Intracranial pressure
Intracranial pressure | |
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Severely high ICP can cause the brain to herniate. | |
Types | Increased, normal, decreased |
Intracranial pressure (ICP) is the pressure exerted by fluids such as
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 the diaphragm and abdominal wall muscles, the latter of which also increases intra-abdominal pressure), the
Intracranial hypertension (IH), also called increased ICP (IICP) or raised intracranial pressure (RICP), 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]
Signs and symptoms of raised intracranial pressure
In general, symptoms and signs that suggest a rise in ICP include
In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include
Irregular respirations occur when injury to parts of the brain interfere with the respiratory drive.
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 cerebral perfusion decrease to a level that results in loss of consciousness. Any further elevations will lead to brain infarction and brain death.[citation needed]
In infants and small children, the effects of ICP differ because their cranial sutures have not closed. In infants, the
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.[6]
Causes of abnormal intracranial pressure
Increased ICP
Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:
- Mass effect such as contusions, subdural or epidural hematoma, or abscesses all tend to deform the adjacent brain.[citation needed]
- Generalized brain swelling can occur in ischemic-anoxia states, 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.[citation needed]
- Obstruction to CSF flow and/or absorption can occur in hemorrhage), or obstruction in cerebral convexities and superior sagittal sinus (decreased absorption).[citation needed]
- Increased CSF production can occur in meningitis, subarachnoid hemorrhage, or choroid plexus tumor.[citation needed]
- Idiopathic or unknown cause (idiopathic intracranial hypertension, a common cause in otherwise well people especially younger women)[citation needed]
- Craniosynostosis
One of the most damaging aspects of
Low ICP
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, 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.[13]
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.[14]
Pathophysiology
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][15] 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.[citation needed]
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.[16]
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 hypothesis.[17][18][19]
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.[19] *This concept only applies to adults, as the presence of fontanelles 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.[19] 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.[20][21]
The Monro–Kellie hypothesis is named after
Diagnosis
The most definitive way of measuring the intracranial pressure is with transducers placed within 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 ICPs. This type of drain is known as an external ventricular drain (EVD).[8] 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.[23]
Treatment
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 of diuretic medication (acetazolamide) is used.[24] 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.[25]
Ventilation
In people who have high ICP due to an acute injury, it is particularly important to ensure adequate
Medication
In the hospital, the blood pressure can be increased in order to increase CPP, increase perfusion, oxygenate tissues, remove wastes, and thereby lessen swelling.
If there is an intact
It is unclear whether mannitol or hypertonic saline is superior, or if they improve outcomes.[29][30]
Struggling, restlessness, and seizures can increase
Surgery
A drastic treatment for increased ICP is
See also
References
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- ^ Sanders MJ and McKenna K. 2001. Mosby’s Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
- ^ a b c Pediatric Head Trauma at eMedicine
- S2CID 11716075.
- ^ Papilledema at eMedicine
- S2CID 6216605.
- ^ a b c d e f "Overview of Adult Traumatic Brain Injuries" (PDF). Orlando Regional Healthcare, Education and Development. 2004. Archived from the original (PDF) on 27 February 2008. Retrieved 16 January 2008.
- ^ Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology at eMedicine
- ^ Initial Evaluation and Management of CNS Injury at eMedicine
- ISBN 978-0-8385-3687-2.
- ISBN 978-0-07-149868-5.
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- PMID 17106628.
- ^ Downie A (2001). "Tutorial: CT in Head Trauma". Archived from the original on 6 November 2005. Retrieved 4 January 2007.
- ^ 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.
- ^ S2CID 1443175. Archived from the originalon 2009-03-21. Retrieved 2008-11-15.
- PMID 33328490.
- PMID 37909235.
- S2CID 206608492.
- PMID 34161530.
- PMID 26250102.
- PMID 16484419.
- ^ a b c Traumatic Brain Injury in Children at eMedicine
- ^ a b c d Head Trauma at eMedicine
- PMID 28712906.
- PMID 26988719.
We observed no mortality benefit or effect on the control of intracranial pressure with the use of hypertonic saline when compared to other solutions.
- S2CID 23859003.
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
- ^ 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.
- PMID 31887790.
External links
- Gruen P (2002). "Monro-Kellie Model". Neurosurgery Infonet. USC Neurosurgery. Archived from the original on 2005-10-26. Retrieved 4 January 2007.
- "Guidelines for the management of severe traumatic brain injury". National Guideline Clearinghouse. Firstgov. 2005. Archived from the original on 2007-03-10. Retrieved 4 January 2007.
- Intracranial Pressure at the U.S. National Library of Medicine Medical Subject Headings (MeSH)