Which condition occurs when blood collects between the dura mater and arachnoid membrane?

Subdural Haemorrhage

A subdural haematoma (SDH) typically occurs owing to injury to the cortical bridging veins that extend radially away from the cortical surface to drain into the dural venous sinuses. Even relatively minor trauma can result in damage to these veins with haemorrhage into this potential, rather than naturally occurring, space between the inner dural layer and arachnoid mater. An SDH has a typical crescentic configuration (Fig. 54.22) due to the absence of anatomical constraint because the haemorrhage is free to extend along the subdural space, coursing over the cerebral convexity. An SDH may extend medially to lie adjacent to the falx and inferiorly towards the floor of the anterior and middle cranial fossae. SDH may also be seen along the tentorium (Fig. 54.23) and evaluation of the multiplanar reconstruction images will assist in visualising these, particularly as a small volume of haemorrhage may be relatively inconspicuous on the axial images. Associated calvarial fractures may or may not be present with SDHs contrary to EDHs when they are usually always present.

The density of SDH on unenhanced CT will depend upon the interval between the initial traumatic event and imaging. If imaging is performed within a few hours, a SDH will appear hyperdense relative to brain parenchyma (seeFig. 54.22). As is the case with EDH, areas of reduced density within a predominantly hyperdense SDH can indicate the presence of active bleeding and further haematoma expansion. A low threshold for repeat imaging in the event of clinical deterioration should be maintained. Acute SDH appearing of only mildly increased density or isodense to brain parenchyma can occasionally be seen in patients with low haematocrit or if there is coexistent arachnoid mater injury that results in CSF leakage into the subdural space.

If the interval between the onset of SDH and imaging is prolonged, then the density of the SDH on initial imaging will be reduced as the clot is degraded. In the subacute period following the initial haemorrhage, from several days up until several weeks, subacute SDHs can vary from being slightly hyperdense to isodense to the brain parenchyma (Fig. 54.24A and B). The density decreases even further when imaging is performed in the chronic phase (from several weeks and longer) (seeFig. 54.24D and E). In addition to a reduction in density of the haematoma, subacute and chronic SDH can be differentiated from acute SDH by the formation of membranes of reactive granulation tissue, which form within the subdural space. These have a typical appearance on imaging, appearing as septations within an iso- to hypodense haematoma (seeFig. 54.24C–E). If there is acute haemorrhage into a chronic SDH, these membranes can limit the distribution of the acute blood products within the chronic haematoma (seeFig. 54.24D and E), giving a characteristic appearance.

Subdural hemorrhage

Subdural hematomas are common sequelae of head trauma and are thought to result from rupture of the bridging veins (veins that drain from the cerebral surface and pierce the dura to enter the adjacent venous sinus). Morphologically they follow the contour of the cerebral surface and can cross the cranial suture lines but not the midline at the falx cerebri and cerebelli. Depending on the size, there is a varying degree of mass effect on the adjacent brain; in the more severe cases, effacement of the adjacent ventricles, midline shift, and various herniation syndromes may occur.

As subdural hematomas age, their imaging appearance changes both on CT and MRI. On CT, acute subdural hematomas appear hyperdense. If the patient remains in a recumbent position, the cellular elements settle to the lower part of the hematoma, which will appear more hyperdense, whereas the “supernatant” is less so. With time, hemoglobin degradation occurs, and the density of the hematoma will decrease, eventually becoming hypodense. During this process there is a transitional stage when the density of the hematoma will be very similar or the same as that of the brain, rendering its detection more difficult. Just as with intraparenchymal hematomas, the density depends on the hematocrit, and in severely anemic patients, even acute subdural hematomas may appear iso- or hypodense, leading to erroneous dating.

