0.2% / year in UK.
500,000 brain injuries/yr in US
- 80% mild, 10% moderate, 10% severe.
- >100,000 of these have some disability
Young men - greatest risk.
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Local vs Diffuse
Diffuse injuries most often result from hypoxia/ischaemic insults due to shock/apnoea after trauma.
- CT may be normal or reveal swelling.s
Multiple punctate haemorrhages may occur.
Diffuse axonal injury

Primary Brain Injuries
(occurs due to energy transfer at impact)

1. Acceleration / Deceleration
Primary cause for brain injury.
Injuring agent does not penetrate skull.
Energy is dissipated by internal movement / gyrations.
--> disruption of neurons
--> tearing of brain substance
--> laceration / contusion on striking dural substances / bony ridges.
May cause diffuse axonal injuries

2. Open Head Injury
Agent enters skull and meninges.
--> direct disruption of tissue.
Severity depends on extent / function of affected area.
Direct damage is less important than energy transfer for prognosis.
- eg if a bullet hits your head, the direct disruption is less important than the shock wave from the bullet's passage (which destroys the entire brain in microseconds).

3. Contusion
May occur during acceleration / deceleration
Or skull inbending at collision point
Severity depends on extent / function of affected area.

4. Contre-coup ('opposite-blow')
Complicated - due to physics of gelatinous bodies (like brain).
When brain accelerate, a positive force is generated at one end.
And immediately a corresponding negative 'vacuum' effect occurs at the other end.
--> disrupts brain / vessels at negative / opposite point.

5. Compression
Uncommon, unless stamped on head or trapped under car when jack fails.
Little momentum transferred to brain, but cranial nerves may be injured.

Secondary Brain Injuries
(occurs after energy transfer complete)
- note ICP physiology

1. Brain Swelling
Brains swell within minutes of injury
Not oedema; is dilation of microcirculation.
I.e. intravascular blood volume expansion.
--> Raised intracranial pressure
Single most important cause of life-threatening ICP rise.

2. Brain Oedema
Does occur, but usually focally.
Eg due to contusion / contra-coup injury.

3. Intracranial haematoma
i) Extradural
ii) Subdural (acute and chronic)
iii) Intra-axial
- fairly common: 20-30% severe brain injuries.
- produced by gyrations of brain exposed to severe acceleration
- poor prognosis (worse than subdural)
- may be pin-point (petechial) if less energy
- or large if greater energy
- majority in frontal and temporal lobes, also commonly in thalami, basal ganglia.
- less commonly in brain stem / cerebellum
- over hours or days can coalesce into an intracerebral haematoma requiring urgent evacuation (20%; detected by repeat CT within 12-24 hrs).

4. Herniation
- cerebri sit above the cerebellum, separated by the tentorium cerebelli.
- midbrain occupies the tentorial hiatus.
- below the cerebellum / midbrain is the brainstem.
- oculomotor n. runs along the edge of the tentorium (parasympathetic pupillary constrictors on surface).

With a cerebral one-sided mass effect, ipsilateral brain herniates infratentorially and across falx.
--> focal brain dysfunction across falx
--> Uncus of temporal lobe squashes midbrain in the tentorial hiatus (eg contralateral hemiplegia; motor tracts cross at foramen magnum; rarely may push opposite side of midbrain against tentorial edge causing ipsilateral hemiplegia / Kernohan's notch syndrome)
--> Ipsilateral third nerve compression (pupillary dilation due to unopposed sympathetic activity)
--> post cerebral artery to visual cortex may stretch / stop flowing.

With diffuse brain swelling symmetrical cephalocaudal herniation occurs.
--> Midbrain spared, but brainstem compromised.
--> stretching of small branches of the basilar artery.
--> ischaemia of RAS, respiratory and cardiac centres
--> may be stimulated first, then shut down..
--> 2ndry 'Duret' brainstem haemorrhages (overstretched, severe, bad news)

Before the GCS, pupillary dilation was the best warning sign of herniation.
Using GCS, herniation should be known long before this time.

5. Hypercarbia
Normally brain vessels dilate when PCO2 rises (adaptive)
- this is usually retained in head injury
If PCO2 rises after injury (eg if lungs injured or sedated)
--> general cerebral vasodilation
--> intracranial pressure may approach MAP
--> depresses consciousness further
--> vicious cycle of increasing vasodilation
This is most likely cause for declining consciousness when no haematoma is found

6. Hypoxia
Injured brain tolerates less hypoxia.
--> Paramount to keep PO2 high.

7. Hypotension
Injured brain tolerates less hypotension
-->preserve normotension

8.  Infection
At risk when:
- Compound skull #
- Penetrating missile
- CSF leakage present eg:
    - tegmentum tympani # (petrous bone); CSF leaks to middle ear and down Eustachian tube).
    - ant cranial fossa #; CSF leaks down nose.

