believe that it relates to brainstem compression. The presence of this response is an
ominous finding that requires urgent intervention.
Focal symptoms of elevated ICP may be caused by local effects in patients with mass
lesions or by herniation syndromes. Herniation results when pressure gradients develop
between two regions of the cranial vault. The most common anatomical locations affected
by herniation syndromes include subfalcine, central transtentorial, uncal transtentorial,
upward cerebellar, cerebellar tonsillar/foramen magnum, and transcalvarial (figure 4)
[3,17]. (See "Stupor and coma in adults", section on 'Neurologic examination' and "Stupor
and coma in adults", section on 'Coma syndromes'.)
One notable false localizing syndrome seen following neurologic injury, referred to as
Kernohan's notch phenomenon, consists of the combination of contralateral pupillary
dilatation and ipsilateral weakness [18,19]. Because the diagnostic accuracy of signs and
symptoms is limited, the findings described above may be inconstant or unreliable in any
given case. Use of radiologic studies may support the diagnosis; however, the most reliable
method of diagnosing elevated ICP is to measure it directly.
ICP MONITORING — Empiric therapy for presumed elevated ICP is unsatisfactory because
CPP cannot be monitored reliably without measurement of ICP. Furthermore, most therapies
directed at lowering ICP are effective for limited and variable periods of time. In addition,
these treatments may have serious side effects. Therefore, while initial steps to control ICP
may, by necessity, be performed without the benefit of ICP monitoring, an important early
goal in management of the patient with presumed elevated ICP is placement of an ICP
monitoring device.
The purpose of monitoring ICP is to improve the clinician's ability to maintain adequate CPP
and oxygenation. The only way to reliably determine CPP (defined as the difference between
MAP and ICP) is to continuously monitor both ICP and blood pressure (BP). In general,
these patients are managed in intensive care units (ICUs) with an ICP monitor and arterial
line. The combination of ICP monitoring and concomitant management of CPP may improve
patient outcomes, particularly in patients with closed head trauma [20-23]. The specific
therapeutic targets for CPP in patients with traumatic brain injury are discussed separately.
(See "Management of acute severe traumatic brain injury", section on 'Cerebral perfusion
pressure'.)
Indications — The diagnosis of elevated ICP generally is based on clinical findings, and
corroborated by imaging studies and the patient's medical history. Closed head injury is one
of the most frequent and best-studied indications for ICP monitoring. Much of the current
practice of ICP monitoring has been derived from clinical experience with closed head
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trauma patients [24]. Indications for ICP monitoring in this indication is discussed in detail
separately. (See "Management of acute severe traumatic brain injury", section on
'Intracranial pressure'.)
Role of computed tomography — Although CT scans may suggest elevated ICP based on
the presence of mass lesions, midline shift, or effacement of the basilar cisterns (picture 2),
patients without these findings on initial CT may have elevated ICP. This was demonstrated
in a prospective study of 753 patients treated at four major head injury research centers in
the United States, which found patients whose initial CT scan did not show a mass lesion,
midline shift, or abnormal cisterns had a 10 to 15 percent chance of developing elevated
ICP during their hospitalization [25].
Other studies have shown that up to one-third of patients with initially normal scans
developed CT scan abnormalities within the first few days after closed head injury [26,27].
Together, these findings demonstrate that ICP can be elevated even in the setting of a
normal initial CT, demonstrating the importance of invasive monitoring in high-risk patients
and the role of follow-up imaging in patients who develop clinical evidence of increased ICP
during hospitalization.
Since ICP monitoring is associated with a small risk of serious complications, including CNS
infection and intracranial hemorrhage, it is reasonable to try to limit its use to patients most
at risk of elevated ICP [28]. In general, invasive monitoring of ICP is indicated in patients
who are [29]:
Suspected to be at risk for elevated ICP
Comatose (Glasgow Coma Scale <8) (table 2)
Diagnosed with a process that merits aggressive medical care
Types of monitors — There are four main anatomical sites used in the clinical
measurement of ICP: intraventricular, intraparenchymal, subarachnoid, and epidural (figure
5) [30]. Noninvasive and metabolic monitoring of ICP has also been studied, but the clinical
value of these methods is unclear at present. Each technique requires a unique monitoring
system, and has associated advantages and disadvantages.
