1 / 40

Head injury

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)

gali
Download Presentation

Head injury

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Head injury FM Brett MD FRCPath

  2. 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

  3. 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

  4. 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

  5. Nature of lesions in HI • Non - missile- RTA • Missile • Distribution of lesions • Focal • Diffuse

  6. Primary damage • scalp laceration • skull fracture • cerebral contusions • ICH • DAI TIME COURSE Immediate Delayed • Secondary damage • ischemia • hypoxia • cerebral oedema • infection

  7. 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

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

  9. Haemorrhage May be EXTRADURALINTRADURAL - subdural, subarachnoid intracerebral

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

  11. Subdural haemorrhage • Usually venous • Rupture of bridging • veins

  12. 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

  13. Traumatic SAH • may result from severe contusions • Fracture of skull can rupture vessels • IVH may enter SAS • RULE OUT ANEURYSM

  14. Cerebral contusions • Superficial bruises of the brain • Frequent but not inevitable after • head injury

  15. 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

  16. 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

  17. 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

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

  19. 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

  20. 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

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

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

  23. 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

  24. 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

  25. 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

  26. 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

  27. 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

  28. ICH herniation Subfalcine herniation Tentorial herniation Tonsillar herniation

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

  30. 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

  31. MISSILE HEAD INJURY • Caused by objects propelled through air • Injury may be: • Depressed • Penetrating • Perforating

  32. 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

  33. 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

  34. 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

More Related