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Evaluation and management of elevated intracranial pressure in adults Authors

Edward R Smith, MD

Sepideh Amin-Hanjani, MD

Section Editor

Michael J Aminoff, MD, DSc

Deputy Editor

Janet L Wilterdink, MD

Disclosures

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

complete.

Literature review current through: Feb 2012. | This topic last updated: Feb 29, 2012.

INTRODUCTION — Elevated intracranial pressure (ICP) is a potentially devastating

complication of neurologic injury. Elevated ICP may complicate trauma, central nervous

system (CNS) tumors, hydrocephalus, hepatic encephalopathy, and impaired CNS venous

outflow (table 1) [1]. Successful management of patients with elevated ICP requires prompt

recognition, the judicious use of invasive monitoring, and therapy directed at both reducing

ICP and reversing its underlying cause.

The evaluation and management of adult patients with elevated ICP will be reviewed here.

Elevated intracranial pressure in children and specific causes and complications of elevated

ICP (eg, ischemic stroke, intracerebral hemorrhage, traumatic brain injury) are discussed

separately. (See "Elevated intracranial pressure in children" and "Management of acute

severe traumatic brain injury", section on 'Intracranial pressure' and "Initial assessment and

management of acute stroke" and "Spontaneous intracerebral hemorrhage: Prognosis and

treatment", section on 'Intracranial pressure control' and "Treatment of aneurysmal

subarachnoid hemorrhage", section on 'Management of complications'.)

PHYSIOLOGY — Intracranial pressure is normally ≤15 mmHg in adults, and pathologic

intracranial hypertension (ICH) is present at pressures ≥20 mmHg. ICP is normally lower in

children than adults, and may be subatmospheric in newborns [2]. Homeostatic

mechanisms stabilize ICP, with occasional transient elevations associated with physiologic

events, including sneezing, coughing, or Valsalva maneuvers.

Intracranial components — In adults, the intracranial compartment is protected by the

skull, a rigid structure with a fixed internal volume of 1400 to 1700 mL. Under physiologic

conditions, the intracranial contents include (by volume) [3]:

Brain parenchyma — 80 percent

Cerebrospinal fluid — 10 percent

Blood — 10 percent

Pathologic structures, including mass lesions, abscesses, and hematomas also may be

present within the intracranial compartment. Since the overall volume of the cranial vault

cannot change, an increase in the volume of one component, or the presence of pathologic

components, necessitates the displacement of other structures, an increase in ICP, or both.

Thus, ICP is a function of the volume and compliance of each component of the intracranial

compartment, an interrelationship known as the Monro-Kellie doctrine [4,5].

The volume of brain parenchyma is relatively constant in adults, although it can be altered

by mass lesions or in the setting of cerebral edema (figure 1). The volumes of CSF and

blood in the intracranial space vary to a greater degree. Abnormal increases in the volume

of any component may lead to elevations in ICP.

CSF is produced by the choroid plexus and elsewhere in the central nervous system (CNS)

at a rate of approximately 20 mL/h (500 mL/day) [6]. CSF is normally resorbed via the

arachnoid granulations into the venous system. Problems with CSF regulation generally

result from impaired outflow caused by ventricular obstruction or venous congestion; the

latter can occur in patients with sagittal (or other) venous sinus thrombosis. Much less

frequently, CSF production can become pathologically increased; this may be seen in the

setting of choroid plexus papilloma. (See "Cerebrospinal fluid: Physiology and utility of an

examination in disease states".)

Cerebral blood flow (CBF) determines the volume of blood in the intracranial space. CBF

increases with hypercapnia and hypoxia. Other determinants of CBF are discussed below.

Autoregulation of CBF may be impaired in the setting of neurologic injury, and may result in

rapid and severe brain swelling, especially in children [7-9].

In summary, the major causes of increased intracranial pressure include:

Intracranial mass lesions (eg, tumor, hematoma)

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

infarction, severe traumatic brain injury)

Increased cerebrospinal fluid (CSF) production, eg, choroid plexus papilloma

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 [11-13].

Another important consideration is that the set-point of autoregulation is also changed in

patients with chronic hypertension. With mild to moderate elevations in blood pressure, the

initial response is arterial and arteriolar vasoconstriction. This autoregulatory process both

maintains tissue perfusion at a relatively constant level and prevents the increase in

pressure from being transmitted to the smaller, more distal vessels [11]. As a result, acute

reductions in blood pressure, even if the final value remains within the normal range, can

produce ischemic symptoms in patients with chronic hypertension (figure 3) [11].

