Head trauma

Definitions

• Mild TBI – GCS 14-15 “concussion”
• Moderate TBI – GCS 9-13
  • 10% of injuries
  • Mortality <20% for isolated moderate TBI but disability higher
  • 40% have abnormal CT scan
  • 8% will require neurosurgical intervention
• Severe TBI – GCS 3-8
  • Mortality approaches 40% (most in first 48 hours)
  • <10% experience good recovery

Categorisation – RANZCR

Introduction

• Male prevalence x 2
• Trimodal
  • 0-4yo
  • 15-24yo
  • >75
• Mortality increases with age at time of injury
• MVA is primary cause in children/young adults
• Falls most common cause in elderly

Pathophysiology

• Cerebral autoregulation
  • Normally maintains stable cerebral blood flow between MAP 50-150
  • Impaired in brain injury
  • CPP <60mmHg is considered the limit of autoregulation in normal humans
  • In absence of ICP monitor, maintain MAP >80
• ICP determined by:
  • Brain volume (<1300mL), CSF (100-150mL) and intravascular blood (100-150mL)
• Normal ICP
  • Adult <10-15
  • Young children 3-7
  • Infants 1.5-6.0

• Secondary neurotoxic cascade
  • Glutamate release with activation of NMDA receptors.etc.
  • Mitochondrial damage, cell death and necrosis
  • Proinflmmatory cytokines to try and clean up damage
• Secondary insults
  • Hypotension, hyperglycaemia, hypoxaemia

• Brain oedema
  • 2 distinct processes
    • Cytotoxic oedema – Large ionic shifts and loss of cellular membrane integrity due to mitochondrial failure and increased free radial production
    • Extracellular oedema – Direct damage to BBB, ionic shifts and alteration of aquaporins
  • Leads to direct compressive damage, vascular compression-induced ischaemia, brain herniation and brain death

• Cerebral blood flow and autoregulation
  • Hypoperfusion phase (first 72 hours)
    • Myogenic autoregulation fails
    • CPP directly dependent on systemic BP
  • Hyperaemic phase (persists for 7-10 days)
    • Autoregulation recovers while intracranial inflammation and medical therapies aimed at targeting adequate CPP result in cerebral hyperaemia and raised ICP
    • Consequence is vasogenic oedema
    • Occurs in 25-30% of patients
  • Vasospastic phase
    • Seen in 10-15% of patients, particularly those with severe primary and secondary injury or traumatic SAH

Herniation

Subfalcine herniation

• Medial surface of affected hemisphere pushed under falx cerebri
• Cingulate gyrus most often involved
• Least severe form and usually clinically silent
• May compress anterior cerebral artery 

Uncal/transtentorial herniation

• Uncus of temporal lobe herniates inferiorly through medial edge of tentorium
• Caused by supratentorial mass or severe cerebral oedema
• On imaging:
  • Contralateral temporal horn dilatation
  • Ipsilateral ambient cistern dilatation
  • Ipsilateral prepontine cistern dilatation

Uncal/transtentorial

• Compression of parasympathetic fibres of CN III
  • Leading to fixed ipsilateral dilated pupil due to unopposed sympathetic tone (ocular motor function impaired late)
• Compression of ipsilateral posterior cerebral artery
  • Compressed between herniating temporal lobe and crus cerebri
  • Medial temporal lobe infarction or medial occipital lobe infarction with visual field defect
• Compression of crus cerebri (cerebral peduncle)
  • Ipsilateral or contralateral paresis
• Occlusion of Sylvian aqueduct
  • Hydrocephalus of 3^rd and lateral ventricles
• Duret haemorrhages
  • Midbrain and upper pons due to tearing of upper branches of basilar artery as midbrain descends
  • Very poor prognostic factor

Central transtentorial herniation

• Occurs with midline lesions and bilateral uncal herniation
• Bilateral pinpoint pupils, bilateral Babinski’s signs and increased muscle tone
• Fixed midpoint pupils, hyperventilation and decorticate posturing follow on

Upward transtentorial herniation

• Due to posterior fossa lesions
• Much less common
• Usually no localising clinical signs but may have:
  • Conjugate downward gaze with absence of vertical eye movements
  • Pinpoint pupils
• On imaging:
  • Spinning top midbrain
  • Narrowing of ambient cisterns
  • Prominence, then flattening, of quadrigeminal cistern (toothless smile appearance)
  • Bilateral dilation of temporal horns and third ventricle

