Head injury

FM Brett MD FRCPath

Head Injury - Facts

• Whether accidental, criminal or suicidalleading cause of death < 45• Accounts 1% of all deaths, 30% traumaticdeaths and 50% of RTA deaths• Severity assessed by GCS

GCS

1. Best eye response - (max 4)2. Best verbal response - (max 5)3. Best motor response - (max 6)

GCS- 13+ mild H I9-12- moderate H I8 or less – severe H I

HI

• May result in LOC• Longer unconscious and deeper coma >likelihood that pt has suffered severe HI• 60% good recovery• Based on US, UK and Netherland figuresfor every 100 HI, 5 VS, 15 severely disabled, 20 minor problems, 60 full recovery

Nature of lesions in HI

• Non - missile- RTA• Missile

Distribution of lesions• Focal• Diffuse

TIME COURSE

Immediate

Delayed

Primary damage• scalp laceration• skull fracture• cerebral contusions• ICH• DAI

Secondary damage• ischemia• hypoxia• cerebral oedema• infection

Pattern of damage in non -missile HIPattern of damage in non -missile HI

FocalFocalScalp- contusion, lacerationSkull - fractureMeninges - haemorrhage, infectionBrain - contusions, laceration, infection

Diffuse damageDiffuse damageBrain, DAI, DVI, HIE, Cerebral oedema

ICH is a complication of 66% of cases of non-missile head injury

HaemorrhageHaemorrhage

May be

EXTRADURAL

INTRADURAL - subdural, subarachnoid intracerebral

EDH

• Found in 2% HI

• Usually associated with skull fracture

• Arterial bleed - usually meningeal vessels

Subdural Subdural haemorrhagehaemorrhage

• Usually venous

• Rupture of bridgingveins

Subdural haematoma: classification

48-72 hours – acute composed of clotted blood

3-20 dys – subacute – mixture of clotted and fluid blood

3 weeks + - chronic encapsulated haematoma

Traumatic SAH

• may result from severe contusions• Fracture of skull can rupture vessels• IVH may enter SAS

• RULE OUT ANEURYSMRULE OUT ANEURYSM

Cerebral contusionsCerebral contusions

• Superficial bruises of the brain

• Frequent but not inevitable afterhead injury

Various types of surface contusions and lacerations

~ Coup – at point of impact~ Contrecoup- diametrically opposite point

of impact~ Herniation – at point of impact between

hernia~ Fracture related to # of skull

Sites of cerebral contusionsSites of cerebral contusions

• Frontal poles• Orbital surfaces of the frontal poles• Temporal poles• lateral and inferior surfaces of occipital poles• cortex adjacent to sylvian fissure

Uncommon types of focal brain damageUncommon types of focal brain damage

• Ischaemic brain damage due to traumaticdissection and thrombosis of vertebral or carotidarteries by hyperextension of the neck• Infarction of pituitary - due to transection of pituitary stalk• pontomedullary rent

InfectionInfection

• complication of skull fracture• Open HI• Incidence is increased even after closedHI as devitalised tissue prone to infection

Diffuse brain injury – term coined by clinicans to describe head-injured patients who have global disruption of neurological function without a lesion on CT scan thatwould account for their clinical state

Implies widespread structural damage which neuropathologically is likely to be traumatic or hypoxic/ischaemic in origin

Diffuse damageDiffuse damage

• DAI - widespread damage to axons in theCNS due to acceleration/deceleration of the head• Pts usually unconscious from moment of impact• Lesser degrees compatible with recovey of consciousness

Primary axotomy

a. b.

Traumatic tearCa++

c. Cytoskeletal disruption

d. Immediatedisconnection

Pathogenesis of DAI

• Primary axotomy - almost immediate

• Large axolemmal tears- influx of CA++- activation of calcium activated proteases- severe cytoskeletal disruption- disconnection

Ca++

Secondary axotomySecondary axotomy

A. B.

C. D.

F. Late disconnection

Cytoskeletal disruption

Membrane sealingstabilised

Increased sensitivity to excitotoxic damage

Activation of Ca++ proteasesespecially calpain

Secondary axotomy

• Ca++ activated proteases focally damage thethe axonal BUTBUT immediate disconnection does not occur • Failure of cellular repair mechanisms or secondary neuronal damage results in axonaldisconnection• Axoplasmic transport continues and results in proximal axonal swelling

Diffuse vascular injuryDiffuse vascular injury

Multiple petechial haemorrhages inthe white matter of the frontal and temporal lobes

Probably results from traction and shearingof parenchymal BV

Brain swelling and raised ICPBrain swelling and raised ICP

Results from:• cerebral vasodilation - inc cerebral blood vol• damage to BV - escape of fluid through BBB• inc water content of neurones and glia- cytotoxiccerebral oedema

Three patterns of brain swelling in Three patterns of brain swelling in HIHI

• Swelling adjacent to contusions

• Diffuse swelling of one cerebral hemispheree.g evacuation of ASDH

• Diffuse swelling both hemispheres

ICH herniation

SubfalcineSubfalcineherniationherniation

Tentorial herniationTentorial herniation

Tonsillar herniationTonsillar herniation

End result of herniation is compression and Duret haemorrhages as seen in the pons

Ischemic damage - likely if:Ischemic damage - likely if:

• clinically evident hypoxia• hypotension with systolic < 80mmHg for at least 15 mins • episodes of inc BP i.e > 30 mm Hg

MISSILE HEAD INJURYMISSILE HEAD INJURY

• Caused by objects propelled through air

Injury may be: • Depressed• Penetrating• Perforating

Traumatic spinal cord injuryTraumatic spinal cord injury

Nature of lesions - Indirect/direct

Distribution - 60-70% cervical, 25% thoracic, 6-15% lumbar.

Fractures C1/2, C4-7, T11-L2

Traumatic spinal cord injuryTraumatic spinal cord injury

Primary damagePrimary damage- - results from cord compressioncontusion, laceration and haemorrhage

Secondary damageSecondary damage - develops over several days and mainly involve physiologic responses to trauma, hypoxia,ischemia

Principal causes of spinal cord compression

~ Lesions in vertebral column- prolapsed disc, kyphoscoliosis, #, Metastatic tumour

~ Spinal extradural lesions – metastatic carcinoma, lymphoma, myeloma,abscess

~ Intradural extramedullary lesions – Meningioma, Schwannoma

~ Intramedullary lesions - Astrocytoma, ependymoma, cyst formation