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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 and pulsates approximately 1mm Hg in a normal healthy adult.[citation needed] 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 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

o 2.1 Pathophysiology o 2.2 Intracranial hypertension o 2.3 Causes o 2.4 Signs and symptoms o 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 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 (eg. 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]

[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 exists.[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, one may administer 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.[19].[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)

[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]

Intracranial pressure

 Dental Dictionary:

intracranial pressureSponsored LinksBrain pressureGet the Answers You're Looking For. Brain pressure www.RightHealth.com/HypertensionHome > Library > Health > Dental Dictionary

n

Pressure that occurs within the cranium. Trauma to the head, inflammation, or infection of the linings of the brain may cause an increase in pressure within the cranium, which is painful, dysfunctional, and may become life-threatening.

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Intracranial pressureTop  Medical Dictionary:

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n. (Abbr. ICP)

Pressure within the cranial cavity.

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Intracranial pressure.

 Wikipedia:

Intracranial pressureTop Home > Library > Miscellaneous > Wikipedia

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 and pulsates approximately 1mm Hg in a normal healthy adult.[citation needed] 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 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

o 2.1 Pathophysiology o 2.2 Intracranial hypertension o 2.3 Causes o 2.4 Signs and symptoms o 2.5 Treatment

3 Low ICP 4 References 5 See also

6 External links

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]

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]

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 (eg. 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.

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.

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]

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 exists.[citation needed]

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, one may administer 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.[19].[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)

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]

Intracranial pressure:  Dr. A. Vincent Thamburaj,   Neurosurgeon, Apollo Hospitals,  Chennai , India.

It is the term applied to the pressure of CSF with in the cranium.

Physiology: 

Normal intracranial pressure in adults is 8 to 18mm Hg and in babies the pressure is 10-20mm less when measured through a lumbar puncture. ICP is not a static state, but one that is influenced by several factors. The recording of ICP shows 2 forms of pressure fluctuations. There is a rise with cardiac systole (due to distention of intracranial arteriolar tree which follows ) and a slower change in pressure with respiration, falling with each inspiration and rising with expiration. Straining, compression of neck veins can also cause sudden, considerable rise in pressure. The conception of the cranium acting as a near rigid container of virtually incompressible substances in the form of brain, blood & CSF in known as the Monro Kellie doctrine. CSF can be displaced through the foramen magnum into spinal theca.

The spinal dural sheath can accept a quantity of CSF as it does not fit the canal closely, being surrounded by a layer of loose areolar tissue & plexus of epidural veins. In addition, in states of increased ICP there is increase in passage of blood through venous emissaries.

Intracranial pressure is a result of at least 2 factors, the volume of the brain (about 1400ml in an adult) being constant. 

(a) CSF which is constantly secreted & after circulating absorbed at an equal rate. CSF circulation is slow (500 to 700 ml/day). At a given time the cranium contains 75 ml of CSF.

(b) Intracranial circulation of blood which is about 1000 litres per day delivered at a pressure of 100 mmHg and at a given time, the cranium contains 75 ml. Any obstruction to venous outflow will entail an increase in the volume of intracranial blood and ICP. As the ICP increases, the cerebral venous pressure increases in parallel so as to remain 2 to 5 mm higher or else the venous system would collapse. Because of this relationship CPP (mean art pressure - venous pressure or mean ICP) can be satisfactorily estimated from mean art pressure - ICP.

Lundberg has described 3 wave patterns ICP waves (A, B, and C waves). A waves are pathological. There is a rapid rise in ICP up to 50-100 mm Hg followed by a variable period during which the ICP remains elevated followed by a rapid fall to the baseline and when they persist for longer periods, they are called 'plateau' waves which are pathological. 'Truncated' or atypical ones, that do not exceed an elevation of 50 mm Hg, are early indicators of neurological deterioration. B & C waves are related to respiration and 'Traube-Hering-Mayer' waves respectively and are of little clinical significance.       