Intraventricular — Intraventricular monitors are considered the "gold standard" of ICP
monitoring catheters. They are surgically placed into the ventricular system and affixed to a
drainage bag and pressure transducer with a three-way stopcock. Intraventricular
monitoring has the advantage of accuracy, simplicity of measurement, and the unique
characteristic of allowing for treatment of some causes of elevated ICP via drainage of CSF.
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The primary disadvantage is infection, which may occur in up to 20 percent of patients. This
risk increases the longer a device is in place [31,32]. Prophylactic catheter changes did not
appear to reduce the risk of infection [32]. (See "Infections of central nervous system
shunts and other devices".)
A further disadvantage of intraventricular systems includes a small (approximately 2
percent) risk of hemorrhage during placement; this risk is greater in coagulopathic patients.
In addition, it may be technically difficult to place an intraventricular drain into a small
ventricle, particularly in the setting of trauma and cerebral edema complicated by
ventricular compression [33].
Intraparenchymal — Intraparenchymal devices consist of a thin cable with an electronic
or fiberoptic transducer at the tip. The most widely used device is the fiberoptic Camino
system. These monitors can be inserted directly into the brain parenchyma via a small hole
drilled in the skull. Advantages include ease of placement, and a lower risk of infection and
hemorrhage (<1 percent) than with intraventricular devices [34-36].
Disadvantages include the inability to drain CSF for diagnostic or therapeutic purposes and
the potential to lose accuracy (or "drift") over several days, since the transducer cannot be
recalibrated following initial placement [30]. In addition, there is a greater risk of
mechanical failure due to the complex design of these monitors. The reliability of
intraparenchymal devices has been debated. One group found only a small (1 mmHg) drift
in a group of 163 patients [37]; however, a second report found that readings varied by >3
mmHg in more than half of the 50 patients studied [38].
Subarachnoid — Subarachnoid bolts are fluid-coupled systems within a hollow screw that
can be placed through the skull adjacent to the dura. The dura is then punctured, which
allows the CSF to communicate with the fluid column and transducer. The most commonly
used subarachnoid monitor is the Richmond (or Becker) bolt; other types include the Philly
bolt, the Leeds screw, and the Landy screw. These devices have low risk of infection and
hemorrhage, but often clog with debris and are unreliable; therefore, they are rarely used.
Additionally, they are believed to be less accurate than ventricular ICP devices [30].
Epidural — Epidural monitors contain optical transducers that rest against the dura after
passing through the skull. They often are inaccurate, as the dura damps the pressure
transmitted to the epidural space, and thus are of limited clinical utility [30,39]. They are
used in the management of coagulopathic patients with hepatic encephalopathy complicated
by cerebral edema. In this setting, use of these catheters is associated with a significantly
lower risk of intracerebral hemorrhage (4 versus 20 and 22 percent for intraparenchymal
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and intraventricular devices) and fatal hemorrhage (1 versus 5 and 4 percent, respectively)
[40]. (See "Acute liver failure: Prognosis and management".)
Waveform analysis — ICP is not a static value; it exhibits cyclic variation based on the
superimposed effects of cardiac contraction, respiration, and intracranial compliance. Under
normal physiologic conditions, the amplitude of the waveform is often small, with B waves
related to respiration and smaller C waves (or Traube-Hering-Mayer waves) related to the
cardiac cycle [10].
Pathological A waves (also called plateau waves) are abrupt, marked elevations in ICP of 50
to 100 mmHg, which usually last for minutes to hours (figure 6). The presence of A waves
signifies a loss of intracranial compliance, and heralds imminent decompensation of
autoregulatory mechanisms [10,41,42]. Thus, the presence of A waves should suggest the
need for urgent intervention to help control ICP.
Noninvasive systems — A number of devices designed to record ICP noninvasively have
been studied, but most have not demonstrated reproducible clinical success or have been
studied in large clinical trials. We do not use these in clinical practice.
Tissue resonance analysis (TRA), an ultrasound-based method, has shown some
promise. In one trial 40 patients underwent both invasive and TRA ICP monitoring,
with good correlation between concomitant invasive and TRA measurements [43].
