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Intracranial Pressure

Intracranial Pressure

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Intracranial pressure

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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 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

Any change in volume greater than 100–120 mL would mean a drastic increase in ICP. is normally fairly constant due to autoregulation. once the ICP has reached around 25 mmHg. the uncus hippocampus becomes compressed against the free edge of the tentorium cerebelli. but to increase. this is due to failure of intracranial compliance. This results in increased cerebral blood volume. However. small increases in brain volume can lead to marked elevations in ICP. Characteristics of stage 2 of intracranial hypertension include . if caused by a unilateral space-occupying lesion (eg.[12] Prognosis is much worse in patients with midline shift than in those without it. [edit] Intracranial hypertension Minimal increases in ICP due to compensatory mechanisms is known as stage 1 of intracranial hypertension. 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). frequently leading to brainstem compression. In uncal herniation. cerebral perfusion falls. Cerebral edema. the pressure of blood flowing to the brain. the ICP has no other resource. 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. 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. and hypoxic conditions are well recognized causes of this secondary injury.[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. which increases ICP. lowering CPP further and causing a vicious cycle. If brainstem compression is involved. Cerebral perfusion pressure (CPP). Traumatic brain injury is a devastating problem with both high subsequent morbidity and high mortality. This results in widespread reduction in cerebral flow and perfusion. When the lesion volume continues to increase beyond the point of compensation. Increased blood pressure can also make intracranial hemorrhages bleed faster. This herniation is often referred to as "coning". In the intensive care unit.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. Midline shift can compress the ventricles and lead to hydrocephalus. hypotension. also increasing ICP. an haematoma) can result in midline shift. Another dire consequence of increased ICP combined with a space-occupying process is brain herniation (usually uncal or tonsilar). eventually leading to ischemia and brain infarction. This is stage 2 of intracranial hypertension. 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]. Severely raised ICP. The body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. it may lead to respiratory depression and is potentially fatal.

If papilledema is protracted.compromise of neuronal oxygenation and systemic arteriolar vasoconstriction to increase MAP and CPP. altered level of consciousness. hyperventilation.. subarachnoid hemorrhage. by Arnold-Chiari malformation). ocular palsies. infectious.g. vomiting without nausea. it may lead to visual disturbances. Neurologic changes seen in increased ICP are mostly due to hypoxia and hypercapnea and are as follows: decreased level of consciousness (LOC). infarction with oedema. . symptoms and signs that suggest a rise in ICP including headache. or obstruction of superior mediastinal or jugular veins. Cheyne-Stokes respirations.g. sluggish dilated pupils and widened pulse pressure. with dramatic changes in ICP with small changes in volume. increase in venous pressure can be due to venous sinus thrombosis. Main article: hydrocephalus • • • • increased CSF production can occur in meningitis. or abscess all tend to deform the adjacent brain. or choroid plexus tumor. it becomes more and more difficult to squeeze blood into the intracranial space. Stage 3 intracranial hypertension is characterised by a sustained increased ICP. generalized brain swelling can occur in ischemic-anoxia states. In stage 3. or hemorrhagic). acute liver failure. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts. The body’s response to a decrease in CPP is to raise blood pressure and dilate blood vessels in the brain. or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption). optic atrophy. extensive meningeal disease (e. hypertensive encephalopathy. as the ICP approaches the MAP. and eventually blindness. hypercarbia. contusions. carcinomatous. and Reye hepatocerebral syndrome. subdural or epidural hematoma. granulomatous. [edit] Causes Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased: • • • • mass effect such as brain tumor. This results in increased cerebral blood volume. eventually leading to ischemia and brain infarction. heart failure. pseudotumor cerebri. back pain and papilledema. e. This results in widespread reduction in cerebral flow and perfusion.. which increases ICP. lowering CPP and perpetuating this vicious cycle. obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain. Idiopathic or unknown cause (idiopathic intracranial hypertension) Cerebral venous sinus thrombosis Acute liver failure[13] [edit] Signs and symptoms In general.

so hyperventilating a patient with a ventilator or bag valve mask can temporarily reduce ICP. bradycardia. In patients who have high ICP it is particularly important to ensure adequate airway. Only when ICP exceeds 40–50 mmHg do CPP and cerebral perfusion decrease to a level that results in loss of consciousness.[16] Inadequate oxygenation also forces brain cells to produce energy using anaerobic metabolism. Cushing's triad involves an increased systolic blood pressure.[17] Hyperventilation is still used if ICP is resistant to other methods of control. and an abnormal respiratory pattern.[citation needed] [edit] Treatment The treatment for IH depends on the etiology. and the Cushing's triad. the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation. the effects of ICP differ because their cranial sutures have not closed. increasing the flow of blood to the brain and causing the ICP to rise. and oxygenation.[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). major considerations in acute treatment of increased ICP relates to the management of stroke and cerebral trauma. A side effect of this is that it could lower pressure of blood to the head. also dilating blood vessels and exacerbating the problem. improving venous drainage. bulge when ICP gets too high. In infants and small children. In addition to management of the underlying causes.[17] Furthermore. Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate. abducens (CrN VI) palsies. which could cause the vessels to rapidly dilate if carbon dioxide levels were returned to normal too quickly. in which breathing is rapid for a period and then absent for a period. ICP can also be lowered by raising the head of the bed. resulting in a reduced and possibly .In addition to the above.[15] Hyperventilation can occur when the brain stem or tegmentum is damaged. breathing.[14] In children. A swollen optic nerve is a reliable sign that ICP exists. blood vessels constrict when carbon dioxide levels are below normal. if mass effect is present with resulting displacement of brain tissue. which produces lactic acid and lowers pH. 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.[6] Conversely. Any further elevations will lead to brain infarction and brain death. or soft spots on the head where the skull bones have not yet fused. additional signs may include pupillary dilatation. the fontanels. a widened pulse pressure. 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. Cheyne-Stokes respiration. a slow heart rate is especially suggestive of high ICP. occurs because of injury to the cerebral hemispheres or diencephalon. In infants. and so is no longer widely used.