Cerebellotonsillar herniation

• Cerebellar tonsils herniate through foramen magnum
• Usually due to posterior fossa mass or midline supratentorial mass
• On imaging:
  • Cerebellar tonsils >5mm below foramen magnum in adults
  • >7mm in children
• Pinpoint pupils, flaccid paralysis and sudden death

The Glasgow Coma Scale

• Motor score alone correlates independently with outcome almost as well as the full score
• Correlates with outcome
• Reliable interobserver
• Effective for measuring recovery or response to treatment over time
• Limitations
  • Measures behavioural responses
  • Does not measure underlying pathophysiology
  • Not useful as a single acute measure of severity as it is a tool to measure disease progression over time
  • May be affected by drugs, alcohol, medications, paralytics, ocular injuries and airway interventions

GCS

• Eyes
  • 4 – Spontaneous
  • 3 – To speech
  • 2 – To pain
  • 1 – No response
• Verbal
  • 5 – Alert and oriented
  • 4 – Disoriented
  • 3 – Speaking but nonsensical
  • 2 – Moans or incomprehensible sounds
  • 1 – No response
• Motor
  • 6 – Follows commands
  • 5 – Localises to pain
  • 4 – Moves or withdraws to pain
  • 3 – Decorticate posturing
  • 2 – Decerebrate posturing
  • 1 – No response

Pupillary response

• Single fixed dilated pupil
  • Suggests intracranial haematoma with uncal herniation
• Bilateral fixed and dilated pupils
  • Increased ICP with poor brain perfusion
  • Bilateral uncal herniation
  • Drug effect (e.g. atropine, sympathomimetic)
  • Severe hypoxia
• Bilateral pinpoint pupils
  • Opioids
  • Central pontine lesions with transtentorial herniation

Posturing

• Decorticate
  • Flexion of upper arms
  • Extension of legs
  • Indicates severe brain injury above the level of the midbrain
• Decerebrate
  • Arm extension and internal rotation
  • Wrist and finger flexion and internal rotation
  • Extension of lower extremities
  • Injury below the midbrain

Imaging

• mTBI and GCS 14-15
  • Intracranial lesion on CT 15% of the time but <1% require neurosurgical intervention
• Cervical spine fractures
  • 8% of comatose TBI patients
  • 4% missed on initial assessment

Imaging classification

• Diffuse injury I (DI-I) – No visible intracranial pathology on CT
• DI II (Diffuse injury)
  • Cisterns present with midline shift 0-5mm and/or
  • Lesion densities present
  • No high or mixed density >25mm
  • May include bony fragments and foreign bodies
• DI III – Swelling
  • Cisterns compressed or absent with midline shift 0-5mm
  • No high or mixed density >25mm
• DI IV – Shift
  • Midline shift > 5mm
  • No high or mixed density >25mm
• Evacuated mass lesion
• Non-evacuated mass lesion
  • HIgh or mixed density lesion >25mm

Head CT decision rules

• New Orleans criteria
  • 100% sensitivity for neurosurgical intervention
  • 5% specific
  • Requires LOC or amnesia to be utilised
• Canadian CT head rule
  • 100% sensitivity for neurosurgical intervention
  • 83% sensitive for intracranial lesion on CT
  • 37% specificity
  • Requires LOC or amnesia to be utilised
• NEXUS
• ACEP guidelines
• NICE guidelines
  • 94% sensitive for neurosurgical intervention
  • 82% sensitive for intracranial lesion on CT
• Neurotraumatology Committee
  • 100% sensitive for both neurosurgical intervention and intracranial lesion on CT

New Orleans criteria

• For patients GCS 15 who have suffered a minor head injury (LOC or amnesia) presenting within 24 hours
  Exclusion criteria: No LOC or amnesia, on anticoagulants or aspirin, <3yo, concurrent injuries that precluded use of CT
• Presence of one of the below indicates CT:
  • Headache
  • Vomiting
  • Age >60
  • Persistent antegrade amnesia
  • Evidence of trauma above the clavicles
  • Seizure
  • Intoxication
• 100% sensitive for intracranial lesion and patients requiring neurosurgical intervention
• 5% specific for intracranial lesion and patients requiring neurosurgical intervention
• Causes unnecessary CT utilisation when compared with CCHR