Cerebral blood flow (CBF): 

The brain accounts for only 2% of total body weight, yet its blood flow represents 15% of resting cardiac output and uses 20% total amount of oxygen consumed. Each 24 hours brain requires 1000 liters in order to obtain 71 lit of oxygen and 100 gm of glucose. The CBF remains constant over a wide range of arterial pressures (between 60 to 150 mm hg) when the mean arterial pressure is increased beyond 150 mm hg there is increased blood flow. CBF ceases when art. mean pressure drops to 20mm Hg. In chronically hypertensive this auto regulation limits appear to be reset.

The exact nature of this auto regulation is not known.

(a) myogenic theory suggests direct reaction of the cerebral arterial smooth muscles to the stretch.

(b) The humoral theory involves regulations by the direct effect of by- products of metabolism

(c) Neurogenic theory rests on perivascular nerves.

The auto regulation is influenced by various factors.

With normal cerebrovascular system and BP, even moderate alterations of pCO2 are capable of markedly altering CBF. Within the range of 30 to 60 mm Hg there is a 2.5% change in CBF as the pCO2 changes by 1 mmHg. With less then 20 and more than 80 mmHg there is no further change. In old age and arteriosclerosis, there is marked decrease in pCO2 influence.

The effects of pO2 are not as marked as CO2 Changes. Moderate variation of O2 above and below the normal level do not affect CBF. pO2 causes constriction of a non ischemic brain along with reduction in CBF. In ischemic hemisphere, increasing the pO2 has no effect. Cerebral vaso dilatation begins with pO2 of 50 mm Hg & CBF increases. When pO2 falls to 30 mmHg, CBF may have tripled.

The ICP influences the CBF through the cerebral perfusion pressure (CPP) which is the difference between mean arterial pressure (MAP) and ICP. Raise in  ICP would lead to a fall in CPP and every effort should be taken to maintain the CPP to 50 mm Hg or more during treatment of raised ICP.

Pathophysiology of increased intracranial pressure:

Increased ICP is defined as a sustained elevation in pressure above 20mm of Hg/cm of H20. 

The craniospinal cavity may be considered as a balloon. During slow increase in volume in a continuous mode, the ICP raises to a plateau level at which the increase level of CSF absorption keeps pace with the increase in volume. Intermittent expansion causes only a transient rise in ICP at first. When sufficient CSF has been absorbed to accommodate the volume the ICP returns to normal. Expansion to a critical volume does however cause persistent raise in ICP which thereafter increases logarithmically with increasing volume Volume - pressure relationship). The ICP finally raises to the level of arterial pressure

which it self begins to increase, accompanied by bradycardia or other disturbances of heart rhythm (Cushing response). This is accompanied by dilatation of small pial arteries and some slowing of venous flow which is followed by pulsatile venous flow.

The rise in ICP to the level of systemic arterial pressure extinguishes cerebral circulation which will restart only if arterial pressure raises sufficiently beyond the ICP to restore CBF. If it fails, brain death occurs.

The cause of raise in ICP and the rate at which it occurs are also important.

Many patients with benign ICT or obstructive hydrocephalus show little or no ill effect, the reason being the brain it self is normal and auto regulation is probably intact.

In patients with parenchymal lesion (tumor, hematoma and contusion), because of the shift of brain and disturbed auto regulation, CBF may by compromised with relatively low levels of ICP.

In acute hydrocephalus, there is rapid deterioration as  there is no time for compensation.

The raise in ICP disturbs brain function by

(1) Reduction in CBF

(2) Transtentorial or foramen magnum herniation resulting in selective compression and ischaemia in the brain stem.

Transtentorial herniation with brainstem compression can lead to clinical deterioration even with adequate CBF. A temporal mass may cause uncal herniation without raised ICP. Similarly a frontal mass can cause axial distortion to impair brainstem perfusion. 

Clinical features if raised ICP:

Raised ICP causes arterial hypertension, bradycardia (Cushing's response) and respiratory changes.

