Brain contusions, internal carotid artery dissection and base of skull fracture
Brain contusion, also known as intracerebral hemorrhage 3, is a common type of traumatic brain injury 2. This injury occurs as a direct result of physical destruction of brain tissue within moments of impact 3. This injury includes damage to the primary brain cells including neurons, astrocytes and oligodendrocytes. Additional secondary injury occurs due to many responses, one of which is the maladaptive physiological 'clean up' process by which endogenous neutrophils and phagocytes release harmful free radicals to the area.
CT is usually the mainstay for imaging in brain contusions. It is preferred over MRI because of three reasons 1:
- Acute hemorrhage is difficult to see on MR
- CT allows support equipment to be taken into the room, unlike MRI
- MR imaging requires more time
Traumatic internal carotid artery dissection (TICAD) is a form of blunt cerebrovascular injury (BCVI) and is commonly caused by motor vehicle accident. In the young adult population, it is a common cause of cerebral ischemic stroke, accounting for approximately 20% of cases 4.
Diagnosis is crucial, however is complicated by the fact that only a minority of patients display immediate neurological symptoms. Furthermore, even symptomatic patients often have an initially normal CT scan. As a result, 80% of patients with TICAD progress to cerebral infarction with one week of onset of symptoms 4.
Aside from CT, other modalities to investigate for suspected TICAD include:
- duplex ultrasonography - may show carotid artery lumen tapering, a false lumen or thrombus
- magnetic resonance imaging/angiography - can visualize vessel-wall irregularity and aneurysmal dilatation
- conventional angiography - gold standard for diagnosis
TICAD can be graded according to the blunt carotid injury grading scale 5. Grading is as follows:
- Grade I: Luminal irregularity or dissection with <25% luminal narrowing
- Grade II: Dissection or intramural hematoma with >25% narrowing, intraluminal thrombus or raised flap
- Grade III: pseudoaneurysm formation
- Grade IV: occlusion of internal carotid artery
- Grade V - transection with free extravasation
These gradings dictate management. Grade I lesions are treated conservatively with anticoagulant therapy. Grade II lesions or higher require intervention, as even Grade II lesions may progress to pseudoaneurym (Grade II lesion) or occlusion (grade IV lesion). Intervention may be with endovascular stent placement and/or surgical intervention.
Base of skull fractures are commonly seen in craniofacial trauma. Up to 24% of patients with blunt head trauma sustain a skull base fracture 6.
Base of skull fractures are clinically relevant due to the possibility of endangerment of nearby structures including:
- Cranial nerves
- Internal carotid artery
- Cavernous sinus
Definitive management for skull base fracture depends on the degree of fracture and the clinical state of the patient. Indications for operative management include:
- Neurological deficits - facial nerve paralysis, hearing loss or blindness
- CSF fistula - manifests as rinorrhea and otorrhea
- Temporal bone fracture
Operative management includes a subtotal petrosectomy. This involves exenteration of the temporal bone air cell tracts and obliteration of the eustachian tube. Once the injured structures are repaired, the remaining cavity is obliterated with an endogenous fat graft and temporalis muscle flap.
In the absence of the above features, conservative, expectant management is carried out. This includes a 5 day course of intravenous antibiotics.
Another point to note, is that nasogastric tube placement is to be avoided in patients with confirmed or suspected base of skull fracture. This is due to the risk of intracranial nasogastric tube placement, whereby the tube traverses into the cranium via a fractured cribriform plate 7.
This patient has a petrous temporal bone fracture. He underwent operative management as described above.
Case contributed by A/Prof. Pramit Phal.