Opinion statement
After brain injury, neurologic intensive care focuses on the detection and treatment of secondary brain insults that may compound the initial injury. Increased intracranial pressure (ICP) contributes to secondary brain injury by causing brain ischemia, hypoxia, and metabolic dysfunction. Because ICP is easily measured at the bedside, it is the target of numerous pharmacologic and surgical interventions in efforts to improve brain physiology and limit secondary injury. However, ICP may not adequately reflect the metabolic health of the underlying brain tissue, particularly in cases of focal brain injury. As a result, ICP control alone may be insufficient to impact patients’ long-term recovery. Further studies are needed to better understand the combination of cerebral, hemodynamic, and metabolic markers that are best utilized to ensure optimal brain and systemic recovery and overall patient outcome after brain injury.
Similar content being viewed by others
References and Recommended Reading
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
Becker DP, Miller JD, Ward JD, et al. The outcome from severe head injury with early diagnosis and intensive management. J Neurosurg. 1977;47:491–502.
Nakagawa K, Smith WS. Evaluation and management of increased intracranial pressure. Continuum. 2011;17:1077–93.
Mokri B. The Monro-Kellie hypothesis: applications in CSF volume depletion. Neurology. 2001;56:1746–8.
Narayan RK, Greenberg RP, Miller JD, et al. Improved confidence of outcome prediction in severe head injury. A comparative analysis of the clinical examination, multimodality evoked potentials, CT scanning, and intracranial pressure. J Neurosurg. 1981;54:751–62.
Eisenberg HM, Frankowski RF, Contant CF, et al. High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg. 1988;69:15–23.
Marmarou A, Anderson RL, Ward JD, et al. Impact of ICP instability and hypotension on outcome in patients with severe head trauma. J Neurosurg. 1991;75:S59–66.
Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. VIII. Intracranial pressure thresholds. J Neurotrauma. 2007;24 Suppl 1:S55–8.
Bratton SL, Chestnut RM, Ghajar J, et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma. 2007;24 Suppl 1:S37–44.
Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367:2471–81. This paper is the only large, randomized controlled study assessing the utility of intracranial pressure monitoring following traumatic brain injury to date.
Kahle KT, Duhaime AC. Intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2013;368:1750.
Ropper A. Brain in a box. N Engl J Med. 2012;367:2539–41.
Schwab S, Aschoff A, Spranger M, et al. The value of intracranial pressure monitoring in acute hemispheric stroke. Neurology. 1996;47:393–8.
Poca MA, Benejam B, Sahuquillo J, et al. Monitoring intracranial pressure in patients with malignant middle cerebral artery infarction: is it useful? J Neurosurg. 2010;112:648–57.
Gardner PA, Engh J, Atteberry D, Moossy JJ. Hemorrhage rates after external ventricular drain placement. J Neurosurg. 2009;110:1021–5.
Lozier AP, Sciacca RR, Romagnoli MF, Connolly ES. Ventriculostomy-related infections: a critical review of the literature. Neurosurgery. 2002;51:170–81.
Vik A, Nag T, Fredriksli OA, et al. Relationship of “dose” of intracranial hypertension to outcome in severe traumatic brain injury. J Neurosurg. 2008;109:678–84.
Sheth KN, Stein DM, Aarabi B, et al. Intracranial pressure dose and outcome in traumatic brain injury. Neurocrit Care. 2013;18:26–32.
Kahraman S, Dutton RP, Hu P, et al. Automated measurement of “pressure times time dose” of intracranial hypertension best predicts outcome after severe traumatic brain injury. J Trauma. 2010;69:110–8.
Bekar A, Gören S, Korfali E, et al. Complications of brain tissue pressure monitoring with a fiberoptic device. Neurosurg Rev. 1998;21:254–9.
Rosner MJ, Coley IB. Cerebral perfusion pressure, intracranial pressure, and head elevation. J Neurosurg. 1986;65:636–41.
Ng I, Lim J, Wong HB. Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation. Neurosurgery. 2004;54:593–8.
Raichle ME, Plum F. Hyperventilation and cerebral blood flow. Stroke. 1972;3:566–75.