however prolonged administration may lead to increase in ICP.[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.[16] Analgesia and sedation (particularly in the pre-hospital. Thus if full sedation alone is ineffective. remove wastes and thereby lessen swelling. and this may also increase the ICP. and seizures can increase metabolic demands and oxygen consumption. oxygenate tissues. but can mask signs of seizures. This type of drain is known as an EVD (extraventricular drain). Sandbags may be used to further limit neck movement. ER.[6]. MAP can be lowered using common antihypertensive agents such as calcium channel blockers.[17] The section of bone removed. as well as increasing blood pressure. 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. removal of this via craniotomy will decrease raised ICP's. Alternatively a synthetic material may be used to replace the removed bone section (see cranioplasty) [edit] Low ICP Main article: Intracranial hypotension . Paralysis allows the cerebral veins to drain more easily. In the hospital.[18] Struggling. and intensive care setting) are used to reduce agitation and metabolic needs of the brain. restlessness. Venous drainage may also be impeded by external factors such as hard collars to immobilise the neck in trauma patients. patients may be paralyzed with drugs such as atracurium. drainage of CSF via lumbar puncture can be used as a treatment.[6] In rare situations when only small amounts of CSF are to be drained to reduce ICP's. increase perfusion. Craniotomies are holes drilled in the skull to remove intracranial hematomas or relieve pressure from parts of the brain. known as a bone flap. 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. A drastic treatment for increased ICP is decompressive craniectomy.[15] When it is necessary to decrease cerebral blood flow.[17] Since hypertension is the body's way of forcing blood into the brain. but these medications may cause low blood pressure and other side 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. This helps to reduce the fluid within the intracranial space. medical professionals do not normally interfere with it when it is found in a head injured patient.[19]. blood pressure can be artificially raised in order to increase CPP.inadequate blood supply to the brain.[6] As raised ICP's may be caused by the presence of a mass. and the drugs can have other harmful effects. 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.

dysfunctional. or infection of the linings of the brain may cause an increase in pressure within the cranium. Trauma to the head.RightHealth. though increased intracranial pressure is a far more common (and far more serious) sign. decreased ICP is the result of lumbar puncture or other medical procedures involving the brain or spinal cord. inflammation.com/Hypertension Home > Library > Health > Dental Dictionary n Pressure that occurs within the cranium. only the intravenous administration of caffeine and theophylline has shown to be particularly useful. the syndrome is self-limiting. and may become life-threatening. Various medical imaging technologies exist to assist in identifying the cause of decreased ICP. Brain pressure www. English▼ . If persistent intracranial hypotension is the result of a lumbar puncture. especially if it is the result of a medical procedure. The symptoms for both conditions are often the same. Often. Main article: Cerebrospinal fluid leak Spontaneous intracranial hypotension may occur as a result of an occult leak of CSF into another body cavity.It is also possible for the intracranial pressure to drop below normal levels. a "blood patch" may be applied to seal the site of CSF leakage. Various medical treatments have been proposed.[20] Intracranial pressure Dental Dictionary: intracranial pressure Sponsored Links Brain pressure Get the Answers You're Looking For. which is painful. More commonly. leading many medical experts to believe that it is the change in pressure rather than the pressure itself causing the above symptoms.

Veterinary Dictionary: ICP Top Home > Library > Animal Life > Veterinary Dictionary Intracranial pressure. ICP) Pressure within the cranial cavity. Wikipedia: Intracranial pressure Top .. (Abbr. • Browse: Unanswered questions | Most-recent questions | Reference library Enter a question or phrase....• • Search unanswered questions. Search: All sources Community Q&A Reference topics • Browse: Unanswered questions | New questions | New answers | Reference library Related Videos: Intracranial pressure Top Medical Dictionary: intracranial pressure Top Home > Library > Health > Medical Dictionary n.

Home > Library > Miscellaneous > Wikipedia Intracranial pressure (ICP) is the pressure in the cranium and thus in the brain tissue and cerebrospinal fluid (CSF).4 Signs and symptoms o 2. valsalva (Queckenstedt's maneuver). blood volume. the upper limit of normal.5 Treatment 3 Low ICP 4 References 5 See also 6 External links The Monro-Kellie hypothesis The pressure-volume relationship between ICP. is elevation of the pressure in the cranium.[5] The principal buffers for increased volumes include both CSF and.[3][4][5] The Monro-Kellie hypothesis states that the cranial compartment is incompressible.2 Intracranial hypertension o 2. treatment to reduce ICP is needed. Intracranial hypertension. and communication with the vasculature (venous and arterial systems). is normally 7–15 mmHg for a supine adult. this pressure is exerted on the brain's intracranial blood circulation vessels. These buffers respond to increases in volume of the remaining intracranial . ICP is measured in millimeters of mercury (mmHg) and. commonly abbreviated IH. such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another. blood. ICP is normally 0–10 mm Hg. and brain tissue. and the volume inside the cranium is a fixed volume. CSF. at 20–25 mm Hg. The cranium and its constituents (blood.[1] Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium. volume of CSF. and brain tissue) create a state of volume equilibrium.[2] Contents [hide] • • • • • • 1 The Monro-Kellie hypothesis 2 Increased ICP o 2. at rest.1 Pathophysiology o 2.[citation needed] CSF pressure has been shown to be influenced by abrupt changes in intrathoracic pressure during coughing (intraabdominal pressure). through the production and absorption of CSF and pulsates approximately 1mm Hg in a normal healthy adult. to a lesser extent. and becomes negative (averaging −10 mmHg) in the vertical position. and cerebral perfusion pressure (CPP) is known as the Monro-Kellie doctrine or the Monro-Kellie hypothesis. ICP is maintained in a tight normal range dynamically.3 Causes o 2.

