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

Last Updated on November 18, 2021 by Andrew Crofton