Radiology in major trauma

Head

Head trauma is responsible for up to 90% of pre-hospital trauma deaths. Some 75% of brain injuries can be classified as mild, 15% as moderate and 10% as severe. The spectrum of head injury ranges from mild concussion to diffuse axonal injury (DAI) incompatible with life; it includes all causes of intracranial haemorrhage.

A CT brain scan is the investigation of choice for all but minor head injuries (see Table 3.8.2 for CT indications in serious head injury). A non-contrast CT brain scan with bone windows is adequate for the detection of intra-cranial haematoma, cerebral oedema with or without midline shift and skull vault fractures ( Figs 3.8.4–3.8.6 ).

The Canadian CT Head Rule for patients with minor head injury also provides guidance for CT brain scanning in patients with minor head injury (Glasgow Coma Scale [GCS] score 13 to 15). This rule found that the presence of any of the high-risk factors ( Table 3.8.3 ) was 100% sensitive for predicting the need for neurological intervention and the presence of medium-risk factors was 97.2% sensitive for detecting clinically important brain injury.

If a compound or depressed fracture of the skull is suspected clinically, a CT brain scan should be performed. A compound depressed skull fracture is considered a neurosurgical emergency because of the increased risk of infection, such as meningitis or brain abscess.

Magnetic resonance imaging (MRI) scan of the brain is the investigation of choice for the diagnosis of DAI. MRI sensitivity for the detection of contusions, shear injury, and extra-axial hematomas is higher than that of CT scan, although it is lower for fractures. It may detect white matter lesions consistent with shear injury in patients presenting with normal CT scan findings ( Fig. 3.8.7 ).

Classification of intracranial haemorrhage

Intracranial bleeding may be classified according to location. This includes: subdural, subarachnoid, extradural, intraventricular or parenchymal bleeding. These commonly coexist in the setting of trauma.

Extradural haematomas are commonly secondary to arterial bleeding due to a skull fracture with subsequent disruption of the middle meningeal artery. The haematoma is ovoid or lentiform and does not cross cranial sutures, but it may cross the midline (see Fig. 3.8.4 ).

Subdural haematomas usually occur as a result of venous bleeding. These haematomas are crescentic in shape, may involve a larger area when compared with an epidural haematoma and may cross cranial sutures, but they do not cross the midline ( Fig. 3.8.8 ).

Subarachnoid haemorrhage may be due to disruption of small subarachnoid vessels or occur by direct extension from a parenchymal contusion/haematoma. Subarachnoid haemorrhage may be visualized in the sulci of the cerebral convexities or within the subarachnoid cisterns at the base of the skull ( Fig. 3.8.9 ).

Intraventricular haemorrhage (see Fig. 3.8.9 ) may be caused by tearing of subependymal veins on the surface of the ventricles or by direct extension from a parenchymal contusion/haematoma. These blood products tend to layer dependently on a CT scan with the patient imaged in a supine position, particularly within the occipital horns of the lateral ventricles.

Cerebral contusions represent foci of bleeding within the parenchyma of the brain. These may occur within superficial grey matter/subcortical white matter due to direct contact from bony protuberances of the calvarium or base of skull. Deeper parenchymal contusions are caused by disruption of intraparenchymal blood vessels. Cerebral contusions commonly increase in size and number within the first 24 hours post-trauma due to continued bleeding (see Fig. 3.8.9 ). These haematomas also develop adjacent oedema, which may increase the associated mass effect on the remainder of the intracranial structures.

Also noteworthy is the increased presentation of patients taking anticoagulation or antiplatelet therapy who fall and suffer head injuries. The bleeding as a result of the injury may progress over 24 hours and may occur in all of the previously noted locations despite both pharmacological and neurosurgical attempts at reversal.

DAI occurs due to acceleration/deceleration forces and is a shearing-type injury to the brain. It may be initially difficult to visualize on a non-contrast CT but can be identified as tiny foci of petechial haemorrhage at the grey/white matter interface, within the corpus callosum or within the brain stem. MRI is the investigation of choice for DAI (see Fig. 3.8.7 )

Non-contrast CT is also capable of identifying areas of acute established infarction. In the setting of trauma, this may be secondary to acute vascular injury or mass effect due to cerebral oedema (see Fig. 3.8.5 ).

Blunt cerebrovascular injury

Blunt injury to the carotid or vertebral vessels (BCVI) occurs in about 0.1% of all trauma patients in the United States. Many of these injuries are diagnosed after the development of symptoms and signs due to central nervous system ischaemia, with neurological morbidity of up to 80% and mortality approaching 40%. However, when asymptomatic patients are screened for BCVI, the incidence rises to 1% for all admitted blunt trauma patients and up to 2.7% for those with an injury severity score (ISS) greater than 15.