Cerebral perfusion pressure — Conditions associated with elevated ICP, including mass

lesions and hydrocephalus, can be associated with a reduction in CPP. This can result in

devastating focal or global ischemia. On the other hand, excessive elevation of CPP can lead

to hypertensive encephalopathy and cerebral edema due to the eventual breakdown of

autoregulation, particularly if the CPP is >120 mmHg [11,14,15]. A higher level of CPP is

tolerated in patients with chronic hypertension because the autoregulatory curve has shifted

to the right (figure 3) [11,15]. (See "Malignant hypertension and hypertensive

encephalopathy in adults", section on 'Mechanisms of vascular injury'.)

Ultimately, global or local reductions in CBF are responsible for the clinical manifestations of

elevated ICP. These manifestations can be further divided into generalized responses to

elevated ICP and herniation syndromes.

CLINICAL MANIFESTATIONS — Global symptoms of elevated ICP include headache,

which is probably mediated via the pain fibers of cranial nerve (CN) V in the dura and blood

vessels, depressed global consciousness due to either the local effect of mass lesions or

pressure on the midbrain reticular formation, and vomiting.

Signs include CN VI palsies, papilledema secondary to impaired axonal transport and

congestion (picture 1), spontaneous periorbital bruising [16] and a triad of bradycardia,

respiratory depression, and hypertension (Cushing's triad, sometimes called Cushing's reflex

or Cushing's response) [3]. While the mechanism of Cushing's triad remains controversial,

many believe that it relates to brainstem compression. The presence of this response is an

ominous finding that requires urgent intervention.

Focal symptoms of elevated ICP may be caused by local effects in patients with mass

lesions or by herniation syndromes. Herniation results when pressure gradients develop

between two regions of the cranial vault. The most common anatomical locations affected

by herniation syndromes include subfalcine, central transtentorial, uncal transtentorial,

upward cerebellar, cerebellar tonsillar/foramen magnum, and transcalvarial (figure 4)

[3,17]. (See "Stupor and coma in adults", section on 'Neurologic examination' and "Stupor

and coma in adults", section on 'Coma syndromes'.)

One notable false localizing syndrome seen following neurologic injury, referred to as

Kernohan's notch phenomenon, consists of the combination of contralateral pupillary

dilatation and ipsilateral weakness [18,19]. Because the diagnostic accuracy of signs and

symptoms is limited, the findings described above may be inconstant or unreliable in any

given case. Use of radiologic studies may support the diagnosis; however, the most reliable

method of diagnosing elevated ICP is to measure it directly.

ICP MONITORING — Empiric therapy for presumed elevated ICP is unsatisfactory because

CPP cannot be monitored reliably without measurement of ICP. Furthermore, most therapies

directed at lowering ICP are effective for limited and variable periods of time. In addition,

these treatments may have serious side effects. Therefore, while initial steps to control ICP

may, by necessity, be performed without the benefit of ICP monitoring, an important early

goal in management of the patient with presumed elevated ICP is placement of an ICP

monitoring device.

The purpose of monitoring ICP is to improve the clinician's ability to maintain adequate CPP

and oxygenation. The only way to reliably determine CPP (defined as the difference between

MAP and ICP) is to continuously monitor both ICP and blood pressure (BP). In general,

these patients are managed in intensive care units (ICUs) with an ICP monitor and arterial

line. The combination of ICP monitoring and concomitant management of CPP may improve

patient outcomes, particularly in patients with closed head trauma [20-23]. The specific

therapeutic targets for CPP in patients with traumatic brain injury are discussed separately.

(See "Management of acute severe traumatic brain injury", section on 'Cerebral perfusion

pressure'.)

Indications — The diagnosis of elevated ICP generally is based on clinical findings, and

corroborated by imaging studies and the patient's medical history. Closed head injury is one

of the most frequent and best-studied indications for ICP monitoring. Much of the current

practice of ICP monitoring has been derived from clinical experience with closed head

trauma patients [24]. Indications for ICP monitoring in this indication is discussed in detail

separately. (See "Management of acute severe traumatic brain injury", section on

'Intracranial pressure'.)

Role of computed tomography — Although CT scans may suggest elevated ICP based on

the presence of mass lesions, midline shift, or effacement of the basilar cisterns (picture 2),

patients without these findings on initial CT may have elevated ICP. This was demonstrated

in a prospective study of 753 patients treated at four major head injury research centers in

the United States, which found patients whose initial CT scan did not show a mass lesion,

midline shift, or abnormal cisterns had a 10 to 15 percent chance of developing elevated

ICP during their hospitalization [25].

