Elevated intracranial pressure and brain herniation

Last updated: October 19, 2023

Summarytoggle arrow icon

Intracranial pressure (ICP) is the pressure that exists within the cranium, including its compartments (e.g., the subarachnoid space and the ventricles). ICP varies as the position of the head changes relative to the body and is periodically influenced by normal physiological factors (e.g., cardiac contractions). Adults in the supine position typically have a physiological ICP of ≤ 15 mm Hg; an ICP of ≥ 20 mm Hg indicates pathological intracranial hypertension. ICP may be elevated in a variety of conditions (e.g., intracranial tumors) and can result in a decrease in cerebral perfusion pressure (CPP) and/or herniation of cerebral structures. Symptoms of elevated ICP are generally nonspecific (e.g., impaired consciousness, headache, vomiting); however, more specific symptoms may be present depending on the affected structures (e.g., Cushing triad if the brainstem is compressed). Findings from brain imaging (e.g., a midline shift) and physical examination (e.g., papilledema) can indicate ICP elevation but may not be able to rule it out. Therefore, ICP monitoring and quantification are vital in at-risk patients. Management usually involves expedited surgery of resectable or drainable lesions, conservative measures (e.g., positioning, sedation, analgesia, and antipyretics), and medical therapy (e.g., hyperosmolar therapy such as mannitol or hypertonic saline, or glucocorticoids). Treatment options for refractory intracranial hypertension include temporary controlled hyperventilation, CSF drainage, and decompressive craniectomy (DC), as well as other advanced medical therapies (e.g., barbiturate coma, therapeutic hypothermia).

Etiologytoggle arrow icon

Pathophysiologytoggle arrow icon

Physiology of ICP [2]

  • Overview
    • Physiological ICP is ≤ 15 mm Hg in adults (in supine position); children generally have a lower ICP.
    • ICP varies depending on the position of the head relative to the rest of the body and is influenced by certain physiological processes (e.g., cardiac contractions, sneezing, coughing, Valsalva maneuver).
    • Volume of intracranial contents [2]
      • Brain: approx. 85%
      • CSF: approx. 10%
      • Blood: approx. 5%
  • Monro-Kellie principle: The sum of volumes of intracranial blood, CSF, and brain within the cranium is constant, which means that an increase in one component volume will be compensated for by a decrease in other(s). [3]
    • Initial compensation allows for an increase in component volume with minimal change in ICP.
    • Once the compensatory mechanisms are exhausted, ICP increases rapidly because of the skull's inability to expand and accommodate the increase in intracranial volume.

Physiology of cerebral blood flow

Therapeutic hyperventilation reduces pCO2↓ cerebral blood flow → ↓ intracranial pressure (used, e.g., when patients with acute cerebral edema are unresponsive to other treatments).

Consequences of elevated ICP

Clinical featurestoggle arrow icon

Subtypes and variantstoggle arrow icon

Cerebral herniation syndromes [7][8]

Subfalcine herniation

Descending transtentorial herniation

Foramen magnum herniation

The following clinical features should raise suspicion for a cerebral herniation syndrome, which can be fatal if not treated promptly: acutely worsening level of consciousness (e.g., coma), pupillary changes (e.g., ipsilateral mydriasis, fixed dilated pupils), new focal neurological deficits (e.g., hemiparesis, decerebrate posturing), and cardiorespiratory compromise (e.g., bradycardia, apnea).

Diagnosticstoggle arrow icon

Neuroimaging (CT head/MRI head) [9]

Clinical examination and imaging may indicate elevated ICP, but cannot rule it out. Additionally, neither allow ICP to be quantified, which is necessary to determine CPP.

Invasive ICP monitoring

  • Invasive monitoring is typically required for confirmation and accurate measurement of ICP.
  • ICP should be evaluated in combination with CPP to guide therapeutic interventions and help prevent secondary brain injury and brain herniation. [10]
  • There are no absolute contraindications for invasive ICP monitoring.
  • Consider the risks versus the benefits in consultation with a specialist.

