Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF). The body has various mechanisms by which it keeps the ICP stable, with CSF pressures varying by about 1 mmHg in normal adults through shifts in production and absorption of CSF. CSF pressure has been shown to be influenced by abrupt changes in intrathoracic pressure during coughing (intraabdominal pressure), valsalva (Queckenstedt's maneuver), and communication with the vasculature (venous and arterial systems). ICP is measured in millimeters of mercury (mmHg) and, at rest, is normally 7–15 mmHg for a supine adult. [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, IICP or raised ICP, is elevation of the pressure in the cranium. ICP is normally 7–15 mm Hg; at 20–25 mm Hg, the upper limit of normal, treatment to reduce ICP may be needed.[2]
Contents
- 1 The Monro-Kellie hypothesis
- 2 Increased ICP
- 2.1 Pathophysiology
- 2.2 Stages of intracranial hypertension
- 2.3 Causes
- 2.4 Signs and symptoms
- 2.5 Treatment
- 3 Low ICP
- 4 See also
- 5 References
- 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 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 brain herniation, 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, CSF hypertension, circulatory hypotension, and hypoxic conditions are well recognized causes of this secondary injury. In the intensive care unit, raised intracranial pressure (intracranial hypertension) is seen frequently after a severe diffuse brain injury (one that occurs over a widespread area) and leads to cerebral ischemia by compromising cerebral perfusion.
Cerebral perfusion pressure (CPP), the pressure of blood flowing to the brain, is normally fairly constant due to autoregulation, but for abnormal mean arterial pressure (MAP) or abnormal ICP the cerebral perfusion pressure is calculated by subtracting the intracranial pressure from the mean arterial pressure: CPP = 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 (e.g. a hematoma) can result in midline shift, a dangerous sequela in which the brain moves toward one side as the result of massive swelling in a cerebral hemisphere. Midline shift can compress the ventricles and lead to hydrocephalus.[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.
Stages of intracranial hypertension
Minimal increases in ICP due to compensatory mechanisms are known as stage 1 of intracranial hypertension. When the lesion volume continues to increase beyond the point of compensation, the ICP has no other resource but to increase. Any change in volume greater than 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 respiration, 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 edema, contusions, subdural or epidural hematoma, or abscesses all tend to deform the adjacent brain.
- generalized brain swelling can occur in ischemic-anoxia states, acute liver failure,[13] hypertensive encephalopathy, hypercarbia, and Reye hepatocerebral syndrome. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
- increase in venous pressure can be due to venous sinus thrombosis, heart failure, or obstruction of superior mediastinal or jugular veins.
- obstruction to CSF flow and/or absorption can occur in hydrocephalus (blockage in ventricles or subarachnoid space at base of brain, e.g., by Arnold-Chiari malformation), extensive meningeal disease (e.g., infection, carcinoma, granuloma, or hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).
Main article: hydrocephalus
- increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor.
- Idiopathic or unknown cause (idiopathic intracranial hypertension)
- craniosynostosis
Signs and symptoms
In general, symptoms and signs that suggest a rise in ICP including headache, vomiting without nausea, ocular palsies, altered level of consciousness, back pain and papilledema. If papilledema is protracted, it may lead to visual disturbances, optic atrophy, and eventually blindness. The headache is classically a morning headache which may wake them from sleep. The brain is relatively poorly supplied by oxygen as a result of mild hypoventilation during the sleeping hours, and also cerebral oedema may worsen during the night due to the lying position. The headache is worse on coughing / sneezing / bending, and progressively worsens over time. There may also be personality or behavioral changes.
In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and the Cushing's triad. Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern.[14] In children, a low heart rate is especially suggestive of high ICP.
Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive. 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.
Papilledema, or the swelling of the optic disc, can be a reliable sign that ICP is elevated. Unlike other conditions that may result in the swelling of the optic disc, it is in the case of papilledema that vision may go largely unaffected.[16]
Treatment
The treatment for IH depends on the etiology. In addition to management of the underlying causes, major considerations in acute treatment of increased ICP relates to the management of stroke and cerebral trauma.
