Medicine:Intracranial pressure

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Short description: Pressure exerted by fluids inside the skull and on the brain

Intracranial pressure
Severely high ICP can cause the brain to herniate.
SpecialtyNeurosurgery, Neurology
TypesIncreased, normal, decreased

Intracranial pressure (ICP) is the pressure exerted by fluids such as cerebrospinal fluid (CSF) inside the skull and on the brain tissue. ICP is measured in millimeters of mercury (mmHg) and at rest, is normally 7–15 mmHg for a supine adult. This equals to 9–20 cmH2O, which is a common scale used in lumbar 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 the diaphragm and abdominal wall muscles, the latter of which also increases intra-abdominal pressure), the valsalva maneuver, and communication with the vasculature (venous and arterial systems).

Intracranial hypertension (IH), also called increased ICP (IICP) or raised 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]

Signs and symptoms of raised intracranial pressure

In general, symptoms and signs that suggest a rise in ICP include 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 that may wake the person up. The brain is relatively poorly supplied by oxygen as a result of mild hypoventilation during the sleeping hours leading to hypercapnia and vasodilation. 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, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and Cushing's triad. Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern.[3] In children, a low heart rate is especially suggestive of high ICP. Intracranial hypertension syndrome is characterized by an elevated ICP, papilledema, and headache with occasional abducens nerve paresis, absence of a space-occupying lesion or ventricular enlargement, and normal cerebrospinal fluid chemical and hematological 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 the cerebral hemispheres or diencephalon.[6] Hyperventilation can occur when the brain stem or tegmentum is damaged.[6]


In infants and small children, the effects of ICP differ because their cranial sutures have not closed. In infants, the fontanels (soft spots on the head where the skull bones have not yet fused) bulge when ICP gets too high. ICP correlates with intraocular 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 abnormal intracranial pressure

Increased ICP

Causes of increased intracranial pressure can be classified by the mechanism in which ICP is increased:

  • Generalized brain swelling can occur in ischemic-anoxia states, acute liver failure,[9] hypertensive encephalopathy, hypercarbia (hypercapnia), and Reye hepatocerebral syndrome. These conditions tend to decrease the cerebral perfusion pressure but with minimal tissue shifts.
  • Craniosynostosis

One of the most damaging aspects of brain 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 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.[13] It is a cause of reflex bradycardia.[14]

Drug-induced intracranial hypertension

Drug-induced intracranial hypertension (DIIH) or medication-induced intracranial hypertension is a condition of higher than normal intracranial pressure with the main cause being a drug.[15] This condition is similar to idiopathic intracranial hypertension, however the etiology in this instance is a drug.[16] The most frequent symptoms are headaches, pulsatile tinnitus, diplopia, and impairment of visual acuity.[15][17] The only observable signs of the condition may be papilledema and bilateral sixth cranial nerve (abducens) palsies.[17]

Low ICP

Main article: Medicine:Cerebrospinal fluid leak

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.[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]

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][20] 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.[21]

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.[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 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.[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 after Edinburgh doctors Alexander Monro and George Kellie.[27]

Diagnosis

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]

Treatment

For long-term or chronic forms of raised ICP, especially idiopathic intracranial hypertension (IIH), a specific type of diuretic 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]

Ventilation

In people 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.[31] 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.[10] Conversely, blood vessels constrict when carbon dioxide levels are below normal, so hyperventilating a person 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.[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 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.