Ocular sonography can provide a noninvasive measure of optic nerve sheath
diameter, which has been found to correlate with intracranial pressure. A number of
studies have found that diameters of 5 to 6 mm have the ability to discriminate
between normal and elevated ICP in patients with intracranial hemorrhage and
traumatic brain injury [44-50].
Transcranial Doppler (TCD) measures the velocity of blood flow in the proximal
cerebral circulation. TCD can be used to estimate ICP based on characteristic
changes in waveforms that occur in response to increased resistance to cerebral
blood flow [51,52]. Generally, TCD is a poor predictor of ICP, although in trauma
patients TCD findings may correlate with outcome at six months [53-55].
Intraocular pressure can be assessed noninvasively using an ultrasonic handheld
optic tonometer. While some evidence suggests that intraocular pressure correlates
with ICP in the absence of oculofacial trauma or glaucoma [56], most other studies'
findings disagree [57-59].
Tympanic membrane displacement (measured using an impedance audiometer) has
been compared to direct monitoring, based on the hypothesis that increased ICP will
transmit a pressure wave to the tympanic membrane via the perilymph [60,61].
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Advanced neuromonitoring — In order to supplement ICP monitoring, several
technologies have recently been developed for the treatment of severe TBI. These
techniques allow for the measurement of cerebral physiologic and metabolic parameters
related to oxygen delivery, cerebral blood flow, and metabolism with the goal of improving
the detection and management of secondary brain injury. These are discussed separately.
(See "Management of acute severe traumatic brain injury", section on 'Advanced
neuromonitoring'.)
Other
GENERAL MANAGEMENT — The best therapy for intracranial hypertension (ICH) is
resolution of the proximate cause of elevated ICP. Examples include: evacuation of a blood
clot, resection of a tumor, CSF diversion in the setting of hydrocephalus, or treatment of an
underlying metabolic disorder.
Regardless of the cause, ICH is a medical emergency, and treatment should be undertaken
as expeditiously as possible. In addition to definitive therapy, there are maneuvers that can
be employed to reduce ICP acutely. Some of these techniques are generally applicable to all
patients with suspected ICH; others (particularly glucocorticoids) are reserved for specific
causes of ICH.
Resuscitation — The urgent assessment and support of oxygenation, blood pressure, and
end-organ perfusion are particularly important in trauma, but applicable to all patients [62-
64]. If elevated ICP is suspected, care should be taken to minimize further elevations in ICP
during intubation through careful positioning, appropriate choice of paralytic agents (if
required), and adequate sedation. Pretreatment with lidocaine has been suggested as a
useful intervention to decrease the rise in ICP associated with intubation; however, good
clinical evidence supporting this approach is limited [65]. (See "Overview of inpatient
management in trauma patients" and "Advanced cardiac life support (ACLS) in adults" and
"Basic life support (BLS) in adults".)
Large shifts in blood pressure should be minimized, with particular care taken to avoid
hypotension. Although it might seem that lower BP would result in lower ICP, this is not the
case. Hypotension, especially in conjunction with hypoxemia, can induce reactive
vasodilation and elevations in ICP. As noted above, pressors have been shown to be safe for
use in most patients with intracranial hypertension, and may be required to maintain CPP
>60 mmHg [20]. (See "Use of vasopressors and inotropes".)
Urgent situations — Life-saving measures may need to be instituted prior to a more
detailed workup (eg, imaging or ICP monitoring) in a patient who presents acutely with
history or examination findings suggestive of elevated ICP. Many of these situations will rely
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upon clinical judgment, but the following combination of findings suggests the need for
urgent intervention [66,67]:
A history that suggests elevated ICP (eg, head trauma, sudden severe headache
typical of subarachnoid hemorrhage)
An examination that suggests elevated ICP (unilateral or bilaterally fixed and dilated
pupil(s), decorticate or decerebrate posturing, bradycardia, hypertension and/or
respiratory depression)
A Glasgow coma scale (GCS) ≤8
Potentially confounding, reversible causes of depressed mental status, hypotension
(SBP <60 mmHg in adults), hypoxemia (PaO2 <60 mmHg), hypothermia (<36ºC),
or obvious intoxication are absent
In such patients osmotic diuretics may be used urgently (see 'Mannitol' below).