9. Hydrocephalus
Blood may leak into CSF if large acceleration
--> damming of CSF
--> hydrocephalus
Usually occurs after 7-10days.

10.  Venous obstruction
Impaired return of blood from brain via internal jugulars.
Ie avoid blocking these veins while nursing.

11. Delayed Traumatic Intracerebral Haematoma
Poorly understood.
Contused brain - loss of autoregulation, venous congestion & hypoxia
--> delayed development or enlargement of haematoma.
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Know GCS
- mild: GCS 14-15
- moderate: 9-13
- severe: 3-8


A period of concussion.
Time to regain consciousness / return GCS to 15 is proportional to acceleration imparted to brain:
- minor if few minutes
- moderate if some hrs
- major may take hundreds of hours
- severe may never return to GCS 15
Patients may then deteriorate again in GCS
- this reflects secondary brain injury events
- must be acted upon with urgency.
- the detection of such patients is the role of neuro obs.

Skull #s

Some pts may be left with post-head-injury syndromes.
- Eg in diffuse axonal injury.

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CT essential.
If pt protected by hyperventilation and diuretics, then saves more time and brain / life than is lost.
--> i.e. operation may be focused.
Also do C-spine; preferable to XRs


Urgent CT indicated if:
- GCS has deteriorated
- conditions below
Rapid CT if:
- GCS is remaining impaired
Same-day CT if:
GCS<12 at examination.

Findings of significance:
- scalp swelling / subgaleal haematoma
- skull #s
- intracranial haematoma & contusions
- mass effect
--> shifts of >5mm often indicate need for surgical evacuation.

See notes on how to evaluate a CT head.

Skull XR
Look for:
1) linear / depressed #s
2) midline position of pineal (if calcified & visible)
3) air-fluid levels in sinuses
4) pneumocephalus
5) facial fractures
6) foreign bodies
Don't obtain this at expense of transferring pt early.
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!Prevent secondary brain injury!

Be concerned with:
1. parenchymal swelling
2. intracranial pressure
3. cerebral perfusion pressure
4. oxygenation of neural elements

Two Tiers of Therapy

First Tier
Sedation and paralytics
External ventricular drains
Parenchymal monitoring
Controlled hyperventilation
Mannitol / hypertonics

Second Tier
Controlled hypothermia
Surgical decompression
Pentobarbital-induced coma

First Aid
Mild Brain Injury
Moderate Injury
Severe Injury
Raised ICP
Care Planning
Penetrating Injury
Care of the Unconscious
Post-trauma Epilepsy
Scalp wounds
Brain death


Are available and should be followed

First Aid
Secure the ABCs.
- maintain BP >90
- maintain Sats >90
- maintain pO2 >60 mmHg
--> outside of these parameters correlates with poorer outcomes.
- resuscitation fluid is N saline / Hartman's; not hypotonic (cause brain oedema)
Beware concurrent c-spine
Bandage wounds.
Record GCS, pupil sizes.


General Assessment
- Vital signs
- Body temp
-Pupil sizes / reactivity
- Whole body for injury.
- Deteriorating?
--> early intervention essential.
--> intubate, hyperventilate, IV diuretic, catheterize, prepare CT / transfer / theatre.
- Stable?
--> continue neuro obs until danger period passed.
Neuro Exam
- Unconscious? Record:
--> mental state & GCS
--> CNs, motor, sensory, coordn.

Mild Brain Injuries
(GCS 14-15)
80% of ED pts; awake, may be amnesic.
Perhaps a brief LOC.
Most recover uneventfully with observation
3% deteriorate unexpectedly and decline must be detected early to prevent sequelae.
CT all with LOC>5mins, amnesia, severe headache, GCS<15 or focal deficit.
If asymptomatic, fully awake and alert, neurologically N, observe for 4hrs and reexamine then discharge to care of observing companion with advice sheet
- return if headache, drowsiness / cognitive decline or focal deficits develop.

Moderate Injuries
(GCS 9-13)
10% of ED pts; usually confused / somnolent, may have focal deficits.
10-20% will deteriorate / lapse into coma.
Obtain a CT and consult relevant surgeon, admit in close observation unit for 12-24hrs.
- get baseline bloods
Follow-up CT at 12-24 hrs if initial CT abnormal or deterioration evident.
If deteriorates and cannot follow simple commands treat as per severe injury.