Other studies have shown that up to one-third of patients with initially normal scans

developed CT scan abnormalities within the first few days after closed head injury [26,27].

Together, these findings demonstrate that ICP can be elevated even in the setting of a

normal initial CT, demonstrating the importance of invasive monitoring in high-risk patients

and the role of follow-up imaging in patients who develop clinical evidence of increased ICP

during hospitalization.

Since ICP monitoring is associated with a small risk of serious complications, including CNS

infection and intracranial hemorrhage, it is reasonable to try to limit its use to patients most

at risk of elevated ICP [28]. In general, invasive monitoring of ICP is indicated in patients

who are [29]:

Suspected to be at risk for elevated ICP

Comatose (Glasgow Coma Scale <8) (table 2)

Diagnosed with a process that merits aggressive medical care

Types of monitors — There are four main anatomical sites used in the clinical

measurement of ICP: intraventricular, intraparenchymal, subarachnoid, and epidural (figure

5) [30]. Noninvasive and metabolic monitoring of ICP has also been studied, but the clinical

value of these methods is unclear at present. Each technique requires a unique monitoring

system, and has associated advantages and disadvantages.

Intraventricular — Intraventricular monitors are considered the "gold standard" of ICP

monitoring catheters. They are surgically placed into the ventricular system and affixed to a

drainage bag and pressure transducer with a three-way stopcock. Intraventricular

monitoring has the advantage of accuracy, simplicity of measurement, and the unique

characteristic of allowing for treatment of some causes of elevated ICP via drainage of CSF.

The primary disadvantage is infection, which may occur in up to 20 percent of patients. This

risk increases the longer a device is in place [31,32]. Prophylactic catheter changes did not

appear to reduce the risk of infection [32]. (See "Infections of central nervous system

shunts and other devices".)

A further disadvantage of intraventricular systems includes a small (approximately 2

percent) risk of hemorrhage during placement; this risk is greater in coagulopathic patients.

In addition, it may be technically difficult to place an intraventricular drain into a small

ventricle, particularly in the setting of trauma and cerebral edema complicated by

ventricular compression [33].

Intraparenchymal — Intraparenchymal devices consist of a thin cable with an electronic

or fiberoptic transducer at the tip. The most widely used device is the fiberoptic Camino

system. These monitors can be inserted directly into the brain parenchyma via a small hole

drilled in the skull. Advantages include ease of placement, and a lower risk of infection and

hemorrhage (<1 percent) than with intraventricular devices [34-36].

Disadvantages include the inability to drain CSF for diagnostic or therapeutic purposes and

the potential to lose accuracy (or "drift") over several days, since the transducer cannot be

recalibrated following initial placement [30]. In addition, there is a greater risk of

mechanical failure due to the complex design of these monitors. The reliability of

intraparenchymal devices has been debated. One group found only a small (1 mmHg) drift

in a group of 163 patients [37]; however, a second report found that readings varied by >3

mmHg in more than half of the 50 patients studied [38].

Subarachnoid — Subarachnoid bolts are fluid-coupled systems within a hollow screw that

can be placed through the skull adjacent to the dura. The dura is then punctured, which

allows the CSF to communicate with the fluid column and transducer. The most commonly

used subarachnoid monitor is the Richmond (or Becker) bolt; other types include the Philly

bolt, the Leeds screw, and the Landy screw. These devices have low risk of infection and

hemorrhage, but often clog with debris and are unreliable; therefore, they are rarely used.

Additionally, they are believed to be less accurate than ventricular ICP devices [30].

Epidural — Epidural monitors contain optical transducers that rest against the dura after

passing through the skull. They often are inaccurate, as the dura damps the pressure

transmitted to the epidural space, and thus are of limited clinical utility [30,39]. They are

used in the management of coagulopathic patients with hepatic encephalopathy complicated

by cerebral edema. In this setting, use of these catheters is associated with a significantly

lower risk of intracerebral hemorrhage (4 versus 20 and 22 percent for intraparenchymal

and intraventricular devices) and fatal hemorrhage (1 versus 5 and 4 percent, respectively)

[40]. (See "Acute liver failure: Prognosis and management".)

Waveform analysis — ICP is not a static value; it exhibits cyclic variation based on the

superimposed effects of cardiac contraction, respiration, and intracranial compliance. Under

normal physiologic conditions, the amplitude of the waveform is often small, with B waves

related to respiration and smaller C waves (or Traube-Hering-Mayer waves) related to the

cardiac cycle [10].