In addition, standard resuscitation techniques should be instituted as soon as possible:
Head elevation
Hyperventilation to a PCO2 of 26 to 30 mmHg
Intravenous mannitol (1 to 1.5 g/kg)
Concomitant with these measures should be aggressive evaluation of the underlying
diagnosis, including neuroimaging, detailed neurologic examination, and history gathering.
Hyperventilation may be contraindicated in the setting of traumatic brain injury and acute
stroke, and is discussed separately (see 'Hyperventilation' below). If appropriate,
ventriculostomy is a rapid means of simultaneously diagnosing and treating elevated ICP.
Monitoring and the decision to treat — If a diagnosis of elevated ICP is suspected and
an immediately treatable proximate cause is not present, then ICP monitoring should be
instituted. The use of ICP monitoring is associated with decreased mortality in patients with
traumatic brain injury [21]. (See "Management of acute severe traumatic brain injury",
section on 'Intracranial pressure'.)
The type of monitoring device employed should be based on an assessment of the
advantages and disadvantages discussed previously (figure 5). (See 'ICP
monitoring' above.)
The goal of ICP monitoring and treatment should be to keep ICP <20 mmHg [68].
Interventions should be utilized only when ICP is elevated above 20 mmHg for >5 to 10
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minutes. As discussed above, brief physiologic elevations in ICP may occur in the setting of
coughing, movement, suctioning, or ventilator asynchrony.
Fluid management — In general, patients with elevated ICP do not need to be severely
fluid restricted [69]. Patients should be kept euvolemic and normo- to hyperosmolar. This
can be achieved by avoiding all free water (including D5W, 0.45 percent (half normal)
saline, and enteral free water) and employing only isotonic fluids (such as 0.9 percent
(normal) saline). Serum osmolality should be kept >280 mOsm/L, and often is kept in the
295 to 305 mOsm/L range. Hyponatremia is common in the setting of elevated ICP,
particularly in conjunction with subarachnoid hemorrhage. (See "Causes of
hyponatremia" and "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic
hormone secretion (SIADH) and reset osmostat", section on 'Subarachnoid hemorrhage'.)
Similarly, the value of colloid compared to crystalloid fluid resuscitation in patients with
elevated ICP has been studied, but findings have been inconclusive with respect to the
superior approach [70]. A subgroup analysis in one large study, however, suggested that in
patients with traumatic brain injury, fluid resuscitation with albumin was associated with a
higher mortality as compared with normal saline [71]. (See "Management of acute severe
traumatic brain injury".)
Hypertonic saline in bolus doses may acutely lower ICP, but further investigations are
required to define a role, if any, for this approach in the management of elevated
intracranial pressure. (See 'Hypertonic saline bolus' below.)
Sedation — Keeping patients appropriately sedated can decrease ICP by reducing
metabolic demand, ventilator asynchrony, venous congestion, and the sympathetic
responses of hypertension and tachycardia [72]. Establishing a secure airway and close
attention to blood pressure allow the clinician to identify and treat apnea and hypotension
quickly.
Propofol has been utilized to good effect in this setting, as it is easily titrated and has a
short half-life, thus permitting frequent neurologic reassessment. (See "Sedative-analgesic
medications in critically ill patients: Selection, initiation, maintenance, and withdrawal".)
Blood pressure control — In general, BP should be sufficient to maintain CPP >60 mmHg.
As discussed above, pressors can be used safely without further increasing ICP. This is
particularly relevant in the setting of sedation, when iatrogenic hypotension can occur.
Hypertension should generally only be treated when CPP >120 mmHg and ICP >20 mmHg.
Caution should be taken to avoid CPP <50 mmHg or, as noted above, normalization of blood
pressure in patients with chronic hypertension in whom the autoregulatory curve has shifted
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to the right (see 'Autoregulation' above). General issues regarding blood pressure
management following stroke are presented elsewhere. (See "Treatment of hypertension in
patients who have had a stroke".)
Position — Patients with elevated ICP should be positioned to maximize venous outflow
from the head. Important maneuvers include reducing excessive flexion or rotation of the
neck, avoiding restrictive neck taping, and minimizing stimuli that could induce Valsalva
responses, such as endotracheal suctioning.