Indications [11][12][13]

Methods to monitor ICP [10][14][15]

Intraventricular catheters; with an external ventricular drain (EVD) and intraparenchymal catheters; (IPC) are most commonly used to monitor ICP, as they have the highest accuracy compared with other monitoring methods.

  • Intraventricular catheter: a monitoring device placed into the ventricles of the brain along with a CSF drainage system (i.e., an EVD) [16]
    • Allows for continuous ICP monitoring and evaluation of intracranial compliance
    • Useful in conditions in which CSF drainage is required for both diagnostic and therapeutic purposes
    • The preferred monitoring method for intracranial lesions associated with hydrocephalus [10]
    • Complications
      • Infections
      • Hemorrhage attributable to the placement of the device
      • Malpositioning and/or accidental removal
      • Blockage with blood or debris
  • Intraparenchymal catheter: a fiberoptic device placed into the brain parenchyma without an accompanying CSF drainage system [17]
    • Allows for continuous ICP monitoring
    • Accuracy and effect on patient outcomes are considered equivalent to intraventricular catheters
    • Lower risk of infection and hemorrhage compared with intraventricular catheters
    • Technical complications: e.g., dislodgement, breakage


  • Generally, ICP > 20 mm Hg indicates intracranial hypertension, which requires treatment. [10]
  • ICP varies in a complex cyclical manner and is influenced by hemodynamic and metabolic factors.
  • Monitor ICP along with MAP to calculate CPP using the formula CPP = MAPICP.

Do not use the ICP value in isolation as a prognostic marker or to inform therapeutic decisions. [10]

Treatmenttoggle arrow icon

Approach [9][10][12][18][19][20]

Stepwise ICP management (based on a multifactorial response) [9][18][21][22]
Step Intervention
Initial steps
  • Identify and expedite the treatment of lesions that are amenable to emergency surgical procedures.
Subsequent step
Elective temporizing step
  • Consider short-term (< 30 minutes) controlled hyperventilation in patients with signs of imminent brain herniation and refractory elevated ICP in the interim while waiting for:
    • Surgical procedures
    • Onset of action of medical therapy
Advanced steps
  • General therapeutic targets: Base treatment decisions on trends identified using repeat assessments of ICP, CPP, and clinical status. [10][12]
    • Target ICP: < 20 mm Hg
    • Target CPP range: 60–70 mm Hg

Conservative therapy [23]

See also “Neuroprotective measures.”

Medical therapy [23]

Overview of hyperosmolar therapies in ICP management [23][30][31][32]
Mannitol HTS
Pharmacology [9][12]
  • Mannitol 20% is most commonly used.
  • Lowers ICP within minutes of administration
  • Peak efficacy: 20–60 minutes after administration
  • Duration of effect: 4–6 hours
  • Multiple concentrations of HTS exist (e.g., 3–23.4%), with highly variable dosages and pharmacokinetics. [23]
  • 23.4% HTS is commonly used.
Therapeutic targets to consider [18][23][24]
  • Symptom-based dosing is recommended for patients with SAH.
  • Serum osmolarity (e.g., 300–320 mOsm/L) or osmolar gap
  • Serum sodium (e.g., 145–155 mEq/L) [9][33][34]
Adverse effects [9][18][20]
Considerations [9]
  • Avoid if systolic BP < 90 mm Hg. [12]

Although hyperosmolar therapies can lower ICP, they have not been shown to improve neurological outcomes in patients with underlying TBI, acute ischemic stroke, ICH, SAH, or hepatic encephalopathy. [23]

Surgical therapy

  • Emergency surgery (if possible): e.g., resection of brain tumor, hematoma evacuation [20]
  • CSF drainage
  • Decompressive craniectomy (DC): removal of a portion of the skull, which allows the brain to expand in volume, thereby reducing ICP [36]
    • Primary DC: removal of a skull flap following evacuation or resection of an intracranial lesion (e.g., brain tumor)
    • Secondary DC: removal of a skull flap without additional surgical procedures to treat refractory elevated ICP
      • Recommended for (controversial): [36]
        • Late refractory elevated ICP: reduced mortality, improved outcomes
        • Early or late refractory elevated ICP: improved control of ICP, reduced neuro-ICU length of stay
        • Large hemispheric stroke (e.g., malignant MCA infarction) in patients with an infarct > 12 cm and within 24–48 hours of symptom onset [24][37]
      • Not recommended for patients with early refractory elevated ICP
    • Multiple approaches have been described in the literature (suboccipital, subtemporal, frontotemporoparietal, etc.) depending on the type and location of the brain lesion. [38]
    • Lowers mortality in TBI without improving neurological or functional outcomes [19]

