Adult Neurosurgery — For Physicians · Module

Neurotrauma & Neurocritical Care

Severe TBI, intracranial pressure, traumatic haematomas, and neurocritical care

Reviewed by — Neurosurgeon · Sidra Medicine, Doha · Last updated:

Overview

Adult neurotrauma and neurocritical care span the spectrum from the polytrauma patient with severe traumatic brain injury to the older patient with a chronic subdural haematoma. The unifying goal is to prevent secondary brain injury, through timely evacuation of surgical mass lesions, control of intracranial pressure and cerebral perfusion, and protocolised neurocritical care.

Traumatic mass lesions (epidural, acute subdural, and intracerebral haematomas) may need urgent evacuation; diffuse injury and refractory intracranial hypertension are managed medically and, selectively, with decompressive craniectomy; chronic subdural haematoma is a distinct, predominantly geriatric entity.

Practice is anchored by the Brain Trauma Foundation severe-TBI and surgical-management guidelines, and shaped by randomised trials of decompressive craniectomy (DECRA, RESCUEicp) and of ICP-monitor-guided care (BEST:TRIP).

References used here

  1. Carney N, Totten AM, O'Reilly C, Ullman JS, Hawryluk GW, Bell MJ, Bratton SL, Chesnut R, Harris OA, Kissoon N, Rubiano AM, Shutter L, Tasker RC, Vavilala MS, Wilberger J, Wright DW, Ghajar J. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6-15.
    Open via DOI Open on PubMed

Severe Traumatic Brain Injury

Severe TBI (Glasgow Coma Scale score 8 or less) is managed, along the lines of the Brain Trauma Foundation guidelines, to prevent secondary brain injury: avoiding hypoxia and hypotension, controlling intracranial pressure, and maintaining cerebral perfusion.

Epidemiology

Incidence
A leading cause of death and acquired disability in young adults, with a rising share in older adults from falls.
Age peak
Bimodal: young adults (road traffic, assault) and older adults (falls).
Location
Focal injury (haematomas, contusions) and/or diffuse injury (diffuse axonal injury, swelling).

Clinical Presentation

  • The Glasgow Coma Scale classifies severity (mild 13–15, moderate 9–12, severe 8 or less); pupillary reactivity and lateralising deficits are assessed alongside the systemic (ATLS) survey.
  • A 'talk-and-deteriorate' course, with initial responsiveness then decline, signals an expanding mass lesion until proven otherwise.

Imaging

  • Non-contrast CT head is the immediate investigation, identifying haematomas, contusions, oedema, midline shift, and effacement of the basal cisterns.
  • CT is repeated for any neurological deterioration or to monitor an evolving injury.

Management

Surgery. Significant mass lesions (epidural, acute subdural, and intracerebral haematomas) are evacuated per surgical guidelines; an external ventricular drain provides CSF diversion and ICP monitoring; decompressive craniectomy is reserved as a tier for refractory intracranial hypertension (see the ICP section).

Adjuvant therapy. Brain Trauma Foundation guidelines anchor care: avoid hypoxia and hypotension, elevate the head, provide analgesia and sedation, use osmotherapy (mannitol or hypertonic saline), set ventilation targets, give seizure prophylaxis where indicated, and treat ICP above threshold while maintaining cerebral perfusion pressure within target.

Considerations. Care is protocolised within a neurocritical-care setting; the BTF 4th-edition guidelines provide the evidence base.

Outcomes

Outcome relates to the initial GCS, age, pupillary reactivity, CT findings, and the avoidance of secondary insults (hypoxia, hypotension, uncontrolled ICP).

By molecular subgroup: Bilaterally unreactive pupils and effaced basal cisterns are poor prognostic signs.

Clinical Pearls

  • Prevent secondary injury: avoid hypoxia and hypotension above all else.
  • GCS of 8 or less defines severe TBI and usually mandates airway protection.
  • Follow the Brain Trauma Foundation guidelines for ICP/CPP-directed care.
  • Get an early CT and repeat it if the patient deteriorates; beware the 'talk and deteriorate' presentation.