On MRI, subdural hematomas exhibit a signal evolution similar to that seen with intraparenchymal hemorrhages, but the pace of evolution is different due to a slower decrease of the oxygen content within the hematoma. Acute subdural hematomas (Fig. 40.67) are initially isointense on T1 and hyperintense on T2, but as deoxyhemoglobin appears, the signal on T2-weighted images becomes hypointense. In the subacute phase, the signal is hyperintense on T1 and hypointense on T2, but in the late subacute stage, the signal will be hyperintense on both T1- and T2-weighted images because of extracellular methemoglobin (Fig. 40.68). It is important to remember that these stages are not separated sharply, and mixed patterns are often seen; this is due to the presence of oxy- and deoxyhemoglobin in the acute stage and intra- and extracellular methemoglobin in the chronic stage. Rebleeding into an existing subdural hematoma may also occur, resulting in the presence of clots of various ages.

Chronic subdural hematomas (Fig. 40.69) are hypointense relative to the brain but, having higher protein content, are mildly hyperintense relative to the CSF on T1-weighted images and hyperintense on T2-weighted images. Hemosiderin deposition is not as prominent as in parenchymal hemorrhages because macrophages tend to be cleared by the meningeal circulation. Chronic subdural hematomas may look similar to hyperacute ones on noncontrast images, but because of their vascular membrane, with gadolinium they exhibit enhancement along their periphery. On CT, chronic subdural hematomas appear as hypodense subdural collections. Mass effect is variable depending on the size of the hematoma and degree of cerebral atrophy. If repeated hemorrhage occurs into the subdural collection, the hyperdense fresh blood is seen within the chronic hypodense collection (Fig. 40.70).

Spinal Epidural and Subdural Hemorrhage

Spinal epidural hemorrhage (SEH) occurs more frequently than spinal subdural hemorrhage (SSH). SEH is more commonly observed in men and has a bimodal distribution, with peaks during childhood andthe fifth and sixth decades of life. Cervical lesions are more common in childhood, whereas thoracic and lumbar lesions predominate in adults. Hemorrhages can be spontaneous but often occur following exertion or trauma. SEH is a complication of both lumbar puncture and epidural anesthesia and is more likely in anticoagulated patients. Other causes include blood dyscrasia, thrombocytopenia, neoplasms, trauma, and vascular malformations. Pregnancy also appears to increase risk for SEH.

SSH is most common in women. It may occur at any age but tends to predominate in the sixth decade. Most occur in the thoracic and lumbar regions. Hemorrhagic diatheses, including treatment with anticoagulants, blood dyscrasias, and thrombocytopenia, are the precipitating factors most commonly associated with SSH. Other factors include trauma, lumbar puncture, vascular malformation, and spinal surgery.

The clinical presentations of SEH and SSH are indistinguishable. The initial symptom is severe back pain at the level of the bleed. Myelopathy or cauda equina syndrome, with motor and sensory findings corresponding to the level of the lesion, develops over hours to days. The diagnosis should be suspected in patients with disorders of coagulation who have undergone recent lumbar puncture and develop back pain or signs of spinal cord or root dysfunction. Patients with a rapidly decreasing platelet count or less than 40,000 platelets/μL are at particular risk of developing SEH or SSH as a complication of lumbar puncture and should receive a platelet transfusion prior to the procedure. Clotting studies and a platelet count are important in the initial evaluation. In SEH and SSH, the CSF may be normal or xanthochromic and may contain increased protein.

MRI can delineate the size and location of the hematoma. In addition, gadolinium-enhanced MRI and MRA may show an underlying vascular malformation. In patients unable to tolerate MRI or where it is unavailable in the acute phase of the illness, myelography with computed tomography (CT) scanning provides an alternative. Myelography can reveal a partial filling defect or complete blockage to the flow of contrast material at the level of the lesion. However, the myelographic appearances of SEH and SSH may be indistinguishable.

Both SEH and SSH are surgical emergencies. Operative treatment is directed toward relief of local pressure and repair of any underlying defect. Laminectomy with evacuation of the clot should be performed as soon as possible to minimize the risk of permanent neurological dysfunction. The prognosis for recovery is better when the preoperative deficits are not severe; timing of surgery appears less important.