Nonsurgical therapy for refractory intracranial hypertension [23]

Controlled hyperventilation

Hyperventilation is primarily used as a temporizing measure for intracranial hypertension refractory to medical therapy. [21]

Controlled hyperventilation should only be used short-term and is not recommended routinely or for prophylaxis. Avoid excessive hyperventilation (PaCO2 < 30 mm Hg), prolonged hyperventilation, and hypoventilation of any kind, as CBF and perfusion may become compromised.

Advanced therapies

These are primarily reserved for patients with persistently refractory intracranial hypertension.

Complicationstoggle arrow icon

Cerebral edema

  • Definition: excess accumulation of fluid within the brain parenchyma as a result of damage to the blood-brain barrier and/or the blood-CSF barrier [48]
Overview of cerebral edema subtypes
Characteristics Vasogenic Cytotoxic Interstitial Osmotic
  • Breakdown of tight endothelial junctions → impaired capillary permeability → extracellular accumulation of fluids
  • Blocked CSF drainage → ↑ ventricular pressure → CSF forced across the ependymal tissue and into the brain parenchymainterstitial fluid accumulation
BBB integrity
  • Breakdown
  • Intact

We list the most important complications. The selection is not exhaustive.

Referencestoggle arrow icon

  1. Tameem A, Krovvidi H. Cerebral physiology. Contin Educ Anaesth Crit Care Pain. 2013; 13 (4): p.113-118.doi: 10.1093/bjaceaccp/mkt001 . | Open in Read by QxMD
  2. Mokri B. The Monro-Kellie hypothesis: Applications in CSF volume depletion. Neurology. 2001; 56 (12): p.1746-1748.doi: 10.1212/wnl.56.12.1746 . | Open in Read by QxMD
  3. Fantini S, Sassaroli A, Tgavalekos KT, Kornbluth J. Cerebral blood flow and autoregulation: current measurement techniques and prospects for noninvasive optical methods. Neurophotonics. 2016; 3 (3): p.031411.doi: 10.1117/1.nph.3.3.031411 . | Open in Read by QxMD
  4. Birg T, Ortolano F, Wiegers EJA, et al. Brain Temperature Influences Intracranial Pressure and Cerebral Perfusion Pressure After Traumatic Brain Injury: A CENTER-TBI Study. Neurocrit Care. 2021; 35 (3): p.651-661.doi: 10.1007/s12028-021-01294-1 . | Open in Read by QxMD
  5. Hackett JG, Abboud FM, Mark AL, Schmid PG, Heistad DD. Coronary vascular responses to stimulation of chemoreceptors and baroreceptors: evidence for reflex activation of vagal cholinergic innervation. Circ Res. 1972; 31 (1): p.8-17.
  6. Shah AK, Fuerst D, Sood S et al. Seizures Lead to Elevation of Intracranial Pressure in Children Undergoing Invasive EEG Monitoring. Epilepsia. 2017; 48 (6): p.1097-1103.doi: 10.1111/j.1528-1167.2006.00975.x . | Open in Read by QxMD
  7. Goetz CG. Textbook of Clinical Neurology. Elsevier ; 2007
  8. Herniation Syndromes. Updated: July 17, 2006. Accessed: March 1, 2017.
  9. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Elsevier Health Sciences ; 2018
  10. Changa AR, Czeisler BM, Lord AS. Management of Elevated Intracranial Pressure: a Review. Curr Neurol Neurosci Rep. 2019; 19 (12): p.99.doi: 10.1007/s11910-019-1010-3 . | Open in Read by QxMD