Stocchetti N, Maas AIR, Chieregato A, van der Plas AA. Hyperventilation in head injury: a review. Chest. 2005;127:1812–27.
Diringer MN, Zazulia AR. Osmotic therapy: fact and fiction. Neurocrit Care. 2004;1:219–33.
Bentsen G, Breivik H, Lundar T, Stubhaug A. Hypertonic saline (7.2 %) in 6 % hydroxyethyl starch reduces intracranial pressure and improves hemodynamics in a placebo-controlled study involving stable patients with subarachnoid hemorrhage. Crit Care Med. 2006;34:2912–7.
White H, Cook D, Venkatesh B. The use of hypertonic saline for treating intracranial hypertension after traumatic brain injury. Anesth Analg. 2006;102:1836–46.
Qureshi AI, Suarez JI. Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension. Crit Care Med. 2000;28:3301–13.
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. Crit Care. 2012;16:R193.
Murad A, Ghostine S, Colohan ART. Controlled lumbar drainage in medically refractory increased intracranial pressure. Acta Neurochir. 2008;102(Suppl):89–91.
Bauer DF, McGwin G, Melton SM, et al. Risk factors for conversion to permanent ventricular shunt in patients receiving therapeutic ventriculostomy for traumatic brain injury. Neurosurgery. 2011;68:85–8.
Rea GL, Rockswold GL. Barbiturate therapy in uncontrolled intracranial hypertension. Neurosurgery. 1983;12:401–4.
Marshall GT, James RF, Landman MP, et al. Pentobarbital coma for refractory intra-cranial hypertension after severe traumatic brain injury: mortality predictions and one-year outcomes in 55 patients. J Trauma. 2010;69:275–83.
Marshall LF, Smith RW, Shapiro HM. The outcome with aggressive treatment in severe head injuries. Part II: acute and chronic barbiturate administration in the management of head injury. J Neurosurg. 1979;50:26–30.
Roberts I, Sydenham E. Barbiturates for acute traumatic brain injury. Cochrane Database Syst Rev. 2012;12, CD000033.
Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomized controlled trials. Lancet Neurol. 2007;6:215–22.
Jüttler E, Schwab S, Schmiedek P, et al. Decompressive surgery for the treatment of malignant infarction of the middle cerebral artery (DESTINY): a randomized, controlled trial. Stroke. 2007;38:2518–25.
Hofmeijer J, Kappelle LJ, Algra A, et al. Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multi-center, open, randomized trial. Lancet Neurol. 2009;8:326–33.
Vahedi K, Vicaut E, Mateo J, et al. Sequential-design, multi-center, randomized, controlled trial of early decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial). Stroke. 2007;38:2506–17.
Geurts M, van der Worp HB, Kappelle LJ, et al. Surgical decompression for space-occupying cerebral infarction: outcomes at 3 years in the randomized HAMLET trial. Stroke. 2013;44:2506–8.
Zhao J, Su YY, Zhang Y, et al. Decompressive hemicraniectomy in malignant middle cerebral artery infarct: a randomized controlled trial enrolling patients up to 80 years old. Neurocrit Care. 2012;17:161–71.
Puetz V, Campos CR, Eliasziw M, et al. Assessing the benefits of hemicraniectomy: what is a favourable outcome? Lancet Neurol. 2007;6:580.
Rahme R, Zuccarello M, Kleindorfer D, et al. Decompressive hemicraniectomy for malignant middle cerebral artery territory infarction: is life worth living? J Neurosurg. 2012;117:749–54.
Danish SF, Barone D, Lega BC, Stein SC. Quality of life after hemicraniectomy for traumatic brain injury in adults: a review of the literature. Neurosurg Focus. 2009;26:E2.
Kolias AG, Kirkpatrick PJ, Hutchinson PJ. Decompressive craniectomy: past, present and future. Nat Rev Neurol. 2013;9:405–15. This review article provides a thorough and comprehensive review of the use of surgical craniectomy for the management of a variety of severe brain injuries and the ethical implications of this procedure.
