Emergency Imaging. Alexander B. Baxter
only find-ing in minor head trauma. Blood that col-lects between the pia and the arachnoid membrane fills cerebral sulci and forms fine serpentine juxtacortical high-density collections. Hemorrhage is also common in the perimesencephalic cisterns. Over a period of days, blood becomes isodense to brain and ultimately resolves.
Traumatic SAH may be limited to cor-tical sulci, the interpeduncular cistern, or the posterior perimesencephalic cisterns. Extensive hemorrhage in the suprasellar and middle cerebral artery cisterns, es-
Fig. 2.10a–d a,b Isolated traumatic subarachnoid hemorrhage. Generalized cerebral swelling with eacement of perimesencephalic cisterns and cortical sulci. Subarachnoid hemorrhage in the interpeduncular and ambi-ent cisterns. Hemorrhage lls numerous frontal and parietal convexity sulci.
c,d Traumatic subarachnoid hemorrhage associated with other cerebral injuries. Generalized cerebral swelling, right frontal cortical contusions, pneumocephalus, clot within the ventricles, and small tentorial subdural hematoma. Traumatic subarachnoid hemorrhage in the interpeduncular cistern and left Sylvian ssure.
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unless associated with significant brain swelling.
CT is the first and often only investiga-tion in the emergency setting; MRI is moresensitive for detection of small hemorrhages,which can be important for accurate progno-sis. Contusions may be subtle or impercep-tible immediately following an acute injury.Delayed hemorrhage, occurring at 12 to 48hours, is known as posttraumatic apoplexyand reflects hypocoagulability that often de-velops following head trauma and resolutionof acute swelling that serves to tamponadesmall vascular injuries (Fig. 2.11).
◆Cerebral Contusion
Cortical contusions result when the brainimpacts upon the irregular contours of theorbital roofs, petrous ridges, and sphe-noid wings in acute acceleration injury.As a result, most contusions are locatedin the cortex and immediate subcorticalwhite matter of the inferior frontal lobes,anterior or inferior temporal lobes, pos-terior cerebellum, dorsal occipital lobes,and frontal and parietal convexities. Theymay be either coup or contrecoup in loca-tion, although the latter are more com-mon. Contusions typically carry a betterprognosis than diuse axonal injury (DAI)
Fig. 2.11a–ea Hemorrhagic right temporal contusion. Right temporal hematoma with adjacent traumatic subarach-noid hemorrhage. Blood within the left sphenoid sinus indicates associated central skull base fracture.b Nonhemorrhagic right and hemorrhagic left contusions. Low-attenuation edema within the right tem-poral lobe and hematoma surrounded by vasogenic edema in the left temporal lobe. Generalized brain swelling with cisternal eacement and traumatic subarachnoid hemorrhage in the interpeduncular and quadrigeminal plate cisterns.
c,dBilateral contusions. Bilateral temporal hemorrhagic and left inferior frontal nonhemorrhagic contusions.e,fRight frontal and left parietal vertex hemorrhagic contusions. Associated right frontal subdural hema-toma, traumatic subarachnoid hemorrhage, and right sided swelling with convexity sulcal eacement.
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tiny perforating vessels. These are located at the gray-white junction of the cerebral hemispheres, the basal ganglia, the corpus callosum, or the dorsolateral midbrain. The depth of the hemorrhage roughly corre-lates with trauma severity.
CT can be normal in DAI, and while MRI is more sensitive for detection of micro-hemorrhages, both techniques are likely to underestimate the extent of axonal in-jury. In patients who survive significant head injury, later Wallerian degeneration of sheared axons, brain atrophy, and ven-tricular enlargement reveal neuronal dam-age that is often not apparent on initial CT (Fig. 2.12).
◆Diuse Axonal Injury
Diuse axonal injury (DAI) is the cerebral neuronal damage that occurs when the brain is subjected to severe rotational and translational forces in trauma. Because gray and white matter densities are not identical, dierential movement of the cor-tex relative to white matter during rapid acceleration shears traversing axons and perforating vessels. DAI is a devastating injury, usually the consequence of high-velocity motor vehicle accidents, and the patient typically suers an immediate loss of consciousness and remains in a persis-tentvegetativestate.
On CT imaging, DAI is revealed by small petechial hemorrhages from laceration of
Fig. 2.12a–da–d Diuse axonal injury. Punctate hemorrhages at the gray-white matter junction involving the an-terior corpus callosum, right thalamus, and left posterior limb of internal capsule. Associated traumatic subarachnoid hemorrhage within the interpeduncular cistern and left quadrigeminal plate cistern.
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evident over the nondependent frontal lobes and tends to have a peaked appear-ance (Mount Fuji sign).
Most cases of pneumocephalus resolve spontaneously and can be observed. An-timicrobial therapy is indicated to pre-vent meningitis when a disrupted sinus or mastoid air cell communicates with the intracranial cavity. When associated with neurologic deterioration, tension pneumo-cephalus can be treated with burr hole de-compression (Fig. 2.13).
◆Pneumocephalus
Intracranial air is always seen after crani-otomy and also occurs in a small percent-age of head trauma patients. If a skull base or calvarial fracture traverses one of the facial sinuses or the mastoid air cells, air is often present in the subdural or subarach-noid space. Rarely, a dural laceration can act like a one-way check valve, permitting inflow of air, but preventing its egress. By this mechanism, intracranial air pressure can exceed tissue pressure and compress the brain. In the supine patient, this is most
Fig. 2.13a–fa–d Pneumocephalus following facial trauma with orbital roof and ethmoid fracture. Small amount of air anterior to theright frontal lobe, between the ethmoid bone and the olfactory cortex, and within the right superior orbit. This air is