Cranial Trauma

Cranial Trauma. Dr Alessandro Aldera Anatomical Pathology.

Learning Objectives. Regarding cerebral trauma, describe the mechanisms, macroscopic appearance, evolution and prognosis of: i. contusions ii. coup an contrecoup injuries iii. subdural haemorrhages iv. extradural haemorrhages v. diffuse axonal injury.

Background:. Significant cause of disability and death Severity and site of injury affect outcome Magnitude and distribution – shape of object, force and whether the head is in motion at the time of injury Broadly classified as: Penetrating, or Blunt.

Types of injury:. Skull fracture Parenchymal injury Contusions Coup and contrecoup Diffuse axonal injury Vascular injury Extradural, subdural, subarachnoid, parenchymal Combinations.

Skull Fractures. I.

Skull fractures:. Classified by the configuration or pattern it displays: Linear Depressed Compound Complications: Brain haemorrhages Infections (abscess/meningitis).

Parenchymal Injuries.

Contusions:. Impact of an object with the head leading to: Collision of brain with skull at site of impact (coup) Opposite side (contrecoup) Both coup and contrecoup injuries are contusions Similar gross and microscopic appearances Crests of gyri most susceptible (cortex along sulci less vulnerable) Rapid tissue displacement  disruption of vascular channels  subsequent haemorrhage, tissue injury and oedema.

Contusions:. Frontal lobes along the orbital gyri and temporal lobes most susceptible Penetration of the brain causes laceration with tissue tearing, vascular disruption, haemorrhage and injury in a linear path.

Acute contusion – haemorrhagic necrosis and oedema Gradually macrophages migrate in and mop up debris Contusions evolves into a yellow plaque with atrophy and gliosis.

Subdural haematoma.

Acute subdural haematoma:. Seen in 12% to 29% of severe TBI Mortality rate of 40% to 60% Rupture of bridging (emissary) veins Individuals with brain atrophy (elderly) are particularly susceptible and can sustain ADH with minor trauma.

A car parked on the side of a road Description automatically generated.

Sequalae:. Initially the subdural haematoma is a flat blood clot not attached to the dura Fibroblast ingrowth causes organization After 10-20 days – outer membrane is formed Then inner membrane forms Subdural becomes entirely encapsulated Further organization leads to formation a sac with a fibrous wall (chronic subdural haematoma).

Extradural haematoma.

Epidural haematoma:. Seen in 2.7-4% of TBI Mortality of approximately 10% Cranial fractures present in 70-90% Most commonly with fractures of the temporal or parietal bones Tearing of middle meningeal artery Bleeding lifts the dura off the skull Convex shape on imaging Symptoms of raised ICP develop rapidly.

Diffuse Axonal Injury.

Diffuse Axonal Injury (DAI):. DAI is a special traumatic lesion Frequently seen in MVAs when the head is unsupported Parts of the of the brain move relative to adjacent parts (shear forces) Rarely a pure lesion (can be difficult to separate from other TBI pathology).

Pathophysiology:. Axons are stretched  changes in axonal cytoskeleton Mitochondria accumulate proximally (spheroids) Mitochondrial dysfunction Leads to axonal rupture Neuroinflammation Wallerian degeneration Multifaceted process Evolution over time Most severe damage is along midline structures.

Clinical:. Severe DAI – unconscious immediately May recover or go into persistent vegetative state Reticular activating substance May have additional widespread vascular injury in severe TBI..

Pathology:. Petechial haemorrhages in: Corpus callosum Dorsolateral brainstem Other areas Due to tearing of blood vessels Microscopically axonal swellings ( spheroids ) are seen BAPP immunohistochemistry.

Pediatric Head Trauma Presented by Jennifer L. Ross, M.D. - ppt ....

Axonal sphenoids (swelling of the axon). Occurs 12-24 hrs after diffuse axonal injury. beta amyloid can accumulate in them with Alzheimer's disease.

Sasi Wallpaper - Cape Town Landscape.