Canadian CT head rule

• Blunt trauma to the head resulting in witnessed LOC, definite amnesia or witnessed disorientation of any duration within the last 24 hours
• GCS 13-15 at presentation with one or more of below require CT*:
  • High-risk for neurosurgical intervention
    • GCS <15 at 2hr
    • Suspected open or depressed skull fracture
    • Age 65 or older
    • >1 episode of vomiting
    • Any sign of basal skull fracture
  • Medium risk factors (for brain injury on CT)
    • Retrograde amnesia >30 minutes
    • Dangerous mechanism (Fall >3 foot or struck pedestrian)
• 83% sensitive and 38% specific for intracranial lesion on CT
• 100% sensitive and 37% specific for neurosurgical intervention
• *If medium risk factors only, can consider period of observation vs. CT

Exclusion criteria for Canadian CT head rule

• Age <16
• ED GCS <13
• Minimal head injury (no LOC, amnesia or disorientation at any stage)
• No clear history of trauma
• Head injury >24 hours ago
• Obvious penetrating skull injury or depressed fracture
• Focal neurological deficit
• Unstable vital signs in major trauma
• Seizure prior to assessment in ED
• Bleeding disorder or use of anticoagulants
• Returned for re-assessment
• Pregnant

NEXUS CT head

• Blunt trauma with minor head injury (GCS 15)
• Excluded penetrating trauma and those undergoing CT anyway
• If any of the following, CT is required:
  • Evidence of significant skull fracture
  • Scalp haematoma
  • Neurological deficit
  • Altered LOC
  • Abnormal behaviour
  • Coagulopathy
  • Persistent vomiting
  • Age 65 or more
• Sensitivity 98.3% for clinically important injuries
• Specificity 13.7%
• Results in increased CT utilisation vs. CCHR

ACEP

• GCS <15 at time of evaluation all get CT
• mTBI with or without LOC with one or more of:
  • GCS <15
  • Focal neurological findings
  • Vomiting 2 or more times
  • Moderate to severe headache
  • Age >65
  • Signs of basal skull fracture
  • Coagulopathy
  • Dangerous mechanism (fall >4 foot)
• mTBI with LOC or amnesia with one or more of:
  • Drug or alcohol intoxication
  • Physical evidence above the clavicles
  • Persistent amnesia
  • Post-traumatic seizures

NICE guideline

• If any of the following, CT within 1 hour:
  • GCS <13 on presentation
  • GCS <15 at 2 hours
  • Suspected open or depressed skull fracture
  • Any sign of basal skull fracture
  • Post-traumatic seizure
  • Focal neurological deficit
  • >1 episode of vomiting
• If any of the following, CT within 8 hours:
  • Warfarin therapy
  • Age >65
  • Bleeding disorder
  • Dangerous mechanism: Pedestrian or cyclist struck, ejected, fall >1m/5 stairs
  • More than 30 minutes retrograde amnesia

Odds ratio for positive CT finding

• GCS score 14 – 2 to 19
• Neurological deficits – 2 to 19
• Signs of basal skull fracture – 10 to 14
• LOC – 2 to 7 (can see equal isolated vomiting, amnesia, post-traumatic seizure)
  • 2% of patients without LOC will have CT finding but <1% will require neurosurgical intervention
• Post-traumatic amnesia – 1.7 to 8
• Headache – 1.4 to 3
• Vomiting – 3 to 5
• Post-traumatic seizure – 2 to 3
• Intoxication – 1
• Anticoagulants – 2 to 8
• Age >65 – 2
• Dangerous mechanism – 2 to 3

Treatment

• Primary goals
  • Maintain cerebral perfusion and oxygenation
    • Optimise intravascular volume
    • Optimise ventilation
  • Prevent secondary injury
    • Correct hypoxia, hypercapnoea, hyperglycaemia, hyperthermia, anaemia or hypoperfusion
    • Recognise and treat raised ICP
    • Arrange neurosurgical intervention if indicated
    • Treat other life-threatening injuries
• SBP <90 and PaO2 <60 at any stage are associated with a 150% increase in mortality risk
• Sedation and analgesia may reduce ICP and prevent transient rises with coughing/gagging/instrumentation
• Prevent and control seizure activity