References used here

  1. Carney N, Totten AM, O'Reilly C, Ullman JS, Hawryluk GW, Bell MJ, Bratton SL, Chesnut R, Harris OA, Kissoon N, Rubiano AM, Shutter L, Tasker RC, Vavilala MS, Wilberger J, Wright DW, Ghajar J. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6-15.
    Open via DOI Open on PubMed
  2. Winn HR (Editor). Youmans and Winn Neurological Surgery. 8th Edition (4-volume set). Elsevier, 2022. ISBN: 978-0-323-66192-8.
  3. Greenberg MS. Greenberg's Handbook of Neurosurgery. 10th Edition. Thieme, 2023. ISBN: 978-1-68420-504-2.

Intracranial Pressure & Decompressive Craniectomy

Raised intracranial pressure (ICP) drives secondary injury after TBI. Management is tiered; monitoring informs treatment, and decompressive craniectomy is a last-tier option whose role is nuanced.

Clinical Presentation

  • Signs of raised ICP and impending herniation (declining GCS, pupillary changes, Cushing response) prompt escalation.
  • ICP is measured by an intraparenchymal monitor or an external ventricular drain; cerebral perfusion pressure (CPP) equals mean arterial pressure minus ICP.

Imaging

  • CT identifies the cause of raised ICP (mass lesion, swelling, hydrocephalus) and guides whether surgery or medical therapy is needed.
  • Effacement of the basal cisterns and midline shift are key radiological markers of mass effect.

Management

Surgery. Decompressive craniectomy reliably lowers ICP, but the trials temper enthusiasm. DECRA (early bifrontotemporoparietal craniectomy for diffuse TBI with refractory ICP) reduced ICP and ICU stay but was associated with worse functional outcomes. RESCUEicp (last-tier craniectomy for refractory raised ICP) reduced mortality, but with more survivors in vegetative or severely disabled states, so it is life-saving while trading mortality for disability and demands careful, individualised decisions and discussion with the family.

Adjuvant therapy. ICP is managed in tiers (sedation, osmotherapy, CSF drainage, ventilation, temperature control). On monitoring: the BEST:TRIP trial found that, in the setting tested, care guided by ICP monitoring was not superior to care guided by serial imaging and clinical examination, although ICP monitoring remains widely used and guideline-supported in appropriate contexts.

Considerations. Decompressive craniectomy decisions weigh survival against the likelihood and acceptability of severe long-term disability.

Outcomes

Craniectomy reliably lowers ICP but does not guarantee a better functional outcome.

By molecular subgroup: DECRA showed worse outcomes with early craniectomy; RESCUEicp showed lower mortality at the cost of more severe disability among survivors.

Clinical Pearls

  • Decompressive craniectomy lowers ICP but does not guarantee better function: see DECRA (worse outcomes) and RESCUEicp (lower mortality, more disability).
  • CPP = MAP − ICP; protect cerebral perfusion while controlling ICP.
  • BEST:TRIP found ICP-monitor-guided care was not superior to imaging/exam-guided care in the studied setting.
  • Escalate ICP therapy in tiers; reserve craniectomy for refractory hypertension.

