Fig. 2.7a–fa,b Acute subdural hematoma. 1.8-cm hyperdense left holohemispheric subdural hematoma with trau-matic subarachnoid hemorrhage, 1.6-cm subfalcine shift, compression of the left lateral ventricle, and trapping of the right lateral ventricle.
c,d Large right subdural hematoma with prominent frontal, parafalcine, and tentorial hyperdense collections.
e,f Window and level in detecting subdural hematoma. (e) CT window = 80 (brain) shows subtle ef-facement of right frontal sulci, but otherwise apparently normal brain. (f) CT window = 170 (subdural). A 5-mm right frontotemporal subdural hematoma is now clearly evident.
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compared with brain and approach thedensity of CSF. Unevacuated hematomasincite a local inflammatory response that leads to formation of a fibrinous capsule and fragile, vascularized membranes. Thesecan rupture spontaneously or with mi-nor trauma, and patients who have had aprevious SDH are at increased risk of hem-orrhage. Delayed bleeding into the subdu-ral space complicates up to one-third ofchronic SDHs and appears as hyperdenseclot within the lower-density hematoma.Rehemorrhage into a chronic SDH may alsoappear convex rather than crescentic due toconfinement by inflammatory membranes.
Blood fluid levels can be seen in chronic or subacute SDH complicated by rehemor-rhage, following lysis of the initial hemato-ma. Acute or subacute SDH in patients who are taking anticoagulants or are otherwise coagulopathic can also show blood fluid levels (Fig. 2.8).
◆ Subacute and Chronic Subdural Hematoma
SDHs evolve over time. Hyperacute hemor-rhage, seen in the rare patient imaged im-mediately after injury, can be hypodense or mixed-density. Most patients are im-aged after coagulation has taken place, and acute SDHs are typically hyperdense and crescentic. As an acute SDH ages, pro-tein degradation occurs, extracellular fluid shifts into the hematoma, and density decreases.
SDHs that are 2 to 3 weeks old may be isodense to the adjacent cortex and dif-ficult to detect, especially when they are small or bilateral. MRI or CT+C is more sen-sitive than NCCT for identification of these subtle hematomas. SDHs of any age can be complicated by rehemorrhage, which can convert a small, well-tolerated subacute SDH into a larger, symptomatic mass.
Three weeks or more after hemorrhage,a SDH is considered chronic. By this time,most simple hematomas are hypodense
Fig. 2.8a–f a,b Subacute subdural hematoma. (a) CT left holohemispheric subdural hematoma, near isodense to cerebral cortex. Eaced left sulci and lateral ventricle with slight left to right subfalcine shift. (b) MRI T1-weighted image more clearly shows extent of subdural hematoma.
c Chronic subdural hematoma. Low-attenuation subdural uid collections with minimal dependent blood products. Underlying cerebral volume loss and moderate symmetric compression of the frontal brain parenchyma.
d Chronic subdural hematoma with rehemorrhage. Left, isodense SDH. Right, low-density SDH with lay-ering blood products.
e,f Complex subdural hematoma. Rehemorrhage with mixed density and lenticular shape due to con-nement of clot by membranes.
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Subdural hygromas have the same CT density as CSF and can be indistinguish-able from chronic subdural hematomas. When isolated and identified in the setting of acute trauma, subdural hygromas are considered a benign consequence of head injury, since most are small and clinically insignificant, and do not require surgi-cal intervention. Subdural hygromas are commonly seenin conjunction with other brain injuries, such as contusion, traumatic subarachnoid hemorrhage, and extra-axial hematomas (Fig. 2.9).
◆Subdural Hygroma
Subdural hygromas are due to CSF that leaksinto the subdural space via either a tear oran irritation of the arachnoid. Subdural hy-gromas are usually bilateral, located overthe anterior frontal or temporal lobes, anddevelop 2 to 3 days after acute head trauma.
Depending on CSF absorption and post-traumatic brain swelling, subdural hygromascan fluctuate in size over time. Atrophy or encephalomalacia aords a potential space for the development of hygromas, whereasparenchymal expansion and fluid reabsorp-tion will speed resolution of the hygroma.
Fig. 2.9a–d a,b Subdural hygroma. (a) CT at time of injury. Mild underlying ventricular and sulcal prominence. (b) CT 48 hours later. Interval appearance of symmetric, low-attenuation bifrontal subdural uid collections. c,d Subdural hygroma associated with cortical contusion, epidural hematoma, and traumatic subarach-noid hemorrhage. Low-attenuation bifrontal subdural collections. High-attenuation subarachnoid hemor-rhage lls the left frontal sulci. Left inferior frontal hemorrhagic contusion. Small right temporo-occipital epidural hematoma containing air.
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pecially in the absence of other traumatic brain injuries (contusion, subdural hema-toma, epidural hematoma) or with minor trauma, is more consistent with subarach-noid hemorrhage due to a ruptured aneu-rysm. It is important to keep in mind that the accident leading to a patient’s head injury may have been precipitated by loss of consciousness due to an aneurysmal hemorrhage. CT or conventional angiog-raphy can be performed to address this possibility.
SAH is associated with increased mor-bidity and mortality in trauma, reflecting its potential to induce vasospasm and itsassociation with more severe mechanismsof head injury. Subarachnoid blood is alsotoxic to the underlying cortex and can inter-fere with normal CSF absorption, which canlead to later complications of chronic hydro-cephalus or superficial siderosis (Fig. 2.10).
◆Traumatic Subarachnoid Hemorrhage
Traumatic subarachnoid hemorrhage (SAH) is a consequence of either direct pial vas-cular injury or extension from a hemor-rhagic cortical contusion, parenchymal hematoma, or extra-axial hematoma. Al-though traumatic SAH is often seen in as-sociation with other brain