but children can tolerate higher pressures for longer periods. shift brain structures.[5] These compensatory mechanisms are able to maintain a normal ICP for any change in volume less than approximately 100–120 mL. directly correlated with poor outcome. an increase in lesion volume (e. For example. and restrict blood supply to the brain.[7] Very high intracranial pressures are usually fatal if prolonged. most commonly due to head injury leading to intracranial hematoma or cerebral edema can crush brain tissue. cause the brain to herniate. is an elevated intracranial pressure.[8] An increase in pressure. epidural hematoma) will be compensated by the downward displacement of CSF and venous blood.constituents.[citation needed] Increased ICP Severely high ICP can cause the brain to herniate.[6] ICP is very likely to cause severe harm if it rises too high. One of the most damaging aspects of brain trauma and other conditions. contribute to hydrocephalus.g. [10] Pathophysiology .[9] It is a cause of reflex bradycardia.

The cranium and the vertebral canal. 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. Intracranial hypertension . hypotension. If brainstem compression is involved. The body’s response to a fall in CPP is to raise systemic blood pressure and dilate cerebral blood vessels. this is due to failure of intracranial compliance. eventually leading to ischemia and brain infarction. and hypoxic conditions are well recognized causes of this secondary injury. However. 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). the uncus hippocampus becomes compressed against the free edge of the tentorium cerebelli. cerebral perfusion falls. This results in increased cerebral blood volume. Cerebral perfusion pressure (CPP).[12] Prognosis is much worse in patients with midline shift than in those without it. small increases in brain volume can lead to marked elevations in ICP. Another dire consequence of increased ICP combined with a space-occupying process is brain herniation (usually uncal or tonsilar). Traumatic brain injury is a devastating problem with both high subsequent morbidity and high mortality. brain. the pressure of blood flowing to the brain. 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. such that the increase in any of its contents. lowering CPP further and causing a vicious cycle. or CSF. 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]. frequently leading to brainstem compression. it may lead to respiratory depression and is potentially fatal. This herniation is often referred to as "coning". this relationship is known as the Monro-Kellie doctrine. will tend to increase the ICP. if caused by a unilateral space-occupying lesion (eg. Severely raised ICP. blood. once the ICP has reached around 25 mmHg. In addition. is normally fairly constant due to autoregulation. an haematoma) can result in midline shift. This results in widespread reduction in cerebral flow and perfusion.[11] One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. In the intensive care unit. any increase in one of the components must be at the expense of the other two. Increased blood pressure can also make intracranial hemorrhages bleed faster. Midline shift can compress the ventricles and lead to hydrocephalus. which increases ICP. a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Cerebral edema. along with the relatively inelastic dura. as well as the slight ability to stretch the falx cerebri between the hemispheres and the tentorium between the hemispheres and the cerebellum. also increasing ICP. form a rigid container. In uncal herniation. 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. Once the ICP approaches the level of the mean systemic pressure.

hyperventilation. and Reye hepatocerebral syndrome. Stage 3 intracranial hypertension is characterised by a sustained increased ICP. heart failure. Any change in volume greater than 100–120 mL would mean a drastic increase in ICP. which increases ICP. This results in widespread reduction in cerebral flow and perfusion. sluggish dilated pupils and widened pulse pressure. or abscess all tend to deform the adjacent brain. pseudotumor cerebri. it becomes more and more difficult to squeeze blood into the intracranial space. as the ICP approaches the MAP. This results in increased cerebral blood volume. or choroid plexus tumor. infarction with oedema. or obstruction of superior mediastinal or jugular veins. extensive meningeal disease (e. Idiopathic or unknown cause (idiopathic intracranial hypertension) Cerebral venous sinus thrombosis Acute liver failure[13] Signs and symptoms .. the ICP has no other resource. but to increase.. lowering CPP and perpetuating this vicious cycle. subarachnoid hemorrhage. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts. Main article: hydrocephalus • • • • increased CSF production can occur in meningitis. Neurologic changes seen in increased ICP are mostly due to hypoxia and hypercapnea and are as follows: decreased level of consciousness (LOC). In stage 3. e. granulomatous. acute liver failure.g.Minimal increases in ICP due to compensatory mechanisms is known as stage 1 of intracranial hypertension. hypercarbia. Characteristics of stage 2 of intracranial hypertension include compromise of neuronal oxygenation and systemic arteriolar vasoconstriction to increase MAP and CPP. The body’s response to a decrease in CPP is to raise blood pressure and dilate blood vessels in the brain. contusions. subdural or epidural hematoma. or hemorrhagic). infectious. with dramatic changes in ICP with small changes in volume. by Arnold-Chiari malformation). increase in venous pressure can be due to venous sinus thrombosis. or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).g. hypertensive encephalopathy. When the lesion volume continues to increase beyond the point of compensation. generalized brain swelling can occur in ischemic-anoxia states. eventually leading to ischemia and brain infarction. Cheyne-Stokes respirations. Causes Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased: • • • • mass effect such as brain tumor. This is stage 2 of intracranial hypertension. carcinomatous. obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain.

