Intracranial pressure

Intracranial pressure
Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue and cerebrospinal fluid
(CSF). The body has various mechanisms by which it keeps the ICP stable, with CSF pressures varying by about 1
mmHg in normal adults through shifts in production and absorption of CSF. CSF pressure has been shown to be
influenced by abrupt changes in intrathoracic pressure during coughing (intraabdominal pressure), valsalva
(Queckenstedt's maneuver), and communication with the vasculature (venous and arterial systems). ICP is measured
in millimeters of mercury (mmHg) and, at rest, is normally 715 mmHg for a supine adult. Changes in ICP are
attributed to volume changes in one or more of the constituents contained in the cranium.
Intracranial hypertension, commonly abbreviated IH, IICP or raised ICP, is elevation of the pressure in the
cranium. ICP is normally 715mm Hg; at 2025mm Hg, the upper limit of normal, treatment to reduce ICP may be
needed.

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.
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.
The principal buffers for increased volumes include 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. These
compensatory mechanisms are able to maintain a normal ICP for any change in volume less than approximately
100120 mL.Wikipedia:Citation needed

Increased ICP
One of the most damaging aspects of brain trauma and other
conditions, directly correlated with poor outcome, is an elevated
intracranial pressure.[1] ICP is very likely to cause severe harm if it
rises too high.[2] Very high intracranial pressures are usually fatal if
prolonged, but children can tolerate higher pressures for longer
periods.[3] 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 brain
herniation, and restrict blood supply to the brain.[4] It is a cause of
reflex bradycardia.[5]

Pathophysiology
The cranium and the vertebral canal, along with the relatively inelastic
Severely high ICP can cause the brain to herniate.
dura, form a rigid container, such that the increase in any of its
contentsbrain, blood, or CSFwill 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

Intracranial pressure
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 25mmHg, 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, CSF hypertension, circulatory 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=MAPICP. 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 bodys 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. a hematoma) 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.[6] 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.

Stages of intracranial hypertension

Minimal increases in ICP due to compensatory mechanisms are 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 100120 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
bodys 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), CheyneStokes respiration, hyperventilation, sluggish dilated pupils and widened
pulse pressure.

Intracranial pressure

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 edema, contusions, subdural or epidural hematoma, or abscesses
all tend to deform the adjacent brain.
generalized brain swelling can occur in ischemic-anoxia states, acute liver failure, hypertensive encephalopathy,
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., infection,
carcinoma, granuloma, or hemorrhage), 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)
craniosynostosis

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. The headache is classically a morning headache which may
wake them from sleep. The brain is relatively poorly supplied by oxygen as a result of mild hypoventilation during
the sleeping hours, and also cerebral oedema may worsen during the night due to the lying position. The headache is
worse on coughing / sneezing / bending, and progressively worsens over time. There may also be personality or
behavioral changes.
In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may
include pupillary dilatation, abducens 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.[7] In children, a low
heart rate is especially suggestive of high ICP.
Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. CheyneStokes
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.[8] Hyperventilation can occur when the brain stem or tegmentum is damaged.
As a rule, patients with normal blood pressure retain normal alertness with ICP of 2540mmHg (unless tissue shifts
at the same time). Only when ICP exceeds 4050mmHg 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.
Papilledema, or the swelling of the optic disc, can be a reliable sign that ICP is elevated. Unlike other conditions that
may result in the swelling of the optic disc, it is in the case of papilledema that vision may go largely unaffected.[9]