Patients with elevated ICP have historically been positioned with the head elevated above
the heart (usually 30 degrees) to increase venous outflow. It should be noted that head
elevation may lower CPP [20,73]; however, given the proven efficacy of head elevation in
lowering ICP, most experts recommend raising the patient's head as long as the CPP
remains at an appropriate level [74].
Fever — Elevated metabolic demand in the brain results in increased cerebral blood flow
(CBF), and can elevate ICP by increasing the volume of blood in the cranial vault.
Conversely, decreasing metabolic demand can lower ICP by reducing blood flow.
Fever increases brain metabolism, and has been demonstrated to increase brain injury in
animal models [75]. Therefore, aggressive treatment of fever, including acetaminophen and
mechanical cooling, is recommended in patients with increased ICP. Intracranial
hypertension is a recognized indication for neuromuscular paralysis in selected patients
[76]. (See "Use of neuromuscular blocking medications in critically ill patients".)
Antiepileptic therapy — Seizures can both complicate and contribute to elevated ICP
[77,78]. Anticonvulsant therapy should be instituted if seizures are suspected; prophylactic
treatment may be warranted in some cases. There are no clear guidelines for the latter, but
examples include high-risk mass lesions, such as those within supratentorial cortical
locations, or lesions adjacent to the cortex, such as subdural hematomas or subarachnoid
hemorrhage.
SPECIFIC THERAPIES — As mentioned previously, the best treatment of elevated ICP is
to address its underlying cause. If this is not possible, a series of steps should be instituted
to reduce ICP in an attempt to improve outcome. In all cases, the clinician should bear in
mind the themes of resuscitation, reduction of intracranial volume, and frequent
reevaluation discussed above.
Mannitol — Osmotic diuretics reduce brain volume by drawing free water out of the tissue
and into the circulation, where it is excreted by the kidneys, thus dehydrating brain
parenchyma [79-82]. The most commonly used agent is mannitol. It is prepared as a 20
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percent solution, and given as a bolus of 1 g/kg. Repeat dosing can be given at 0.25 to 0.5
g/kg as needed, generally every six to eight hours. Use of any osmotic agent should be
carefully evaluated in patients with renal insufficiency.
The effects are usually present within minutes, peak at about one hour, and last 4 to 24
hours [29,83]. Some have reported a "rebound" increase in ICP; this probably occurs when
mannitol, after repeated use, enters the brain though a damaged blood-brain barrier and
reverses the osmotic gradient [84,85]. Useful parameters to monitor in the setting of
mannitol therapy include serum sodium, serum osmolality, and renal function.
Concerning findings associated with the use of mannitol include serum sodium >150 meq,
serum osmolality >320 mOsm, or evidence of evolving acute tubular necrosis (ATN). In
addition, mannitol can lower systemic BP, necessitating careful use if associated with a fall
in CPP. Patients with known renal disease may be poor candidates for osmotic diuresis. (See
"Complications of mannitol therapy".)
Other diuretics — Furosemide, 0.5 to 1.0 mg/kg intravenously, may be given with
mannitol to potentiate its effect. However, this effect can also exacerbate dehydration and
hypokalemia [86-88].
Glycerol and urea were used historically to control ICP via osmoregulation; however, use of
these agents has decreased because equilibration between brain and plasma levels occurs
more quickly than with mannitol. Furthermore, glycerol has been shown to have a
significant rebound effect and to be less effective in ICP control [89,90].
Hypertonic saline bolus — Hypertonic saline in bolus doses may acutely lower ICP;
however, the effect of this early intervention on long-term clinical outcomes remains unclear
[91-98]. The volume and tonicity of saline (7.2 to 23.4 percent) used in these reports have
varied widely. As an example, one controlled trial randomly assigned 226 patients with
traumatic brain injury to prehospital resuscitation with 250 mL hypertonic saline (7.5
percent) or the same volume of Ringer's lactate [91]. Survival until hospital discharge, six-
month survival, and neurologic function six months after injury were similar in both groups.
Mannitol and hypertonic saline have been compared in at least five randomized trials of
patients with elevated ICP from a variety of causes (traumatic brain injury, stroke, tumors)
[98-102]. A meta-analysis of these trials found that hypertonic saline appeared to have
greater efficacy in managing elevated ICP, but clinical outcomes were not examined [103].
