| Intracranial pressure | |
|---|---|
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| Severely high ICP can cause the brain toherniate. | |
| Specialty | Neurosurgery,Neurology |
| Types | Increased, normal, decreased |
Intracranial pressure (ICP) is the pressure exerted by fluids such ascerebrospinal fluid (CSF) inside theskull and on thebrain tissue. ICP is measured in millimeters of mercury (mmHg) and at rest, is normally 7–15 mmHg for asupine adult. This equals to 9–20cmH2O, which is a commonscale used inlumbar punctures.[1] The body has various mechanisms by which it keeps the ICP stable, with CSF pressures varying by about 1 mmHg in normal adults through shifts in production and absorption of CSF.
Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium. CSF pressure has been shown to be influenced by abrupt changes in intrathoracic pressure during coughing (which is induced by contraction of thediaphragm andabdominal wall muscles, the latter of which also increases intra-abdominal pressure), thevalsalva maneuver, and communication with thevasculature (venous andarterial systems).
Intracranial hypertension (IH), also calledincreased ICP (IICP) orraised intracranial pressure (RICP), refers to elevated pressure in the cranium. 20–25 mmHg is the upper limit of normal at which treatment is necessary, though it is common to use 15 mmHg as the threshold for beginning treatment.[2]
In general, symptoms and signs that suggest a rise in ICP includeheadache,vomiting withoutnausea,ocular palsies,altered level of consciousness,back pain andpapilledema. If papilledema is protracted, it may lead to visual disturbances,optic atrophy, and eventually blindness. The headache is classically a morning headache that may wake the person up. The brain is relatively poorly supplied by oxygen as a result of mildhypoventilation during the sleeping hours leading tohypercapnia andvasodilation.Cerebral edema may worsen during the night due to the lying position. The headache is worse on coughing, sneezing, or bending, and progressively worsens over time. There may also be personality or behavioral changes.[clarification needed]
In addition to the above, ifmass effect is present with resulting displacement of brain tissue, additional signs may includepupillary dilatation,abducens palsies, andCushing's triad. Cushing's triad involves an increasedsystolic blood pressure, a widenedpulse pressure,bradycardia, and an abnormal respiratory pattern.[3] In children, a low heart rate is especially suggestive of high ICP.[citation needed]Intracranial hypertension syndrome is characterized by an elevated ICP,papilledema, andheadache with occasionalabducensnerveparesis, absence of a space-occupying lesion or ventricular enlargement, and normalcerebrospinal fluid chemical andhematological constituents.[4][5]
Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive.Biot's respiration, in which breathing is rapid for a period and then absent for a period, occurs because of injury to thecerebral hemispheres ordiencephalon.[6]Hyperventilation can occur when thebrain stem ortegmentum is damaged.[6]
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 does CPP and cerebralperfusion decrease to a level that results in loss of consciousness. Any further elevations will lead tobrain infarction andbrain death.[citation needed]
In infants and small children, the effects of ICP differ because theircranial sutures have not closed. In infants, thefontanels (soft spots on the head where the skull bones have not yet fused) bulge when ICP gets too high. ICP correlates withintraocular pressure (IOP) but seems to lack the accuracy necessary for close management of intracranial pressure in the acute post-traumatic period.[7]
Papilledema (swelling of the optic disc) can be a reliable sign of elevated ICP. Unlike other conditions that may result in the swelling of the optic disc, it is in the case of papilledema that vision may go largely unaffected.[8]
Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:
One of the most damaging aspects ofbrain trauma and other conditions, directly correlated with poor outcome, is an elevated intracranial pressure.[10] ICP is very likely to cause severe harm if it rises too high.[11] Very high intracranial pressures are usually fatal if prolonged, but children can tolerate higher pressures for longer periods.[12] An increase in pressure, most commonly due to head injury leading tointracranial hematoma orcerebral edema, can crush brain tissue, shift brain structures, contribute tohydrocephalus, causebrain herniation, and restrict blood supply to the brain.[13] It is a cause ofreflex bradycardia.[14]
Drug-induced intracranial hypertension (DIIH) ormedication-induced intracranial hypertension is a condition of higher than normal intracranial pressure with the main cause being adrug.[15] This condition is similar toidiopathic intracranial hypertension, however the etiology in this instance is a drug.[16] The most frequent symptoms areheadaches,pulsatile tinnitus,diplopia, and impairment ofvisual acuity.[15][17] The only observable signs of the condition may bepapilledema and bilateralsixth cranial nerve (abducens) palsies.[17]
Spontaneous intracranial hypotension may occur as a result of an occult leak of CSF at the level of the spine, into another body cavity. More commonly, decreased ICP is the result of lumbar puncture or other medical procedure involving the 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.[citation needed]
If persistent intracranial hypotension is the result of a lumbar puncture, ablood patch may be applied to seal the site of CSF leakage. Various medical treatments have been proposed; only the intravenous administration ofcaffeine andtheophylline has shown to be particularly useful.[18]
The International Classification of Headache Disorders (ICHD) Third Edition diagnostic criteria for spontaneous intracranial hypotension includes any headache attributed to low CSF pressure (low CSF opening pressure) or CSF leakage (evidence of CSF leakage on imaging). Further, the headache must have a temporal relation to the low CSF pressure or leakage and the headache cannot be better explained by another ICHD diagnosis. The final criteria is that in the rare cases of spontaneous intracranial hypotension with no headache present, the neurologic symptoms that are present must be attributable to low CSF or explained by the diagnosis of spontaneous intracranial hypotension.[19]
Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly constant due to autoregulation, but for abnormalmean 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][20] One of the main dangers of increased ICP is that it can causeischemia 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 systemicblood pressure and dilate cerebralblood 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 makeintracranial hemorrhages bleed faster, also increasing ICP.[citation needed]
Severely raised ICP, if caused by a unilateral space-occupying lesion (e.g. ahematoma) can result inmidline shift, a dangeroussequela in which the brain moves toward one side as the result of massive swelling in acerebral hemisphere. Midline shift can compress theventricles and lead tohydrocephalus.[21]
The pressure–volume relationship between ICP, volume of CSF, blood, and brain tissue, andcerebral perfusion pressure (CPP) is known as the Monro–Kellie doctrine or hypothesis.[22][23][24]
The Monro–Kellie hypothesis states that the cranial compartment is inelastic and that the volume inside the cranium is fixed. 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.[24]*This concept only applies to adults, as the presence offontanelles and open suture lines in infants that have not yet fused means there is potential for a change in size and intracranial volume.
