Increased intracranial pressure is a rise in the pressure inside the skull that can result from or cause brain

injury.

Causes

Increased intracranial pressure can be due to a rise in cerebrospinal fluid pressure. It can also be due to
increased pressure within the brain matter caused by a mass (such as a tumor), bleeding into the brain or
fluid around the brain, or swelling within the brain matter itself.

An increase in intracranial pressure is a serious medical problem. The pressure itself can damage the brain
or spinal cord by pressing on important brain structures and by restricting blood flow into the brain.

Many conditions can increase intracranial pressure. Common causes include:

 Aneurysm rupture and subarachnoid hemorrhage

 Brain tumor
 Encephalitis
 Hydrocephalus (increased fluid around the brain)
 Hypertensive brain hemorrhage
 Intraventricular hemorrhage
 Meningitis
 Severe head injury
 Subdural hematoma
 Status epilepticus
 Stroke

Symptoms

Infants:

 Drowsiness
 Separated sutures
 Bulging of the soft spot on top of the head (bulging fontanelle)
 Vomiting

Older children and adults:

 Behavior changes
 Decreased consciousness
 Headache
 Lethargy
 Neurological problems
 Seizures
 Vomiting

Exams and Tests

A health care provider will usually make this diagnosis at the patient's bedside in an emergency room or
hospital. Primary care doctors may sometimes spot early symptoms of increased intracranial pressure
such as headache, seizures, or neurological problems.

An MRI or CT scan of the head can often determine the cause and confirm the diagnosis.

Intracranial pressure may be measured during a spinal tap (lumbar puncture). It can also be measured
directly by using a device that is drilled through the skull or a tube (catheter) that is inserted inside the
brain.

Treatment

Sudden increased intracranial pressure is an emergency. The person will be treated in the intensive care
unit of the hospital. The health care team will measure and monitor the patient's neurological and vital
signs, including temperature, pulse, breathing rate, and blood pressure.

Treatment may include:

 Breathing support
 Draining of cerebrospinal fluid to lower pressure in the brain
 Medications to decrease swelling
 Rarely, removal of part of the skull

If a tumor, hemorrhage, or other underlying problem has caused the increase in intracranial pressure, the
cause should be treated as appropriate.

For information regarding treatment for certain causes of increased intracranial pressure, see:

 Hydrocephalus
 Normal pressure hydrocephalus

Outlook (Prognosis)

Sudden increased intracranial pressure is a serious and often deadly condition. If the underlying cause of
the raised intracranial pressure can be treated, then the outlook is generally better.

If the increased pressure pushes on important brain structures and blood vessels, it can lead to serious,
permanent problems or even death.

Possible Complications

 Death
 Permanent neurological problems
 Reversible neurological problems
 Seizures
 Stroke

When to Contact a Medical Professional

A health care provider will usually make this diagnosis in an emergency room or hospital.

Prevention

This condition usually cannot be prevented. If you have a persistent headache, blurred vision, changes in
your level of alertness, neurological problems, or seizures, seek medical attention as soon as possible.

Alternative Names

ICP; Intracranial pressure - increased; Intracranial hypertension; Acute increased intracranial pressure;
Sudden increased intracranial pressure

References

Ling GSF. Traumatic brain injury and spinal cord injury. In: Goldman L, Ausiello D, eds. Cecil Medicine.
23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 422.

Update Date: 12/21/2009

Updated by: David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine,
Department of Medicine, University of Washington School of Medicine; Daniel B. Hoch, PhD, MD,
Assistant Professor of Neurology, Harvard Medical School, Department of Neurology, Massachusetts
General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.
Intracranial hypertension, commonly abbreviated IH, is elevation of the pressure in the
cranium. ICP is normally 7–15 mm Hg; at 20–25 mm Hg, the upper limit of normal, treatment to
reduce ICP is needed.[2]

Increased ICP

Severely high ICP can cause the brain to herniate.

