Multitrauma with diffuse axonal injury, temporal bone fractures and traumatic caroticocavernous fistula

Brain and Skull

• Scalp haematomas.
• Diffuse sulcal effacement. No hydrocephalus.
• Diffuse axonal injury (pons, body/splenium of corpus callosum).
• Small posterior falcine subdural.
• Subarachnoid haemorrhage.
• Small volume of intraventricular haemorrhage.
• Left temporal extradural haemorrhage and pneumocephalus.
• Right longitudinally-orientated petrous temporal bone fracture sparing the otic capsule with ossicular chain disruption, haemomastoid and extension into the external auditory meatus. There is also extension into the right parietal and occipital bones.
• Left parietal bone fracture extending through the mastoid air cells and petrous temporal bone into the external auditorauditory meatus. Ossicular chain is intact. Otic capsule sparing.
• Left base of skull fracture extending into the clivus, sphenoid bone, left foramen lacerum and left carotid canal. Possible extension into the right carotid canal. Haemosphenoid.
• Fracture of the nasal septum.
• Hard palate fracture.
• Medial left maxillary antrum fracture.
• Gas from the base of skull fracture in the soft tissues of the face.
• Oral cavity packing material.

C-Spine

• ETT, NGT, Guedels.
• Subarachnoind blood in the superior cervical spine.
• Gas from the base of skull fractures.
• No cervical spine fracture.

This case demonstrates why MRI is the modality of choice for assesing for DAI. This patient had a normal CT Brain but evidence of haemorrhagic and non-haemorrhagic DAI on MRI.

On MRI, there are multiple foci of abnormal high FLAIR signal in the inferior frontal lobes bilaterally as well as within the genu, body and splenium of the corpus callosum. These represent non-haemorrhagic DAI lesions.

Punctate hypointense foci within the bilateral frontal lobes on Gradientgradient echo are in keeping with regions of punctate haemorrhagic foci.

Diffuse axonal injury:

Diffuse axonal injury (DAI) is due to traumatic stretching of axons, usually due to sudden deceleration. DAI is characterised by multiple focal lesions. These typically occur at the grey-white matter junction (particularly in the frontotemporal lobes), the corpus callosum (particulary the splenium), and the brainstem. Less common locations include the: basal ganglia; internal/external capsule; corona radiata and the cerebellar peduncles. In general, the deeper the abnormalities, the more severe the injury (see Grading of diffuse axonal injury).

The appearance of DAI lesions depends on whether they are haemorrhagic or not. Haemorrhagic lesions will appear hyperdense on CT whilst non-haemorrhagic lesions will be hypodense. The size of lesions can range from millimetremillimetres to centimeters.

MRI is the modality of choice for assessing DAI as many patients with a normal CT will have DAI visible on MRI – greater than 30% of patients with a negative CT will have a positive MRI¹. CT is particularly insensitive for non-haemorrhagic lesions.

DAI should be considered if the clinical findings are disproportionate to the imaging findings.

Cerebral contusions and diffuse axonal injury result from different mechanisms.

Cerebral contusions occur when the head strikes a solid object and comes to an abrupt stop. The brain continues to move for a short amount of time and hits the inside of the skull. Thus the classic location for cerebral contusions is the brain surface, most commonly the anterior inferior frontal and temporal lobes.

The aetiology of diffuse axonal injury is different. It occurs due to shearing injury resulting in axonal stretching. When the head strikes an object, the cortex moves at a different speed compared to the white matter and structures deep in the brain. Thus DAI injures typically occur at the grey-white matter junction.

The main difference on imaging between cerebral contusions and DAI is the location of the lesions – contusions typically involve the cortex and there is often associated extra-axial blood, whilst DAI typically involves the grey-white matter junction.  

Temporal bone fracture:

Traditionally petrous temporal bone fractures were classified as either longitudinal (parallel to the long axis of the petrous ridge) or transverse (perpendicular to the petrous ridge), with many fractures involving both transverse and longitudinal components². 

There is now a newer system of classification which is more predictive of complications associated with temporal bone fractures^2,3. This classifies fractures as either otic capsule sparing or otic capsule violating^2,3. Otic capsule violating fractures course through the osseous labyrinth and are more commonly associated with complications such as sensorineural nearing loss, cerebrospinal fluid otorrhoea and facial nerve injury than otic capsule-sparing fractures^2,3.

Ossicle dislocations are more common than fractures of the ossicles². Incudostapedial dislocation is the most common dislocation whilst the incus is the most commonly fractured ossicle². The axial plane provides the best view to evaluate for ossicular dislocation².

Temporal bone fractures and their complications are often able to be readily identified on routine CT. Dedicated temporal bone CT is only required if there is a high degree of clinical suspicion of fractures but no fracture is identified on the routine CT². Signs that are suggestive of an underlying fracture include: opacification of the mastoid air cells, external ear canal, or the middle ear; air-fluid level in the sphenoid sinus; pneumocephalus adjacent to the temporal bone; an extraaxial fluid collection or brain injury; and air in the glenoid fossa of the temporomandibular joint².

If the fracture extends into the carotid canal a CTA to evaluate the internal carotid artery is recommended. CT Venogram should be considered if the fracture extends into the dural venous sinuses or jugular bulb. Both carotid and dural venous sinus injuries are rare.

Patients with temporal bone fractures are more likely to have an intracranial injury and so this must be inspected for⁴.

Carotid dissection:

Vascular injuries to the neck are usually the result of penetrating trauma but can also occur from blunt trauma. Injuries can range from vessel spasm to transection. Blunt trauma is more likely to result in dissection and occlusion.

CTA has a high sensitivity and specifityspecificity for detecting dissecton. Direct changes of carotid dissection on CTA include irregularity of the vessel wall and psuedoaneurysm formation. The classic presentation, although uncommon, in patients with internal carotid dissection is: local pain, headache, ipsilateral Horner syndrome, ischaemic stroke and retinal ischaemia.