Intracranial pressure

From Wikipedia, the free encyclopedia

Jump to: navigation, search
Intracranial pressure, (ICP), is the pressure in the cranium and thus in the brain
tissue and cerebrospinal fluid (CSF); this pressure is exerted on the brain's
intracranial blood circulation vessels. ICP is maintained in a tight normal range
dynamically, through the production and absorption of CSF. Because the entire
system is contained by bone and strong ligamentous connections, the pressures of
the body, such as those caused by straining, exercise, and coughing, do not affect
the brain or its environment.[citation needed] ICP is measured in millimeters of
mercury (mmHg) and, at rest, is normally 7�15 mmHg for a supine adult, and becomes
negative (averaging -10 mmHg) in the vertical position.[1] Changes in ICP are
attributed to volume changes in one or more of the constituents contained in the
cranium.

Intracranial hypertension, commonly abbreviated IH, is elevation of the pressure

in the cranium. ICP is normally 0�10 mm Hg; at 20�25 mm Hg, the upper limit of
normal, treatment to reduce ICP is needed.[2]

Contents [hide]
1 The Monro-Kellie hypothesis
2 Increased ICP
2.1 Pathophysiology
2.2 Intracranial hypertension
2.3 Causes
2.4 Signs and symptoms
2.5 Treatment
3 Low ICP
4 References
5 See also
6 External links

[edit] The Monro-Kellie hypothesis

The pressure-volume relationship between ICP, volume of CSF, blood, and brain
tissue, and cerebral perfusion pressure (CPP) is known as the Monro-Kellie
doctrine or the Monro-Kellie hypothesis.[3][4][5]

The Monro-Kellie hypothesis states that the cranial compartment is incompressible,

and the volume inside the cranium is a fixed volume. The cranium and its
constituents (blood, CSF, and brain tissue) create a state of volume equilibrium,
such that any increase in volume of one of the cranial constituents must be
compensated by a decrease in volume of another.[5]

The principal buffers for increased volumes include both CSF and, to a lesser
extent, blood volume. These buffers respond to increases in volume of the
remaining intracranial constituents. For example, an increase in lesion volume
(e.g. epidural hematoma) will be compensated by the downward displacement of CSF
and venous blood.[5] These compensatory mechanisms are able to maintain a normal
ICP for any change in volume less than approximately 100�120 mL.[citation needed]

[edit] 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 body, along with the relatively inelastic dura, form
a rigid container, such that the increase in any of its contents�brain, blood, or
CSF�will 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.

Traumatic brain injury is a devastating problem with both high mortality and high
subsequent morbidity. Injury to the brain occurs both at the time of the initial
trauma (the primary injury) and subsequently due to ongoing cerebral ischemia (the
secondary injury). Cerebral edema, hypotension, and axonal 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 causing blood flow 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, 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 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.

Highly increased ICP, if caused by a one-sided space-occupying process (eg. an

haematoma) can result in midline shift, a dangerous condition 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 buildup of CSF.[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 cerebellar), in which the brain is squeezed
past structures within the skull, severely compressing it. If brainstem
compression is involved, it may lead to decreased respiratory drive and is
potentially fatal. This herniation is often referred to as "coning".

Major causes of morbidity due to increased 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 further and causing a 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]

[edit] Signs and symptoms

In general, symptoms and signs that suggest a rise in ICP including headache,
nausea, vomiting, ocular palsies, altered LOC, 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.

[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]

Struggling, restlessness, and seizures can increase metabolic demands and oxygen
consumption, as well as increasing blood pressure.[18].[16] 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)

A swollen optic nerve is a reliable sign that ICP exists.

[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: Spontaneous 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.[19]