References used here

  1. Cooper DJ, Rosenfeld JV, Murray L, Arabi YM, Davies AR, D'Urso P, Kossmann T, Ponsford J, Seppelt I, Reilly P, Wolfe R. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364(16):1493-1502.
    Open via DOI Open on PubMed
  2. Hutchinson PJ, Kolias AG, Timofeev IS, Corteen EA, Czosnyka M, Timothy J, Anderson I, Bulters DO, Belli A, Eynon CA, Wadley J, Mendelow AD, Mitchell PM, Wilson MH, Critchley G, Sahuquillo J, Unterberg A, Servadei F, Teasdale GM, Pickard JD, Menon DK, Murray GD, Kirkpatrick PJ; RESCUEicp Trial Collaborators. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension. N Engl J Med. 2016;375(12):1119-1130.
    Open via DOI Open on PubMed
  3. Chesnut RM, Temkin N, Carney N, Dikmen S, Rondina C, Videtta W, Petroni G, Lujan S, Pridgeon J, Barber J, Machamer J, Chaddock K, Celix JM, Cherner M, Hendrix T; Global Neurotrauma Research Group. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367(26):2471-2481.
    Open via DOI Open on PubMed
  4. Carney N, Totten AM, O'Reilly C, Ullman JS, Hawryluk GW, Bell MJ, Bratton SL, Chesnut R, Harris OA, Kissoon N, Rubiano AM, Shutter L, Tasker RC, Vavilala MS, Wilberger J, Wright DW, Ghajar J. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6-15.
    Open via DOI Open on PubMed

Acute Epidural Haematoma

An epidural (extradural) haematoma is blood between the dura and the skull, classically from a temporal skull fracture lacerating the middle meningeal artery. The 'lucid interval', a brief recovery before deterioration, is a hallmark but is not always present.

Clinical Presentation

  • Head trauma with a possible lucid interval followed by decline; uncal herniation produces an ipsilateral dilated pupil and contralateral weakness.
  • A 'talk-and-deteriorate' presentation is classic and must be recognised early.

Imaging

  • CT shows a biconvex (lens-shaped) hyperdense extra-axial collection, typically temporoparietal, that does not cross suture lines (but can cross the midline).
  • An associated skull fracture is common.

Management

Surgery. Prompt surgical evacuation (craniotomy) is indicated for a significant epidural haematoma. Per the Brain Trauma Foundation surgical-management guideline, an EDH greater than 30 cm³ should be evacuated regardless of GCS, and urgent evacuation is recommended for a comatose patient (GCS <9) with anisocoria. Small EDHs without significant mass effect or deficit may be observed with serial imaging.

Adjuvant therapy. Reverse any coagulopathy and provide neurocritical-care monitoring.

Considerations. Outcome is excellent when evacuation precedes secondary injury, so the 'talk-and-deteriorate' patient must not be missed.

Outcomes

With prompt evacuation before herniation, and in the absence of severe underlying brain injury, the prognosis is generally very good.

By molecular subgroup: Delay to evacuation after herniation markedly worsens outcome.

Clinical Pearls

  • Classic biconvex hyperdensity that does not cross sutures.
  • The lucid interval is classic but inconsistent, so don't rely on its absence.
  • BTF surgical guideline: evacuate EDH >30 cm³, and urgently if comatose with anisocoria.
  • Outcome is excellent if treated before herniation.

References used here

  1. Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW, Servadei F, Walters BC, Wilberger JE; Surgical Management of Traumatic Brain Injury Author Group. Surgical management of acute epidural hematomas. Neurosurgery. 2006;58(3 Suppl):S7-S15.
    Open on PubMed
  2. Greenberg MS. Greenberg's Handbook of Neurosurgery. 10th Edition. Thieme, 2023. ISBN: 978-1-68420-504-2.

Acute Subdural Haematoma

An acute subdural haematoma is blood between the dura and the arachnoid, usually from torn bridging veins or cortical lacerations, and is often associated with significant underlying brain injury. It carries a worse prognosis than an epidural haematoma.

Clinical Presentation

  • Depressed consciousness after trauma, frequently with a lateralising deficit; the clinical picture is often dominated by the underlying brain injury.
  • Anticoagulant or antiplatelet use increases the risk and severity.

Imaging

  • CT shows a crescent-shaped (concave) hyperdense extra-axial collection following the convexity, crossing suture lines but not the midline; thickness and midline shift are quantified.
  • Associated contusions and swelling are common and worsen prognosis.

Management

Surgery. Surgical evacuation (craniotomy, sometimes with decompressive craniectomy) is indicated for a significant acute subdural haematoma. Per the Brain Trauma Foundation surgical-management guideline, an ASDH with a thickness greater than 10 mm or a midline shift greater than 5 mm should be evacuated regardless of GCS; a comatose patient with a smaller ASDH is managed with ICP monitoring and surgery if indicated.

