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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

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jul 2021. | This topic last updated: Apr 26, 2019.

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 ICP 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 (ICP) in children: Clinical manifestations and diagnosis" and
"Management of acute moderate and severe traumatic brain injury", section on 'Intracranial
pressure management' and "Initial assessment and management of acute stroke" and
"Aneurysmal subarachnoid hemorrhage: Treatment and prognosis", section on 'Early
complications' and "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis",
section on 'Intracranial pressure management'.)

PHYSIOLOGY
ICP 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.

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 (CSF) – 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/hour (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 ICP include:

● Intracranial mass lesions (eg, tumor, hematoma)

● Cerebral edema (such as in acute hypoxic-ischemic encephalopathy, large cerebral


infarction, severe traumatic brain injury)

● Increased CSF production (eg, choroid plexus papilloma)

● 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 ICH (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 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.

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 (BP),
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
BP, 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 "Moderate to severe hypertensive retinopathy 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 triad, sometimes called Cushing reflex or
Cushing response) [3]. While the mechanism of Cushing triad remains controversial, 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 anatomic 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 cerebral perfusion
pressure (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 mean
arterial pressure [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 moderate and severe traumatic brain injury", section on 'Hemodynamic
management'.)

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 trauma patients
[24]. Indications for ICP monitoring in patients with traumatic brain injury are discussed in
detail separately. (See "Management of acute moderate and severe traumatic brain injury",
section on 'Intracranial pressure management'.)

Since ICP monitoring is associated with a small risk of serious complications, including central
nervous system (CNS) infection and intracranial hemorrhage, it is reasonable to try to limit its
use to patients most at risk of elevated ICP [25]. In general, invasive monitoring of ICP is
indicated in patients who are [26]:

● Suspected to be at risk for elevated ICP


● Comatose (Glasgow Coma Scale [GCS] <8) ( table 2)
● Diagnosed with a process that merits aggressive medical care

Although computed tomography (CT) scans may suggest elevated ICP based on the presence of
mass lesions, midline shift, or effacement of the basilar cisterns ( image 1), 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 [27].
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 [28,29]. 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.

Types of monitors — There are four main anatomic 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 cerebrospinal fluid (CSF).

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 cerebrospinal fluid 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 and
intraventricular devices, respectively) and fatal hemorrhage (1 versus 5 and 4 percent,
respectively) [40]. (See "Acute liver failure in adults: Management and prognosis".)

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 ( waveform 1). 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 not been
studied in large clinical trials. We do not use these in clinical practice.

● 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 (CBF) [43,44].
Generally, TCD is a poor predictor of ICP, although in trauma patients TCD findings may
correlate with outcome at six months [45-48].

● 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 [49].

● Ocular sonography can provide a noninvasive measure of optic nerve sheath diameter,
which has been found to correlate with ICP. 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 [50-56].

● 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 [57], most other studies' findings disagree
[58-60].

● 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 [61,62].

Advanced neuromonitoring — In order to supplement ICP monitoring, several technologies


have been developed for the treatment of severe traumatic brain injury. These techniques allow
for the measurement of cerebral physiologic and metabolic parameters related to oxygen
delivery, CBF, and metabolism with the goal of improving the detection and management of
secondary brain injury. These are discussed separately. (See "Management of acute moderate
and severe traumatic brain injury", section on 'Advanced neuromonitoring'.)

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, cerebrospinal
fluid (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 (BP), and
end-organ perfusion are particularly important in trauma, but applicable to all patients [63-65].
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 [66]. (See "Overview of inpatient management of the adult trauma
patient" and "Advanced cardiac life support (ACLS) in adults" and "Adult basic life support (BLS)
for health care providers".)

Large shifts in BP 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 ICH, and may be required to maintain cerebral perfusion pressure (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 upon clinical
judgment, but the following combination of findings suggests the need for urgent intervention
[67,68]:

● 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 and reversible causes of depressed mental status, such as


hypotension (systolic BP [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 moderate and severe traumatic brain
injury", section on 'Intracranial pressure management'.)

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 [69]. Interventions
should be utilized only when ICP is elevated above 20 mmHg for >5 to 10 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 [70]. 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 hypotonic hyponatremia in adults" and "Treatment
of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset
osmostat", section on 'Subarachnoid hemorrhage'.)

Similarly, the value of colloid compared with crystalloid fluid resuscitation in patients with
elevated ICP has been studied, but findings have been inconclusive with respect to the superior
approach [71]. 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 [72]. (See "Management of acute moderate and 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 ICP. (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 [73]. Establishing a secure airway and close attention to BP 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 adults: 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 BP in
patients with chronic hypertension in whom the autoregulatory curve has shifted to the right
(see 'Autoregulation' above). General issues regarding BP management following stroke are
presented elsewhere. (See "Antihypertensive therapy for secondary stroke prevention".)