A very common treatment for long-term, especially idiopathic, cranial hypertension is medication with a special diuretic, especially one prescribed by a neurologist.
In patients who have high ICP due to an acute injury, it is particularly important to ensure adequate airway, breathing, and oxygenation. Inadequate blood oxygen levels (hypoxia) or excessively high carbon dioxide levels (hypercapnia) cause cerebral blood vessels to dilate, increasing the flow of blood to the brain and causing the ICP to rise.[17] 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 was formerly a part of the standard treatment of traumatic brain injuries, but the induced constriction of blood vessels limits blood flow to the brain at a time when the brain may already be ischemic—hence it is no longer widely used.[18] 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.[18] Hyperventilation is still used if ICP is resistant to other methods of control, or there are signs of brain herniation, because the damage herniation can cause is so severe that it may be worthwhile to constrict blood vessels even if doing so reduces blood flow. ICP can also be lowered by raising the head of the bed, improving venous drainage. A side effect of this is that it could lower pressure of blood to the head, resulting in a reduced and possibly inadequate blood supply to the brain. Venous drainage may also be impeded by external factors such as hard collars to immobilize the neck in trauma patients, and this may also increase the ICP. Sandbags may be used to further limit neck movement.
In the hospital, the blood pressure can be artificially increased in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes, and thereby lessen swelling.[18] Since hypertension is the body's way of forcing blood into the brain, medical professionals do not normally interfere with it when it is found in a patient with a head injury.[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, osmotherapy may be carried out by administering IV mannitol to create a hypertonic solution within the blood to draw water out of the neurons. This helps to reduce the fluid within the intracranial space; however, prolonged administration may lead to increase in ICP.[19]
Struggling, restlessness, and seizures can increase metabolic demands and oxygen consumption, as well as increasing blood pressure.[17][20] 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.[17] 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. There are many clinical studies of non-invasive intracranial pressure measurement methods currently being proposed, aimed at finding reliable and accurate ways to measure ICP non-invasively. Such methods could improve diagnostics of traumatic brain injury and many other conditions associated with intracranial hypertension.
Craniotomies are holes drilled in the skull to remove intracranial hematomas or relieve pressure from parts of the brain.[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,[21] 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.[18] 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.[22]
See also
- Brain Trauma Foundation
- Neurocritical care
- Cushing's triad
- Traumatic brain injury
- external ventricular drain
- Non-invasive intracranial pressure measurement methods
References
- ^ a b Steiner LA, Andrews PJ (2006). "Monitoring the injured brain: ICP and CBF". British Journal of Anaesthesia 97 (1): 26–38. doi:10.1093/bja/ael110. PMID 16698860.
- ^ Ghajar J (September 2000). "Traumatic brain injury". Lancet 356 (9233): 923–9. doi:10.1016/S0140-6736(00)02689-1. PMID 11036909.
- ^ Monro A (1783). Observations on the structure and function of the nervous system. Edinburgh: Creech & Johnson.
- ^ Kellie G (1824). "Appearances observed in the dissection of two individuals; death from cold and congestion of the brain". Trans Med Chir Sci Edinb 1: 84–169.
- ^ a b c Mokri B (June 2001). "The Monro-Kellie hypothesis: applications in CSF volume depletion". Neurology 56 (12): 1746–8. doi:10.1212/WNL.56.12.1746. PMID 11425944.
- ^ a b c d e f Orlando Regional Healthcare, Education and Development. 2004. "Overview of Adult Traumatic Brain Injuries." Accessed January 16, 2008.
- ^ Dawodu S. 2005. "Traumatic Brain Injury: Definition, Epidemiology, Pathophysiology" Emedicine.com.Accessed January 4, 2007.
- ^ Tolias C and Sgouros S. 2006. "Initial Evaluation and Management of CNS Injury." Emedicine.com. Accessed January 4, 2007.