  11. Le Roux P, Menon DK, Citerio G, et al. Consensus Summary Statement of the International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care. Neurocrit Care. 2014; 21 (S2): p.1-26.doi: 10.1007/s12028-014-0041-5 . | Open in Read by QxMD
  12. Wagner KE et al.. Trauma. Oper Neurosurg. 2019; 17 (Supplement_1): p.S45-S75.doi: 10.1093/ons/opz089 . | Open in Read by QxMD
  13. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2016; 80 (1): p.6-15.doi: 10.1227/neu.0000000000001432 . | Open in Read by QxMD
  14. Kristiansson H et al.. Measuring Elevated Intracranial Pressure through Noninvasive Methods. J Neurosurg Anesthesiol. 2013; 25 (4): p.372-385.doi: 10.1097/ana.0b013e31829795ce . | Open in Read by QxMD
  15. Dimitriou J et al.. Comparison of Complications in Patients Receiving Different Types of Intracranial Pressure Monitoring: A Retrospective Study in a Single Center in Switzerland. World Neurosurg. 2016; 89: p.641-646.doi: 10.1016/j.wneu.2015.11.037 . | Open in Read by QxMD
  16. Fried HI, Nathan BR, Rowe AS, et al. The Insertion and Management of External Ventricular Drains: An Evidence-Based Consensus Statement. Neurocrit Care. 2016; 24 (1): p.61-81.doi: 10.1007/s12028-015-0224-8 . | Open in Read by QxMD
  17. Volovici V, Huijben JA, Ercole A, et al. Ventricular Drainage Catheters versus Intracranial Parenchymal Catheters for Intracranial Pressure Monitoring-Based Management of Traumatic Brain Injury: A Systematic Review and Meta-Analysis. J Neurotrauma. 2019; 36 (7): p.988-995.doi: 10.1089/neu.2018.6086 . | Open in Read by QxMD
  18. Winn HR. Youmans and Winn Neurological Surgery. Elsevier ; 2016
  19. Hutchinson PJ, Kolias AG, Timofeev IS, et al. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension. N Engl J Med. 2016; 375 (12): p.1119-1130.doi: 10.1056/nejmoa1605215 . | Open in Read by QxMD
  20. Esquenazi Y, Lo VP, Lee K. Critical Care Management of Cerebral Edema in Brain Tumors. J Intensive Care Med. 2016; 32 (1): p.15-24.doi: 10.1177/0885066615619618 . | Open in Read by QxMD
  21. Rabinstein AA et al. Neurological Emergencies. Springer International Publishing ; 2020
  22. Schizodimos T, Soulountsi V, Iasonidou C, Kapravelos N. An overview of management of intracranial hypertension in the intensive care unit. J Anesth. 2020; 34 (5): p.741-757.doi: 10.1007/s00540-020-02795-7 . | Open in Read by QxMD
  23. Cook AM, Morgan Jones G, Hawryluk GWJ, et al. Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients. Neurocrit Care. 2020; 32 (3): p.647-666.doi: 10.1007/s12028-020-00959-7 . | Open in Read by QxMD
  24. Torbey MT, Bösel J, Rhoney DH, et al. Evidence-Based Guidelines for the Management of Large Hemispheric Infarction. Neurocrit Care. 2015; 22 (1): p.146-164.doi: 10.1007/s12028-014-0085-6 . | Open in Read by QxMD
  25. Burgess S, Abu-Laban RB, Slavik RS, Vu EN, Zed PJ. A Systematic Review of Randomized Controlled Trials Comparing Hypertonic Sodium Solutions and Mannitol for Traumatic Brain Injury. Ann Pharmacother. 2016; 50 (4): p.291-300.doi: 10.1177/1060028016628893 . | Open in Read by QxMD
  26. Miyoshi Y, Kondo Y, et al. Effects of hypertonic saline versus mannitol in patients with traumatic brain injury in prehospital, emergency department, and intensive care unit settings: a systematic review and meta-analysis. Journal of Intensive Care. 2020; 8 (1).doi: 10.1186/s40560-020-00476-x . | Open in Read by QxMD