In patients who have high ICP it is particularly important to ensure adequate airway. which could cause the vessels to rapidly dilate if carbon dioxide levels were returned to normal too quickly.In general. or soft spots on the head where the skull bones have not yet fused. and oxygenation. A swollen optic nerve is a reliable sign that ICP exists. Only when ICP exceeds 40–50 mmHg do CPP and cerebral perfusion decrease to a level that results in loss of consciousness. patients with normal blood pressure retain normal alertness with ICP of 25– 40 mmHg (unless tissue shifts at the same time). In addition to management of the underlying causes.[citation needed] Treatment The treatment for IH depends on the etiology. in which breathing is rapid for a period and then absent for a period. In infants and small children. the fontanels. Cushing's triad involves an increased systolic blood pressure. and an abnormal respiratory pattern. If papilledema is protracted.[6] Conversely. major considerations in acute treatment of increased ICP relates to the management of stroke and cerebral trauma.[17] Furthermore. back pain and papilledema. bulge when ICP gets too high. a widened pulse pressure. optic atrophy. the effects of ICP differ because their cranial sutures have not closed. bradycardia. Any further elevations will lead to brain infarction and brain death.[15] Hyperventilation can occur when the brain stem or tegmentum is damaged. symptoms and signs that suggest a rise in ICP including headache. the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation. which produces lactic acid and lowers pH. altered level of consciousness. it may lead to visual disturbances. also dilating blood vessels and exacerbating the problem. blood vessels constrict when carbon dioxide levels are below normal. occurs because of injury to the cerebral hemispheres or diencephalon. 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. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate. ocular palsies.[17] . increasing the flow of blood to the brain and causing the ICP to rise. breathing. and the Cushing's triad. abducens (CrN VI) palsies. Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive.[15] As a rule. vomiting without nausea. additional signs may include pupillary dilatation. if mass effect is present with resulting displacement of brain tissue. a slow heart rate is especially suggestive of high ICP. Cheyne-Stokes respiration. In addition to the above.[14] In children. and so is no longer widely used. and eventually blindness.[16] Inadequate oxygenation also forces brain cells to produce energy using anaerobic metabolism. In infants.

resulting in a reduced and possibly inadequate blood supply to the brain. restlessness. remove wastes and thereby lessen swelling. but can mask signs of seizures.[6]. 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. ER. Paralysis allows the cerebral veins to drain more easily. patients may be paralyzed with drugs such as atracurium.[6] As raised ICP's may be caused by the presence of a mass. This helps to reduce the fluid within the intracranial space.Hyperventilation is still used if ICP is resistant to other methods of control.[17] The section of bone removed. blood pressure can be artificially raised in order to increase CPP. removal of this via craniotomy will decrease raised ICP's. In the hospital. MAP can be lowered using common antihypertensive agents such as calcium channel blockers. however prolonged administration may lead to increase in ICP. improving venous drainage. 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.[6] In rare situations when only small amounts of CSF are to be drained to reduce ICP's. but these medications may cause low blood pressure and other side effects. oxygenate tissues. and seizures can increase metabolic demands and oxygen consumption. ICP can also be lowered by raising the head of the bed. and the drugs can have other harmful effects. Sandbags may be used to further limit neck movement. A side effect of this is that it could lower pressure of blood to the head. 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. one may administer IV mannitol to create a hypertonic solution within the blood to draw water out of the neurons. A drastic treatment for increased ICP is decompressive craniectomy.[19].[17] Since hypertension is the body's way of forcing blood into the brain. 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. as well as increasing blood pressure.[16] Analgesia and sedation (particularly in the pre-hospital. Thus if full sedation alone is ineffective. increase perfusion. known as a bone flap. Craniotomies are holes drilled in the skull to remove intracranial hematomas or relieve pressure from parts of the brain.[18] Struggling.[6] If there is an intact blood brain barrier. medical professionals do not normally interfere with it when it is found in a head injured patient. and this may also increase the ICP. Alternatively a synthetic material may be used to replace the removed bone section (see cranioplasty) .[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. and intensive care setting) are used to reduce agitation and metabolic needs of the brain. Venous drainage may also be impeded by external factors such as hard collars to immobilise the neck in trauma patients.[15] When it is necessary to decrease cerebral blood flow. drainage of CSF via lumbar puncture can be used as a treatment. This type of drain is known as an EVD (extraventricular drain).

(a) CSF which is constantly secreted & after circulating absorbed at an equal rate. Straining. The conception of the cranium acting as a near rigid container of virtually incompressible substances in the form of brain. The spinal dural sheath can accept a quantity of CSF as it does not fit the canal closely. A. The symptoms for both conditions are often the same. If persistent intracranial hypotension is the result of a lumbar puncture. Apollo Hospitals. ICP is not a static state. CSF circulation is slow (500 to 700 ml/day). Vincent Thamburaj. the syndrome is self-limiting. Chennai . It is the term applied to the pressure of CSF with in the cranium. blood & CSF in known as the Monro Kellie doctrine. There is a rise with cardiac systole (due to distention of intracranial arteriolar tree which follows ) and a slower change in pressure with respiration. Intracranial pressure is a result of at least 2 factors.Low ICP Main article: Intracranial hypotension It is also possible for the intracranial pressure to drop below normal levels. compression of neck veins can also cause sudden. though increased intracranial pressure is a far more common (and far more serious) sign. a "blood patch" may be applied to seal the site of CSF leakage. in states of increased ICP there is increase in passage of blood through venous emissaries. decreased ICP is the result of lumbar puncture or other medical procedures involving the brain or spinal cord. Often. CSF can be displaced through the foramen magnum into spinal theca. Various medical imaging technologies exist to assist in identifying the cause of decreased ICP. The recording of ICP shows 2 forms of pressure fluctuations. India. the volume of the brain (about 1400ml in an adult) being constant. leading many medical experts to believe that it is the change in pressure rather than the pressure itself causing the above symptoms.[20] Intracranial pressure: Dr. falling with each inspiration and rising with expiration. Neurosurgeon . but one that is influenced by several factors. Various medical treatments have been proposed. being surrounded by a layer of loose areolar tissue & plexus of epidural veins. Main article: Cerebrospinal fluid leak Spontaneous intracranial hypotension may occur as a result of an occult leak of CSF into another body cavity. In addition. especially if it is the result of a medical procedure. 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. More commonly. At a given time the cranium contains 75 ml of CSF. considerable rise in pressure. . only the intravenous administration of caffeine and theophylline has shown to be particularly useful.