Pathological A waves (also called plateau waves) are abrupt, marked elevations in ICP of 50

to 100 mmHg, which usually last for minutes to hours (figure 6). The presence of A waves

signifies a loss of intracranial compliance, and heralds imminent decompensation of

autoregulatory mechanisms [10,41,42]. Thus, the presence of A waves should suggest the

need for urgent intervention to help control ICP.

Noninvasive systems — A number of devices designed to record ICP noninvasively have

been studied, but most have not demonstrated reproducible clinical success or have been

studied in large clinical trials. We do not use these in clinical practice.

Tissue resonance analysis (TRA), an ultrasound-based method, has shown some

promise. In one trial 40 patients underwent both invasive and TRA ICP monitoring,

with good correlation between concomitant invasive and TRA measurements [43].

Ocular sonography can provide a noninvasive measure of optic nerve sheath

diameter, which has been found to correlate with intracranial pressure. A number of

studies have found that diameters of 5 to 6 mm have the ability to discriminate

between normal and elevated ICP in patients with intracranial hemorrhage and

traumatic brain injury [44-50].

Transcranial Doppler (TCD) measures the velocity of blood flow in the proximal

cerebral circulation. TCD can be used to estimate ICP based on characteristic

changes in waveforms that occur in response to increased resistance to cerebral

blood flow [51,52]. Generally, TCD is a poor predictor of ICP, although in trauma

patients TCD findings may correlate with outcome at six months [53-55].

Intraocular pressure can be assessed noninvasively using an ultrasonic handheld

optic tonometer. While some evidence suggests that intraocular pressure correlates

with ICP in the absence of oculofacial trauma or glaucoma [56], most other studies'

findings disagree [57-59].

Tympanic membrane displacement (measured using an impedance audiometer) has

been compared to direct monitoring, based on the hypothesis that increased ICP will

transmit a pressure wave to the tympanic membrane via the perilymph [60,61].

Advanced neuromonitoring — In order to supplement ICP monitoring, several

technologies have recently been developed for the treatment of severe TBI. These

techniques allow for the measurement of cerebral physiologic and metabolic parameters

related to oxygen delivery, cerebral blood flow, and metabolism with the goal of improving

the detection and management of secondary brain injury. These are discussed separately.

(See "Management of acute severe traumatic brain injury", section on 'Advanced

neuromonitoring'.)

Other

GENERAL MANAGEMENT — The best therapy for intracranial hypertension (ICH) is

resolution of the proximate cause of elevated ICP. Examples include: evacuation of a blood

clot, resection of a tumor, CSF diversion in the setting of hydrocephalus, or treatment of an

underlying metabolic disorder.

Regardless of the cause, ICH is a medical emergency, and treatment should be undertaken

as expeditiously as possible. In addition to definitive therapy, there are maneuvers that can

be employed to reduce ICP acutely. Some of these techniques are generally applicable to all

patients with suspected ICH; others (particularly glucocorticoids) are reserved for specific

causes of ICH.

Resuscitation — The urgent assessment and support of oxygenation, blood pressure, and

end-organ perfusion are particularly important in trauma, but applicable to all patients [62-

64]. If elevated ICP is suspected, care should be taken to minimize further elevations in ICP

during intubation through careful positioning, appropriate choice of paralytic agents (if

required), and adequate sedation. Pretreatment with lidocaine has been suggested as a

useful intervention to decrease the rise in ICP associated with intubation; however, good

clinical evidence supporting this approach is limited [65]. (See "Overview of inpatient

management in trauma patients" and "Advanced cardiac life support (ACLS) in adults" and

"Basic life support (BLS) in adults".)

Large shifts in blood pressure should be minimized, with particular care taken to avoid

hypotension. Although it might seem that lower BP would result in lower ICP, this is not the

case. Hypotension, especially in conjunction with hypoxemia, can induce reactive

vasodilation and elevations in ICP. As noted above, pressors have been shown to be safe for

use in most patients with intracranial hypertension, and may be required to maintain CPP

>60 mmHg [20]. (See "Use of vasopressors and inotropes".)