One of the most damaging aspects of brain trauma and other conditions, directly correlated with
poor outcome, is an elevated intracranial pressure.[6] ICP is very likely to cause severe harm if it
rises too high.[7] Very high intracranial pressures are usually fatal if prolonged, but children can
tolerate higher pressures for longer periods.[8] An increase in pressure, most commonly due to
head injury leading to intracranial hematoma or cerebral edema can crush brain tissue, shift brain
structures, contribute to hydrocephalus, cause the brain to herniate, and restrict blood supply to
the brain.[9] It is a cause of reflex bradycardia.[10]

[edit] Pathophysiology

The cranium and the vertebral canal, along with the relatively inelastic dura, form a rigid
container, such that the increase in any of its contents; brain, blood, or CSF, will tend to increase
the ICP. In addition, any increase in one of the components must be at the expense of the other
two; this relationship is known as the Monro-Kellie doctrine. Small increases in brain volume do
not lead to immediate increase in ICP because of the ability of the CSF to be displaced into the
spinal canal, as well as the slight ability to stretch the falx cerebri between the hemispheres and
the tentorium between the hemispheres and the cerebellum. However, once the ICP has reached
around 25 mmHg, small increases in brain volume can lead to marked elevations in ICP; this is
due to failure of intracranial compliance.
Traumatic brain injury is a devastating problem with both high subsequent morbidity and high
mortality. Injury to the brain occurs both at the time of the initial trauma (the primary injury) and
subsequently due to ongoing cerebral ischemia (secondary injury). Cerebral edema, hypotension,
and hypoxic conditions are well recognized causes of this secondary injury. In the intensive care
unit, raised intracranial pressure (intracranial hypertension) is seen frequently after a severe
diffuse brain injury (one that occurs over a widespread area) and leads to cerebral ischemia by
compromising cerebral perfusion.

Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly
constant due to autoregulation, but for abnormal mean arterial pressure (MAP) or abnormal ICP
the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the
mean arterial pressure: CPP = MAP − ICP .[1][11] One of the main dangers of increased ICP is that
it can cause ischemia by decreasing CPP. Once the ICP approaches the level of the mean
systemic pressure, cerebral perfusion falls. The body’s response to a fall in CPP is to raise
systemic blood pressure and dilate cerebral blood vessels. This results in increased cerebral
blood volume, which increases ICP, lowering CPP further and causing a vicious cycle. This
results in widespread reduction in cerebral flow and perfusion, eventually leading to ischemia
and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed
faster, also increasing ICP.

Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. an haematoma) can
result in midline shift, a dangerous sequela in which the brain moves toward one side as the
result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles
and lead to hydrocephalus.[12] Prognosis is much worse in patients with midline shift than in
those without it. Another dire consequence of increased ICP combined with a space-occupying
process is brain herniation (usually uncal or tonsilar). In uncal herniation, the uncus
hippocampus becomes compressed against the free edge of the tentorium cerebelli, frequently
leading to brainstem compression. If brainstem compression is involved, it may lead to
respiratory depression and is potentially fatal. This herniation is often referred to as "coning".

Major causes of morbidity due to raised intracranial pressure are due to global brain infarction as
well as decreased respiratory drive due to brain herniation.

[edit] Intracranial hypertension

Minimal increases in ICP due to compensatory mechanisms is known as stage 1 of intracranial

hypertension. When the lesion volume continues to increase beyond the point of compensation,
the ICP has no other resource, but to increase. Any change in volume greater than 100–120 mL
would mean a drastic increase in ICP. This is stage 2 of intracranial hypertension. Characteristics
of stage 2 of intracranial hypertension include compromise of neuronal oxygenation and
systemic arteriolar vasoconstriction to increase MAP and CPP. Stage 3 intracranial hypertension
is characterised by a sustained increased ICP, with dramatic changes in ICP with small changes
in volume. In stage 3, as the ICP approaches the MAP, it becomes more and more difficult to
squeeze blood into the intracranial space. The body’s response to a decrease in CPP is to raise
blood pressure and dilate blood vessels in the brain. This results in increased cerebral blood
volume, which increases ICP, lowering CPP and perpetuating this vicious cycle. This results in
widespread reduction in cerebral flow and perfusion, eventually leading to ischemia and brain
infarction. Neurologic changes seen in increased ICP are mostly due to hypoxia and hypercapnea
and are as follows: decreased level of consciousness (LOC), Cheyne-Stokes respirations,
hyperventilation, sluggish dilated pupils and widened pulse pressure.