Severe Injuries
(GCS 3-8)
Greatest risk of morbidity and mortality
- 'wait and see' approach = disastrous -> be prompt.
Cardiopulmonary resuscitation is immediately required
- hypoxia and hypotension -> 75% mortality.
- hypotension --> 60 vs 25% mortality.
Airway & Breathing
Early intubation and 100% O2 ventilation (sats >98%)
- hyperventilate with caution if acute neurological deterioration (below)
Hypotension is only secondary to brain injury when near terminal medullary failure is occurring.
- establish euvolaemia ASAP
- DPL/FAST is preferred if unconscious
- CT head is obtained after laparotomy / definitive BP control.
Restoring euvolaemia can allow sudden improvement in GCS.
Do not use hypotonic fluid
D as per primary survey
- perform GCS / pupil exam prior to sedating the pt; don't use long-acting agents.
Doll's eye movements, calorics and corneal responses are deferred to a neurosurgeon.
Perform serial GCS, pupils, lateralization in the secondary survey
Emergency CT head & repeat it if deteriorates & routinely at 12-24 hrs if contusion/haematoma on initial scan.
Best to get a CT head before operating for evacuation (saves time).

Raised ICP

ICP Monitoring if
1. severe TBI and CT abnormal
2. severe TBI, normal CT, and 2+ risk factors (posturing on exam, age>40, haemodynamic instability)
Placed by Neurosx
Concurrent ventricular access in same device allows drainage of CSF to alleviate ICP.

Suspect if deteriorating
- most will not have a haemorrhage.
- but if so...

Get haemorrhages drained.
- extensive craniotomy often reqd for subdurals
- craniotomy essential for extradurals to stop all bleeding.
--> know that intracranial bleeding is clotty and tenacious, and a burrhole will not be sufficient.
--> burrholes may be diagnostic when there is no CT.


i) normalise PO2, PCO2
- PO2 >70, PCO2 30-40.
- hyperventilation to <30mmHG reduces ICP but can worsen ischaemia and loses effect after a few hours, so reserve until urgent and be brief as possible.

ii) nurse head up

- helps venous drainage

iii) maintain osmolarity

- 290-310osm
- ie caution with crystalloids.
- if critical, use frusemide and mannitol to keep in upper part of range.
- mannitol: 20% solution; a sugary alcohol.
--> works best as boluses, e.g. 0.25-1 g/kg, indicated if acute neuro deterioration during observation and not hypotensive en-route to CT
--> works by rheology (flow); decrease in haematocrit and blood viscosity through plasma expansion, increases cerebral blood low and oxygen delivery, while osmotic effect withdraws sodium and water from cerebrum.
- effect lasts 6h

iv) preserve normotension

- certainly systolic 100-200.
- difficult as to stricter control - brain may require some increase in pressure.

v)  ICP Monitoring
- Calculate CPP : CPP = MAP = ICP.
- CPP >60 reqd to maintain homeostasis of neural elements.

v) paralyse and intubate

- If ICP high (>20mmHg), and not sedated, add sedation.
--> Then commence draining CSF

vi) Controlled hyperventilation
Control cerebral perfusion by altering CO2 in bloodstream on ABG (cerebral autoregulation)
- high CO2 causes vasodilation; brain sees need for more oxygen
but if CO2 driven too low; then excessive vasoconstriction can be harmful or cause stroke.
Critical balance lies between PCO2 of 30-35mmHg

Second-tier therapies
Used sparingly: multitude of complications
- coagulopathy, dysregulatoin, increased infections.
MDT and team decision on whether worthwhile

Barbiturate coma
Reduces neural element metabolism.

Controlled hypothermia

Reduces neural element metabolism to a minimum.
Target temp 33-35o
Must be paralyzed to prevent shivering.

Decompressive Craniectomy
Removal of skull bone flap 12-15cm; typically bifrontal.
Duroplasty (enlarge dural space) using pericranium or bioengineered product

What about steroids
- no benefit; not indicated

Care Planning

Allow Home If:

- don't warrant admission (below)
- mild injury
- fully conscious
- oriented
- no skull #
- <10 mins LOC
- relative / friend to observe
- return if headache, repeated vomiting, confusion, drowsiness
- get reviewed in day or 2 ideally.

Admit If (in general):
- skull # / penetrating injury
- moderate/severe injury
- significant associated injury
- not oriented 2hrs after impact
- any abnormal neurology
- abnormal GCS
- significant intoxication
- any abnormality on CT

Urgent CT If:
- skull #
- not oriented at 2 hrs
- LOC >10mins
- GCS not improving
- GCS deteriorating(!)

