Most skull base fractures are identified on noncontrast head CT obtained for evalu-ation of head trauma. High-energy impact and fractures that traverse the carotid ca-nals or cavernous sinus can be associated with carotid or vertebral injury, including dissection and pseudoaneurysm. Vascular injury places the patient at increased risk for secondary embolic cerebral infarct, which can be prevented with anticoagula-tion. Because of this risk, CT angiography with helical thin-section imaging is gener-ally advised in this group (Fig. 2.5).
◆Skull Fracture
A calvarial fracture does not reliably pre-dict underlying brain injury, and a normal skull radiograph does not exclude intra-cranial injury. Calvarial fractures that are depressed more than 5 mm are usually elevated surgically. Epidural hematoma is associated with fractures that traverse the course of the middle meningeal artery. Skull base fractures are associated with high-energy trauma and with more severe brain injury; the most common locations include the petrous temporal bone, the ba-siocciput, the sphenoid bone, and the eth-moid bone.
Anterior skull base fractures traverse the paranasal sinuses and orbit, and they can disrupt the cribriform plate and optic canals. Clinical consequences include CSF rhinorrhea, periorbital ecchymosis (“rac-coon eyes”), and olfactory or optic nerve damage. Trauma to the central skull base, usually from lateral impact, results in pe-trous temporal bone fractures and may be associated with CSF otorrhea, hemotympa-
Fig. 2.5a–da,b Calvarial fracture. Left frontal calvarial fracture with small subjacent epidural hematoma and minimal intracranial air. The fracture fragment is elevated one-half calvarial width relative to the remainder of the skull.
c,d Skull base fracture. Nondisplaced longitudinal right temporal bone fracture that traverses the basi-sphenoid (clivus) and basiocciput. Blood is present in the sphenoid sinus and the right mastoid air cells. A small amount of air is present in the posterior fossa.
e,f Depressed skull fracture. Right parietal calvarial fracture with 1.8-cm depression and subjacent corti-cal contusion.
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mogeneous, swirling appearance due to a mixture of clotted and unclotted blood.
Venous epidural hematomas, which ac-count for approximately 10% of EDHs, arethe consequence of dural venous sinus dis-ruption or, rarely, diploic vein or arachnoidgranulation rupture. They are low-pressurehemorrhages that typically do not enlargeover time and rarely require evacuation. Incontrast to arterial hematomas, traumaticvenous EDHs often occur in children andare not necessarily associated with skullfractures. They are most commonly seenin the middle cranial fossa adjacent to thegreater wing of the sphenoid bone, wherevenous EDHs are due to disruption of thesphenoparietal venous sinus. They also mayfollow injury to the sagittal or transverse si-nuses and can traverse the tentorium at theocciput or the falx at the vertex (Fig. 2.6).
◆Epidural Hematoma
Most epidural hematomas (EDH) are of arterial origin and result from calvarial fractures that cross branches of the middle meningeal artery. Hemorrhage under arte-rial pressure separates the outer layer of the dura from the skull, creating an extraparen-chymal intracranial mass that compresses the adjacent brain, leading to ischemia and potential compartmental herniation. Epi-dural hematomas can enlarge rapidly and, if not treated, are often rapidly fatal. With early evacuation, however, the prognosis is good; the skull absorbs most of the energy of impact as it fractures, sparing the under-lying brain parenchyma from direct injury.
An acute EDH is a smooth, hyperdense biconvex extraparenchymal blood col-lection, limited by the coronal sutures, to which the dura is especially adherent. Hyperacute, active bleeding has an inho-
Fig. 2.6a–f a–d Arterial epidural hematoma. Hyperdense, right parietal, lenticular, extraparenchymal hematoma with maximal thickness 2.7 cm. Ipsilateral cortical sulcal and lateral ventricular compression with minimal subfalcine shift. Contralateral anterior temporal lobe hemorrhagic contusion. Right parietal vertex scalp hematoma and laceration.
e,f Venous epidural hematoma. Lenticular (1-cm) extraparenchymal mixed-density hemorrhage adja-cent to the right sphenotemporal buttress with mild compression of the anterior temporal lobe. Right preseptal periorbital and temporal scalp hematoma. The underlying brain parenchyma is normal, and the perimesencephalic cisterns are patent.
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ity of the brain to tamponade low-pressure hemorrhages. In such patients, enlarged extracerebral space limits the degree of pa-renchymal compression and ischemia.
Acute SDHs are crescentic, hyperdense, and usually homogeneous. They can ex-tend along the entire hemisphere and are confined by the falcine and tentorial dural reflections. In contrast to most EDHs, SDH is not limited by calvarial sutures. Venous hemorrhage is usually more gradual than arterial bleeding, and SDHs can develop more slowly than EDHs. Nonetheless, large SDHs can cause acute and severe neurolog-ic deterioration and often require urgent evacuation. Hematoma thickness or sub-falcine shift of 2 cm or greater is associated with a particularly poor prognosis.
The density of subdural clot can overlap with that of calvarial bone on narrow CT windows optimized for evaluation of brain parenchyma, and small subdural hemato-mas can be dicult to detect. To avoid this error, head CT obtained for trauma should always be viewed at both narrow and wide (subdural) window settings (Fig. 2.7).
◆Acute Subdural Hematoma
Acute subdural hematomas (SDHs) occurwhen cortical veins that traverse the subdu-ral space are torn under cerebral accelerationor rotation. Blood accumulates between theinner (meningeal) layer of the dura, which isfirmly attached to the skull, and the smooth arachnoid membrane loosely adherent tothe surface of the brain. Uncommonly, a pri-mary parenchymal or subarachnoid hemor-rhage can disrupt the arachnoid membraneand rupture into the subdural space. SDH isassociated with a skull fracture in less than50% of cases and is typically a “contrecoup”injury that results from recoil of the brainaway from the inner surface of the skull op-posite the site of impact.
Especially in younger patients, an acute SDH indicates significant energy transfer and is frequently associated with severe parenchymal brain injury, brain hernia-tion, and cerebral ischemia. SDH due to minor trauma is more common in the el-derly and in patients with cerebral atrophy.