• Signs and symptoms of raised ICP
  • Change in mental status
  • Worsening headache
  • Nausea/vomiting
  • Lethargy
  • Hypertension
  • Coma
  • Bradycardia
  • Agonal respirations
  • Change in pupillary response
  • Focal neurological deficits
  • Decorticate/decerebrate posturing
  • CT signs
    • Attenuation of visibility of sulci and gyri
    • Compressed lateral ventricles
    • Poor grey/white differentiation
  • Papilloedema takes time to develop

Goal-directed therapy checklist

• C-spine precautions
• Maintain airway, intubate GCS <8
• SpO2 >90, PaO2>60, PaCO2 35-45
• SBP >110, MAP >80, N/S, blood products and vasopressors as required
• GCS before paralytics and motor/sensation for all limbs
• State head + C-spine CT
• Repeat exam for raised ICP (GCS drop of 2 points warrants Ix)
• Maintain normoglycaemia 6-10
• Control temp 36-38.3
• Give anticonvulsant if GCS <11, acute seizure with injury or abnormal head CT scan (in liaison with neurosurgeons – Leviteracetam 1000mg IV/PO then 500mg BD for 7 days

Goal-directed therapy checklist

• Reduce ICP with conservative means
• Mannitol 1g/kg IV bolus if evidence of/concern for raised ICP (hypertonic saline 250mL 3% saline over 30 minutes if refractory)
• ICP monitoring and CSF diversion if GCS <9
  • CPP >60
  • ICP <20
• Sodium 135-140
• INR <1.4
• Platelets >75
• Hb >80
• DVT prophylaxis within 2-3 days of injury (d/w Neurosurg)
• Nutrition

• Airway and breathing
  • Treat any condition that compromises ventilation
  • GCS <8 require intubation
  • Early intubation to facilitate rapid and safe transfer to CT is warranted
  • Prolonged hypocapnoea (>6 hours) causes cerebral vasoconstriction and worsens cerebral ischaemia
  • Target SpO2 90%, PaO2 >60 and PaCO2 35-45
  • PEEP >15 may impair cerebral venous return
  • Weaning from ventilation should occur once cerebral oedema resolved, control of ICP achieved and adequate CPP

• Neurogenic Pulmonary oedema
  • Dramatic clinical syndrome that occurs in most patients with severe TBI
  • Centrally-mediated sympathetic overactivity leads to sudden onset pulmonary oedema, hypoxia, low filling pressures, poor lung compliance, bilateral lung infiltrates
  • Usually 2-8 hours following injury
  • Treatment is supportive
  • Diuretics are effective but must be titrated carefully to avoid underperfusing brain

• Circulation
  • SBP >100 for 50-69yo and >110 for 15-49yo and >70yo
  • Permissive hypotension worsens outcomes
  • Isolated head injury rarely causes hypotension unless preterminal (through combination of sympathetic surge and myocardial dysfunction)
  • Treat pain to prevent severe hypertension
• Temperature
  • Elevated temperature drives metabolic demand and glutamate release
  • Evidence for hypothermia not substantial and therefore not recommended
  • Targeting 33-35 for at least 72 hours and up to 7 days in severe head injury vs. 37 showed no improvement in neurological outcome at 6 months

• Seizure treatment and prophylaxis
  • Treat acute seizures as per seizure guideline (aggressively)
  • Prophylactic phenytoin 18mg/kg IV at 25mg/min or keppra 1000mg load IV then 500mg BD
    • If GCS <11, abnormal head CT or acute seizure after the injury (BTF)
    • No great evidence for benefit (LITFL)
  • This reduces the occurrence of post-traumatic seizures within the first week
  • Steroids have no role

• Risk factors for post-traumatic seizures (LITFL)
  • GCS <10
  • Cortical contusion
  • Depressed skull fracture
  • Subdural, epidural or intracerebral haematoma
  • Penetrating wound
  • Seizure within 24 hours of injury

• Sedation
  • Opioids affect pupil responses and are relatively contraindicated as a result
  • Sole propofol is preferred as immediately reversible with cessation, may have neuroprotective effect, anticonvulsant effect, does not affect pupils directly and does not accumulate
  • Prolonged use results in tachyphylaxis and significant caloric loading from lipid vector
  • If large doses are provided, propofol infusion syndrome is a potential outcome

