Traumatic Brain Injury (TBI) Management


The management of Traumatic Brain Injury (TBI) is focused on the prevention of secondary injury


  • prevention of secondary injury is the goal
  • secure airway by rapid sequence intubation (early intubation of probable benefit but not proven)
  • establish normal breathing (normocapnia unless neurological deterioration documented)
  • circulation (aggressively avoid hypotension; use crystalloid fluids – avoid albumin solutions)
  • protect c-spine
  • timely transport to a neurosurgical unit


  • manage with an ATLS protocol
  • focussed neurological assessment: GCS, pupils, extent of extremity movements, examine head (e.g. haemotympanum, periorbital or mastoid ecchymosis, CSF rhinorrhoea, otorrhoea)
  • haemodynamically stable -> CT
  • haemodynamically unstable -> laparotomy, thoracotomy, diagnostic burrholes if there is lateralising neurology (e.g. fixed dilated pupil)


  • determined by lesions
  • small haematomas usually observed (<10mm)
  • haematomas/contusions involving the middle cranial fossa are higher risk (can cause herniation without a rise in ICP)
  • penetrating injuries: bullets -> massive destruction, knives -> minimal mass effect but high risk of infection and CSF leak


  • standard monitoring required plus invasive pressure monitoring
  • ICP monitoring mandatory for severe TBI + abnormal CT as intracranial hypertension develops in 60% (see ICP monitor document)
  • EVDs vs Codmans (both have advantages and disadvantages)


  • evacuation of mass lesions
  • decompressive craniectomy (controversial, the DECRA study showed harm with early, aggressive decompression)



  • avoid hypoxaemia
    — titrated FiO2
    — PEEP up to 15cmH2O doesn’t increase ICP significantly
  • avoid hypotension and hypvolaemia
    — use saline and avoid albumin
    — use vasopressors
    — treat anaemia

Specific therapy


  • avoid intracranial hypertension
    — sustained ICP > 20mmHg causes ischaemia
  • maintain CPP of 60mmHg
    — higher produces more ARDS
    — lower produces a fall in brain tissue PO2


  • head up 30 degrees position
  • sedation and analgesia
  • neuromuscular blockade
    — helps control ICP
    — increases risk of pneumonia and critical illness polyneuropathy
  • vent CSF via EVD if raised ICP
  • mild hyperventilation to maintain normocarbia
    — aim for PaCO2 35mmHg


  • osmotherapies
    — mannitol 0.25-1g/kg Q3hrly
    — hypertonic saline (3%) 3 mL/kg over 10 min or 10-20 mL 20% saline


  • barbiturate coma
    — decreases cerebral metabolic rate, but can cause hypotension and has long half life
  • therapeutic hypothermia
    — lowers ICP but not shown to change outcome (POLAR study is currently in progress)
  • aggressive hyperventilation
    — causes cerebral vasoconstriction
    — not used except in rescue situation (e.g. patient coning)
  • decompressive craniectomy
  • lumbar CSF drainage


  • avoidance of hyperthermia
    — increase in neuronal death when > 39 C during first 24 hours
    — aggressively cool if T >39 C
  • seizure prophylaxis
    — phenytoin or levitiracetam during first 7 days, but generally on midazolam and propofol
    — no evidence of benefit

Supportive care and Monitoring

  • DVT prophylaxis
    — TEDS + IPC
    — can usually use LMWH and UFH within 2-3 days of injury (discuss with neurosurgeon)
  • nutrition
    — early feeding important because of high metabolic requirement
  • sedation
    —  permits manipulation of ventilation, optimisation of cerebral metabolic rate (CMRO2), cerebral blood flow (CBF), and intracranial pressure (ICP)
    — also provides anxiolysis, treatment of withdrawal syndromes and seizure control

References and links


Journal articles

  • Flower O, Hellings S. Sedation in traumatic brain injury. Emerg Med Int. 2012;2012:637171. doi: 10.1155/2012/637171. PMC3461283.
  • Haddad SH, Arabi YM. Critical care management of severe traumatic brain injury in adults. Scand J Trauma Resusc Emerg Med. 2012 Feb 3;20:12. PMC3298793.
  • Helmy A, Vizcaychipi M, Gupta AK. Traumatic brain injury: intensive care management. Br J Anaesth. 2007 Jul;99(1):32-42. PMID: 17556349.

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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