John M. Barkley
L. Anne Hayman
Pedro J. Diaz-Marchan
Our discussion of the pathophysiology and imaging appearances of brain injury will now turn to the extraaxial space. As discussed earlier, the dura is a layer of tissue intimately applied to the inner table of the skull and periosteum. The arachnoid is a network of tissue between the outer dura and inner pia—which lines the cortex of the brain. A fundamental understanding of the dural vascular anatomy, including the middle meningeal artery and dural venous sinuses allows one to predict the etiology of an extra-axial hematoma (3).
The subdural space is a potential space that becomes evident radiologically if there is fluid, hemorrhage or purulent material between the dura and arachnoid. Subdural collections are confined to the dural reflections and will not cross midline, although they may cross sutures. These boundaries are helpful if the collection is small and indeterminate. The midline dural reflection is the falx cerebri. Separating the cerebrum and cerebellum is the falx cerebelli. Subdural collections near the midline or cerebellum, may layer on these dural reflections. Sometimes it is difficult to characterize a collection as subdural or epidural in location.
Furthermore, it may be difficult to characterize a hematoma as above or below the falx cerebri. In these instances, the indeterminate collections should be referred to as simply extra-axial.
A subdural hematoma is an extra-axial collection of blood that may occur if there is traumatic injury to the bridging veins beneath the dura (Figure 11-9). These bridging veins travel within the subdural space, toward the main dural sinuses.
Acceleration and deceleration forces may lead to tearing of the bridging veins and subsequently, a subdural hematoma. Arterial injury may rarely cause a subdural hematoma. Following vessel injury, blood collects between the dura and arachnoid. An acute subdural hematoma appears hyperdense (bright) on a noncontrast CT of the brain. It is often crescent-shaped and conforms to the inner table of the skull on axial images. Unlike the epidural space that is confined and may exert a tamponade effect to limit the size of the hematoma, subdural hematomas may become large because of the relatively unconfined nature of the subdural space, subarachnoid space and underlying brain. Because subdural hematomas may cross sutures, they are often seen layering along an entire hemisphere. If large enough, these hematomas will exert mass effect on the underlying brain, causing effacement of sulci, ventricles or even midline shift. Severe midline shift may progress to subfalcine herniation as described previously.
The natural evolution of a subdural hematoma may be followed with serial CT scans. The hematoma will become isodense (similar density) when compared to brain, making it difficult to detect between 5–20 days after injury (Figure 11-10). This decrease in density of a subdural hematoma is due to breakdown of hemoglobin and protein products within the collection. These subacute collections are subtle on imaging and secondary signs such as mass effect and sulcal effacement must be searched for in order to diagnose them. Eventually these collections will become chronic and appear hypodense (dark) compared to underlying brain more than 3 weeks after injury (1, 2). Occasionally, a subacute or chronic subdural hematoma will rebleed, causing a heterogeneous appearance to the collection, with mixed areas of hyper and hypodensity. These collections composed of acute hemorrhage superimposed on chronic blood products appear as a blood-fluid levels in the supine patient. The blood-fluid level is due to differences in density of the blood, or the hematocrit effect. This leads to an appearance of acute, bright blood inferior to the more chronic, serous collection layering dependently.
The mortality rate from traumatic subdural hematomas may be lowered from 90 percent to 30 percent if diagnosis and treatment occur in a timely fashion, usually within the first 4 hr (4). The timing of surgical intervention depends on many factors such as co-existing injuries and the neurological status of the patient. Patients who receive early surgical evacuation of a symptomatic SDH have an improved neurological outcome with relief from increasing intracranial pressure (5).
Subdural hygromas are collections within the subdural space that are hypodense, much like chronic subdural hematomas. They are collections of cerebrospinal fluid (CSF) that result from traumatic leakage from the surface of the brain after injury to the arachnoid membrane (2). It may be difficult to distinguish a chronic subdural hematoma from a subdural hygroma or an expanded extra-axial space. This issue often arises when imaging elderly patients, who have some degree of atrophy and expansion of the extra-axial spaces.
MRI is helpful in these cases, for subdural hygromas and expanded extra-axial spaces will have identical signal characteristics with the CSF in the ventricles and cisterns on all MRI pulse sequences. Subdural hematomas, even if chronic will typically differ from CSF on one or more pulse sequences.
Original: Brain Injury Medicine. Principles and Practice
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