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
- Focuses on the prevention of secondary injury
- See Traumatic Brain Injury (TBI) Management
PROGNOSIS
References and Links
CCC Neurocritical Care Series
Emergencies: Brain Herniation, Eclampsia, Elevated ICP, Status Epilepticus, Status Epilepticus in Paeds
DDx: Acute Non-Traumatic Weakness, Bulbar Dysfunction, Coma, Coma-like Syndromes, Delayed Awakening, Hearing Loss in ICU, ICU acquired Weakness, Post-Op Confusion, Pseudocoma, Pupillary Abnormalities
Neurology: Anti-NMDA Encephalitis, Basilar Artery Occlusion, Central Diabetes Insipidus, Cerebral Oedema, Cerebral Venous Sinus Thrombosis, Cervical (Carotid / Vertebral) Artery Dissections, Delirium, GBS vs CIP, GBS vs MG vs MND, Guillain-Barre Syndrome, Horner’s Syndrome, Hypoxic Brain Injury, Intracerebral Haemorrhage (ICH), Myasthenia Gravis, Non-convulsive Status Epilepticus, Post-Hypoxic Myoclonus, PRES, Stroke Thrombolysis, Transverse Myelitis, Watershed Infarcts, Wernicke’s Encephalopathy
Neurosurgery: Cerebral Salt Wasting, Decompressive Craniectomy, Decompressive Craniectomy for Malignant MCA Syndrome, Intracerebral Haemorrhage (ICH)
— SCI: Anatomy and Syndromes, Acute Traumatic Spinal Cord Injury, C-Spine Assessment, C-Spine Fractures, Spinal Cord Infarction, Syndomes,
— SAH: Acute management, Coiling vs Clipping, Complications, Grading Systems, Literature Summaries, ICU Management, Monitoring, Overview, Prognostication, Vasospasm
— TBI: Assessment, Base of skull fracture, Brain Impact Apnoea, Cerebral Perfusion Pressure (CPP), DI in TBI, Elevated ICP, Limitations of CT, Lund Concept, Management, Moderate Head Injury, Monitoring, Overview, Paediatric TBI, Polyuria incl. CSW, Prognosis, Seizures, Temperature
ID in NeuroCrit. Care: Aseptic Meningitis, Bacterial Meningitis, Botulism, Cryptococcosis, Encephalitis, HSV Encephalitis, Meningococcaemia, Spinal Epidural Abscess
Equipment/Investigations: BIS Monitoring, Codman ICP Monitor, Continuous EEG, CSF Analysis, CT Head, CT Head Interpretation, EEG, Extradural ICP Monitors, External Ventricular Drain (EVD), Evoked Potentials, Jugular Bulb Oxygen Saturation, MRI Head, MRI and the Critically Ill, Train of Four (TOF), Transcranial Doppler
Pharmacology: Desmopressin, Hypertonic Saline, Levetiracetam (Keppra), Mannitol, Midazolam, Sedation in ICU, Thiopentone
MISC: Brainstem Rules of 4, Cognitive Impairment in Critically Ill, Eye Movements in Coma, Examination of the Unconscious Patient, Glasgow Coma Scale (GCS), Hiccoughs, Myopathy vs Neuropathy, Neurology Literature Summaries, NSx Literature Summaries, Occulocephalic and occulovestibular reflexes, Prognosis after Cardiac Arrest, SIADH vs Cerebral Salt Wasting, Sleep in ICU
- Brain Trauma Foundation Guidelines – Guidelines for the Management of Severe TBI
- ICN Podcast — 87. TBI – Introduction (2013)
- Swadron SP, LeRoux P, Smith WS, Weingart SD. Emergency neurological life support: traumatic brain injury. Neurocrit Care. 2012 Sep;17 Suppl 1:S112-21. PMID: 22975830
Critical Care
Compendium
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
Hi
IS the Marshall score used to classify DAI’s or all TBI’s? My understanding is that it is used to classify all types of TBI’s
Thanks
Hi James
You are right that the Marshall score is a TBI classification – it’s use here was to show how it grades severity of DAI.
A problem of with the Marshal score is that it doesn’t include all types of TBI (e.g. traumatic subarachnoid haemorrhage), so in practice we often use it in the context of predominant DAI.
Some references with a brief discussion is on Radiopaedia: https://radiopaedia.org/articles/marshall-classification-of-traumatic-brain-injury
Cheers
Chris