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.[32] 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 person with a head injury.[6] When it is necessary to decrease cerebral blood flow, MAP can be lowered using common antihypertensive agents such as calcium channel blockers.[10]

If there is an intact blood–brain barrier, osmotherapy (mannitol or hypertonic 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]


Surgery

A drastic treatment for increased ICP is decompressive craniectomy,[36] 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.[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 (see cranioplasty)

See also

References

  1. ↑ 1.0 1.1 "Monitoring the injured brain: ICP and CBF". British Journal of Anaesthesia 97 (1): 26–38. July 2006. doi:10.1093/bja/ael110. PMID 16698860. 
  2. ↑ "Traumatic brain injury". Lancet 356 (9233): 923–929. September 2000. doi:10.1016/S0140-6736(00)02689-1. PMID 11036909. 
  3. ↑ Sanders MJ and McKenna K. 2001. Mosby's Paramedic Textbook, 2nd revised Ed. Chapter 22, "Head and Facial Trauma." Mosby.
  4. ↑ "Intracranial hypertension syndrome in systemic lupus erythematosus: Clinical analysis and review of the literature". J. Huazhong Univ. Sci. Technol. Med. Sci. 29 (1): 107–11. February 2009. doi:10.1007/s11596-009-0123-3. PMID 19224175. 
  5. ↑ Sismanis A (August 1987). "Otologic manifestations of benign intracranial hypertension syndrome: diagnosis and management". Laryngoscope 97 (8 Pt 2 Suppl 42): 1–17. doi:10.1288/00005537-198708001-00001. PMID 3302575. 
  6. ↑ 6.0 6.1 6.2 Pediatric Head Trauma at eMedicine
  7. ↑ "Correlation of intraocular pressure with intracranial pressure in children with severe head injuries". Pediatric Critical Care Medicine 11 (5): 593–598. September 2010. doi:10.1097/PCC.0b013e3181ce755c. PMID 20081553. 
  8. ↑ Papilledema at eMedicine
  9. ↑ "AASLD position paper: the management of acute liver failure". Hepatology 41 (5): 1179–1197. May 2005. doi:10.1002/hep.20703. PMID 15841455. 
  10. ↑ 10.0 10.1 10.2 "Overview of Adult Traumatic Brain Injuries". Orlando Regional Healthcare, Education and Development. 2004. http://www.orlandoregional.org/pdf%20folder/overview%20adult%20brain%20injury.pdf. 
  11. ↑ Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology at eMedicine
  12. ↑ Initial Evaluation and Management of CNS Injury at eMedicine
  13. ↑ "Pathology of Brain Damage After Head Injury". Head Injury (4th ed.). McGraw-Hill. 2000. pp. 133–54. ISBN 978-0-8385-3687-2. 
  14. ↑ First Aid for the USMLE Step 1 2008 (First Aid for the Usmle Step 1). McGraw-Hill Medical. 2007. p. 254. ISBN 978-0-07-149868-5. https://archive.org/details/firstaidforusmle00taol/page/254. 
  15. ↑ 15.0 15.1 Tan, Marcus G.; Worley, Brandon; Kim, Whan B.; ten Hove, Martin; Beecker, Jennifer (April 2020). "Drug-Induced Intracranial Hypertension: A Systematic Review and Critical Assessment of Drug-Induced Causes". American Journal of Clinical Dermatology 21 (2): 163–172. doi:10.1007/s40257-019-00485-z. ISSN 1175-0561. PMID 31741184. http://link.springer.com/10.1007/s40257-019-00485-z. 
  16. ↑ Friedman, Deborah I. (2005-02-01). "Medication-Induced Intracranial Hypertension in Dermatology". American Journal of Clinical Dermatology 6 (1): 29–37. doi:10.2165/00128071-200506010-00004. ISSN 1179-1888. PMID 15675888. 
  17. ↑ 17.0 17.1 Jain, Kewal K. (2021), Jain, Kewal K., ed., "Drug-Induced Intracranial Hypertension", Drug-induced Neurological Disorders (Cham: Springer International Publishing): pp. 169–180, doi:10.1007/978-3-030-73503-6_12, ISBN 978-3-030-73503-6 