Further clinical trials are required to clarify the appropriate role of hypertonic saline infusion
versus mannitol in the management of elevated ICP [104]. (See "Management of acute
severe traumatic brain injury", section on 'Osmotic therapy'.)
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Glucocorticoids — Glucocorticoids were associated with a worse outcome in a large
randomized clinical trial of their use in moderate to severe head injury [105,106]. They
should not be used in this setting. (See "Management of acute severe traumatic brain
injury".)
In addition, glucocorticoids are not considered to be useful in the management of cerebral
infarction or intracranial hemorrhage. (See "Spontaneous intracerebral hemorrhage:
Prognosis and treatment".)
In contrast, glucocorticoids may have a role in the setting of intracranial hypertension
caused by brain tumors and CNS infections. (See "Management of vasogenic edema in
patients with primary and metastatic brain tumors" and "Treatment and prognosis of brain
abscess" and "Dexamethasone to prevent neurologic complications of bacterial meningitis in
adults".)
Hyperventilation — Use of mechanical ventilation to lower PaCO2 to 26 to 30 mmHg has
been shown to rapidly reduce ICP through vasoconstriction and a decrease in the volume of
intracranial blood; a 1 mmHg change in PaCO2 is associated with a 3 percent change in CBF
[107]. Hyperventilation also results in respiratory alkalosis, which may buffer post-injury
acidosis [107]. The effect of hyperventilation on ICP is short-lived (1 to 24 hours) [108-
110]. Following therapeutic hyperventilation, the patient's respiratory rate should be
tapered back to normal over several hours to avoid a rebound effect [111].
Therapeutic hyperventilation should be considered as an urgent intervention when elevated
ICP complicates cerebral edema, intracranial hemorrhage, and tumor. Hyperventilation
should not be used on a chronic basis, regardless of the cause of increased ICP.
Hyperventilation should be minimized in patients with traumatic brain injury or acute stroke.
In these settings, vasoconstriction may cause a critical decrease in local cerebral perfusion
and worsen neurologic injury, particularly in the first 24 to 48 hours [24,108,110,112-115].
Thus, the need for hyperventilation should be carefully considered, and prophylactic
hyperventilation in the absence of elevated ICP should be avoided. (See "Management of
acute severe traumatic brain injury", section on 'Hyperventilation'.)
Barbiturates — The use of barbiturates is predicated on their ability to reduce brain
metabolism and cerebral blood flow, thus lowering ICP and exerting a neuroprotective effect
[116-119]. Pentobarbital is generally used, with a loading dose of 5 to 20 mg/kg as a bolus,
followed by 1 to 4 mg/kg per hr [120,121]. Treatment should be assessed based on ICP,
CPP, and the presence of unacceptable side effects. Continuous EEG monitoring is generally
used; EEG burst suppression is an indication of maximal dosing.
Page 15
The therapeutic value of this maneuver is somewhat unclear. In a randomized trial of 73
patients with elevations in ICP refractory to standard therapy, patients treated with
pentobarbital were 50 percent more likely to have their ICP controlled. However, there was
no difference in clinical outcomes between groups [122]. In general, the use of barbiturates
is a "last-ditch" effort, as several studies show that their ability to lower ICP does not
appear to affect outcomes [107,123].
Barbiturate therapy can be complicated by hypotension, possibly requiring vasopressor
support. The use of barbiturates is also associated with a loss of the neurologic examination,
requiring accurate ICP, hemodynamic, and often EEG monitoring to guide therapy.
Therapeutic hypothermia — First reported as a treatment for brain injury in the 1950s,
induced or therapeutic hypothermia has remained a controversial issue in the debate
concerning the management of elevated ICP [107,124,125]. It is not currently
recommended as a standard treatment for increased intracranial pressure in any clinical
setting.
Hypothermia decreases cerebral metabolism and may reduce CBF and ICP. Initial studies of
hypothermia were limited by systemic side effects, including cardiac arrhythmias and severe
coagulopathy. However, later work suggested that hypothermia can lower ICP and may
improve patient outcomes [126]. Hypothermia also appeared to be effective in lowering ICP
after other therapies have failed [127,128].