- ^ Graham DI and Gennareli TA. Chapter 5, "Pathology of Brain Damage After Head Injury" In, Cooper P and Golfinos G. 2000. Head Injury, 4th Ed. Morgan Hill, New York.
- ^ Deepak A. Rao; Le, Tao; Bhushan, Vikas (2007). First Aid for the USMLE Step 1 2008 (First Aid for the Usmle Step 1). McGraw-Hill Medical. ISBN 0-07-149868-0. Page 254
- ^ Duschek S, Schandry R (2007). "Reduced brain perfusion and cognitive performance due to constitutional hypotension". Clinical Autonomic Research 17 (2): 69–76. doi:10.1007/s10286-006-0379-7. PMC 1858602. PMID 17106628.
- ^ Downie A. 2001. "Tutorial: CT in Head Trauma" Accessed January 4, 2007.
- ^ Polson J, Lee WM (2005). "AASLD position paper: the management of acute liver failure". Hepatology 41 (5): 1179–97. doi:10.1002/hep.20703. PMID 15841455.
- ^ Sanders MJ and McKenna K. 2001. Mosby’s Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
- ^ a b c Singh J and Stock A. 2006. "Head Trauma." Emedicine.com. Accessed January 4, 2007.
- ^ http://emedicine.medscape.com/article/1217204-overview
- ^ a b c Su F and Huh J. 2006. "Neurointensive Care for Traumatic Brain Injury in Children." Emedicine.com. Accessed January 4, 2007.
- ^ a b c d Shepherd S. 2004. "Head Trauma." Emedicine.com. Accessed January 4, 2007.
- ^ Trauma.org 2000. "TRAUMA.ORG: Neurotrauma: Control of Intracranial Hypertension" Trauma.org. Accessed March 18, 2009.
- ^ Bechtel K. 2004. "Pediatric Controversies: Diagnosis and Management of Traumatic Brain Injuries." Trauma Report. Supplement to Emergency Medicine Reports, Pediatric Emergency Medicine Reports, ED Management, and Emergency Medicine Alert. Volume 5, Number 3. Thomsom American Health Consultants.
- ^ Sahuquillo J, Arikan F (2006). "Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury". In Sahuquillo, Juan. Cochrane Database Syst Rev (1): CD003983. doi:10.1002/14651858.CD003983.pub2. PMID 16437469.
- ^ Paldino M, Mogilner AY, Tenner MS (December 2003). "Intracranial hypotension syndrome: a comprehensive review". Neurosurg Focus 15 (6): ECP2. doi:10.3171/foc.2003.15.6.8. PMID 15305844.
External links
- Gruen P. 2002. "Monro-Kellie Model" Neurosurgery Infonet. USC Neurosurgery. Accessed January 4, 2007.
- National Guideline Clearinghouse. 2005. Guidelines for the management of severe traumatic brain injury. Firstgov. Accessed January 4, 2007.
- Intracranial Pressure at the US National Library of Medicine Medical Subject Headings (MeSH)
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Nervous system physiology: neurophysiology / clinical neurophysiology
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| Primarily CNS |
- Arousal
- Intracranial pressure
- Lateralization of brain function
- Sleep
- Memory
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| Primarily PNS |
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| Both |
| Evoked potential |
- Bereitschaftspotential
- P300
- Auditory evoked potential
- Somatosensory evoked potentials
- Visual evoked potential
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| Other short term |
- Neurotransmission
- Chronaxie
- Membrane potential
- Action potential
- Postsynaptic potential
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| Long term |
- Axoplasmic transport
- Neuroregeneration/Nerve regeneration
- Neuroplasticity/Synaptic plasticity
- Long-term potentiation
- Long-term depression
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| Other |
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anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp
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noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr
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proc, drug (N1A/2AB/C/3/4/7A/B/C/D)
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anat (h/r/t/c/b/l/s/a)/phys (r)/devp/prot/nttr/nttm/ntrp
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noco/auto/cong/tumr, sysi/epon, injr
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