[edit] Causes

Causes of increased intracranial pressure can be classified by the mechanism in which ICP is
increased:

 mass effect such as brain tumor, infarction with oedema, contusions, subdural or epidural
hematoma, or abscess all tend to deform the adjacent brain.
 generalized brain swelling can occur in ischemic-anoxia states, acute liver failure, hypertensive
encephalopathy, pseudotumor cerebri, hypercarbia, and Reye hepatocerebral syndrome. These
conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
 increase in venous pressure can be due to venous sinus thrombosis, heart failure, or
obstruction of superior mediastinal or jugular veins.
 obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or
subarachnoid space at base of brain, e.g., by Arnold-Chiari malformation), extensive meningeal
disease (e.g., infectious, carcinomatous, granulomatous, or hemorrhagic), or obstruction in
cerebral convexities and superior sagittal sinus (decreased absorption).

Main article: hydrocephalus

 increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus
tumor.
 Idiopathic or unknown cause (idiopathic intracranial hypertension)
 Cerebral venous sinus thrombosis
 Acute liver failure[13]
 craniosynostosis

[edit] Signs and symptoms

In general, symptoms and signs that suggest a rise in ICP including headache, vomiting without
nausea, ocular palsies, altered level of consciousness, back pain and papilledema. If papilledema
is protracted, it may lead to visual disturbances, optic atrophy, and eventually blindness.

In addition to the above, if mass effect is present with resulting displacement of brain tissue,
additional signs may include pupillary dilatation, abducens (CrN VI) palsies, and the Cushing's
triad. Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure,
bradycardia, and an abnormal respiratory pattern.[14] In children, a slow heart rate is especially
suggestive of high ICP.

Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive.
Cheyne-Stokes respiration, in which breathing is rapid for a period and then absent for a period,
occurs because of injury to the cerebral hemispheres or diencephalon.[15] Hyperventilation can
occur when the brain stem or tegmentum is damaged.[15]

As a rule, patients with normal blood pressure retain normal alertness with ICP of 25–40 mmHg
(unless tissue shifts at the same time). Only when ICP exceeds 40–50 mmHg do CPP and
cerebral perfusion decrease to a level that results in loss of consciousness. Any further elevations
will lead to brain infarction and brain death.

In infants and small children, the effects of ICP differ because their cranial sutures have not
closed. In infants, the fontanels, or soft spots on the head where the skull bones have not yet
fused, bulge when ICP gets too high.

A swollen optic nerve is a reliable sign that ICP is elevated.[citation needed]

[edit] Treatment

The treatment for IH depends on the etiology. In addition to management of the underlying
causes, major considerations in acute treatment of increased ICP relates to the management of
stroke and cerebral trauma.

In patients who have high ICP it is particularly important to ensure adequate airway, breathing,
and oxygenation. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide
levels (hypercapnia) cause cerebral blood vessels to dilate, increasing the flow of blood to the
brain and causing the ICP to rise.[16] Inadequate oxygenation also forces brain cells to produce
energy using anaerobic metabolism, which produces lactic acid and lowers pH, also dilating
blood vessels and exacerbating the problem.[6] Conversely, blood vessels constrict when carbon
dioxide levels are below normal, so hyperventilating a patient with a ventilator or bag valve
mask can temporarily reduce ICP. Hyperventilation used to be part of standard management of
traumatic brain injuries but the constriction of blood vessels limits blood flow to the brain in a
time when the brain may already be ischemic, and so is no longer widely used.[17] Furthermore,
the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation,
which could cause the vessels to rapidly dilate if carbon dioxide levels were returned to normal
too quickly.[17] Hyperventilation is still used if ICP is resistant to other methods of control, or
there are signs of brain herniation because the damage herniation can cause is so severe that it
may be worthwhile to constrict blood vessels even if doing so reduces blood flow. ICP can also
be lowered by raising the head of the bed, improving venous drainage. A side effect of this is that
it could lower pressure of blood to the head, resulting in a reduced and possibly inadequate blood
supply to the brain. Venous drainage may also be impeded by external factors such as hard
collars to immobilise the neck in trauma patients, and this may also increase the ICP. Sandbags
may be used to further limit neck movement.

