Evaluation and Management of Elevated Intracranial Pressure in Adults - UpToDate PDF

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Evaluation and management of elevated intracranial pressure in adults
Authors: Edward R Smith, MD, Sepideh AminHanjani, 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: Sep 2018. | This topic last updated: Jun 21, 2017.
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 (ICP) in
children: Clinical manifestations and diagnosis" and "Management of acute severe traumatic brain injury", section
on 'Intracranial pressure management' and "Initial assessment and management of acute stroke" and "Treatment
of aneurysmal subarachnoid hemorrhage", section on 'Management of complications' and "Spontaneous
intracerebral hemorrhage: Treatment and prognosis", section on 'Intracranial pressure management'.)
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.
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 MonroKellie doctrine [4,5].
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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 [79].
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
● 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.
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 [1113].
Another important consideration is that the setpoint 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 "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's triad, sometimes called Cushing's reflex or Cushing's response) [3]. While the mechanism of
Cushing's 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 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 [2023]. 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 '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 beststudied
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 this indication is discussed in
detail separately. (See "Management of acute severe traumatic brain injury", section on 'Intracranial pressure
management'.)
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 [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 <8) (table 2)
● Diagnosed with a process that merits aggressive medical care
Although 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 onethird 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 highrisk patients and the role of followup imaging in patients who develop clinical evidence of
increased ICP during hospitalization.
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 threeway 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.
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 [3436].
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 fluidcoupled 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) 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 TraubeHeringMayer
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 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 [43,44]. Generally, TCD is a poor predictor of ICP, although in trauma
patients TCD findings may correlate with outcome at six months [4548].
● Tissue resonance analysis (TRA), an ultrasoundbased 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 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 [5056].
● 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 [5860].
● 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 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'.)
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 endorgan perfusion
are particularly important in trauma, but applicable to all patients [6365]. 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 "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 — Lifesaving 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, 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 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 to 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 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 [73].
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 halflife, thus
permitting frequent neurologic reassessment. (See "Sedativeanalgesic 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 blood pressure in patients
with chronic hypertension in whom the autoregulatory curve has shifted to the right (see 'Autoregulation' above).
General issues regarding blood pressure management following stroke are presented elsewhere. (See
"Antihypertensive therapy to prevent recurrent stroke or transient ischemic attack".)
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. Intracranial hypertension is a recognized indication for neuromuscular paralysis in
selected patients [77]. (See "Clinical use of neuromuscular blocking agents in critically ill patients".)
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 highrisk 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
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 [8083]. 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 about one hour, and last 4 to 24 hours [26,84]. Some
have reported a "rebound" increase in ICP; this probably occurs when mannitol, after repeated use, enters the
brain though a damaged bloodbrain barrier and reverses the osmotic gradient [85,86]. 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".)
Hypertonic saline bolus — With growing familiarity of use and accumulation of these data, hypertonic saline
has increasingly been employed as a first line agent, supplanting mannitol at numerous institutions.
Hypertonic saline in bolus doses can acutely lower ICP; however, the effect of this early intervention on longterm
clinical outcomes remains unclear [8795]. 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 [87]. Survival until hospital discharge, sixmonth 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 [96].
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) [94,97100]. Metaanalyses 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 [101,102]. Further clinical trials are required to clarify the
appropriate role of hypertonic saline infusion versus mannitol in the management of elevated ICP [103,104].
The role of hypertonic saline in the management of elevated ICP in traumatic brain injury is discussed separately.
(See "Management of acute severe traumatic brain injury", section on 'Osmotic 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 [105107].
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 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: Treatment and prognosis".)
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 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 CBF [112]. Hyperventilation also results in respiratory alkalosis,
which may buffer postinjury acidosis [112]. The effect of hyperventilation on ICP is shortlived (1 to 24 hours)
[113115]. 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 [24,113,115,117120]. 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 'Ventilation'.)
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 [121124]. 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 [125,126]. 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.
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 "lastditch" 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].
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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 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 [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 (TBI), but
it’s role has not been well established in that setting. (See "Management of acute 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 intracranial hypertension refractory to other
therapies.
Removal of CSF — When hydrocephalus is identified, a ventriculostomy should be inserted (figure 6). 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 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 MonroeKellie doctrine. There
is a growing body of literature supporting the efficacy of decompressive craniectomy in certain clinical situations
[137146]. 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
[149156]. 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 [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 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 ICP in individual
disease settings, including trauma, cerebrovascular disease, and other conditions are discussed separately. As
examples:
● (See "Management of acute severe traumatic brain injury", section on 'Intracranial pressure management'.)
● (See "Spontaneous intracerebral hemorrhage: Treatment and prognosis", section on 'Intracranial pressure
management'.)
● (See "Treatment of aneurysmal subarachnoid hemorrhage", section on 'Intracranial pressure'.)
● (See "Intracranial epidural hematoma in adults", section on 'Intracranial pressure'.)
● (See "Subdural hematoma in adults: Prognosis and management", section on 'Increased intracranial
pressure'.)
● (See "Decompressive hemicraniectomy for malignant middle cerebral artery territory infarction".)
● (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", section on
'Acute treatment of elevated ICP'.)
● (See "Neurologic complications of bacterial meningitis in adults", section on 'Increased intracranial
pressure'.)
● (See "Clinical management and monitoring during antifungal therapy of the HIVinfected patient with
cryptococcal meningoencephalitis", 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 12.0
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 spaceoccupying 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.
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).
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.
Papilledema
Papilledema, characterized by blurring of the optic disc margins, loss of
physiologic cupping, hyperemia, and fullness of the veins, in a 5yearold girl
with intracranial hypertension due to vitamin A intoxication.
Courtesy of Gerald Striph, MD.
Transtentorial herniation
Data from: Plum F, Posner JB. The Diagnosis of Stupor and Coma III. FA Davis, Philadelphia 1995. p. 103.
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.
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).
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.
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.
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.
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). Equity Ownership/Stock Options (Spouse): Trust (The portfolio may include medical or drug
companies). 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.
Conflict of interest policy

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