  27. Chen H, Song Z, Dennis JA. Hypertonic saline versus other intracranial pressure-lowering agents for people with acute traumatic brain injury. Cochrane Database of Systematic Reviews. 2020.doi: 10.1002/14651858.cd010904.pub3 . | Open in Read by QxMD
  28. Quintard H, Meyfroidt G, Citerio G. Hyperosmolar Agents for TBI: All Are Equal, But Some Are More Equal Than Others?. Neurocrit Care. 2020; 33 (2): p.613–614.doi: 10.1007/s12028-020-01063-6 . | Open in Read by QxMD
  29. Cook AM, Shutter L. Response to Drs. Quintard, et al.. Neurocrit Care. 2020; 33 (2): p.615-616.doi: 10.1007/s12028-020-01064-5 . | Open in Read by QxMD
  30. Rowland MJ, Veenith T, Hutchinson PJ, Perkins GD. Osmotherapy in traumatic brain injury. The Lancet Neurology. 2020; 19 (3): p.208.doi: 10.1016/s1474-4422(20)30003-x . | Open in Read by QxMD
  31. Mangat HS. Hypertonic saline infusion for treating intracranial hypertension after severe traumatic brain injury. Critical Care. 2018; 22 (1): p.37.doi: 10.1186/s13054-018-1963-7 . | Open in Read by QxMD
  32. Boone M, Oren-Grinberg A, Robinson T, Chen C, Kasper E. Mannitol or hypertonic saline in the setting of traumatic brain injury: What have we learned?. Surgical Neurology International. 2015; 6 (1): p.177.doi: 10.4103/2152-7806.170248 . | Open in Read by QxMD
  33. Wagner I, Hauer E-M, Staykov D, et al. Effects of Continuous Hypertonic Saline Infusion on Perihemorrhagic Edema Evolution. Stroke. 2011; 42 (6): p.1540-1545.doi: 10.1161/strokeaha.110.609479 . | Open in Read by QxMD
  34. Wells DL, Swanson JM, Wood GC, et al. The relationship between serum sodium and intracranial pressure when using hypertonic saline to target mild hypernatremia in patients with head trauma. Critical Care. 2012; 16 (5): p.R193.doi: 10.1186/cc11678 . | Open in Read by QxMD
  35. Ryken TC, McDermott M, Robinson PD, et al. The role of steroids in the management of brain metastases: a systematic review and evidence-based clinical practice guideline. J Neurooncol. 2009; 96 (1): p.103-114.doi: 10.1007/s11060-009-0057-4 . | Open in Read by QxMD
  36. Hawryluk GWJ, Rubiano AM, Totten AM, et al. Guidelines for the Management of Severe Traumatic Brain Injury: 2020 Update of the Decompressive Craniectomy Recommendations. Neurosurgery. 2020; 87 (3): p.427-434.doi: 10.1093/neuros/nyaa278 . | Open in Read by QxMD
  37. Honeybul S, Ho KM, Gillett G. Outcome Following Decompressive Hemicraniectomy for Malignant Cerebral Infarction. Stroke. 2015; 46 (9): p.2695-2698.doi: 10.1161/strokeaha.115.010078 . | Open in Read by QxMD
  38. Bullock MR, Chesnut R, Ghajar J, et al. Guidelines for the Surgical Management of Traumatic Brain Injury Author Group. Neurosurgery. 2006; 58 (3): p.S2-vi-S2-vi.doi: 10.1093/neurosurgery/ . | Open in Read by QxMD
  39. Godoy DA, Seifi A, Garza D, Lubillo-Montenegro S, Murillo-Cabezas F. Hyperventilation Therapy for Control of Posttraumatic Intracranial Hypertension. Frontiers in Neurology. 2017; 8: p.250.doi: 10.3389/fneur.2017.00250 . | Open in Read by QxMD