yet its blood flow represents 15% of resting cardiac output and uses 20% total amount of oxygen consumed. When pO2 falls to 30 mmHg. even moderate alterations of pCO2 are capable of markedly altering CBF. With normal cerebrovascular system and BP. there is marked decrease in pCO2 influence. Lundberg has described 3 wave patterns ICP waves (A. Cerebral vaso dilatation begins with pO2 of 50 mm Hg & CBF increases. that do not exceed an elevation of 50 mm Hg. Cerebral blood flow (CBF): The brain accounts for only 2% of total body weight. B. 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. The exact nature of this auto regulation is not known. (b) The humoral theory involves regulations by the direct effect of by.products of metabolism (c) Neurogenic theory rests on perivascular nerves. pO2 causes constriction of a non ischemic brain along with reduction in CBF. 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. CBF may have tripled. In old age and arteriosclerosis. and C waves). CBF ceases when art. 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 . increasing the pO2 has no effect. The auto regulation is influenced by various factors. Any obstruction to venous outflow will entail an increase in the volume of intracranial blood and ICP. 'Truncated' or atypical ones. 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. A waves are pathological. With less then 20 and more than 80 mmHg there is no further change. the cranium contains 75 ml. The effects of pO2 are not as marked as CO2 Changes.(b) Intracranial circulation of blood which is about 1000 litres per day delivered at a pressure of 100 mmHg and at a given time. (a) myogenic theory suggests direct reaction of the cerebral arterial smooth muscles to the stretch. Pathophysiology of increased intracranial pressure: . The ICP influences the CBF through the cerebral perfusion pressure (CPP) which is the difference between mean arterial pressure (MAP) and ICP. B & C waves are related to respiration and 'Traube-Hering-Mayer' waves respectively and are of little clinical significance. mean pressure drops to 20mm Hg.5% change in CBF as the pCO2 changes by 1 mmHg. As the ICP increases. are early indicators of neurological deterioration. Moderate variation of O2 above and below the normal level do not affect CBF. they are called 'plateau' waves which are pathological. Each 24 hours brain requires 1000 liters in order to obtain 71 lit of oxygen and 100 gm of glucose.ICP. In chronically hypertensive this auto regulation limits appear to be reset. Within the range of 30 to 60 mm Hg there is a 2. In ischemic hemisphere.

Similarly a frontal mass can cause axial distortion to impair brainstem perfusion.pressure relationship). Transtentorial herniation with brainstem compression can lead to clinical deterioration even with adequate CBF. A temporal mass may cause uncal herniation without raised ICP. The midbrain involvement result in Chyne-Stokes respiration. there is sustained hyperventilation. bradycardia (Cushing's response) and respiratory changes. hematoma and contusion). If it fails. the ICP raises to a plateau level at which the increase level of CSF absorption keeps pace with the increase in volume. In acute hydrocephalus. there is rapid deterioration as there is no time for compensation.Increased ICP is defined as a sustained elevation in pressure above 20mm of Hg/cm of H20. Clinical features if raised ICP: Raised ICP causes arterial hypertension. When sufficient CSF has been absorbed to accommodate the volume the ICP returns to normal. because of the shift of brain and disturbed auto regulation. 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. The craniospinal cavity may be considered as a balloon. Many patients with benign ICT or obstructive hydrocephalus show little or no ill effect. Expansion to a critical volume does however cause persistent raise in ICP which thereafter increases logarithmically with increasing volume (Volume . In patients with parenchymal lesion (tumor. 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. The cause of raise in ICP and the rate at which it occurs are also important. Intermittent expansion causes only a transient rise in ICP at first. It is traditionally accepted that hypertension and bradycardia are due to ischaemia or pressure on the brainstem. The ICP finally raises to the level of arterial pressure which it self begins to increase. CBF may by compromised with relatively low levels of ICP. 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 reason being the brain it self is normal and auto regulation is probably intact. The respiratory changes depend on the level of brainstem involved. When midbrain and pons are involved. This is accompanied by dilatation of small pial arteries and some slowing of venous flow which is followed by pulsatile venous flow. There is rapid and shallow respiration when upper medulla involvement with ataxic breathing in the . brain death occurs. accompanied by bradycardia or other disturbances of heart rhythm (Cushing response). During slow increase in volume in a continuous mode.

(2) Other most commonly used devices are the hollow screw and bolt devices. Insertion of ventricular catheter is not always simple and can cause hemorrhage and infection (5%). There is nothing to achieve in monitoring ICP in the patients with GCS of less than 3. 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. if any. Richmond screw and Becker bolt are used extra durally. (b) Low BP (c) Those who require ventilation. The clinical monitoring is age old and time tested. Pulmonary edema seems to be due to increased sympathetic activity as a result of the effects of raised ICP on the hypothalamus. tympanic membrane displacement. It employs a fibre optic system to detect the distortion of a tiny mirror within with balloon system. (3) Ladd device is currently in wide use. give a clue. Ladd fiber optic system has been used extra cutaneously. and the sub dural catheter. (2) Transcranial doppler. Bradycardia. A fluid filled catheter in the subdural space. Invasive methods: (1) Intraventricular monitoring remains one of the popular techniques. Additional advantage is the potential for draining CSF therapeutically. pupillary dilation are normally accepted as signs of increased ICP. (3) Manual feeling the craniotomy flap or skull defect. connected to arterial pressure monitoring system is cost effective and serves the purpose adequately. Several devices have been described for measuring ICP through open fontanel. Methods: Non invasive methods: (1) Clinical deterioration in neurological status is widely considered as sign of increased ICP. especially in patients with ventriculomegaly. extradural and even extra cutaneously. It can be used in the subdural . medulla or cervical spinal cord.final stages. increased pulse pressure. . and ultrasound 'time of flight' techniques have been advocated.