Raised ICP

• If deteriorating GCS, obtain repeat CT to examine for progressively expanding haematoma
• First-tier
  • Head up 30 degrees (drops MAP), sedation, analgesia, NM blockade, vent CSF if drain in and target PaCO2 35

• Second-tier
  • Mannitol
    • Lowers ICP, improves cerebral blood flow, CPP and brain metabolism
    • Free radical scavenger
    • Has effect generally within 30 minutes
    • Expands plasma volume and can improve oxygen-carrying capacity
    • 0.25-1g/kg repeat boluses q3h (not constant infusion)
    • No dose-dependent effect seen so many clinicians start with 0.25g/kg
    • Results in net intravascular volume loss over time due to diuretic effect
      • Relatively contraindicated in haemorrhage and hypotension
      • Monitor input/output carefully
  • Hypertonic saline
    • Useful alternative if not adequately fluid resuscitated or hypotensive
    • BTF recommends mannitol as first-line
    • 250mL 3% saline over 30 minutes
    • Monitor serum sodium and osmolality
  • CAN BE GIVEN SERIALLY AND TOGETHER

• Final tier
  • Barbiturate coma
    • Reduce cerebral metabolism and ICP but no mortality benefit in trials
    • Titration to burst suppression is suggested but often difficult to achieve due to haemodynamic effects
  • Therapeutic hypothermia (lowers ICP but does not improve outcomes – POLAR study)
  • Aggressive hyperventilation in rescue situation
  • Decompressive craniectomy
  • Lumbar CSF drainage

• Cerebral perfusion pressure management
  • Indications
    • Abnormal CT and GCS <9
    • Normal CT and two or more of:
      • Age >40
      • Unilateral or bilateral motor posturing
      • SBP <90
  • Maintain CPP 55-60 to adequately perfuse brain tissue
  • Increasing CPP >70 may result in injury to other organs e.g. ARDS
  • If undergoing emergency surgery e.g. orthopaedic repair, management of CPP is crucial during large shifts of central volume due to surgical bleeding

• Raised ICP management
  • ICP >20 increases morbidity and mortality
  • Can utilise positioning (although head up will reduce MAP), mannitol, hypertonic saline, direct CSF diversion and ofcourse surgical evacuation
  • Acute sustained rise in ICP or neurological deterioration always warrants repeat CT as 10% of patients suffer a delayed haemorrhage

• SIADH, cerebral salt wasting and neurogenic DI are all possibilities
  • Close monitoring of serum sodium and osmolality is crucial

• Close monitoring of neurological status
  • Either full assessment, or simply GCS/pupils/lateralising signs is crucial and any deterioration in any of these must be considered life-threatening intracranial hypertension or tentorial herniation until proven otherwise
• ICP monitoring (see BTF powerpoint)
  • Codman monitors (either intraparenchymal or intraventricular) can be inserted at bedside but suffer from baseline drift significant after 5 days, inability to re-zero and inability to drain CSF
• When calculating CPP:
  • Both MAP and ICP should be referenced to external auditory meatus (corresponds to Circle of Willis)
• Continue ICP monitoring until patient stabilised, ICP <20-25cmH20 persistently and cerebral oedema resolved on CT
  • This is usually within 7 days

Specific injuries

• Skull fractures
  • Categorised
    • Basilar vs. skull convexity
    • Linear vs. depressed vs. comminuted
    • Open vs. Closed
  • Fractures that cross the middle meningeal artery, a major venous sinus or linear occipital fractures have high intracerebral complication rates
  • Indications for antibiotics (Vancomycin 1g IV and Ceftriaxone 2g IV)
    • Open or depressed
    • Involve a sinus
    • Pneumocephalus
  • Skull fracture depressed > thickness of skull usually require operative repair

• Basilar skull fracture
  • High risk factor for intracranial injury
  • Most common involves petrous portion of temporal bone, external auditory canal and tympanic membrane
    • Associated with dural tearing with CSF rhinorrhoea/otorrhoea
  • Vertigo, decreased hearing and seventh nerve palsies are signs of basilar skull fracture
  • To confirm CSF leak, send for beta-transferrin identification
  • Require antibiotics in consult with neurosurgery (Ceftriaxone 2g IV and vancomycin 1g IV), elevate head to 30 degrees
  • Lumbar drains may be placed +- repair by neurosurgery or ENT