It is traditionally accepted that hypertension and bradycardia are due to ischaemia or pressure on the brainstem. There is also a suggestion that they could be due to removal of supratentorial inhibition of brainstem vasopressor centers due to cerebral ischaemia and that bradycardia is independent of the rise in blood pressure.

The respiratory changes depend on the level of brainstem involved. The midbrain involvement result in Chyne-Stokes respiration. When midbrain and pons are involved, there is sustained hyperventilation. There is rapid and shallow respiration when upper medulla involvement with ataxic breathing in the final stages.

Pulmonary edema seems to be due to increased sympathetic activity as a result of the effects of raised ICP on the hypothalamus, medulla or cervical spinal cord.    

ICP monitoring:

ICP monitoring is most often used in head trauma in the following situations:

1) GCS less than 8

2) Drowsy with CT findings (operative or non operative)

3) Post op hematoma evacuation

4) High risk patients  (a) Above 40 yrs. (b) Low BP (c) Those who require ventilation.

There is nothing to achieve in monitoring ICP in the patients with GCS of less than 3.

Methods:

Non invasive methods:

(1) Clinical deterioration in neurological status is widely considered as sign of increased ICP. Bradycardia, increased pulse pressure, pupillary dilation are normally accepted as signs of increased ICP. The clinical monitoring is age old and time tested.

(2) Transcranial doppler, tympanic membrane displacement, and ultrasound 'time of flight' techniques have been advocated. Several devices have been described for measuring ICP through open fontanel. Ladd fiber optic system has been used extra cutaneously.

(3) Manual feeling the craniotomy flap or skull defect, if any, give a clue.

Invasive methods:

(1) Intraventricular monitoring remains one of the popular techniques, especially in patients with ventriculomegaly. Additional advantage is the potential for draining CSF therapeutically. Insertion of ventricular catheter is not always simple and can cause hemorrhage and infection (5%).

(2) Other most commonly used devices are the hollow screw and bolt devices, and the sub dural catheter. Richmond screw and Becker bolt are used extra durally. A fluid filled catheter in the subdural space, connected to arterial pressure monitoring system is cost effective and serves the purpose adequately.

(3) Ladd device is currently in wide use. It employs a fibre optic system to detect the distortion of a tiny mirror within with balloon system. It can be used in the subdural , extradural and even extra cutaneously.

(4) A mechanically coupled surface monitoring device is the 'cardio search pneumatic sensor' used subdurally or extradurally. These systems are not widely used.

(5) Electronic devices (Camino & Galtesh design) are getting popular world over. Intraparenchymal probes, the measured pressure may be compartmentalized and not necessarily representative of real ICP. In addition to ICP monitoring, modern intraparenchymal sensors help study the chemical environment of the site of pathology.

(6) Fully implantable devices are valuable in a small group who requires long term ICP monitoring for brain tumors, hydrocephalus or other chronic brain diseases. Cosmon intrcranial pressure telesensor can be implanted as a part of shunt system. Ommaya reservoir is an alternative which can be punctured & CSF pressure readings are obtained.

(7) Lumbar puncture and measurement of CSF pressure for obvious reasons is not recommended.

Benefits of ICP monitoring:

There is no doubt that ICP monitoring helps in management of conditions where one expects prolonged intracranial hypertension. Monitoring is the only means by which therapy can be selectively employed and the effectiveness of therapy can be accurately studied.

1) Where ever clinical monitoring is not possible, such as during hyper ventilation therapy and high dose barbiturate therapy, ICP monitoring helps.

2) Pre op monitoring helps in assessment of NPH before a shunting procedure.

3) Cerebral perfusion pressure (CPP), regulation of cerebral blood flow, and volume, CSF absorption capacity, brain compensatory reserve, and content of vasogenic events can be studied with ICP monitoring. Some of these parameters help in prediction of prognosis of survival following head injury and optimization of' 'CPP guided therapy'.

4) It can provide additional assessment of brain death. Brain perfusion effectively ceases in nearly all, once ICP exceeds diastolic blood pressure.