These systems are not widely used. modern intraparenchymal sensors help study the chemical environment of the site of pathology. 2) Pre op monitoring helps in assessment of NPH before a shunting procedure. Treatment of increased ICP: There is no doubt the best treatment for increased ICP is the removal of the causative lesion such as tumors. regulation of cerebral blood flow. 4) It can provide additional assessment of brain death. The effective maintenance requires a dedicated team effort. Monitoring is the only means by which therapy can be selectively employed and the effectiveness of therapy can be accurately studied. 3) Cerebral perfusion pressure (CPP). Intraparenchymal probes. In addition to ICP monitoring. 1) Where ever clinical monitoring is not possible. hydrocephalus or other chronic brain diseases. 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'. brain compensatory reserve. such as during hyper ventilation therapy and high dose barbiturate therapy. Ommaya reservoir is an alternative which can be punctured & CSF pressure readings are obtained. ICP monitoring helps. Post operative increased ICP should be uncommon these days with increased use of microscope and special techniques to avoid brain retraction. CSF absorption capacity. a basal meningioma once completely removed. and volume. either due to intraoperative injury to veins and post operative diuretic therapy as practiced in some centers. Brain perfusion effectively ceases in nearly all. and hemorrhage. hydrocephalus. (7) Lumbar puncture and measurement of CSF pressure for obvious reasons is not recommended. (5) Electronic devices (Camino & Galtesh design) are getting popular world over. and hematomas. 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. . infection. As we so often see. The problems of ICP monitoring are cost. the measured pressure may be compartmentalized and not necessarily representative of real ICP. (6) Fully implantable devices are valuable in a small group who requires long term ICP monitoring for brain tumors. has a smooth post op period. once ICP exceeds diastolic blood pressure. Benefits of ICP monitoring: There is no doubt that ICP monitoring helps in management of conditions where one expects prolonged intracranial hypertension.(4) A mechanically coupled surface monitoring device is the 'cardio search pneumatic sensor' used subdurally or extradurally. Cosmon intrcranial pressure telesensor can be implanted as a part of shunt system.

There is one school which questions the very existence of increased ICP. When there is clinical deterioration such as pupillary dilatation or widened pulse . hyper baric O2. Debate continues in the II line of management as well. 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 still a debate whether increased ICP is the cause or result of the brain damage.140 mmHg. Adequate analgesia is often forgotten. although there is no experimental proof for the same. Prolonged hyperventilation should be avoided and becomes in.35 mmHg and pO2 of 120 . 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. 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. Clinical and ICP monitoring will help. thereby reducing CBF and reduce ICP.urea Anesthetic agents . Some prefer measures to induce cerebral vasoconstriction. hypoxia or electrolyte disturbance. it is a must even in unconscious patients. In addition it causes hypo tension due to decreased venous return .Hyperventilation. The following therapeutic measures are available. It is claimed a pCO2 under 20 results in ischemia. 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 both compliment each other. The present trend is to maintain normal ventilation with pCO2 in the range of 30 . glycerol . Not all the midline shift seen in CTs indicate increased ICP. hypothermia Osmotherapy . It just means ICP was high during the shift. The shift takes longer to reverse even after ICP returns to normal . 2) II line of management Induced cerebral vasoconstriction . 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.Barbiturates. Etomidate.effective after about 24 hrs. Treatment is aimed at preventing the secondary events.Mannitol. 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. Some prefer osmotherapy alone as the II line. Careful attention to nutrition and electrolytes. Surgical decompression -Many do not recommend decompressive surgery. bladder and bowel functions and appropriate treatment of infections are instituted promptly. gamma hydroxybutyrate. Some go for both.

They basically induce cerebral vasoconstriction and reduce the cerebral blood volume and the ICP. hypothermia are still in experimental stage. cerebral metabolic requirements and thereby cerebral blood volume are reduced resulting in the reduction of ICP. It may also act as a free radical scavenger. hyperventilation may be instituted (preferably with an Ambu bag) until the ICP comes down. 1) It increases the erythrocyte flexibility. In addition it reduces brain metabolism and energy demand which facilitate better healing. Mannitol is still the magic drug to reduce to ICP. Diuretics such as frusemide. but have no prophylactic value. but only if used properly: it is the most common osmotic diuretic used. 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. . intraaxial lesions respond better than extra axial lesions. mannitol with draws water across the ependyma of the ventricles in a manner analogous to that produced by ventricular drainage. As one would have observed. A loading dose of 10mg/kg over 30 minutes and 1-3mg/kg every hour is widely employed. Glycerol and urea are hardly used these days. Mannitol effect on ICP is maximal 1/2 hr after infusion and lasts for 3 or 4 hrs as a rule. c) Barbiturates can lower the ICP when other measures fail. In small doses it protects the brain from ischemic insults due to increased erythrocyte flexibility. Hyper baric O2. that frusemide compliments mannitol and increases the output. When repeated doses are required. Some claim. especially in Japan . so that it reduces circulatory overload. b) Osmotherapy is useful in the cytotoxic edema stage. Facilities for close monitoring of ICP and hemodynamic instability should accompany any barbiturate therapy. Several theories have been advanced concerning the mechanism by which it reduces ICP. The traditional dose is 1 gm/kg/24 hr of 20% to 25% i. either as a bolus or more commonly intermittently. or is due to recurrence of increased ICP. by increasing the serum osmolality.pressure. the base line serum osmolality gradually increases and when this exceeds 330 mosm/1 mannitol therapy should cease. The correct dose is the smallest dose which will have sufficient effect on ICP. where blood brain barrier integrity is impaired and there is no significant effect on normal brain. Mannitol is not inert and harmless. Phenobarbital is most widely used. d) High dose steroid therapy was popular some years ago and still used by some. 3) Another theory is. It restores cell wall integrity and helps in recovery and reduce edema. There is no role for dehydration. Some give frusemide before mannitol. either alone or in conjunction with mannitol help to hasten its excretion and reduce the baseline serum osmolality prior to next dose. Barbiturates and other anesthetic agents reduce CBF and arterial pressure thereby reducing ICP. 2) The diuretic effect is mainly around the lesion. They inhibit free radical mediated lipid peroxidation and suppress cerebral metabolism. Further use is ineffective and likely to induce renal failure. when capillary permeability is intact.v. 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.