  18. ↑ "Intracranial hypotension syndrome: a comprehensive review". Neurosurgical Focus 15 (6): ECP2. December 2003. doi:10.3171/foc.2003.15.6.8. PMID 15305844. 
  19. ↑ "Spontaneous Intracranial Hypotension". The New England Journal of Medicine 385 (23): 2173–2178. December 2021. doi:10.1056/NEJMra2101561. PMID 34874632. 
  20. ↑ "Reduced brain perfusion and cognitive performance due to constitutional hypotension". Clinical Autonomic Research 17 (2): 69–76. April 2007. doi:10.1007/s10286-006-0379-7. PMID 17106628. 
  21. ↑ "Tutorial: CT in Head Trauma". 2001. http://www.radiology.co.uk/srs-x/tutors/cttrauma/tutor.htm. 
  22. ↑ Observations on the structure and function of the nervous system. Edinburgh: Creech & Johnson. 1783. 
  23. ↑ "Appearances observed in the dissection of two individuals; death from cold and congestion of the brain". Trans Med Chir Sci Edinb 1: 84–169. 1824. 
  24. ↑ 24.0 24.1 24.2 "The Monro-Kellie hypothesis: applications in CSF volume depletion". Neurology 56 (12): 1746–1748. June 2001. doi:10.1212/WNL.56.12.1746. PMID 11425944. http://www.neurology.org/cgi/content/full/56/12/1746. Retrieved 2008-11-15. 
  25. ↑ "An update to the Monro-Kellie doctrine to reflect tissue compliance after severe ischemic and hemorrhagic stroke". Scientific Reports 10 (1): 22013. December 2020. doi:10.1038/s41598-020-78880-4. PMID 33328490. Bibcode: 2020NatSR..1022013K. 
  26. ↑ "Tissue Compliance and Intracranial Pressure Responses to Large Intracerebral Hemorrhage in Young and Aged Spontaneously Hypertensive Rats". Hypertension 81 (1): 151–161. January 2024. doi:10.1161/HYPERTENSIONAHA.123.21628. PMID 37909235. 
  27. ↑ "A hotbed of medical innovation: George Kellie (1770-1829), his colleagues at Leith and the Monro-Kellie doctrine". Journal of Medical Biography 22 (2): 93–100. May 2014. doi:10.1177/0967772013479271. PMID 24585579. 
  28. ↑ "Noninvasive intracranial pressure monitoring methods: a critical review". Arquivos de Neuro-Psiquiatria 79 (5): 437–446. May 2021. doi:10.1590/0004-282x-anp-2020-0300. PMID 34161530. 
  29. ↑ "Interventions for idiopathic intracranial hypertension". The Cochrane Database of Systematic Reviews 2015 (8). August 2015. doi:10.1002/14651858.CD003434.pub3. PMID 26250102. 
  30. ↑ "Effects of dexamethasone on cerebral perfusion and water diffusion in patients with high-grade glioma". AJNR. American Journal of Neuroradiology 27 (2): 402–408. February 2006. PMID 16484419. 
  31. ↑ Traumatic Brain Injury in Children at eMedicine
  32. ↑ 32.0 32.1 32.2 32.3 Head Trauma at eMedicine
  33. ↑ "A Comparison of Pharmacologic Therapeutic Agents Used for the Reduction of Intracranial Pressure After Traumatic Brain Injury". World Neurosurgery 106: 509–528. October 2017. doi:10.1016/j.wneu.2017.07.009. PMID 28712906. 
  34. ↑ "Hypertonic saline in severe traumatic brain injury: a systematic review and meta-analysis of randomized controlled trials". CJEM 18 (2): 112–120. March 2016. doi:10.1017/cem.2016.12. 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.". 
  35. ↑ "A Systematic Review of Randomized Controlled Trials Comparing Hypertonic Sodium Solutions and Mannitol for Traumatic Brain Injury: Implications for Emergency Department Management". The Annals of Pharmacotherapy 50 (4): 291–300. April 2016. doi:10.1177/1060028016628893. PMID 26825644. "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". 
  36. ↑ "Decompressive craniectomy for the treatment of high intracranial pressure in closed traumatic brain injury". The Cochrane Database of Systematic Reviews 2019 (12). December 2019. doi:10.1002/14651858.CD003983.pub3. PMID 31887790. 



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