The problems of ICP monitoring are cost, infection, and hemorrhage. The effective maintenance requires a dedicated team effort.  

Treatment of increased ICP:

There is no doubt the best treatment for increased ICP is the removal of the causative lesion such as tumors, hydrocephalus, and hematomas.

Post operative increased ICP should be uncommon these days with increased use of microscope and special techniques to avoid brain retraction. As we so often see, a basal meningioma once completely removed, has a smooth post op period, whereas a convexity or even falx meningioma may be easily removed but post operative period may be stormy, mainly due to impairment of venous drainage, either due to intraoperative injury to veins and post operative diuretic therapy as practiced in some centers.

There is still a debate whether increased ICP is the cause or result of the brain damage. Many feel both compliment each other. There is one school which questions the very existence of increased ICP. Not all the midline shift seen in CTs indicate increased ICP. It just means ICP was high during the shift. The shift takes longer to reverse even after ICP returns to normal . It is widely accepted the increased ICP is a temporary phenomenon lasting for a short time unless there is a fresh secondary injury due to a clot, hypoxia or electrolyte disturbance.

Treatment is aimed at preventing the secondary events. Clinical and ICP monitoring will help.

The following therapeutic measures are available.

1) I line of management:

General measures form the I line of treatment essentially making the patient comfortable and ABC of trauma management are effectively instituted. Careful attention to

nutrition and electrolytes, bladder and bowel functions and appropriate treatment of infections are instituted promptly.

Adequate analgesia is often forgotten; it is a must even in  unconscious patients.  

2) II line of management 

Induced cerebral vasoconstriction - Hyperventilation, hyper baric O2, hypothermia

Osmotherapy - Mannitol, glycerol ,urea

Anesthetic agents - Barbiturates, gamma hydroxybutyrate, Etomidate, 

Surgical decompression -Many do not recommend decompressive surgery.

This aims at combating increased ICP which is assumed when there is neurological deterioration or if ICP monitoring is available and the ICP goes above 25 cm of H2O.

There is a small group of surgeons who start the II line in conditions where ICP is expected to raise without waiting for a rise. Many feel that institution of measures to reduce ICP invariably compromises CBF and wait for the raise in ICP before starting the II line of management. 

Debate continues in the II line of management as well. Some prefer osmotherapy alone as the II line. Some prefer measures to induce cerebral vasoconstriction, thereby reducing CBF and reduce ICP. Some go for both.

a) Hyperventilation aims at keeping the pCO2 down to 30-25 mm Hg so that CBF falls and cerebral blood volume is reduced and thereby reducing the ICP. Prolonged hyperventilation should be avoided and becomes in- effective after about 24 hrs. In addition it causes hypo tension due to decreased venous return . It is claimed a pCO2 under 20 results in ischemia, although there is no experimental proof for the same. 

The present trend is to maintain normal ventilation with pCO2 in the range of 30 - 35 mmHg and pO2 of 120 - 140 mmHg. When there is clinical deterioration such as pupillary dilatation or widened pulse pressure, hyperventilation may be instituted (preferably with an Ambu bag) until the ICP comes down.

Hyper baric O2, hypothermia are still in experimental stage, especially in Japan . They basically induce cerebral vasoconstriction and reduce the cerebral blood volume and the ICP.

b) Osmotherapy is useful in the cytotoxic edema stage, when capillary permeability is intact, by increasing the serum osmolality. Mannitol is still the magic drug to reduce to ICP, but only if used properly: it is the most common osmotic diuretic used. It may also act as a free radical scavenger.

Mannitol is not inert and harmless. Glycerol and urea are hardly used these days. Several theories have been advanced concerning the mechanism by which it reduces ICP.

  1) It increases the erythrocyte flexibility, which decreases blood viscosity and causes a reflex vasoconstriction that reduces cerebral blood volume and decreases ICP and may reduce CSF production by the choroids plexus. In small doses it protects the brain from ischemic insults due to increased erythrocyte flexibility. 