The principal buffers for increased volumes include CSF and, to a lesser extent, blood volume. These buffers respond to increases in volume of the remaining intracranial constituents. For example, an increase in lesion volume (e.g., epidural hematoma) will be compensated by the downward displacement of CSF and venous blood.[24] Additionally, there is some evidence that brain tissue itself may provide an additional buffer for elevated ICP in circumstances of acute intracranial mass effect via cell volume regulation.[25][26]
The Monro–Kellie hypothesis is named afterEdinburgh doctorsAlexander Monro andGeorge Kellie.[27]
The most definitive way of measuring the intracranial pressure is with transducers placed within the brain. Acatheter can be surgically inserted into one of the brain'slateral ventricles and can be used to drain CSF (cerebrospinal fluid) in order to decrease ICPs. This type of drain is known as anexternal ventricular drain (EVD).[10] This is rarely required outside brain injury and brain surgery settings.[citation needed]
In situations when only small amounts of CSF are to be drained to reduce ICP's (e.g. in idiopathic intracranial hypertension), drainage of CSF via lumbar puncture can be used as a treatment.Non-invasive measurement of intracranial pressure is being studied.[28]
The treatment for ICP depends on the cause. 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.[citation needed]
For long-term or chronic forms of raised ICP, especially idiopathic intracranial hypertension (IIH), a specific type ofdiuretic medication (acetazolamide) is used.[29] In cases of confirmed brain neoplasm, dexamethasone is given to decrease ICP. Although the exact mechanism is unknown, current research shows that dexamethasone is capable of decreasing peritumoral water content and local tissue pressure to decrease ICP.[30]
In people who have high ICP due to an acute injury, it is particularly important to ensure adequateairway, breathing, andoxygenation. Inadequate blood oxygen levels (hypoxia) or excessively highcarbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate, increasing the flow of blood to the brain and causing the ICP to rise.[31] Inadequate oxygenation also forces brain cells to produce energy usinganaerobic metabolism, which produceslactic acid and lowerspH, also dilating blood vessels and exacerbating the problem.[10] Conversely, blood vessels constrict when carbon dioxide levels are below normal, sohyperventilating a person with aventilator orbag valve mask can temporarily reduce ICP. Hyperventilation was formerly a part of the standard treatment oftraumatic brain injuries, but the induced constriction of blood vessels limits blood flow to the brain at a time when the brain may already be ischemic—hence it is no longer widely used.[32] 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.[32] Hyperventilation is still used if ICP is resistant to other methods of control, or there are signs ofbrain herniation, because the damage herniation can cause is so severe that it may be worthwhile to constrict blood vessels even if doing so reduces blood flow. ICP can also be lowered by raising the head of the bed, improving venous drainage. A side effect of this is that it could lower pressure of blood to the head, resulting in a reduced and possibly inadequate blood supply to the brain. Venous drainage may also be impeded by external factors such as hard collars to immobilize the neck in trauma patients, and this may also increase the ICP. Sandbags may be used to further limit neck movement.[citation needed]
In the hospital, the blood pressure can be increased in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes, and thereby lessen swelling.[32] Sincehypertension 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 person with a head injury.[6] When it is necessary to decrease cerebral blood flow, MAP can be lowered using commonantihypertensive agents such ascalcium channel blockers.[10]
If there is an intactblood–brain barrier,osmotherapy (mannitol orhypertonic saline) may be used to decrease ICP.[33]
It is unclear whether mannitol or hypertonic saline is superior, or if they improve outcomes.[34][35]
Struggling, restlessness, and seizures can increasemetabolic demands and oxygen consumption, as well as increasing blood pressure.[31][36] Analgesia and sedation are used to reduce agitation and metabolic needs of the brain, but these medications may cause low blood pressure and other side effects.[10] Thus if full sedation alone is ineffective, people may beparalyzed with drugs such asatracurium. Paralysis allows the cerebral veins to drain more easily, but can mask signs ofseizures, and the drugs can have other harmful effects.[31] Paralysing drugs are only introduced if patients are fully sedated (this is essentially the same as ageneral anaesthetic)[citation needed]
Craniotomies are holes drilled in the skull with the help ofcranial drills to removeintracranial hematomas or relieve pressure from parts of the brain.[10] As raised ICP's may be caused by the presence of a mass, removal of this via craniotomy will decrease raised ICP's.[citation needed]
A drastic treatment for increased ICP isdecompressive craniectomy,[37] in which a part of the skull is removed and thedura mater is expanded to allow the brain to swell without crushing it or causingherniation.[32] 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 (seecranioplasty)[citation needed]
{{citation}}: CS1 maint: work parameter with ISBN (link)We observed no mortality benefit or effect on the control of intracranial pressure with the use of hypertonic saline when compared to other solutions.
based on limited data, clinically important differences in mortality, neurological outcomes, and ICP reduction were not observed between HTS or mannitol in the management of severe TBI
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