Urgent situations — Life-saving measures may need to be instituted prior to a more

detailed workup (eg, imaging or ICP monitoring) in a patient who presents acutely with

history or examination findings suggestive of elevated ICP. Many of these situations will rely

upon clinical judgment, but the following combination of findings suggests the need for

urgent intervention [66,67]:

A history that suggests elevated ICP (eg, head trauma, sudden severe headache

typical of subarachnoid hemorrhage)

An examination that suggests elevated ICP (unilateral or bilaterally fixed and dilated

pupil(s), decorticate or decerebrate posturing, bradycardia, hypertension and/or

respiratory depression)

A Glasgow coma scale (GCS) ≤8

Potentially confounding, reversible causes of depressed mental status, hypotension

(SBP <60 mmHg in adults), hypoxemia (PaO2 <60 mmHg), hypothermia (<36ºC),

or obvious intoxication are absent

In such patients osmotic diuretics may be used urgently (see 'Mannitol' below).

In addition, standard resuscitation techniques should be instituted as soon as possible:

Head elevation

Hyperventilation to a PCO2 of 26 to 30 mmHg

Intravenous mannitol (1 to 1.5 g/kg)

Concomitant with these measures should be aggressive evaluation of the underlying

diagnosis, including neuroimaging, detailed neurologic examination, and history gathering.

Hyperventilation may be contraindicated in the setting of traumatic brain injury and acute

stroke, and is discussed separately (see 'Hyperventilation' below). If appropriate,

ventriculostomy is a rapid means of simultaneously diagnosing and treating elevated ICP.

Monitoring and the decision to treat — If a diagnosis of elevated ICP is suspected and

an immediately treatable proximate cause is not present, then ICP monitoring should be

instituted. The use of ICP monitoring is associated with decreased mortality in patients with

traumatic brain injury [21]. (See "Management of acute severe traumatic brain injury",

section on 'Intracranial pressure'.)

The type of monitoring device employed should be based on an assessment of the

advantages and disadvantages discussed previously (figure 5). (See 'ICP

monitoring' above.)

The goal of ICP monitoring and treatment should be to keep ICP <20 mmHg [68].

Interventions should be utilized only when ICP is elevated above 20 mmHg for >5 to 10

minutes. As discussed above, brief physiologic elevations in ICP may occur in the setting of

coughing, movement, suctioning, or ventilator asynchrony.

Fluid management — In general, patients with elevated ICP do not need to be severely

fluid restricted [69]. Patients should be kept euvolemic and normo- to hyperosmolar. This

can be achieved by avoiding all free water (including D5W, 0.45 percent (half normal)

saline, and enteral free water) and employing only isotonic fluids (such as 0.9 percent

(normal) saline). Serum osmolality should be kept >280 mOsm/L, and often is kept in the

295 to 305 mOsm/L range. Hyponatremia is common in the setting of elevated ICP,

particularly in conjunction with subarachnoid hemorrhage. (See "Causes of

hyponatremia" and "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic

hormone secretion (SIADH) and reset osmostat", section on 'Subarachnoid hemorrhage'.)

Similarly, the value of colloid compared to crystalloid fluid resuscitation in patients with

elevated ICP has been studied, but findings have been inconclusive with respect to the

superior approach [70]. A subgroup analysis in one large study, however, suggested that in

patients with traumatic brain injury, fluid resuscitation with albumin was associated with a

higher mortality as compared with normal saline [71]. (See "Management of acute severe

traumatic brain injury".)

Hypertonic saline in bolus doses may acutely lower ICP, but further investigations are

required to define a role, if any, for this approach in the management of elevated

intracranial pressure. (See 'Hypertonic saline bolus' below.)

Sedation — Keeping patients appropriately sedated can decrease ICP by reducing

metabolic demand, ventilator asynchrony, venous congestion, and the sympathetic

responses of hypertension and tachycardia [72]. Establishing a secure airway and close

attention to blood pressure allow the clinician to identify and treat apnea and hypotension

quickly.

Propofol has been utilized to good effect in this setting, as it is easily titrated and has a

short half-life, thus permitting frequent neurologic reassessment. (See "Sedative-analgesic

medications in critically ill patients: Selection, initiation, maintenance, and withdrawal".)

Blood pressure control — In general, BP should be sufficient to maintain CPP >60 mmHg.

As discussed above, pressors can be used safely without further increasing ICP. This is

particularly relevant in the setting of sedation, when iatrogenic hypotension can occur.

Hypertension should generally only be treated when CPP >120 mmHg and ICP >20 mmHg.

Caution should be taken to avoid CPP <50 mmHg or, as noted above, normalization of blood

pressure in patients with chronic hypertension in whom the autoregulatory curve has shifted

to the right (see 'Autoregulation' above). General issues regarding blood pressure

management following stroke are presented elsewhere. (See "Treatment of hypertension in

patients who have had a stroke".)