Whitfield PC, Patel H, Hutchinson PJ, et al. Bifrontal decompressive craniectomy in the management of posttraumatic intracranial hypertension. Br J Neurosurg. 2001;15:500–7.
Aarabi B, Hesdorffer DC, Ahn ES, et al. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg. 2006;104:469–79.
Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364:1493–502.
Attia J, Cook DJ. Prognosis in anoxic and traumatic coma. Crit Care Clin. 1998;14:497–511.
Sahuquillo J, Martínez-Ricarte F, Poca MA. Decompressive craniectomy in traumatic brain injury after the DECRA trial. Where do we stand? Curr Opin Crit Care. 2013;19:101–6.
Austinat M, Braeuninger S, Pesquero JB, et al. Blockade of bradykinin receptor B1 but not bradykinin receptor B2 provides protection from cerebral infarction and brain edema. Stroke. 2009;40:285–93.
Raslan F, Schwarz T, Meuth SG, et al. Inhibition of bradykinin receptor B1 protects mice from focal brain injury by reducing blood–brain barrier leakage and inflammation. J Cereb Blood Flow Metab. 2010;30:1477–86.
Albert-Weissenberger C, Stetter C, Meuth SG, et al. Blocking of bradykinin receptor B1 protects from focal closed head injury in mice by reducing axonal damage and astroglia activation. J Cereb Blood Flow Metab. 2012;32:1747–56.
Shakur H, Andrews P, Asser T, et al. The BRAIN TRIAL: a randomised, placebo controlled trial of a Bradykinin B2 receptor antagonist (Anatibant) in patients with traumatic brain injury. Trials. 2009;10:109.
Kunz M, Nussberger J, Holtmannspoetter M, et al. Bradykinin in blood and CSF after acute cerebral lesions: correlations with cerebral edema and intracranial pressure. J Neurotrauma. 2013; [Ahead of print].
Deutsch ER, Espinoza TR, Atif F, et al. Progesterone’s role in neuroprotection: a review of the evidence. Brain Res. 2013;1530:82–105.
Shahrokhi N, Khaksari M, Soltani Z, et al. Effect of sex steroid hormones on brain edema, intracranial pressure, and neurologic outcomes after traumatic brain injury. Eur J Neurol. 2010;88:414–21.
Yan F, Hu Q, Chen J, Wu C, Gu C, Chen G. Progesterone attenuates early brain injury after subarachnoid hemorrhage in rats. Neurosci Lett. 2013;543:163–7.
Wright DW, Kellermann AL, Hertzberg VS, et al. ProTECT: a randomized clinical trial of progesterone for acute traumatic brain injury. Ann Emerg Med. 2007;49:391–402.
Simard JM, Chen M, Tarasov KV, et al. Newly expressed SUR1-regulated NC (Ca-ATP) channel mediates cerebral edema after ischemic stroke. Nat Med. 2006;12:433–40.
Simard JM, Woo SK, Schwartzbauer GT, Gerzanich V. Sulfonylurea receptor 1 in central nervous system injury: a focused review. J Cereb Blood Flow Metab. 2012;32:1699–717.
Sheth KN. Novel approaches to the primary prevention of edema after ischemia. Stroke. 2013;44:S136.
Compliance with Ethics Guidelines
Conflict of Interest
Danielle K. Sandsmark declares that she has no conflict of interest.
Kevin N. Sheth declares that he has no conflict of interest.
Human and Animal Rights and Informed Consent
This article does not contain any studies with animal subjects performed by any of the authors. With regard to the authors’ research cited in this paper, all procedures were followed in accordance with the ethical standards of the responsible committee on human experimentation and with the Helsinki Declaration of 1975, as revised in 2000 and 2008.
Author information
Authors and Affiliations
Corresponding author
Additional information
This article is part of the Topical Collection on Critical Care Neurology
Rights and permissions
About this article
Cite this article
Sandsmark, D.K., Sheth, K.N. Management of Increased Intracranial Pressure. Curr Treat Options Neurol 16, 272 (2014). https://doi.org/10.1007/s11940-013-0272-3
Published:
DOI: https://doi.org/10.1007/s11940-013-0272-3