Intracranial pressure

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.
A very common treatment for long-term, especially idiopathic, cranial hypertension is medication with a special
diuretic, especially one prescribed by a neurologist.
In patients who have high ICP due to an acute injury, 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.[10] 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. 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 was formerly a part of the standard treatment of traumatic
brain injuries, but the induced constriction of blood vessels limits blood flow to the brain at a time when the brain
may already be ischemichence it is no longer widely used.[11] 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. 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 immobilize the neck in trauma patients, and this may also
increase the ICP. Sandbags may be used to further limit neck movement.
In the hospital, the blood pressure can be artificially increased in order to increase CPP, increase perfusion,
oxygenate tissues, remove wastes, and thereby lessen swelling. 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 patient with a head injury.
When it is necessary to decrease cerebral blood flow, MAP can be lowered using common antihypertensive agents
such as calcium channel blockers. If there is an intact bloodbrain barrier, osmotherapy may be carried out 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.[12]
Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption, as well as
increasing blood pressure.[13] 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. 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. 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). 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.
There are many clinical studies of non-invasive intracranial pressure measurement methods currently being
proposed, aimed at finding reliable and accurate ways to measure ICP non-invasively. Such methods could improve
diagnostics of traumatic brain injury and many other conditions associated with intracranial hypertension.
Craniotomies are holes drilled in the skull to remove intracranial hematomas or relieve pressure from parts of the
brain. As raised ICP's may be caused by the presence of a mass, removal of this via craniotomy will decrease raised

Intracranial pressure
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. 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)

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.

References
[1] Orlando Regional Healthcare, Education and Development. 2004. "Overview of Adult Traumatic Brain Injuries." (http:/ / www.
orlandoregional. org/ pdf folder/ overview adult brain injury. pdf) Accessed January 16, 2008.
[2] Dawodu S. 2005. "Traumatic Brain Injury: Definition, Epidemiology, Pathophysiology" (http:/ / www. emedicine. com/ pmr/ topic212. htm)
Emedicine.com.Accessed January 4, 2007.
[3] Tolias C and Sgouros S. 2006. "Initial Evaluation and Management of CNS Injury." (http:/ / www. emedicine. com/ med/ topic3216. htm)
Emedicine.com. Accessed January 4, 2007.
[4] Graham DI and Gennareli TA. Chapter 5, "Pathology of Brain Damage After Head Injury" In, Cooper P and Golfinos G. 2000. Head Injury,
4th Ed. Morgan Hill, New York.
[5] Page 254
[6] Downie A. 2001. "Tutorial: CT in Head Trauma" (http:/ / www. radiology. co. uk/ srs-x/ tutors/ cttrauma/ tutor. htm) Accessed January 4,
2007.
[7] Sanders MJ and McKenna K. 2001. Mosbys Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
[8] Singh J and Stock A. 2006. "Head Trauma." (http:/ / www. emedicine. com/ ped/ topic929. htm) Emedicine.com. Accessed January 4, 2007.
[9] http:/ / emedicine. medscape. com/ article/ 1217204-overview
[10] Su F and Huh J. 2006. "Neurointensive Care for Traumatic Brain Injury in Children." (http:/ / www. emedicine. com/ ped/ topic3082. htm)
Emedicine.com. Accessed January 4, 2007.
[11] Shepherd S. 2004. "Head Trauma." (http:/ / www. emedicine. com/ med/ topic2820. htm) Emedicine.com. Accessed January 4, 2007.
[12] Trauma.org 2000. "TRAUMA.ORG: Neurotrauma: Control of Intracranial Hypertension" (http:/ / www. trauma. org/ archive/ neuro/
icpcontrol. html) Trauma.org. Accessed March 18, 2009.
[13] Bechtel K. 2004. "Pediatric Controversies: Diagnosis and Management of Traumatic Brain Injuries." Trauma Report. Supplement to
Emergency Medicine Reports, Pediatric Emergency Medicine Reports, ED Management, and Emergency Medicine Alert. Volume 5, Number
3. Thomsom American Health Consultants.

Intracranial pressure

External links
Gruen P. 2002. "Monro-Kellie Model" Neurosurgery Infonet. USC Neurosurgery (http://uscneurosurgery.com/
infonet/glossary/m/monro kellie model.htm). Accessed January 4, 2007.
National Guideline Clearinghouse. 2005. Guidelines for the management of severe traumatic brain injury. (http://
www.guideline.gov/summary/summary.aspx?doc_id=3794&nbr=003020&string=intracranial+AND+
pressure) Firstgov. Accessed January 4, 2007.
Intracranial Pressure (http://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?mode=&term=Intracranial+
Pressure) at the US National Library of Medicine Medical Subject Headings (MeSH)

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