Position — Patients with elevated ICP should be positioned to maximize venous outflow

from the head. Important maneuvers include reducing excessive flexion or rotation of the

neck, avoiding restrictive neck taping, and minimizing stimuli that could induce Valsalva

responses, such as endotracheal suctioning.

Patients with elevated ICP have historically been positioned with the head elevated above

the heart (usually 30 degrees) to increase venous outflow. It should be noted that head

elevation may lower CPP [20,73]; however, given the proven efficacy of head elevation in

lowering ICP, most experts recommend raising the patient's head as long as the CPP

remains at an appropriate level [74].

Fever — Elevated metabolic demand in the brain results in increased cerebral blood flow

(CBF), and can elevate ICP by increasing the volume of blood in the cranial vault.

Conversely, decreasing metabolic demand can lower ICP by reducing blood flow.

Fever increases brain metabolism, and has been demonstrated to increase brain injury in

animal models [75]. Therefore, aggressive treatment of fever, including acetaminophen and

mechanical cooling, is recommended in patients with increased ICP. Intracranial

hypertension is a recognized indication for neuromuscular paralysis in selected patients

[76]. (See "Use of neuromuscular blocking medications in critically ill patients".)

Antiepileptic therapy — Seizures can both complicate and contribute to elevated ICP

[77,78]. Anticonvulsant therapy should be instituted if seizures are suspected; prophylactic

treatment may be warranted in some cases. There are no clear guidelines for the latter, but

examples include high-risk mass lesions, such as those within supratentorial cortical

locations, or lesions adjacent to the cortex, such as subdural hematomas or subarachnoid

hemorrhage.

SPECIFIC THERAPIES — As mentioned previously, the best treatment of elevated ICP is

to address its underlying cause. If this is not possible, a series of steps should be instituted

to reduce ICP in an attempt to improve outcome. In all cases, the clinician should bear in

mind the themes of resuscitation, reduction of intracranial volume, and frequent

reevaluation discussed above.

Mannitol — Osmotic diuretics reduce brain volume by drawing free water out of the tissue

and into the circulation, where it is excreted by the kidneys, thus dehydrating brain

parenchyma [79-82]. The most commonly used agent is mannitol. It is prepared as a 20

percent solution, and given as a bolus of 1 g/kg. Repeat dosing can be given at 0.25 to 0.5

g/kg as needed, generally every six to eight hours. Use of any osmotic agent should be

carefully evaluated in patients with renal insufficiency.

The effects are usually present within minutes, peak at about one hour, and last 4 to 24

hours [29,83]. Some have reported a "rebound" increase in ICP; this probably occurs when

mannitol, after repeated use, enters the brain though a damaged blood-brain barrier and

reverses the osmotic gradient [84,85]. Useful parameters to monitor in the setting of

mannitol therapy include serum sodium, serum osmolality, and renal function.

Concerning findings associated with the use of mannitol include serum sodium >150 meq,

serum osmolality >320 mOsm, or evidence of evolving acute tubular necrosis (ATN). In

addition, mannitol can lower systemic BP, necessitating careful use if associated with a fall

in CPP. Patients with known renal disease may be poor candidates for osmotic diuresis. (See

"Complications of mannitol therapy".)

Other diuretics — Furosemide, 0.5 to 1.0 mg/kg intravenously, may be given with

mannitol to potentiate its effect. However, this effect can also exacerbate dehydration and

hypokalemia [86-88].

Glycerol and urea were used historically to control ICP via osmoregulation; however, use of

these agents has decreased because equilibration between brain and plasma levels occurs

more quickly than with mannitol. Furthermore, glycerol has been shown to have a

significant rebound effect and to be less effective in ICP control [89,90].

Hypertonic saline bolus — Hypertonic saline in bolus doses may acutely lower ICP;

however, the effect of this early intervention on long-term clinical outcomes remains unclear

[91-98]. The volume and tonicity of saline (7.2 to 23.4 percent) used in these reports have

varied widely. As an example, one controlled trial randomly assigned 226 patients with

traumatic brain injury to prehospital resuscitation with 250 mL hypertonic saline (7.5

percent) or the same volume of Ringer's lactate [91]. Survival until hospital discharge, six-

month survival, and neurologic function six months after injury were similar in both groups.

Mannitol and hypertonic saline have been compared in at least five randomized trials of

patients with elevated ICP from a variety of causes (traumatic brain injury, stroke, tumors)

[98-102]. A meta-analysis of these trials found that hypertonic saline appeared to have

greater efficacy in managing elevated ICP, but clinical outcomes were not examined [103].