  2) The diuretic effect is mainly around the lesion, where blood brain barrier integrity is impaired and there is no significant effect on normal brain. As one would have observed, intraaxial lesions respond better than extra axial lesions.

  3) Another theory is, mannitol with draws water across the ependyma of the ventricles in a manner analogous to that produced by ventricular drainage.

The traditional dose is 1 gm/kg/24 hr of 20% to 25% i.v. either as a bolus or more commonly intermittently. 

There is no role for dehydration. Mannitol effect on ICP is maximal 1/2 hr after infusion and lasts for 3 or 4 hrs as a rule. The correct dose is the smallest dose which will have sufficient effect on ICP. When repeated doses are required, the base line serum osmolality gradually increases and when this exceeds 330 mosm/1 mannitol therapy should cease. Further use is ineffective and likely to induce renal failure. Diuretics such as frusemide, either alone or in conjunction with mannitol help to hasten its excretion and reduce the baseline serum osmolality prior to next dose. Some claim, that frusemide compliments mannitol and increases the output. Some give frusemide before mannitol, so that it reduces circulatory overload. The so called rebound phenomenon is due to reversal of osmotic gradient as a result of progressive leak of the osmotic agent across defective blood brain barrier, or is due to recurrence of increased ICP.

c) Barbiturates can lower the ICP when other measures fail; but have no prophylactic value. They inhibit free radical mediated lipid peroxidation and suppress cerebral metabolism; cerebral metabolic requirements and thereby cerebral blood volume are reduced resulting in the reduction of ICP. 

Phenobarbital is most widely used. A loading dose of 10mg/kg over 30 minutes and 1-3mg/kg every hour is widely employed. Facilities for close monitoring of ICP and hemodynamic instability should accompany any barbiturate therapy.

d) High dose steroid therapy was popular some years ago and still used by some. It restores cell wall integrity and helps in recovery and reduce edema. Barbiturates and other anesthetic agents reduce CBF and arterial pressure thereby reducing ICP. In addition it reduces brain metabolism and energy demand which facilitate better healing.

Surgical decompression:

Decompressive craniotomies such as sub temporal decompression are recommended only in highly selected patients these days. Herniation of brain thro' defect, cause further injury, further edema and further increased ICP. But in occasional cases, when every other measure has failed, such decompression craniotomy may be justified.

There are occasional reports from few centers  recommending such procedures.

Medicine is an ever changing field. Standard and safety precautions must be followed. But

as new research and clinical experience broaden our knowledge, changes in treatment and drugs therapy become necessary or appropriate. Ultimately it is the responsibility of treating surgeon relying on his experience and knowledge of the patient to decide the best for the patient.

Intracranial pressureIntracranial pressure, (ICP), is the pressure exerted by the cranium

on the brain tissue, cerebrospinal fluid (CSF), and the brain's circulating blood volume. ICP is a dynamic phenomenon constantly fluctuating in response to activities such as exercise, coughing, straining, arterial pulsation, and respiratory cycle. 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. 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.

Intracranial pressure 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 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. These compensatory mechanisms are able to maintain a normal ICP for any change in volume less than approximately 100–120 mL.

Intracranial pressure 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. ICP is very likely to cause severe harm if it rises too high. Very high intracranial pressures are usually fatal if prolonged, but children can tolerate higher pressures for longer periods. 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. It is a cause of reflex bradycardia.

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 . 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. 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.

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 increace 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 LOC, Cheyne-Stokes respirations, hyperventilation, sluggish dilated pupils and widened pulse pressure.

Intracranial pressure Causes of increased ICP

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

Intracranial pressure Signs and symptoms of increased ICP

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

Intracranial pressure Treatment of increased ICP

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. 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 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. 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 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. 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. When it is necessary to decrease cerebral blood flow, MAP can be lowered using common antihypertensive agents such as calcium channel blockers.

Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption, as well as increasing blood pressure.. 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.

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 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)

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

Intracranial pressure Low ICP

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.