at 20–25 mm Hg. coughing. commonly abbreviated IH. further edema and further increased ICP. Herniation of brain thro' defect. cause further injury. The cranium and its constituents (blood. changes in treatment and drugs therapy become necessary or appropriate.g. and becomes negative (averaging −10 mmHg) in the vertical position. These buffers respond to increases in volume of the remaining intracranial constituents. and cerebral perfusion pressure (CPP) is known as the Monro-Kellie doctrine or the Monro-Kellie hypothesis. blood. such decompression craniotomy may be justified. epidural . treatment to reduce ICP is needed. and respiratory cycle. such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another. ICP is normally 0–10 mm Hg. (ICP). But in occasional cases. Medicine is an ever changing field. when every other measure has failed. and brain tissue. volume of CSF. There are occasional reports from few centers recommending such procedures. But as new research and clinical experience broaden our knowledge. and the brain's circulating blood volume. straining.Surgical decompression : Decompressive craniotomies such as sub temporal decompression are recommended only in highly selected patients these days. Ultimately it is the responsibility of treating surgeon relying on his experience and knowledge of the patient to decide the best for the patient. CSF. the upper limit of normal. is normally 7–15 mmHg for a supine adult. arterial pulsation. For example. The principal buffers for increased volumes include both CSF and. Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium. cerebrospinal fluid (CSF). an increase in lesion volume (e. blood volume. The Monro-Kellie hypothesis states that the cranial compartment is incompressible. is elevation of the pressure in the cranium. ICP is a dynamic phenomenon constantly fluctuating in response to activities such as exercise. to a lesser extent. at rest. Intracranial hypertension. Intracranial pressure Intracranial pressure. and the volume inside the cranium is a fixed volume. is the pressure exerted by the cranium on the brain tissue. Intracranial pressure The Monro-Kellie hypothesis The pressure-volume relationship between ICP. ICP is measured in millimeters of mercury (mmHg) and. and brain tissue) create a state of volume equilibrium. Standard and safety precautions must be followed.

but children can tolerate higher pressures for longer periods. Traumatic brain injury is a devastating problem with both high mortality and high subsequent morbidity. Very high intracranial pressures are usually fatal if prolonged. It is a cause of reflex bradycardia. Pathophysiology The cranium and the vertebral body. contribute to hydrocephalus. and axonal hypoxic conditions are . or CSF— will increase the ICP. Cerebral edema. and restrict blood supply to the brain. Intracranial pressure Increased ICP Severely high ICP can cause the brain to herniate. form a rigid container. small increases in brain volume can lead to marked elevations in ICP. hypotension. once the ICP has reached around 25 mmHg. blood. ICP is very likely to cause severe harm if it rises too high. 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). is an elevated intracranial pressure. shift brain structures. In addition. most commonly due to head injury leading to intracranial hematoma or cerebral edema can crush brain tissue. cause the brain to herniate. as well as the slight ability to stretch the falx cerebri between the hemispheres and the tentorium between the hemispheres and the cerebellum. One of the most damaging aspects of brain trauma and other conditions. any increase in one of the components must be at the expense of the other two. An increase in pressure. directly correlated with poor outcome. 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. this relationship is known as the Monro-Kellie doctrine. These compensatory mechanisms are able to maintain a normal ICP for any change in volume less than approximately 100–120 mL. such that the increase in any of its contents—brain. along with the relatively inelastic dura.hematoma) will be compensated by the downward displacement of CSF and venous blood. However.

severely compressing it. Any change in volume greater than 100–120 mL would mean a drastic increase in ICP. When the lesion volume continues to increase beyond the point of compensation. This results in increased cerebral blood volume. One of the main dangers of increased ICP is that it can cause ischemia by decreasing CPP. it becomes more and more difficult to squeeze blood into the intracranial space. This results in increased cerebral blood volume. Neurologic changes seen in increased ICP are mostly due to hypoxia and hypercapnea and are as follows: decreased LOC. In the intensive care unit. sluggish dilated pupils and widened pulse pressure. If brainstem compression is involved. is normally fairly constant due to autoregulation. The body’s response to a decrease in CPP is to raise blood pressure and dilate blood vessels in the brain. also increasing ICP. with dramatic changes in ICP with small changes in volume. Once the ICP approaches the level of the mean systemic pressure. Characteristics of stage 2 of intracranial hypertension include compromise of neuronal oxygenation and systemic arteriolar vasoconstriction to increace MAP and CPP. Highly increased ICP. Another dire consequence of increased ICP combined with a space-occupying process is brain herniation (usually uncal or cerebellar). as the ICP approaches the MAP. Midline shift can compress the ventricles and lead to buildup of CSF. The body’s response to a decrease in CPP is to raise blood pressure and dilate blood vessels in the brain. in which the brain is squeezed past structures within the skull. This results in widespread reduction in cerebral flow and perfusion. which increases ICP. the pressure causing blood flow to the brain. eventually leading to ischemia and brain infarction. eventually leading to ischemia and brain infarction. Increased blood pressure can also make intracranial hemorrhages bleed faster. lowering CPP further and causing a vicious cycle. hyperventilation. In stage 3. Stage 3 intracranial hypertension is characterised by a sustained increased ICP. Cerebral perfusion pressure (CPP). if caused by a one-sided space-occupying process (eg. it may lead to decreased respiratory drive and is potentially fatal. the ICP has no other resource. lowering CPP further and causing a vicious cycle. This results in widespread reduction in cerebral flow and perfusion. 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. which increases ICP.well recognized causes of this secondary injury. but to increase. . 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. This is stage 2 of intracranial hypertension. it becomes more and more difficult to squeeze blood into the intracranial space. This herniation is often referred to as "coning". a dangerous condition in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. an haematoma) can result in midline shift. 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 . Prognosis is much worse in patients with midline shift than in those without it. Cheyne-Stokes respirations.