Further clinical trials are required to clarify the appropriate role of hypertonic saline infusion

versus mannitol in the management of elevated ICP [104]. (See "Management of acute

severe traumatic brain injury", section on 'Osmotic therapy'.)

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

randomized clinical trial of their use in moderate to severe head injury [105,106]. They

should not be used in this setting. (See "Management of acute severe traumatic brain

injury".)

In addition, glucocorticoids are not considered to be useful in the management of cerebral

infarction or intracranial hemorrhage. (See "Spontaneous intracerebral hemorrhage:

Prognosis and treatment".)

In contrast, glucocorticoids may have a role in the setting of intracranial hypertension

caused by brain tumors and CNS infections. (See "Management of vasogenic edema in

patients with primary and metastatic brain tumors" and "Treatment and prognosis of brain

abscess" and "Dexamethasone to prevent neurologic complications of bacterial meningitis in

adults".)

Hyperventilation — Use of mechanical ventilation to lower PaCO2 to 26 to 30 mmHg has

been shown to rapidly reduce ICP through vasoconstriction and a decrease in the volume of

intracranial blood; a 1 mmHg change in PaCO2 is associated with a 3 percent change in CBF

[107]. Hyperventilation also results in respiratory alkalosis, which may buffer post-injury

acidosis [107]. The effect of hyperventilation on ICP is short-lived (1 to 24 hours) [108-

110]. Following therapeutic hyperventilation, the patient's respiratory rate should be

tapered back to normal over several hours to avoid a rebound effect [111].

Therapeutic hyperventilation should be considered as an urgent intervention when elevated

ICP complicates cerebral edema, intracranial hemorrhage, and tumor. Hyperventilation

should not be used on a chronic basis, regardless of the cause of increased ICP.

Hyperventilation should be minimized in patients with traumatic brain injury or acute stroke.

In these settings, vasoconstriction may cause a critical decrease in local cerebral perfusion

and worsen neurologic injury, particularly in the first 24 to 48 hours [24,108,110,112-115].

Thus, the need for hyperventilation should be carefully considered, and prophylactic

hyperventilation in the absence of elevated ICP should be avoided. (See "Management of

acute severe traumatic brain injury", section on 'Hyperventilation'.)

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

metabolism and cerebral blood flow, thus lowering ICP and exerting a neuroprotective effect

[116-119]. Pentobarbital is generally used, with a loading dose of 5 to 20 mg/kg as a bolus,

followed by 1 to 4 mg/kg per hr [120,121]. Treatment should be assessed based on ICP,

CPP, and the presence of unacceptable side effects. Continuous EEG monitoring is generally

used; EEG burst suppression is an indication of maximal dosing.

The therapeutic value of this maneuver is somewhat unclear. In a randomized trial of 73

patients with elevations in ICP refractory to standard therapy, patients treated with

pentobarbital were 50 percent more likely to have their ICP controlled. However, there was

no difference in clinical outcomes between groups [122]. In general, the use of barbiturates

is a "last-ditch" effort, as several studies show that their ability to lower ICP does not

appear to affect outcomes [107,123].

Barbiturate therapy can be complicated by hypotension, possibly requiring vasopressor

support. The use of barbiturates is also associated with a loss of the neurologic examination,

requiring accurate ICP, hemodynamic, and often EEG monitoring to guide therapy.

Therapeutic hypothermia — First reported as a treatment for brain injury in the 1950s,

induced or therapeutic hypothermia has remained a controversial issue in the debate

concerning the management of elevated ICP [107,124,125]. It is not currently

recommended as a standard treatment for increased intracranial pressure in any clinical

setting.

Hypothermia decreases cerebral metabolism and may reduce CBF and ICP. Initial studies of

hypothermia were limited by systemic side effects, including cardiac arrhythmias and severe

coagulopathy. However, later work suggested that hypothermia can lower ICP and may

improve patient outcomes [126]. Hypothermia also appeared to be effective in lowering ICP

after other therapies have failed [127,128].

Hypothermia can be achieved using whole body cooling, including lavage and cooling

blankets, to a goal core temperature of 32 to 34ºC. The best method of cooling (local versus

systemic), the optimal target core temperature, and the appropriate duration of treatment

are not known [129]. It appears that rewarming should be accomplished over a period of

less than 24 hours [130].

The value of therapeutic hypothermia has been best assessed in patients after traumatic

brain injury (TBI), but it’s role has not been well established in that setting. (See

"Management of acute severe traumatic brain injury", section on 'Induced hypothermia' and

"Elevated intracranial pressure in children", section on 'Hypothermia'.)

