traumatic Injuries

Question 1

What are the three most common causes of truamatic head injury

Answer 1

Heamorrhage, penetrating injury, Diffuse

Question 2

What is concussion?

Answer 2

Is a clinical term as pathological term isn’t understood, but is typically associated with loss of reflexes, unconscienceness and temporary respiratory arrest

Question 3

What is the downside of hard skull prtecting brain

Answer 3

Is very hard so rapid change in momentum can cause contussions

Question 4

What is the site of impact called

Answer 4

Coup and on oppisite side is called countercoup

Question 5

What are the secondary effects of traumatic injury

Answer 5

- Acute
	○ Ischemia
	○ Hypoxia
	○ Raised ICP (not quite acute, slightly delayed)
- Delayed/Chronic
	○ Infection
	○ Epilepsy

Question 6

Different types of skull fractures

Answer 6

Linear, depressed, comminuted

Question 7

What are the most common sites of contussion

Answer 7

inferior frontal lobe and inferiorlateral temporal lobe due to the base of the skull having a stepwise nature

Question 8

What is the pathogenesis of a contussion

Answer 8

Will leave a yellow scar, atrophy and brain shrinking, often at tips of gyri and also accumualte heamidesorin

Question 9

Different types of heamorrhage

Answer 9

Epidural, sub-dural, sub arachnoid and intracerebral

Question 10

What region is at risk of tearing in lacerations by foreign objects

Answer 10

The ponto-medullary region can tear and heamorrhage leading to instantaneous death

Question 11

What is diffuse Axonal injury

Answer 11

Damage and atrophy/death of axons due to raised ICP, ischemia, haemorrhage, hypoxia and laceration and small vessel heamorrhage

Question 12

What can be seen macroscopically from DAI

Answer 12

Corpus collasum atrophy, enlarged ventricles

Question 13

What is the pathogenesis of DAI

Answer 13

Swelling of neurons, axon rupture/blockage leading to protein accumulation in the soma and hence cells swell, known as neuronal spheriods

Question 14

Consequences of brain injury

Answer 14

Infection, hydrocephalus, epilepsy and chronic truamatic encephalopathy

Question 15

What is seen with chronic truamatic encephalopathy

Answer 15

Recurrent knocks(trauma and concussion) to the head leading to neuronal loss, tau and a-beta plaque formation, scar tissue which can lead to brain atrophy and predisposition to epilepsy

Question 16

Consequences of raised ICP

Answer 16

Initial compensation from reduced Blood flow and CSF (total of 150ml), once this compensation fails then herniation and pressure must be released to prevent death

Question 17

Causes of raised ICP

Answer 17

• Trauma
• Tumour
• Infarction
• Haemorrhage
• Infection
• Cerebral Oedema
• CSF occlusions

Question 18

Describe central oedema

Answer 18

Is either vasogenic of cytotoxic

Question 19

Vasogenic odema

Answer 19

Is compromised BBB leading to swelling, can be treated with steriods, hypocapneo and isotonic solutions

Question 20

Cytotoxic odema

Answer 20

Caused by cell swelling as a consequence of direct cell damage leading to compromised membrane and ion channel failure, doesn’t respond to steroids and can be caused by stroke/haemorrhage

Question 21

What is Cushing’s Triad

Answer 21

Response to raised ICP, increased Respiration, increased blood pressure and bradycardia

Question 22

Common signs in sub-falcrine herniation

Answer 22

Headache, nausea and vomiting. Usually a sign of predisposition to other hernations

Question 23

Common signs in transtentorial herniation

Answer 23

Contralateral Third nerve palsy (ptosis, mydriasis and occulamotor dysfunction (down and out). Typically PNS will go first in ischemia. There will also be compression of ippsilateral PCA hence honomynous heminopia with macular sparing. Compression of Reticular Activating system and therefore LOC. Also Kurnahan’s Notch and loss of motor function