Hypothermia can be achieved using whole body cooling, including lavage and cooling
blankets, to a goal core temperature of 32 to 34ºC. The best method of cooling (local versus
systemic), the optimal target core temperature, and the appropriate duration of treatment
are not known [129]. It appears that rewarming should be accomplished over a period of
less than 24 hours [130].
The value of therapeutic hypothermia has been best assessed in patients after traumatic
brain injury (TBI), but it’s role has not been well established in that setting. (See
"Management of acute severe traumatic brain injury", section on 'Induced hypothermia' and
"Elevated intracranial pressure in children", section on 'Hypothermia'.)
Given the uncertainties surrounding the appropriate use of therapeutic hypothermia in
patients with elevated ICP, this treatment should be limited to clinical trials, or to patients
with intracranial hypertension refractory to other therapies.
Removal of CSF — When hydrocephalus is identified, a ventriculostomy should be inserted
(figure 7). Rapid aspiration of CSF should be avoided because it may lead to obstruction of
the catheter opening by brain tissue. Also, in patients with aneurysmal subarachnoid
Page 16
hemorrhage, abrupt lowering of the pressure differential across the aneurysm dome can
precipitate recurrent hemorrhage.
CSF should be removed at a rate of approximately 1 to 2 mL/minute, for two to three
minutes at a time, with intervals of two to three minutes in between until a satisfactory ICP
has been achieved (ICP <20 mmHg) or until CSF is no longer easily obtained. Slow removal
can also be accomplished by passive gravitational drainage through the ventriculostomy. A
lumbar drain is generally contraindicated in the setting of high ICP due to the risk of
transtentorial herniation.
Decompressive craniectomy — Decompressive craniectomy removes the rigid confines of
the bony skull, increasing the potential volume of the intracranial contents and
circumventing the Monroe-Kellie doctrine. There is a growing body of literature supporting
the efficacy of decompressive craniectomy in certain clinical situations [131-140].
Importantly, it has been demonstrated that in patients with elevated ICP, craniectomy alone
lowered ICP 15 percent, but opening the dura in addition to the bony skull resulted in an
average decrease in ICP of 70 percent [141]. Decompressive craniectomy also appears to
improve brain tissue oxygenation [142].
Observational data suggest that rapid and sustained control of ICP, including the use of
decompressive craniectomy, improves outcomes in trauma, stroke, and subarachnoid
hemorrhage in carefully selected cases [143-150]. The indications for decompressive
craniectomy in these settings are discussed separately. (See "Decompressive
hemicraniectomy for malignant middle cerebral artery territory infarction" and "Management
of acute severe traumatic brain injury", section on 'Decompressive craniectomy'.) Obvious
mass lesions associated with an elevated ICP should be removed, if possible.
Potential complications of surgery include herniation through the skull defect, spinal fluid
leak, wound infection, and epidural and subdural hematoma [151].
Paradoxical transtentorial herniation is an uncommon but potentially lethal complication in
patients with hemicraniectomy and a large skull defect who subsequently undergo lumbar
puncture (LP) or CSF drainage [152,153]. This results from the combined effects of
atmospheric pressure with the negative pressure of the LP or ventriculostomy. It has also
been described as a delayed complication three to five months after decompressive
craniectomy for cerebral infarction in the absence of LP or ventriculostomy [154]. Marked
decompression of the skin and dura over the skull defect accompany and may precede
neurologic signs of herniation. Standard treatments to lower ICP can hasten herniation.
Instead, the patient should be placed supine or in the Trendelenburg position, CSF drains
Page 17
should be clamped, crystalloid fluid should be administered intravenously, and an epidural
blood patch placed for patients with dural leak.
SUMMARY — The best therapy for intracranial hypertension is resolution of the proximate
cause of elevated ICP. Regardless of the cause, treatment should be undertaken as
expeditiously as possible, and should be based on the principles of resuscitation, reduction
of the volume of the intracranial contents, and reassessment. The role of evidence-based
guidelines in the clinical management of elevated ICP is evolving [155]. However, it is
important to remember that individual patients respond differently to different therapies;
therefore, interventions should be based on careful assessment of the individual clinical
scenario rather than on strict protocols.