In the hospital, blood pressure can be artificially raised in order to increase CPP, increase
perfusion, oxygenate tissues, remove wastes and thereby lessen swelling.[17] Since hypertension
is the body's way of forcing blood into the brain, medical professionals do not normally interfere
with it when it is found in a head injured patient.[15] When it is necessary to decrease cerebral
blood flow, MAP can be lowered using common antihypertensive agents such as calcium
channel blockers.[6] If there is an intact blood brain barrier, osmotherapy may be prescribed by
administering IV mannitol to create a hypertonic solution within the blood to draw water out of
the neurons. This helps to reduce the fluid within the intracranial space, however prolonged
administration may lead to increase in ICP.[18]

Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption,
as well as increasing blood pressure.[16][19] Analgesia and sedation (particularly in the pre-
hospital, ER, and intensive care setting) are used to reduce agitation and metabolic needs of the
brain, but these medications may cause low blood pressure and other side effects.[6] Thus if full
sedation alone is ineffective, patients may be paralyzed with drugs such as atracurium. Paralysis
allows the cerebral veins to drain more easily, but can mask signs of seizures, and the drugs can
have other harmful effects.[16] Paralysing drugs are only introduced if patients are fully sedated
(this is essentially the same as a general anaesthetic)

Intracranial pressure can be measured continuously with intracranial transducers. A catheter can
be surgically inserted into one of the brain's lateral ventricles and can be used to drain CSF
(cerebrospinal fluid) in order to decrease ICP's. This type of drain is known as an EVD
(extraventricular drain).[6] In rare situations when only small amounts of CSF are to be drained to
reduce ICP's, drainage of CSF via lumbar puncture can be used as a treatment.

Craniotomies are holes drilled in the skull to remove intracranial hematomas or relieve pressure
from parts of the brain.[6] As raised ICP's may be caused by the presence of a mass, removal of
this via craniotomy will decrease raised ICP's.

A drastic treatment for increased ICP is decompressive craniectomy, in which a part of the skull
is removed and the dura mater is expanded to allow the brain to swell without crushing it or
causing herniation.[17] The section of bone removed, known as a bone flap, can be stored in the
patient's abdomen and resited back to complete the skull once the acute cause of raised ICP's has
resolved. Alternatively a synthetic material may be used to replace the removed bone section
(see cranioplasty)

[edit] Low ICP

Main article: Intracranial hypotension

It is also possible for the intracranial pressure to drop below normal levels, though increased
intracranial pressure is a far more common (and far more serious) sign. The symptoms for both
conditions are often the same, leading many medical experts to believe that it is the change in
pressure rather than the pressure itself causing the above symptoms.

Main article: Cerebrospinal fluid leak

Spontaneous intracranial hypotension may occur as a result of an occult leak of CSF into another
body cavity. More commonly, decreased ICP is the result of lumbar puncture or other medical
procedures involving the brain or spinal cord. Various medical imaging technologies exist to
assist in identifying the cause of decreased ICP. Often, the syndrome is self-limiting, especially
if it is the result of a medical procedure. If persistent intracranial hypotension is the result of a
lumbar puncture, a "blood patch" may be applied to seal the site of CSF leakage. Various
medical treatments have been proposed; only the intravenous administration of caffeine and
theophylline has shown to be particularly useful.[20]

Increased intracranial pressure - Overview

 Overview
 Symptom
 Treatment
 Prevention
 All Information

Alternative Names

ICP; Intracranial pressure - increased; Intracranial hypertension; Acute increased intracranial

pressure; Sudden increased intracranial pressure

Definition of Increased intracranial pressure:

Increased intracranial pressure is a rise in the pressure inside the skull that can result from or
cause brain injury.

Causes, incidence, and risk factors:

Increased intracranial pressure can be due to a rise in cerebrospinal fluid pressure. It can also be
due to increased pressure within the brain matter caused by a mass (such as a tumor), bleeding
into the brain or fluid around the brain, or swelling within the brain matter itself.

