Transcript CNS-trauma-med

Head injury
FM Brett
MD FRCPath
At the end of this lecture you should be able to:
1. Know basic facts about the incidence of head injury
2. Know the difference between focal and diffuse injury
3. Know the difference between missile and non-missile head injury
4. Be able to classify ICH
5. Know the difference between traumatic and spontaneous SAH
6. Be able to list the complications of Raised ICP
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)
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
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
Nature of lesions in HI
• Non - missile- RTA
• Missile
Distribution of lesions
• Focal
• Diffuse
Primary damage
TIME COURSE
• scalp laceration
• skull fracture
• cerebral contusions
• ICH
• DAI
Immediate
Delayed
Secondary damage
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ischemia
hypoxia
cerebral oedema
infection
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
ICH is a complication
of 66% of cases of nonmissile head injury
Haemorrhage
May be
EXTRADURAL
INTRADURAL - subdural,
subarachnoid
intracerebral
EDH
• Found in 2% HI
• Usually associated
with skull fracture
• Peak 10-30 yrs
• Rare < 2 and >60
• Arterial bleed usually meningeal
vessels
Subdural haemorrhage
• Usually venous
• Rupture of bridging
veins
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
SAH
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•
•
•
•
•
Berry aneurysm
Traumatic
Infectious
Fusiform aneurysm
AVM
CAA
CIRCLE OF WILLIS
Berry aneurysms
Congenital
Risk of bleeding inc;
• Hypertension
• AVM
• systemic vascular
disease
• defects collagen
• polcystic renal disease
Traumatic SAH
• may result from severe contusions
• Fracture of skull can rupture vessels
• IVH may enter SAS
• RULE OUT ANEURYSM
Cerebral contusions
• Superficial bruises of the brain
• Frequent but not inevitable after
head 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 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 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
Infection
• complication of skull fracture
• Open HI
• Incidence is increased even after closed
HI 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 that
would account for their clinical state
Implies widespread structural damage
which neuropathologically is likely to be
traumatic or hypoxic/ischaemic in origin
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 recovery of
consciousness
Pathogenesis of DAI
• Primary axotomy - almost immediate
• Large axolemmal tears- influx of CA++
- activation of calcium activated proteases
- severe cytoskeletal disruption- disconnection
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
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
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
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
ICH Herniation
Subfalcine
herniation
Tentorial herniation
Tonsillar herniation
End result of herniation is compression and Duret
haemorrhages as seen in the pons
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 INJURY
• Caused by objects propelled through air
Injury may be:
• Depressed
• Penetrating
• Perforating
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
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
CONCLUSIONS
~ HI – leading cause of death under age of 45
~ Can be missile or non-missile.
~ Distribution of lesions – focal or diffuse.
~ ICH may be extradural or intradural
~ SAH may be traumatic or spontaneous
~ Main complication of HI is raised ICP.