• Cerebral contusion and ICH
  • Contusions most common in subfrontal cortex > frontal and temporal lobes > occipital lobes
  • ICH can occur days later, often at site of resolving contusion
    • More common if coagulopathic
  • Obtain serial CT’s if any change in mental status occurs

• Subarachnoid haemorrhage
  • Traumatic due to disruption of parenchyma and subarachnoid vessels
  • Most common CT finding in moderate to severe TBI
  • Three-fold higher risk of mortality (42% vs. 14%)
  • CT most sensitive for traumatic SAH at 6-8 hours after injury
  • Early CT before this can miss this serious injury

• Extradural haematoma
  • Blunt trauma to temporoparietal region with associated skull fracture and middle meningeal artery disruption is most common cause
  • Parieto-occipital or posterior fossa trauma causing tears of venous sinuses can also cause this
  • Classic lucid period followed by demise (although this occurs in the minority – 20%)
  • Biconvex haematoma due to high pressure arterial bleeding
  • Herniation can occur within hours
  • Early recognition and evacuation improves morbidity and mortality
  • Underlying parenchymal injury is often absent and full recovery can be expected if evacuated prior to herniation or neurological deficit
  • DOES NOT cross suture lines (remember image of subdural across whole hemisphere)
  • May not have LOC and 50% of patients have only very brief LOC

• Subdural haematoma
  • Sudden acceleration-deceleration with rupture of bridging dural veins
  • Collects more slowly due to venous bleeding but often associated with underlying parenchymal damage
  • Much higher mortality than extradurals (3x; 75% vs. 20-30%)
  • Elderly, chronic alcoholics are more susceptible due to room to move
  • Children <2 are also at increased risk of this
  • Acute symptoms develop within 14 days of injury
  • After 2 weeks, chronic subdural haematoma is used
  • In elderly or alcoholics, often present with altered sensorium and often no history of trauma
  • Acute subdurals – CT shows hyperdense, crescent-shaped lesions that cross suture lines (but not midline)
  • Subacute subdurals – Isodense and more difficult to identify (contrast improves this)
  • Chronic subdurals – Hypodense (dark) due to iron in blood having been metabolised
  • When is surgery indicated?
    • UpToDate consensus guidelines state surgery is indicated if:
      • Clot >10mm or midline shift >5mm regardless of GCS
      • GCS drop of 2 or more
      • Asymmetric or fixed dilated pupils
      • Refractory raised ICP
    • Non-operative treatment recommended for:
      • GCS <9 and not falling, clot <10mm, midline shift <5mm, no pupillary abnormalities and no intracranial hypetension
    • Decision is predicated on previous functional status, age and comorbidities

• Diffuse axonal injuries
  • Disruption of axonal fibres in white matter and brainstem
  • Sharing forces due to sudden deceleration
  • MVA or shaken baby
  • If severe, oedema can develop rapidly
  • Classic CT findings
    • Nothing
    • Punctate haemorrhagic injury along grey-white junction of cerebral cortex and in deep white matter
    • Treatment is limitation of secondary injury

• Penetrating injury
  • Bullets produce cavities 3-4x larger than their diameter
  • GCS can be used to prognosticate outcome for non-intoxicated gunshot wounds to the brain
    • >8 and reactive pupils have 25% mortality
    • <5 have 100% mortality
  • Intubate, vancomycin 1g IV and ceftriaxone 2g IV
  • Stab injuries only damage contacted structures but require the above and obvious surgical consult for removal

Mild TBI

• Pathophysiology
  • Ionic shift with momentary disruption in function and subsequent upregulation of ion channel density
  • After a single injury, the ion channel density returns to normal over time
  • Repeated injuries leads to increased resting number of ion channels leaving the brain vulnerable to overactivation, neuronal toxicity and cell death
  • Large ionic shifts can also cause mitochondrial dysfunction and depletion of intracellular energy stores
    • Get metabolic mismatch with neuronal dysfunction
  • Chronic traumatic encephalopathy is hypothesised to occur due to repeated head injuries in sports
  • Second impact syndrome can occur in the setting of second concussion prior to recovery from first with rapid cerebral oedema and death