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Topic 1659 Version 8.0
Page 26
Causes of intracranial hypertension
Intracranial hemorrhage
Tramatic brain injury
Ruptured aneurysm
Arteriovenous malformation
Other vascular anomalies
Central nervous system infections
Neoplasm
Vasculitis
Ischemic infarcts
Hydrocephalus
Idiopathic intracranial hypertension (pseudotumor cerebri)
Idiopathic
Page 27
Intracranial compensation for an expanding mass lesion
Page 29
Data from Pathophysiology and management of the intracranial vault. In: Textbook of Pediatric Intensive Care, 3rd ed, Rogers, MC (Ed), Williams and Wilkins 1996. p. 646; figure 18.1.
Page 30
The relationship between intracranial volume and pressure is nonlinear
Page 32
An initial increase in volume results in a small increase in pressure because of intracranial
compensation (blue line). Once intracranial compensation is exhausted, additional increases
in intracranial volume result in a dramatic rise in intracranial pressure (red line).
Page 33
Cerebral autoregulation in hypertension
Page 35
Schematic representation of autoregulation of cerebral blood flow in normotensive and
hypertensive subjects. In both groups, initial increases or decreases in mean arterial
pressure are associated with maintenance of cerebral blood flow due to appropriate changes
in arteriolar resistance. More marked changes in pressure are eventually associated with
loss of autoregulation, leading to a reduction (with hypotension) or an elevation (with
marked hypertension) in cerebral blood flow. These changes occur at higher pressures in
patients with hypertension, presumably due to arteriolar thickening. Thus, aggressive
antihypertensive therapy will produce cerebral ischemia at a higher mean arterial pressure
in patients with underlying hypertension. Redrawn from Kaplan, NM, Lancet 1994; 344:1335.
Page 38
Papilledema, characterized by blurring of the optic disc margins, loss of physiologic cupping,
hyperemia, and fullness of the veins, in a 5-year-old girl with intracranial hypertension due
to vitamin A intoxication. Courtesy of Gerald Striph, MD.
Page 39
Transtentorial herniation
Page 41
Data from Pulm, F, Posner, JB. The Diagnosis of Stupor and Coma III. FA Davis, Philadelphia 1982. p. 103.
Page 42
Radiographic findings suggestive of elevated ICP
Page 44
Evidence of contusions with surrounding edema (top arrow), effacement of cisterns (middle
arrow), and effacement of sulci (lowest arrow).
Page 45
Glasgow coma scale
Eye opening
Spontaneous 4
Response to verbal command 3
Response to pain 2
No eye opening 1
Best verbal response
Oriented 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
No verbal response 1
Best motor response
Obeys commands 6
Localizing response to pain 5
Withdrawal response to pain 4
Flexion to pain 3
Extension to pain 2
No motor response 1
Page 46
The GCS is scored between 3 and 15, 3 being the worst, and 15 the best. It is composed of
three parameters: best eye response (E), best verbal response (V), and best motor
response (M). The components of the GCS should be recorded individually; for example,
E2V3M4 results in a GCS score of 9. A score of 13 or higher correlates with mild brain
injury; a score of 9 to 12 correlates with moderate injury; and a score of 8 or less
represents severe brain injury.
Page 47
Intracranial pressure monitors
Page 49
Ventriculostomy allows both ICP monitoring and therapeutic drainage of cerebrospinal fluid
(CSF). Subdural and intraparenchymal monitors cannot be used to drain CSF.
Page 52
Interpreting ICP waveforms: A waves. The most clinically significant ICP waveforms are A
waves, which may reach elevations of 50 to 100 mm Hg, persist for 5 to 20 minutes, then
drop sharply - signaling exhaustion of the brain's compliance mechanisms. A waves may
come and go, spiking from temporary rises in thoracic pressure or from any condition that
increases ICP beyond the brain's compliance limits. Activities, such as sustained coughing or
straining during defecation, can cause temporary elevations in thoracic pressure. Reproduced
with permission from: Nursing Procedures, 4th Ed. Lippincott Williams & Wilkins, 2004. Copyright © 2004 Lippincott Williams & Wilkins.
Page 53
External ventricular drain
Page 55
An external ventricular drain (EVD) is a small catheter inserted through the skull usually
into the lateral ventricle, which is typically connected to a closed collecting device to allow
for drainage of cerebrospinal fluid. The EVD can also be connected to a transducer that
records intracranial pressure.
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