Given the uncertainties surrounding the appropriate use of therapeutic hypothermia in

patients with elevated ICP, this treatment should be limited to clinical trials, or to patients

with intracranial hypertension refractory to other therapies.

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

(figure 7). Rapid aspiration of CSF should be avoided because it may lead to obstruction of

the catheter opening by brain tissue. Also, in patients with aneurysmal subarachnoid

hemorrhage, abrupt lowering of the pressure differential across the aneurysm dome can

precipitate recurrent hemorrhage.

CSF should be removed at a rate of approximately 1 to 2 mL/minute, for two to three

minutes at a time, with intervals of two to three minutes in between until a satisfactory ICP

has been achieved (ICP <20 mmHg) or until CSF is no longer easily obtained. Slow removal

can also be accomplished by passive gravitational drainage through the ventriculostomy. A

lumbar drain is generally contraindicated in the setting of high ICP due to the risk of

transtentorial herniation.

Decompressive craniectomy — Decompressive craniectomy removes the rigid confines of

the bony skull, increasing the potential volume of the intracranial contents and

circumventing the Monroe-Kellie doctrine. There is a growing body of literature supporting

the efficacy of decompressive craniectomy in certain clinical situations [131-140].

Importantly, it has been demonstrated that in patients with elevated ICP, craniectomy alone

lowered ICP 15 percent, but opening the dura in addition to the bony skull resulted in an

average decrease in ICP of 70 percent [141]. Decompressive craniectomy also appears to

improve brain tissue oxygenation [142].

Observational data suggest that rapid and sustained control of ICP, including the use of

decompressive craniectomy, improves outcomes in trauma, stroke, and subarachnoid

hemorrhage in carefully selected cases [143-150]. The indications for decompressive

craniectomy in these settings are discussed separately. (See "Decompressive

hemicraniectomy for malignant middle cerebral artery territory infarction" and "Management

of acute severe traumatic brain injury", section on 'Decompressive craniectomy'.) Obvious

mass lesions associated with an elevated ICP should be removed, if possible.

Potential complications of surgery include herniation through the skull defect, spinal fluid

leak, wound infection, and epidural and subdural hematoma [151].

Paradoxical transtentorial herniation is an uncommon but potentially lethal complication in

patients with hemicraniectomy and a large skull defect who subsequently undergo lumbar

puncture (LP) or CSF drainage [152,153]. This results from the combined effects of

atmospheric pressure with the negative pressure of the LP or ventriculostomy. It has also

been described as a delayed complication three to five months after decompressive

craniectomy for cerebral infarction in the absence of LP or ventriculostomy [154]. Marked

decompression of the skin and dura over the skull defect accompany and may precede

neurologic signs of herniation. Standard treatments to lower ICP can hasten herniation.

Instead, the patient should be placed supine or in the Trendelenburg position, CSF drains

should be clamped, crystalloid fluid should be administered intravenously, and an epidural

blood patch placed for patients with dural leak.

SUMMARY — The best therapy for intracranial hypertension is resolution of the proximate

cause of elevated ICP. Regardless of the cause, treatment should be undertaken as

expeditiously as possible, and should be based on the principles of resuscitation, reduction

of the volume of the intracranial contents, and reassessment. The role of evidence-based

guidelines in the clinical management of elevated ICP is evolving [155]. However, it is

important to remember that individual patients respond differently to different therapies;

therefore, interventions should be based on careful assessment of the individual clinical

scenario rather than on strict protocols.

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Topic 1659 Version 8.0

GRAPHICS

Causes of intracranial hypertension

Intracranial hemorrhage

Tramatic brain injury

Ruptured aneurysm

Arteriovenous malformation

Other vascular anomalies

Central nervous system infections

Neoplasm

Vasculitis

Ischemic infarcts

Hydrocephalus

Idiopathic intracranial hypertension (pseudotumor cerebri)

Idiopathic

Intracranial compensation for an expanding mass lesion

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, 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 5-year-old girl with intracranial hypertension due

to vitamin A intoxication. Courtesy of Gerald Striph, MD.

Transtentorial herniation

Data from Pulm, F, Posner, JB. The Diagnosis of Stupor and Coma III. FA Davis, Philadelphia 1982. p. 103.

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).

Glasgow coma scale

Eye opening

Spontaneous 4

Response to verbal command 3

Response to pain 2

No eye opening 1

Best verbal response

Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Best motor response

Obeys commands 6

Localizing response to pain 5

Withdrawal response to pain 4

Flexion to pain 3

Extension to pain 2

No motor response 1

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.

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.

Pathol 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.

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