  40. Clark J, Ellens N, Figueroa B. The use of barbiturate-induced coma during cerebrovascular neurosurgery procedures: A review of the literature. Brain Circulation. 2015; 1 (2): p.140.doi: 10.4103/2394-8108.172887 . | Open in Read by QxMD
  41. Roberts I, Sydenham E. Barbiturates for acute traumatic brain injury. Cochrane Database of Systematic Reviews. 2012: p.CD000033.doi: 10.1002/14651858.cd000033.pub2 . | Open in Read by QxMD
  42. Crompton EM, Lubomirova I, Cotlarciuc I, Han TS, Sharma SD, Sharma P. Meta-Analysis of Therapeutic Hypothermia for Traumatic Brain Injury in Adult and Pediatric Patients. Crit Care Med. 2017; 45 (4): p.575-583.doi: 10.1097/ccm.0000000000002205 . | Open in Read by QxMD
  43. Andrews PJ, Sinclair HL, Rodríguez A, et al. Therapeutic hypothermia to reduce intracranial pressure after traumatic brain injury: the Eurotherm3235 RCT. Health Technol Assess (Rockv). 2018; 22 (45): p.1-134.doi: 10.3310/hta22450 . | Open in Read by QxMD
  44. Watson HI, Shepherd AA, Rhodes JKJ, Andrews PJD. Revisited: A Systematic Review of Therapeutic Hypothermia for Adult Patients Following Traumatic Brain Injury. Crit Care Med. 2018; 46 (6): p.972-979.doi: 10.1097/ccm.0000000000003125 . | Open in Read by QxMD
  45. Andrews et al.. Hypothermia for Intracranial Hypertension after Traumatic Brain Injury. New England Journal of Medicine. 2015; 373 (25): p.2403-2412.doi: 10.1056/nejmoa1507581 . | Open in Read by QxMD
  46. Chen H, Wu F, Yang P, Shao J, Chen Q, Zheng R. A meta-analysis of the effects of therapeutic hypothermia in adult patients with traumatic brain injury. Critical Care. 2019; 23 (1): p.396.doi: 10.1186/s13054-019-2667-3 . | Open in Read by QxMD
  47. Karnatovskaia LV, Lee AS, Festic E, Kramer CL, Freeman WD. Effect of Prolonged Therapeutic Hypothermia on Intracranial Pressure, Organ Function, and Hospital Outcomes Among Patients with Aneurysmal Subarachnoid Hemorrhage. Neurocrit Care. 2014; 21 (3): p.451-461.doi: 10.1007/s12028-014-9989-4 . | Open in Read by QxMD
  48. Marmarou A. A review of progress in understanding the pathophysiology and treatment of brain edema. Neurosurg Focus. 2007; 22 (5): p.E1.
  49. Liebeskind DS, Jüttler E, Shapovalov Y, Yegin A, Landen J, Jauch EC. Cerebral Edema Associated With Large Hemispheric Infarction. Stroke. 2019; 50 (9): p.2619-2625.doi: 10.1161/strokeaha.118.024766 . | Open in Read by QxMD
  50. Donkin JJ, Vink R. Mechanisms of cerebral edema in traumatic brain injury: therapeutic developments. Curr Opin Neurol. 2010; 23 (3): p.293-299.doi: 10.1097/wco.0b013e328337f451 . | Open in Read by QxMD
  51. Rao JVI, Vengamma B, Naveen T, Naveen V. Lead encephalopathy in adults. J Neurosci Rural Pract. 2014; 5 (2): p.161-163.doi: 10.4103/0976-3147.131665 . | Open in Read by QxMD
  52. Dalby T, Wohl E, Dinsmore M, Unger Z, Chowdhury T, Venkatraghavan L. Pathophysiology of Cerebral Edema—A Comprehensive Review. Journal of Neuroanaesthesiology and Critical Care. 2020; 08 (03): p.163-172.doi: 10.1055/s-0040-1721165 . | Open in Read by QxMD
  53. Increased Intracranial Pressure. Updated: October 22, 2015. Accessed: March 1, 2017.

Icon of a lockAccess full content

Sign up and get unlimited access.
 Evidence-based content, created and peer-reviewed by physicians. Read the disclaimer