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 [20,74]; 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 [75].

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 [76]. Therefore, aggressive treatment of fever, including acetaminophen and
mechanical cooling, is recommended in patients with increased ICP. ICH is a recognized
indication for neuromuscular paralysis in selected patients [77]. (See "Neuromuscular blocking
agents in critically ill patients: Use, agent selection, administration, and adverse effects".)

Antiseizure therapy — Seizures can both complicate and contribute to elevated ICP [78,79].
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.

Osmotic therapy and diuresis — With growing familiarity of use, hypertonic saline has
increasingly been employed as a first-line agent, supplanting mannitol at numerous
institutions.

Hypertonic saline bolus — Hypertonic saline in bolus doses can acutely lower ICP; however,
the effect of this early intervention on long-term clinical outcomes remains unclear [80-88]. 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 [80]. Survival until hospital discharge, six-month survival, and neurologic
function six months after injury were similar in both groups. In a retrospective review of
patients treated at a single study, the safety and efficacy of 14.6 and 23.4 percent saline boluses
appeared to be similar [89].

Mannitol and hypertonic saline have been compared in at least eight randomized trials of
patients with elevated ICP from a variety of causes (traumatic brain injury, stroke, tumors)
[87,90-93]. Meta-analyses of these trials have found that hypertonic saline appears to have
greater efficacy in managing elevated ICP, but clinical outcomes have not been systematically
examined [94,95]. Further clinical trials are required to clarify the appropriate role of hypertonic
saline infusion versus mannitol in the management of elevated ICP [96,97].

The role of hypertonic saline in the management of elevated ICP in traumatic brain injury is
discussed separately. (See "Management of acute moderate and severe traumatic brain injury",
section on 'Osmotic therapy'.)

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
[98-101]. The most commonly used agent is mannitol. It is prepared as a 20 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 approximately one hour, and last 4 to 24
hours [26,102]. 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 [103,104]. 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 blood pressure (BP), necessitating careful use if associated with a
fall in cerebral perfusion pressure (CPP). Patients with known renal disease may be poor
candidates for osmotic diuresis. (See "Complications of mannitol therapy".)

Other agents — 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
[105-107].

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 [108,109].

Glucocorticoids — Glucocorticoids were associated with a worse outcome in a large


randomized clinical trial of their use in moderate to severe head injury [110,111]. They should
not be used in this setting. (See "Management of acute moderate and 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: Acute
treatment and prognosis".)

By contrast, glucocorticoids may have a role in the setting of intracranial hypertension (ICH)
caused by brain tumors and central nervous system (CNS) infections. (See "Management of
vasogenic edema in patients with primary and metastatic brain tumors" and "Treatment and
prognosis of bacterial 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 cerebral
blood flow (CBF) [112]. Hyperventilation also results in respiratory alkalosis, which may buffer
post-injury acidosis [112]. The effect of hyperventilation on ICP is short-lived (1 to 24 hours)
[113-115]. Following therapeutic hyperventilation, the patient's respiratory rate should be
tapered back to normal over several hours to avoid a rebound effect [116].

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 [24,113,115,117-120]. 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 moderate and
severe traumatic brain injury", section on 'Ventilation'.)

Barbiturates — The use of barbiturates is predicated on their ability to reduce brain


metabolism and CBF, thus lowering ICP and exerting a neuroprotective effect [121-124].
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 hour [125,126]. Treatment should be assessed based on ICP, CPP, and the
presence of unacceptable side effects. Continuous electroencephalography (EEG) monitoring is
generally used; EEG burst suppression is an indication of maximal dosing.

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 [127]. 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 [112,128].

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. In this
setting, thiopental has been reported to produce hypokalemia with induction and rebound
hyperkalemia on drug cessation [129].

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 [112,130,131]. It is not currently recommended as
a standard treatment for increased ICP 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 [132]. Hypothermia also appeared to be effective in lowering ICP after other
therapies have failed [133,134].

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
[135]. It appears that rewarming should be accomplished over a period of less than 24 hours
[136].

The value of therapeutic hypothermia has been best assessed in patients after traumatic brain
injury, but its role has not been well established in that setting. (See "Management of acute
moderate and severe traumatic brain injury", section on 'Hypothermia' and "Elevated
intracranial pressure (ICP) in children: Management", section on 'Temperature control'.)

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 ICH
refractory to other therapies.

Removal of CSF — When hydrocephalus is identified, a ventriculostomy should be inserted (


figure 6). Rapid aspiration of cerebrospinal fluid (CSF) should be avoided because it may lead
to obstruction of the catheter opening by brain tissue. Also, in patients with aneurysmal
subarachnoid 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 [137-146]. 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 [147]. Decompressive craniectomy also appears to improve brain tissue oxygenation
[148].

