Traumatic Brain Injury (TBI) Overview

OVERVIEW

Traumatic brain injury (TBI) is an insult to the brain from an external mechanical force, potentially leading to an altered level of consciousness and permanent or temporary impairment of cognitive, physical, and psychosocial functions.

  • TBI accounts for >30% of trauma deaths and is the leading cause of disability in people under 40
  • bimodal distribution
    — young adult males
    — elderly

CAUSES

Blunt or penetrating

  • Falls (most common cause)
  • MVC (cause of most TBI deaths)
  • violence and assaults
  • industrial accidents
  • sport

Consider:

  • NAI in children
  • elder abuse
  • domestic violence

PRIMARY INJURY

  •  Primary injury occurs at the time of the traumatic incident
  • Mechanisms
    • Impact loading – Collision of the head with a solid object at a tangible speed (contact forces)
    • Impulsive loading – Sudden motion without significant physical contact (inertial forces or acceleration/ deceleration injury)
    • Static loading – Loading in which the effect of speed of occurrence may not be significant
  • cause brain tissue deformation through:
    — compression
    — tension (stretch)
    — shearing
  • leading to direct cellular and tissue injury:
    — cell membrane disruption and ion channel dysfuntion
    — blood-brain barrier and vascular disruption
    — altered autoregulation
    — local inflammation

SECONDARY INJURY

  • occurs hours to days after the initial insult and is a major determinant of the patients ultimate neurological outcome
  • attributable to further cellular damage from the effects of primary injuries
  • numerous neurochemical mediators:
    — oxygen free radicals
    — excitatory amino acids and endogenous opioid peptides, cytokines and other inflammatory agents
    —  increased metabolism in the injured brain due to increased circulating levels of catecholamines from TBI-induced stimulation of the sympathoadrenomedullary axis and serotonergic system
    — depression in glucose utilization
    — increase in extracellular potassium may lead to edema
    — decrease in intracellular magnesium may contribute to calcium influx
  • leads to neuronal degeneration and poor outcome

Intracranial

  • seizure
  • delayed haematoma or rebleed
  • SAH
  • vasospasm
  • hydrocephalus
  • neuroinfection

Systemic

  • hypoxia
  • hypotension
  • hypo/hypercapnia
  • hyperthermia
  • hypo/hyperglycaemia
  • hypo/hypernatraemia
  • hyperosmolarity
  • infection

GRADING OF HEAD INJURY

Mild

  • GCS 13-15
  • ‘brief LOC’, nausea, cognitive, behavioural and emotional disturbance

Moderate

  • GCS 9-12 after non-surgical resuscitation

Severe

  • GCS < 8 after non-surgical resuscitation

INDICATIONS FOR IMAGING

Definite

  • LOC for > 5 minutes
  • focal neurological findings
  • seizure
  • failure of mental status to improve over time in an alcohol-intoxicated patient
  • penetrating skull injuries
  • signs of a basal or depressed skull fracture
  • coagulopathy
  • previous shunt-treated hydrocephalus
  • infants and children
  • age > 60

New Orleans Criteria for CT post minor HI

  • headache
  • vomiting
  • > 60 yrs
  • drug or alcohol intoxification
  • deficits in STM
  • evidence of trauma above the clavicles

Canadian CT head rules

High Risk features

  • GCS < 15 for 2 hours post injury
  • suspected open or depressed skull fracture
  • more than 2 episodes of vomiting
  • physical evidence of basal skull fracture
  • age > 65
  • coagulopathy

Medium Risk features

  • antero-grade amnesia for more than 30 min prior to injury
  • dangerous mechanism:
    — pedestrian vs motor vehicle
    — ejection from vehicle
    — fall from > than 3 feet

TYPES OF TBI

Skull Fracture

  • from contact force
  • usually associated with a brief loss of consciousness
  • linear: lateral convexities of skull
  • depressed: blunt force from an object with a small surface area (hammer)
  • BOS: severe blunt trauma to forehead or occiput

Subdural Haematoma

  • tearing of bridging veins
  • haematoma spreads over cortical surface within dural reflections of falx cerebri which prevents expansion to the contralateral hemisphere
  • often associated with cerebral contusions underneath

Epidural Haematoma

  • usually from middle meningeal artery tear with associated skull fracture
  • most are temporal or parietal but can occur in frontal and occipital lobes (rare in posterior fossa)
  • classic lenticular shape
  • uncommon in infants, toddlers c/o skull is deformable and not likely to fracture
  • uncommon in adults > 60 years as dura extremely adherent to skull

Subarachnoid Haematoma

  • does not produce a haematoma or mass effect
  • may cause post-traumatic vasospasm

Cerebral Contusions

  • heterogenous lesions comprising of punctate haemorrhage, oedema and necrosis
  • inferior frontal cortex and anterior temporal lobes where the inner table of skull is very irregular
  • do evolve over time (may not see on first CT) -> can cause significant mass effect with herniation
  • may cause headache -> elevated ICP and coma

Diffuse Axonal Injury

  • lacerations or punctate contusions at the interface between grey and white matter
  • caused by a rotational vector of injury
  • common cause of persistent vegetative state or prolonged coma
  • Marshall Classification of DAI on CT:
    • I – no CT abnormalities (normal)
    • II – cisterns present, mid line shift < 5mm, no high risk/mixed density lesion > 25mm3 (abnormal)
    • III – cisterns compressed, mid line shift < 5mm, no high risk/mixed density lesion > 25mm3 (swelling)
    • IV – cisterns compressed, > 5mm of mid line shift, high risk/mixed density lesion > 25mm3 (shift)

RISK FACTORS FOR POST-TRAUMATIC SEIZURES

  • GCS<10
  • Cortical contusion
  • Depressed skull fracture
  • Subdural, epidural or intracerebral haematoma
  • Penetrating head wound
  • Seizure within 24 hours of injury

PHYSIOLOGICAL MONITORING

TBI MANAGEMENT

PROGNOSIS

References and Links


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and 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 two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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