Etiology
The primary etiology of both acute and chronic subdural hematomas (SDH) is trauma.[15] Less commonly, SDHs are associated with rupture of a cerebral aneurysm or vascular malformation (i.e., arteriovenous malformation or dural fistula).[16][17] There are also case reports in the literature of spontaneous SDHs associated with cerebral hypotension and malignancy.[18][19][20]
Pathophysiology
Acute subdural hematomas (SDH) typically result from torsional or shear forces causing disruption of bridging cortical veins emptying into the dural venous sinuses. This causes SDHs to form along the brain convexities.[1][21][22] Direct force to the skull and brain may cause contusions or lacerations, and typically results in bleeding from a subdural vessel near the temporal pole.[22][1] In some cases, arterial injury may occur, resulting in rapid neurologic decline and poor chances for recovery.[1] As intracranial pressure rises, cerebral perfusion pressures and cerebral blood flow may fall and ischemic injury occurs. Timely hematoma evacuation may prevent the pathophysiologic cycle that otherwise leads to ischemia and neuronal death.[23] In many circumstances, associated injuries (contusions, epidural hematoma, diffuse axonal injury) affect neurologic recovery. Chronic SDHs become symptomatic from direct compression of underlying brain, and usually do not result in the cascade of ischemia and secondary neuronal injury.[24][1] Patients usually have a degree of underlying brain atrophy and may have a history of alcoholism or coagulopathy.[1]
Like acute SDHs, chronic SDHs form from rupture of a bridging cortical vein, where they are suspended beyond the trabeculae of the arachnoid space. Because there is brain atrophy, there is considerable room for these hematomas to enlarge before they cause symptoms. As the hematoma develops, the dura undergoes an inflammatory reaction due to exposure to blood and fibrin products, which results in formation of neomembranes that may give chronic SDHs a loculated appearance.[25][1] Chronic SDHs are believed to result from slow venous bleeding, typically from bridging veins on the cerebral surface, but the pathophysiologic process is likely more complex and remains incompletely understood.[26] This can occur due to traumatic events, anatomic changes that result in cranio-cerebral disproportion (i.e. brain-shrinkage with age), intracranial hypotension, or through anatomic manipulation (cranial surgery).[26][27] Chronic SDHs tend to enlarge over time. This is thought to be due to either osmotic gradients that encourage the flow of cerebrospinal fluid across neomembranes into a hyperosmotic hematoma or repeated hemorrhage from the vascularized neomembranes.[1] As this collection forms in a potential space, and given that the bleeding derives from low-pressure venous blood, the hematoma takes time to develop, which explains why many patients become symptomatic weeks after the initial injury.[26]
Classification
Computed tomography appearance[1]
Subdural hematomas (SDH) can be divided into 4 types:
Acute SDH (<3 days old, diffusely hyperdense)
Subacute SDH (3-21 days old, heterogeneously hyperdense/isodense)
Chronic SDH (>21 days old, diffusely hypodense)
Acute-on-chronic SDH (areas of hyperdensity within hypodense hematoma).
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