Adjuvant therapy. Manage the frequently severe underlying brain injury and ICP, and urgently reverse any coagulopathy.

Considerations. Prognosis is driven by the underlying brain injury, the patient's age, and the time to evacuation more than by the clot alone.

Outcomes

Worse than an epidural haematoma because of the associated parenchymal injury; rapid evacuation and ICP control matter.

By molecular subgroup: Older age, lower GCS, and delayed evacuation predict worse outcomes.

Clinical Pearls

  • Crescent-shaped and crosses suture lines (unlike EDH), but not the midline.
  • BTF thresholds — evacuate if thickness >10 mm or midline shift >5 mm.
  • The underlying brain injury, not just the clot, drives prognosis.
  • Reverse anticoagulation urgently.

References used here

  1. Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW, Servadei F, Walters BC, Wilberger JE; Surgical Management of Traumatic Brain Injury Author Group. Surgical management of acute subdural hematomas. Neurosurgery. 2006;58(3 Suppl):S16-S24.
    Open on PubMed
  2. Greenberg MS. Greenberg's Handbook of Neurosurgery. 10th Edition. Thieme, 2023. ISBN: 978-1-68420-504-2.

Chronic Subdural Haematoma

A chronic subdural haematoma (cSDH) is an encapsulated, liquefied collection that develops over weeks, predominantly in older adults, often after minor or unremembered trauma and associated with brain atrophy and antithrombotic use.

Clinical Presentation

  • Insidious headache, confusion, gait disturbance, focal deficit, or cognitive decline; symptoms commonly fluctuate.
  • It is an important and treatable cause of reversible cognitive and gait decline in older adults.

Imaging

  • CT shows a crescentic, often hypodense or mixed-density extra-axial collection over the convexity — sometimes bilateral — with mass effect.
  • Membranes and acute-on-chronic components (mixed density) are common.

Management

Surgery. A symptomatic cSDH with mass effect is typically treated by surgical drainage — most commonly burr-hole drainage, where placing a subdural drain reduces recurrence. Middle meningeal artery embolisation has emerged as an adjunct or alternative: the multicentre randomised MAGIC-MT trial (Liu et al., 2024) evaluated MMA embolisation added to usual care (burr-hole drainage or nonsurgical treatment) for nonacute subdural haematoma, part of a growing evidence base defining its role.

Adjuvant therapy. Review and manage antithrombotic medication and its reversal, and treat seizures if they occur.

Considerations. Recurrence is not uncommon; a subdural drain reduces it. Many small, asymptomatic cSDHs are simply observed.

Outcomes

Generally good functional recovery after drainage in selected patients; recurrence and the frailty of an older population are the main challenges.

By molecular subgroup: Bilateral collections, marked atrophy, and continued antithrombotic therapy are associated with higher recurrence.

Clinical Pearls

  • Older adults after minor or unremembered trauma, often on antithrombotics.
  • Burr-hole drainage with a subdural drain reduces recurrence.
  • Middle meningeal artery embolisation is an emerging adjunct under active randomised study (e.g. MAGIC-MT).
  • Always check and manage anticoagulation, and consider cSDH in any older patient with new cognitive or gait decline.

References used here

  1. Liu J, Ni W, Zuo Q, Yang H, Peng Y, et al.; MAGIC-MT Investigators. Middle Meningeal Artery Embolization for Nonacute Subdural Hematoma. N Engl J Med. 2024;391(20):1901-1912.
    Open via DOI Open on PubMed
  2. Greenberg MS. Greenberg's Handbook of Neurosurgery. 10th Edition. Thieme, 2023. ISBN: 978-1-68420-504-2.
  3. Winn HR (Editor). Youmans and Winn Neurological Surgery. 8th Edition (4-volume set). Elsevier, 2022. ISBN: 978-0-323-66192-8.