The Denver Modification of Screening criteria ( Table 3.8.4 ) provide both risk factors as well as symptoms and signs for BCVI. CT angiography (CTA) is now the investigation of choice for the diagnosis of BCVI. Table 3.8.5 shows a grading scale for BCVI as proposed by Biffi et al.

Table 3.8.4

Denver modification of screening criteria for blunt cerebrovascular injury

Symptoms/signs of BCVI

Arterial haemorrhage

Cervical bruit

Expanding cervical haematoma

Focal neurological deficit

Neurological findings incongruous with CT scan findings

Ischaemic stroke on secondary CT scan

Risk factors for BCVI

High-energy transfer mechanism with:

Le Fort 2 or 3 fractures

Cervical spine fracture patterns: subluxation, fractures extending into the foramen transversarium, fractures of C1–C3

Basilar skull fractures with carotid canal involvement

Diffuse axonal injury with GCS score <7

Near hanging with anoxic brain injury

BCVI , Blunt cerebrovascular injury; CT , computed tomography.

Table 3.8.5

Grading scale for blunt cerebrovascular injury

Grade 1: intimal irregularity with <25% narrowing

Grade 2: dissection or intramural haematoma with >25% narrowing

Grade 3: pseudoaneurysm

Grade 4: occlusion of lumen

Grade 5: transection with extravasation

A dissection of the right vertebral artery due to blunt trauma in a patient with bilateral facet dislocation is shown in E-Fig. 3.8.1 ; E-Fig. 3.8.2 demonstrates dissection of the right internal carotid artery with a large associated pseudoaneurysm; and E-Fig. 3.8.3 shows a posterior inferior cerebellar artery infarct in a patient with a vertebral artery dissection.

Facial injury

Facial trauma may range from relatively minor undisplaced nasal bone fractures to the life-threatening problems of airway protection and haemorrhage associated with mid-facial (Le Fort) fractures. Underlying cerebral injury may also be associated with frontal bone fractures.

The commonest injury to the mid-face is the blowout fracture caused by a direct blow to the orbit, which results in a fracture of the orbital floor or the medial wall of the orbit in the region of the paper-thin lamina papyracea ( E-Fig. 3.8.4 ). There may be tenderness over the fractured bone associated with diplopia due to entrapment of orbital contents or (less commonly) visual disturbance due to globe or optic nerve injury. These fractures are best seen on CT scans with multi-planar reconstructions. Blowout fractures with entrapment of orbital contents require surgical elevation.

Mandibular fractures are usually obvious clinically because of pain, malocclusion and drooling. Mandibular fractures may be difficult to demonstrate on standard PA and oblique x-ray views. A panoramic view or orthopantomogram (OPG) is more useful, but CT of the mandible provides optimal demonstration of mandibular fractures, including those involving the mandibular neck, condyle and temporomandibular joint (TMJ) ( E-Fig. 3.8.5 ). Dislocation of the TMJ is also optimally diagnosed on CT ( E-Fig. 3.8.6 ).

Fractures of the zygoma are classified as (1) tripod fractures and (2) isolated fractures of the zygomatic arch. The tripod fracture or zygomatico-maxillary fracture separates the malar eminence of the zygoma from its frontal, temporal and maxillary attachments. Tripod fractures are usually caused by a significant force to the body of the zygoma or malar eminence. The three fractures that constitute the tripod fracture are located in the inferior orbital margin, the lateral orbital margin or the zygomaticofrontal suture and the zygomatic arch. These fractures are best viewed on CT scans ( Fig. 3.8.10 ).

The Le Fort fractures are caused by direct trauma to the mid-face. The Le Fort 1 fracture involves the maxilla at the level of the nasal floor and will allow mobility of the palate (‘floating palate’) ( Fig. 3.8.11 ). The Le Fort 2 fracture passes through the nasal bones as well as the medial, inferior and lateral walls of the maxillary antrum. The Le Fort 3 or ‘craniofacial dysjunction/floating face’ fracture involves the nasal bones, the medial and lateral orbital walls and the zygomatic arch.

Frontal sinus fractures commonly occur as a result of direct force and are often compound, with the risk of associated intracranial infection. There may be an associated intracranial haematoma or cerebral contusion. A CT scan will best evaluate these fractures and determine the involvement of the posterior sinus wall. These fractures often require surgical exploration for debridement and repair.