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 [149-156]. The indications for decompressive
craniectomy in these settings are discussed separately (see "Malignant cerebral hemispheric
infarction with swelling and risk of herniation" and "Management of acute moderate and 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 [157].

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 [158,159]. 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 [160]. Marked decompression of the skin and
dura over the skull defect accompanies 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 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 (ICH) 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. Interventions should be based on careful assessment
of the individual clinical scenario rather than on strict protocols. Specific recommendations
regarding the assessment and treatment of elevated intracranial pressure (ICP) in individual
disease settings, including trauma, cerebrovascular disease, and other conditions, are
discussed separately. As examples:

● (See "Management of acute moderate and severe traumatic brain injury", section on
'Intracranial pressure management'.)

● (See "Spontaneous intracerebral hemorrhage: Acute treatment and prognosis", section on


'Intracranial pressure management'.)

● (See "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis".)

● (See "Intracranial epidural hematoma in adults", section on 'Intracranial pressure'.)

● (See "Subdural hematoma in adults: Prognosis and management".)

● (See "Malignant cerebral hemispheric infarction with swelling and risk of herniation".)

● (See "Cerebral venous thrombosis: Treatment and prognosis", section on 'Elevated


intracranial pressure and herniation'.)

● (See "Management of vasogenic edema in patients with primary and metastatic brain
tumors".)

● (See "Neurologic complications of bacterial meningitis in adults", section on 'Increased


intracranial pressure'.)

● (See "Clinical management and monitoring during antifungal therapy for cryptococcal
meningoencephalitis in patients with HIV", section on 'Monitoring of intracranial pressure'.)

● (See "Acute liver failure in adults: Management and prognosis", section on 'Cerebral
edema'.)

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Topic 1659 Version 14.0
GRAPHICS

Causes of intracranial hypertension*

Traumatic brain injury/intracranial hemorrhage


Subdural, epidural, or intraparenchymal hemorrhage
Ruptured aneurysm
Diffuse axonal injury
Arteriovenous malformation or other vascular anomalies

Central nervous system infections (eg, encephalitis, meningitis, abscess)

Ischemic stroke

Neoplasm

Vasculitis

Hydrocephalus

Hypertensive encephalopathy 

Idiopathic intracranial hypertension (pseudotumor cerebri)

* For further information on clinical manifestations, diagnosis, or treatment of these conditions, refer to specific UpToDate topics.

Graphic 69683 Version 9.0


Intracranial compensation for mass

Normally, the intracranial components are in equilibrium as shown in chamber 1.


Initially, the volume of a space-occupying lesion is compensated for by displacement of
blood and CSF  and ICP remains normal (chamber 2). When the limits of this
 compensation is reached; any additional increase in the volume of the mass lesion is
accompanied by a corresponding increase in ICP (chamber 3, decompensated phase).

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.

Graphic 65853 Version 5.0


The relationship between intracranial volume and pressure is
nonlinear

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).

Graphic 54602 Version 2.0


Cerebral autoregulation in hypertension

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. Management of hypertensive emergencies. Lancet 1994; 344:1335.

Graphic 57676 Version 4.0


Papilledema

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.

Graphic 50378 Version 1.0


Transtentorial herniation

Data from: Plum F, Posner JB. The Diagnosis of Stupor and Coma III. FA Davis, Philadelphia 1995. p. 103.

Graphic 76974 Version 5.0


Glasgow Coma Scale (GCS)

  Score

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

Total  

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.

Graphic 81854 Version 9.0


Radiographic findings suggestive of elevated ICP

Evidence of contusions with surrounding edema (top arrow), effacement of cisterns


(middle arrow), and effacement of sulci (lowest arrow).

Graphic 67017 Version 3.0


Intracranial pressure monitors

Ventriculostomy allows both ICP monitoring and therapeutic drainage of cerebrospinal fluid (CSF).
Subdural and intraparenchymal monitors cannot be used to drain CSF.

Graphic 78630 Version 1.0


Pathologic A waves

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.

Graphic 61774 Version 4.0


External ventricular drain

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.

Graphic 56391 Version 2.0


Contributor Disclosures
Edward R Smith, MD Nothing to disclose Sepideh Amin-Hanjani, MD Nothing to disclose Michael J
Aminoff, MD, DSc Equity Ownership/Stock Options: Trust [The portfolio may include medical or drug
companies]. Consultant/Advisory Boards: Brain Neurotherapy Bio [Parkinson disease]. Janet L Wilterdink,
MD Nothing to disclose

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

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