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) 2. Best verbal response - (max 5) 3. Best motor response - (max 6) GCS- 13+ mild H I 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

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 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 non- missile head injury

Haemorrhage May be EXTRADURAL INTRADURAL - subdural, subarachnoid intracerebral

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

Subdural haemorrhage Usually venous Rupture of bridging veins

Subdural haematoma: classification 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 ANEURYSM 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 recovey of consciousness

Primary axotomy a. b. Traumatic tear Ca++ c.c. Cytoskeletal disruption d. Immediate disconnection

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

Ca++ Secondary axotomy A. B. C. D. F. Late disconnection Cytoskeletal disruption Membrane sealing stabilised Increased sensitivity to excitotoxic damage Activation of Ca++ proteases especially calpain

Secondary axotomy Ca++ activated proteases focally damage the BUT 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 Subfalcineherniation 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 % cervical, 25% thoracic, 6-15% lumbar. Fractures C1/2, C4-7, T11-L2

Traumatic spinal cord injury Primary damage - Primary damage - results from cord compression contusion, laceration and haemorrhage Secondary damage Secondary 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