• Diagnosis
  • Clinical and symptoms can be delayed
  • Biomarkers
    • S100B serum levels rise and fall rapidly so time from injury is crucial
    • 94-100% sensitive for detecting injury
    • ACEP provides Level C recommendation that if level <0.1microgram/L within 4 hours of injury, CT is not required
  • Cognitive screening
    • Mini-Cog or Quick confusion scale can be performed to grade level of concussion but not validated in ED setting
    • Quick confusion scale (abnormal <12)
      • What year is it? – 2
      • What month is it? – 2
      • State short key phrase and ask patient to immediately repeat it
      • What time is it? – 2
      • Count backwards from 20 to 1 – 2 points
      • Say months in reverse – 2 points
      • Repeat key phrase – 5 points
  • Practical steps
    • Step 1: Plausible mechanism identified
      • Blunt force trauma
      • Acceleration-deceleration
      • Explosion/blast
    • Step 2: Signs and symptoms immediately
      • LOC, post-traumatic amnesia or confusion
      • Subtler symptoms are sometimes included in this i.e. slowed thinking/feeling dazed but these reduce specificity
    • Step 3: Consider potential confounders
      • Alternative Dx: Cervical strain, chronic pain, deconditioning, analgesic medication use, post-traumatic stress, depression, developmental disorders
      • Drinking/drugs
• Prognosis
  • 1/5 patients with mTBI suffer symptoms beyond 1 month
  • Little evidence for objective impairment in cognition or function long-term
  • Most patients are back to baseline within 1-2 weeks (2-4 weeks for children/adolescents)

• Treatment and disposition
  • Initial relative rest (cognitive and physical) for 24-48 hours
  • Avoid aspirin and NSAID’s after acute injury
  • Discharge to care of a responsible adult and provide instructions to both patient and ‘carer’
  • Return for increasing symptoms, headaches, altered mental status, nausea or vomiting
  • Refer to OT service for ongoing concussion management
  • Gradual return-to-activity program
    • Symptoms are the only reliable guide to recovery
    • Guide is to increase activity/stimulation at a pace that does not worsen existing symptoms or generate new symptoms
    • May be more structured for those returning to school, work, sport or military service
    • No return to physical collision sports until completely recovered

Special considerations

• Post-concussive syndrome
  • 20-40% of patients suffer symptoms at 3 months and 15% at 1 year
  • Most common symptoms
    • Headaches, dizziness, reduced concentration, memory impairment, judgement problems, sleep disorders, irritability, fatigue, visual disturbance, depression and anxiety
  • Clinical findings at time of injury do not reliably predict this
  • Can overlap with PTSD
  • Neuropsychological testing and ongoing symptom checking/sympomatic care is indicated

• Recurrent concussions
  • 3 or more concussions poses risk for long-term sequelae, especially in adolescents and young children
  • Almost all cases of second impact syndrome have occurred in young athletes
    • 60-80% mortality
    • Loss of autoregulation, ion imbalance and rapid cerebral oedema
  • Chronic traumatic encephalopathy
    • Early onset of memory loss and depression
    • Tau protein deposition is seen

• Oral anticoagulants
  • ICH if on warfarin with elevated INR have 89% mortality rate
  • Overall preinjury anticoagulation has increased OR 2.4 for mortality
  • All should undergo head CT
  • If on warfarin need immediate reversal
    • Vit K 10mg IV
    • FFP 1U (150-300mL IV)
    • Prothrombinex 50IU/kg
• Antiplatelets (from surgicalcriticalcare.net)
  • Do CT on all* and cease antiplatelet
  • Risk of low dose aspirin has not been determine
  • OR for intracranial lesion after mild head injury on antiplatelets is 2.6
  • Clopidogrel is a potent risk factor
  • If on aspirin – Do not give desmopressin or platelets *
  • If on ADP-inhibitors
    • Do not administer platelets to patients who will NOT undergo neurosurgical procedure regardless of other findings
    • If neurosurgical procedure planned
      • Check baseline platelet function assay (PFA) and administer 1 U of apheresis platelets (6-10 pack) at time of maximal desired benefit
      • If unknown medication history and high-risk patient treat as if on ADP-inhibitor
• Beware delayed haemorrhage and if discharging home, educate re: risk of this and need to be able to get medical assistance rapidly
• If active bleeding and renal dysfunction consider desmopressin 0.3mcg/kg IV in 50mL N/S or cryoprecipitate 1U IV stat

Decompressive craniectomy (BTF)