An increase in intracranial pressure is a serious medical problem. The pressure itself can damage
the brain or spinal cord by pressing on important brain structures and by restricting blood flow
into the brain.

Many conditions can increase intracranial pressure. Common causes include:

 Aneurysm rupture and subarachnoid hemorrhage

 Brain tumor
 Encephalitis
 Hydrocephalus (increased fluid around the brain)
 Hypertensive brain hemorrhage
 Intraventricular hemorrhage
  Meningitis
 Severe head injury
 Subdural hematoma
 Status epilepticus
 Stroke

Subdural hematoma

 Reviewed last on: 12/21/2009

 David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of
Medicine, University of Washington School of Medicine; Daniel B. Hoch, PhD, MD, Assistant
Professor of Neurology, Harvard Medical School, Department of Neurology, Massachusetts
General Hospital. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.

References

Ling GSF. Traumatic brain injury and spinal cord injury. In: Goldman L, Ausiello D, eds. Cecil
Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 422.

Related Articles

 Central nervous system

 Head injury
 Subdural hematoma
 Meningitis

Increased Intracranial Pressure

Intracranial pressure (ICP) is the pressure in the skull that results from the volume of three
essential components: cerebrospinal fluid (CSF), intracranial blood volume and central nervous
system tissue. The normal intracranial pressure is between 5-15 mmHg. This is slightly lower
than the mean systemic arterial pressure but considerably higher than venous pressure.

The intact cranium is essentially inexpandable containing about 1400 grams of central nervous
system (CNS) or brain tissue, 75 ml of blood and about 75 ml of cerebrospinal fluid (CSF).
These three components of the cranial vault maintain a state of equilibrium. Their pressure and
volume determine the condition of balance. According to Monro-Kellie hypothesis, any
increase in one of these elements must be balanced or compensated by a proportional
constriction either or both of the other two components such as decreasing the volume of
cerebral blood flow, shifting CSF flow (into the spinal canal) or increasing CSF absorption.
Absence of these compensatory changes results to increased intracranial pressure. Once ICP
reaches around 25 mmHg marked elevation in intracranial pressure will be noted.

CSF is formed from the blood by the choroid plexuses, which are hanging at the roof of the
brain’s ventricles. From the point where it is produced, it flows through the aqueduct of Sylvius
to the fourth ventricles. Three apertures (opening) are found in the fourth ventricle which serves
as passageway going to the subarachnoid spaces in the brain and spinal cord. These openings are
Foramina of Magendie (median aperture) and two Foramina of Luschka (lateral apertures). A
presence of tumor in choroid plexus may cause an overproduction of CSF. If the passageway of
CSF is obstructed or brain tissue damage during surgery occurs, elevated ICP is inevitable.

Normally, a change in CSF and blood volume occurs. For instance, during exhalation a
temporary rise in intrathoracic pressure occurs. This impairs cerebral venous drainage and
thereby reabsorption of CSF. An increase in ICP might likely occur, unless the blood will be
expelled or the brain tissue will shrink (compensatory mechanism). If no compensation will
occur, based on Monro-Kellie hypothesis, a slight increase in intracranial pressure will take
place. The same process occurs during Valsalva maneuver (forcible exhalation against a closed
glottis), sneezing, coughing and straining at stool. This is the main reason why people with
increase ICP and at risk for cerebral hemorrhage are instructed to avoid these instances.

Presence of carbon dioxide can also increase ICP. Carbon dioxide is a potent vasodilator that
dilates aretrioles (including those in the chorionic plexus in the brain) which elevates cerebral
blood volume and ICP.

Etiology

CSF – hydrocephalus

 Overproduction of CSF

1. Meningitis
2. Subarachnoid hemorrhage
3. Brain tumor

 Impediment of CSF flow

1. Narrowed foramina of Magendie and Luschka

2. Obstruction in the Aqueduct of Sylvius
3. Arnold-Chiari disorder

 Interference with CSF absorption

 1. Surgery

CNS tissue

 Head injury
 Cerebral edema

Blood

 Cerebral venous sinus thrombosis

 Hematoma
 Increased carbon dioxide partial pressure

Sources:

1. Medical Surgical Nursing by Smeltzer and Bare

2. Pathophysiology by Nowak and Handford