hypertensive encephalopathy. In addition to the above. Idiopathic or unknown cause (idiopathic intracranial hypertension) Cerebral venous sinus thrombosis Acute liver failure Intracranial pressure Signs and symptoms of increased ICP In general. optic atrophy. extensive meningeal disease (e. contusions. if mass effect is present with resulting displacement of brain tissue. hypercarbia. infarction with oedema. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts. nausea.g. ocular palsies. • increase in venous pressure can be due to venous sinus thrombosis. • generalized brain swelling can occur in ischemic-anoxia states.. altered level of consciousness. If papilledema is protracted. or hemorrhagic). symptoms and signs that suggest a rise in ICP including headache. e. granulomatous. back pain and papilledema. heart failure. Cushing's triad involves an increased systolic blood . and eventually blindness. or obstruction of superior mediastinal or jugular veins.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. • • • • Main article: hydrocephalus increased CSF production can occur in meningitis. pseudotumor cerebri. acute liver failure. subdural or epidural hematoma. or choroid plexus tumor. vomiting. • obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain. by Arnold-Chiari malformation). it may lead to visual disturbances. subarachnoid hemorrhage. infectious. and Reye hepatocerebral syndrome. abducens (CrN VI) palsies. or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).g.. or abscess all tend to deform the adjacent brain. carcinomatous. and the Cushing's triad. additional signs may include pupillary dilatation.

In infants and small children. bradycardia. resulting in a reduced and possibly inadequate blood supply to the brain. and so is no longer widely used. Hyperventilation can occur when the brain stem or tegmentum is damaged. in which breathing is rapid for a period and then absent for a period. Any further elevations will lead to brain infarction and brain death. In addition to management of the underlying causes. Venous drainage may also be impeded by external factors such as hard collars to immobilise the neck in trauma patients. which produces lactic acid and lowers pH. breathing. Furthermore. increasing the flow of blood to the brain and causing the ICP to rise. Hyperventilation is still used if ICP is resistant to other methods of control. Sandbags may be used to further limit neck movement. the brain adjusts to the new level of carbon dioxide after 48 to 72 hours of hyperventilation. 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. Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. 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. which could cause the vessels to rapidly dilate if carbon dioxide levels were returned to normal too quickly. the fontanels. and this may also increase the ICP. In infants. a widened pulse pressure. occurs because of injury to the cerebral hemispheres or diencephalon. and an abnormal respiratory pattern. so hyperventilating a patient with a ventilator or bag valve mask can temporarily reduce ICP. As a rule. also dilating blood vessels and exacerbating the problem. Only when ICP exceeds 40– 50 mmHg do CPP and cerebral perfusion decrease to a level that results in loss of consciousness. A side effect of this is that it could lower pressure of blood to the head. improving venous drainage. In children. In patients who have high ICP it is particularly important to ensure adequate airway. Intracranial pressure Treatment of increased ICP The treatment for IH depends on the etiology. a slow heart rate is especially suggestive of high ICP. . blood vessels constrict when carbon dioxide levels are below normal. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate. major considerations in acute treatment of increased ICP relates to the management of stroke and cerebral trauma. the effects of ICP differ because their cranial sutures have not closed. bulge when ICP gets too high. patients with normal blood pressure retain normal alertness with ICP of 25–40 mmHg (unless tissue shifts at the same time). Conversely. or soft spots on the head where the skull bones have not yet fused. Cheyne-Stokes respiration. and oxygenation. Inadequate oxygenation also forces brain cells to produce energy using anaerobic metabolism. ICP can also be lowered by raising the head of the bed.pressure.

When it is necessary to decrease cerebral blood flow. removal of this via craniotomy will decrease raised ICP's. oxygenate tissues. restlessness. blood pressure can be artificially raised in order to increase CPP. medical professionals do not normally interfere with it when it is found in a head injured patient. patients may be paralyzed with drugs such as atracurium. known as a bone flap. Thus if full sedation alone is ineffective. 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. .In the hospital. The section of bone removed. Craniotomies are holes drilled in the skull to remove intracranial hematomas or relieve pressure from parts of the brain. Analgesia and sedation (particularly in the pre-hospital. but can mask signs of seizures.. As raised ICP's may be caused by the presence of a mass. and seizures can increase metabolic demands and oxygen consumption. increase perfusion. In rare situations when only small amounts of CSF are to be drained to reduce ICP's. ER. This type of drain is known as an EVD (extraventricular drain). MAP can be lowered using common antihypertensive agents such as calcium channel blockers. 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. drainage of CSF via lumbar puncture can be used as a treatment. 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. Paralysis allows the cerebral veins to drain more easily. though increased intracranial pressure is a far more common (and far more serious) sign. but these medications may cause low blood pressure and other side effects. and the drugs can have other harmful effects. 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. Struggling. leading many medical experts to believe that it is the change in pressure rather than the pressure itself causing the above symptoms.. Intracranial pressure Low ICP It is also possible for the intracranial pressure to drop below normal levels. Since hypertension is the body's way of forcing blood into the brain. as well as increasing blood pressure. remove wastes and thereby lessen swelling. The symptoms for both conditions are often the same. A drastic treatment for increased ICP is decompressive craniectomy. 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. and intensive care setting) are used to reduce agitation and metabolic needs of the brain.

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