The usual mechanism that produces an acute subdural hematoma is a high-speed impact to the skull. This causes brain tissue to accelerate or decelerate relative to the fixed dural structures, tearing blood vessels.
Often, the torn blood vessel is a vein that connects the cortical surface of the brain to a dural sinus (termed a bridging vein). In elderly persons, the bridging veins may already be stretched because of brain atrophy (shrinkage that occurs with age).
Alternatively, a cortical vessel, either a vein or small artery, can be damaged by direct injury or laceration. An acute subdural hematoma due to a ruptured cortical artery may be associated with only minor head injury, possibly without an associated cerebral contusion. In one study, the ruptured cortical arteries were found to be located around the sylvian fissure. [3]
The head trauma may also cause associated brain hematomas or contusions, subarachnoid hemorrhage, and diffuse axonal injury. Secondary brain injuries may include edema, infarction, secondary hemorrhage, and brain herniation.
Typically, low-pressure venous bleeding from bridging veins dissects the arachnoid away from the dura, and the blood layers out along the cerebral convexity. Cerebral injury results from direct pressure, increased intracranial pressure (ICP), or associated intraparenchymal insults.
In the subacute phase, the clotted blood liquefies. Occasionally, the cellular elements layer can appear on CT imaging as a hematocrit-like effect. In the chronic phase, cellular elements have disintegrated, and a collection of serous fluid remains in the subdural space. In rare cases, calcification develops.
Much less common causes of subdural hematoma involve coagulopathies and ruptured intracranial aneurysms. Subdural hematomas have even been reported to be caused by intracranial tumors.
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Acute right-sided subdural hematoma associated with significant midline shift (ie, subfalcine herniation) shown on CT scan.
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Bilateral chronic subdural hematomas shown on CT scan. Midline shift is absent because of bilateral mass effect. Subdural hematoma is bilateral in 20% of patients with chronic subdural hematoma.
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An acute subdural hematoma is shown in this intraoperative photograph. Note the frontotemporoparietal flap used. The hematoma is currant jelly–like in appearance.
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A left-sided acute subdural hematoma (SDH). Note the high signal density of acute blood and the (mild) midline shift of the ventricles.
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A left-sided chronic subdural hematoma (SDH). Note the effacement of the left lateral ventricle.
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Chronic subdural hematomas (SDHs) are commonly bilateral and have areas of acute bleeding, which result in heterogeneous densities. Note the lack of midline shift due to the presence of bilateral hematomas.
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An isodense subdural hematoma (SDH). Note that no sulcal markings are below the inner table of the skull on the right side. This hematoma has scattered areas of hyperdense, or acute, blood within it.
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Isodense subdural hematoma (SDH) as pictured with MRI. MRI can more readily reveal smaller SDHs, and, on MRI, the imaging of the blood products change characteristically over time.
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Atrophy of the brain, resulting in a space between the brain surface and the skull, increases the risk of subdural hematoma (SDH).
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An acute subdural hematoma (SDH) as a complication of a craniotomy. Note the significant mass effect with midline shift.
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Acute subdural hematoma. Note the bright (white) image properties of the blood on this noncontrast cranial CT scan. Note also the midline shift. Image courtesy of J. Stephen Huff, MD
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Subacute subdural hematoma. The crescent-shaped clot is less white than on CT scan of acute subdural hematoma. In spite of the large clot volume, this patient was awake and ambulatory. Image courtesy of J. Stephen Huff, MD.
