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Head injury. FM Brett MD FRCPath. Head Injury - Facts Whether accidental, criminal or suicidal leading cause of death < 45 Accounts 1% of all deaths, 30% traumatic deaths and 50% of RTA deaths Severity assessed by GCS. GCS 1. Best eye response - (max 4)

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slide1

Head injury

FM Brett

MD FRCPath

slide2

Head Injury - Facts

  • Whether accidental, criminal or suicidal
  • leading cause of death < 45
  • Accounts 1% of all deaths, 30% traumatic
  • deaths and 50% of RTA deaths
  • Severity assessed by GCS
slide3

GCS

1. Best eye response - (max 4)

2. Best verbal response - (max 5)

3. Best motor response - (max 6)

GCS- 13+ mild H I

9-12- moderate H I

8 or less – severe H I

slide4

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 figures
  • for every 100 HI, 5 VS, 15 severely disabled, 20 minor problems, 60 full recovery
slide5

Nature of lesions in HI

  • Non - missile- RTA
  • Missile
  • Distribution of lesions
  • Focal
  • Diffuse
slide6

Primary damage

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

TIME COURSE

Immediate

Delayed

  • Secondary damage
  • ischemia
  • hypoxia
  • cerebral oedema
  • infection
slide7

Pattern of damage in non -missile HI

Focal

Scalp- contusion, laceration

Skull - fracture

Meninges - haemorrhage, infection

Brain - contusions, laceration, infection

Diffuse damage

Brain, DAI, DVI, HIE, Cerebral oedema

slide9

Haemorrhage

May be

EXTRADURALINTRADURAL - subdural,

subarachnoid

intracerebral

slide10

EDH

  • Found in 2% HI
  • Usually associated
  • with skull fracture
  • Arterial bleed -
  • usually meningeal
  • vessels
slide11

Subdural haemorrhage

  • Usually venous
  • Rupture of bridging
  • veins
slide12

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

slide13

Traumatic SAH

  • may result from severe contusions
  • Fracture of skull can rupture vessels
  • IVH may enter SAS
  • RULE OUT ANEURYSM
slide14

Cerebral contusions

  • Superficial bruises of the brain
  • Frequent but not inevitable after
  • head injury
slide15

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

slide17

Sites 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
slide19

Uncommon types of focal brain damage

  • Ischaemic brain damage due to traumatic
  • dissection and thrombosis of vertebral or carotid
  • arteries by hyperextension of the neck
  • Infarction of pituitary - due to transection
  • of pituitary stalk
  • pontomedullary rent
slide20

Infection

  • complication of skull fracture
  • Open HI
  • Incidence is increased even after closed
  • HI as devitalised tissue prone to infection
slide21

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 that

would account for their clinical state

Implies widespread structural damage

which neuropathologically is likely to be

traumatic or hypoxic/ischaemic in origin

slide22

Diffuse damage

  • DAI - widespread damage to axons in the
  • CNS due to acceleration/deceleration of the
  • head
  • Pts usually unconscious from moment of
  • impact
  • Lesser degrees compatible with recovey of
  • consciousness
slide23

Primary axotomy

a.b.

Ca++

Traumatic tear

c.

Cytoskeletal disruption

d.

Immediate

disconnection

slide24

Pathogenesis of DAI

  • Primary axotomy - almost immediate
  • Large axolemmal tears- influx of CA++
  • - activation of calcium activated proteases
  • - severe cytoskeletal disruption- disconnection
slide25

Secondary axotomy

Ca++

B.

A.

Activation of Ca++ proteases

especially calpain

Membrane sealing

stabilised

D.

C.

Cytoskeletal disruption

Increased sensitivity to

excitotoxic damage

F.

Late disconnection

slide26

Secondary axotomy

  • Ca++ activated proteases focally damage the
  • the axonal BUT immediate disconnection does
  • not occur
  • Failure of cellular repair mechanisms or
  • secondary neuronal damage results in axonal
  • disconnection
  • Axoplasmic transport continues and results in
  • proximal axonal swelling
slide27

Diffuse vascular injury

Multiple petechial haemorrhages in

the white matter of the frontal and

temporal lobes

Probably results from traction and shearing

of parenchymal BV

slide29

Brain 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- cytotoxic
  • cerebral oedema
slide31

Three patterns of brain swelling in

  • HI
  • Swelling adjacent to contusions
  • Diffuse swelling of one cerebral hemisphere
  • e.g evacuation of ASDH
  • Diffuse swelling both hemispheres
slide32

ICH herniation

Subfalcine

herniation

Tentorial herniation

Tonsillar herniation

slide36

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
slide37

MISSILE HEAD INJURY

  • Caused by objects propelled through air
  • Injury may be:
  • Depressed
  • Penetrating
  • Perforating
slide38

Traumatic spinal cord injury

Nature of lesions - Indirect/direct

Distribution - 60-70% cervical,

25% thoracic, 6-15% lumbar.

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

slide39

Traumatic spinal cord injury

Primary damage- results from cord compression

contusion, laceration and haemorrhage

Secondary damage - develops over several days and

mainly involve physiologic responses to trauma, hypoxia,

ischemia

slide40

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