Transfer to neurosurg If:
- GCS <10 at 4 hours.
- GCS not improved over 4 hrs
- GCS deteriorating

Tell the neurosurgeon:
- age, mechanism and time
- resp and cardiovascular status
- results of neuro exam, incl GCS (esp motor), pupils.
- associated injuries
- diagnostic study results
- hypotension/hypoxia treatment

Principles of surgical management
Targets a localized insult.
Epidural, subdural, parenchymal haematomas, and SAH.

Urgent operation If:
- intracranial haematoma and ICP up.
- depressed skull #
- contaminated compound wound

Surgery: Extradural
Classic lucid interval exists in 50%
Arise from arteries, veins, sinus, dura bridging veins and bone.
Indicated drainage if:
1. volume >30 cm3; regardless of clinical presentation (usually will be deficits)
-->the sooner the better.
2. Volume <30cm3 and midline shift >5mm or shear thickness a5mm+
3. Neurosx may decide to do it anyway if GCS<8 and no other clear contributing factors.

Surgery: Subdurals
More common than extradural
Arise from venous bleeding.
Indicated drainage if:
1. Thickness >1cm
2. Midline shift > 5mm
3. Otherwise a declining GCS 2 pts
Craniotomy, as soon as possible.

Surgery: Parenchymal lesions
Most common.
Intimately associated with neuronal destruction.
Indicated drainage if:
1. GCS 6-8 and contusions in frontal / temporal >20cm3 with midline shift >5mm or obliterated cisterns.
2. Contusion >50cm3
Contraindicated if devastating brain injury that will not benefit.
Middle and posterior fossa lesions
- smaller regions but proximity with the brain stem
- less tolerant indications; even smaller lesions e.g. cerebellum >20cm3

General surgeon craniotomy?
Exceptionally the need for life-saving haematoma evacuation is imminent
- in a rural setting a trained surgeon may undertake craniotomy under neurosurgeon advice.
- this desperation measure is extreme and only justified in this very specific setting.

Later operation If:
- Perstistent CSF leak beyond 24hrs
- Hydrocephalus
- Chronic subdurdal / hygroma and impairment.
  (hygroma is a post-traumatic CSF sequestration)

Penetrating Brain Injury
E = 1/2mv^2
- E = kinetic energy; m=mass; v=velocity

1. Full careful exam
2. CT head / radiology
3. CT angiogram for traumatic aneurysm / vascular injury if SAH, intraparenchymal haematoma or trajectory concern.
4. ICP monitoring often useful; associated diffuse cerebral oedema.
5. Clean up entrance / exit but don't debride bone or fragments some distance from entrance site
6. Repair air sinus injury, CSF leak when stable.
7. Broad spectrum antibiotics 1-6 weeks.
8. Consider early anti-epileptics.

Care of the Unconscious

As for forgoing measures
Also attend to nutrition, hydration, skin.
Pulmonary cares
- physio / intubation / tracheostomy cares

If unconscious for >6hrs of post-traumatic amnesia for 48hrs
--> get formal neuropsychological assessment.
Many of these pts will require rehab

Post-trauma epilepsy
May be generalised or partial.

5% in non-missile injuries
Higher if one of:
- missile injuries (30-40%)
- early seizure (24hrs-7days)
- intracranial haematoma
Or higher if 2 of:
- dural penetration
- depressed skull #
- intracranial infection
- focal neurology
- post traumatic epilepsy >24hrs
Natural History
560% develop it in 1st yr, 13% in 2nd, 8% in 3rd, 2-4% per yr thereafter.
Phenytoin reduces seizure rate in first week but not thereafter.
Phytoin employed acutely: 1g IV at <50mg/minute, maintained at 100mg/8hrs with dose titration to serum levels
- add diazepam / lorazepam if ongoing seizures
- control rapidly: prolonged seizures 30-60m cause secondary injury.

Scalp wounds
Blood loss may be extensive, especially in children
- but won't generally cause adult shock.
- apply pressure and ligate large vessels.
Inspect the wound for foreign bodies
- major cause of infection
- inspect for CSF leak, skull #

Brain Death
Certification of this is sometimes reqd - relevant for organ donation.
Leave this to experienced clinicians in no way involved with the organ transplantation.
Be especially careful in children (remarkable recovery ability)
Brain dead if
a) cerebral angio shows no circulation beyond clinoid processes OR
b) all of:
- GCS = 3
- total apnoea for 3mins with arterial PCOS 40mmHg or greater
- body temp >36
- no sedation on board, temp corrected
- no pupillary, corneal or gag reflexes
- no ocular deviation with cold caloric stimulation, no Doll's eyes reflex
- only spinal reflexes evident on painful stimulation of periphery.
Ancillary investigations
EEG (no activity at high gain)
CBF studies
ICP measurement (exceeds MAP for >1hr)
Atropine without change in heart response.

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