Head Injury

Question 0

History of CT Scanning

Answer 0

Allan cormack and Godfrey hounsfield

1979 Nobel prize for medicine.

Question 1

Epidemiology of head injury

Answer 1

1million AnE attendances per yr –> 135,000 people admitted
- 85% minor, 10% moderate and 5% severe.
2x risk in men

Question 2

General principles of head CT

Answer 2

Asymmetry is bad - deviations from normal anatomy is bad

Must always correlate clinical findings with CT image.

Question 3

Indications for neurosurgical involvement in a head injury

Answer 3

Persistent GCS <8 or delayed deterioration of GCS (motor response)
Unaccounted for confusion after 4hrs or progressive focal neurology
Seizure without full recovery
Definite or suspected penetrating injury
Cerebrospinal fluid leak

Question 4

Indications for use of CT in head injury

Answer 4

Reduced GCS 30mins after event.

OR if amnesia or LOC if >65yrs/high impact/coagulopathy

Question 5

Assessing a head CT

Answer 5

‘Blood Can Be Very Bad’ –> blood, cistern, brain, ventricles, bone
Check if specific windows have been included to look for brain, bone and blood

Question 6

Blood on head CT

Answer 6

Fresh blood is hyper dense (white) on CT
1–2 weeks is isodense with brain tissue
2-3 weeks is hypodense with brain tissue

Question 8

Cisterna on head CT

Answer 8

Potential spaces formed by collections of CSF – important indicators of increased ICP or bleeding
cisterna include –> Sylvian, quadrigeminal, interhemispheric, supraseller and circumesencephalic

Question 9

CT signs of trauma to brain tissue

Answer 9

Cortex is normally lighter and inhomogeneous appearance
Consider –> Symmetry (Midline falx and ventricles evenly spaced on either side), Grey/white matter differentiation (loss is early sign of CVA/ischemia or neoplastic oedema),
Midline shift or effacement of sulci (unilateral or bilateral)

Question 10

Communicating Hydrocephalus

Answer 10

Free exit from ventricles with a blockage at the level of the archnoid granulations – all ventricles will be enlarged

Question 11

Non-communicating Hydrocephalus

Answer 11

Obstruction in the outflow from the lateral ventricles causing ventricular enlargement – some ventricles enlarged depending on the location of the blockage

Question 12

Skull fractures on CT

Answer 12

Do not confuse with suture (close by 35) – best seen in bone window
Can effect vault or base of skull

Question 13

Types of haemorrhage after traumatic brain injury (5)

Answer 13

Extradural Subdural
Subarachnoid Intracerebral
Intraventricular

Question 14

CT findings in TBI

Answer 14

Bleeding
ICP (conpressed cisterna, compressed ventricles or hydrocephalus, midline shift or effaced sulci)
Pneumocephalus or foreign body
Fractures –> linear or depressed skull fractures

Question 15

Extradural haematoma

Answer 15

15-20% mortality, biconvex and does not cross suture lines, 85% arterial laceration (middle meningeal) but can be venous
lucid interval then LOC. Usually occurs over cerebral convexity

Question 16

Subdural haematoma

Answer 16

60-80% mortality if acute, lower if chronic, crescent, slow onset headache and confusion. Usually over cerebral convexity
Crosses suture lines. From surface or bridging vessels Does not cause hydrocephalus. Common in alcoholics, often causes fluctuating deficits.

Question 17

Subarachnoid haematoma

Answer 17

50% mortality, fresh blood in CSF, thunderclap headache

85% aneurysmal but can be traumatic – hydrocephalus develops in 20% of cases

Question 18

Intracerebral haematoma

Answer 18

40% mortality, blood in parenchyme, headache, vomiting and focal neurology. Due to sudden deceleration of the head (RTA), occurs where the head impacts on bony prominences

Question 19

Intraventricular haematoma

Answer 19

associated with high energy TBI – poor outcome, also occurs in premature infants
Can be secondary to ICH or SAH and both can lead to hydrocephalus

Question 20

Hydrocephalus

Answer 20

CSF is produced at the chonoid plexi in the lateral ventricles at 0.5-1ml/min –> blockage will lead to increasing pressure with potential for tonsilar herniation and death