• Bifrontal DC is not recommended to improve outcomes as measured by GOS-Extended at 6 months post-injury in patients with diffuse injury (without mass lesions) and with ICP >20 for >15 minutes within a 1 hour period that are refractory to first-tier therapies
  • Has been shown to reduce ICP and minimise days in ICU
• Large frontotemporoparietal DC is preferred to a small one for reduced mortality and improved neurological outcomes in patients with severe TBI

Decompressive craniectomy

• RESCUEicp trial (2016)
  • Unilateral for large mass lesions or bifrontal DC for diffuse oedema resulted in:
    • Reduced death (26.9 vs. 48.9%)
    • Increased vegetative state (8.5 vs 2.1%)
    • Of 100 patients treated with DC, 22 more survivors (6 in vegetative state, 8 lower severe disability and 8 upper severe disability or better)
    • Improved functional outcome with surgery at 12 months on ordinal analysis
    • Further study required
    • 37% underwent DC despite being in medical arm due to failed barbiturate coma
• DECRA trial
  • Bifrontal DC only with worse functional outcome and no difference in mortality
  • Reduced ICP and ICU LOS

Neurogenic hypertension

• Common beyond day 5
• Centrally mediated and may be associated with ECG changes or supraventricular arrhythmias
• Usually self-limiting and correlates with severity of injury
• Beta-blockers and/or clonidine recommended
• Vasodilators are relatively contraindicated in head injury

CRASH-I trial

• Adults with head injury
• Methylpred 2g load then 0.4g/hr over 48 hours
• Steroid group mortality at 2 weeks = 21% vs. 18% for placebo
• 6 month f/u favoured placebo for mortality and severe disability
• DO NOT GIVE steroids in this situation

CRASH-2 trial

• TXA within 3 hours in unstable trauma patients with major extracranial bleeding
• Reduced death by 30%
• Excluded patients with isolated TBI

CRASH-3 trial

• Lancet 2019
• Inclusion
  • Adults with TBI within 3 hours
  • GCS 12 or lower or any intracranial bleeding on CT
  • No major extracranial bleeding
• Time limit reduced from 8 to 3 hours halfway through and primary endpoint changed halfway through to head injury death at 28 days for patients treated within 3 hours
• Patients with GCS 3 and those with bilateral unreactive pupils were in prespecified sensitivity analysis due to very poor prognosis and effect of reducing effect size to null if included
• Risk of head injury related death was 18.5% in TXA group vs. 19.8% in placebo group
• If GCS 3 and bilateral unreactive pupils excluded resulted in 12.5% head injury-related death in TXA group vs. 14% in placebo group
• Neither of these outcomes met statistical significance
• Significant reduction on subsequent analysis in mild-moderate head injury group but no reduction in severe head injury
• Found to be more effective in less head injured patients
• No evidence of adverse events or complications
• No increase in disability among survivors in TXA group

SCAT-5

• Standardised tool for evaluating concussion
• Any athlete with suspected concussion must be removed from play and not return that day
• Immediate assessment
  • Red flag check – Neck pain, paraesthesia, severe headache, seizure, LOC, vomiting, agitated
  • Observable signs
  • Memory assessment
  • GCS
  • Cervical spine assessment

• Medical assessment
  • Athlete background
  • Symptom evaluation
  • Cognitive screening – Orientation, immediate memory, concentration
  • Neurological screen – Reading, C-spine movement, double vision, finger-nose, tandem gait
  • Delayed recall
  • Decision

• Concussion advice
  • Rest for a few days with avoidance of behaviours that worsen symptoms
  • Avoid alcohol
  • Avoid prescription/OTC medications
  • Avoid aspirin/NSAID’s
  • Do not drive until cleared by medical professional
  • Gradually increase activity levels after a few days as long as symptoms do not worsen
  • Only start graduated return to sport once symptoms resolved and can perform normal activities of daily life

• Graduated return to sport
  • Light aerobic exercise
  • Sport-specific exercise
  • Non-contact training drills
  • Full contact practice
  • Return to match
• Graduated return to school
  • Normal activities of daily living
  • School activities at home e.g. reading
  • Return to school part-time
  • Return to school full-time

Modified Brain Injury Guideline

Fairly strong, mostly retrospective evidence for reduction in repeat CT usage and reduced length of stay while also maintaining safety.

Useful for determining which patients need NSx consultation, admission and/or repeat CT head after TBI with ICH.

Last Updated on October 29, 2024 by Andrew Crofton