Subdural Hematoma

Subdural hematoma is the result of bleeding over the surface of the brain, beneath the dura. Subdural hematoma may be acute or chronic. Acute subdural hematoma usually occurs after severe, high-impact injuries and is often associated with contusions of the adjacent areas of the brain. If the subdural hematoma is small (<5 mm in thickness) and the patient is stable clinically, a period of observation may be reasonable. If conservative management is elected, careful clinical observation and follow-up imaging are needed, because there is potential for the subdural hematoma to enlarge. Craniotomy to remove the hematoma is necessary if there is significant mass effect with raised ICP. At surgery, the hematoma is found to have a solid, jelly-like consistency.

Chronic subdural hematoma represents the gradual accumulation of liquefied hematoma in the subdural space, occurring over 2 or more weeks. Chronic subdural hematoma is usually present in elderly persons, who have more prominent subdural spaces as a result of cerebral atrophy. Chronic subdural hematoma, occurs most commonly after minor head injury. Sometimes the patient and family cannot even recall when the injury occurred. Over time, the hematoma gradually enlarges as a result of repeated episodes of minor bleeding and/or the drawing of fluid into the hematoma as a result of an osmotic effect. As in other forms of intracranial hemorrhage, risks of chronic subdural hematoma are elevated in individuals with coagulopathy caused by liver disease or anticoagulant medications. Surgery is often required and may involve either burr hole drainage or a craniotomy. At surgery, a chronic subdural hematoma is liquefied and is described as having a “crank case oil” appearance. The prognosis is guarded, and there is substantial risk of recurrent subdural hematoma that necessitates further surgery. Figure 103-2 shows bilateral chronic subdural hematomas.

Subdural hematoma may have both acute and chronic components if there is ongoing bleeding in the subdural space. The presence of a mixed acute and chronic subdural hematoma is readily identified on CT (Figure 103-3).

Subdural Hematoma

Subdural hematoma (SDH) develops due to rupture of the bridging veins on the surface of the brain. Although SDH is often precipitated by trauma (which may be quite minor, particularly in the elderly), it can also occur spontaneously. Strategies to reverse coagulopathy are similar to those outlined earlier in the section on spontaneous ICH. An SDH may progressively expand, causing brain compression and eventual herniation. Urgent neurosurgical intervention is frequently required for such patients, and there is a corresponding need for rapid correction of any hemostatic defects (see later discussion). Traumatic SDH is discussed further in the section on traumatic brain injury.

Background

Subdural hematomas are caused more frequently by venous rather than arterial damage and are often self-limiting because of the slow bleeding process. However, if the hematoma is large, mass pressure effect may take place, shifting cerebral structures and causing edema in the parenchyma of the brain, resulting in a poor clinical outcome. In addition, the possibility of herniation exists with large subdural hematomas or with hematomas that continue to enlarge after injury. Subdural hematomas arise deep to the dura but external to the arachnoid membrane, and the untreated hematoma may become subacute or chronic. Acute subdural hematoma is more common in older age groups because the veins are less resilient and more easily damaged. Patients taking anticoagulants and patients with alcoholism are also prone to acute subdural hematoma.139,224,275,281

Definition/Background

Acute subdural hematoma (SDH) is a form of traumatic brain injury in which blood collects between the dura and the arachnoid. It results from tears in the bridging veins and is among the most lethal of all head injuries. It has been reported to occur in 5%–25% of patients who have severe head injuries. It typically appears hyperdense on noncontrast CT studies. With time, subdural hematomas evolve and become isodense to the underlying cortex, suggestive of subacute SDHs.

In contrast to acute subdural hematoma, chronic subdural hematoma is not always related to head trauma. It is thought to result from a slow effusion of venous blood into the subdural space. This subsequently results in the formation of a membrane within the subdural space. Repeated episodes of slow bleeding results in multiple such membranes, and subsequently compartmentalized subdural collections. Unlike an acute subdural hematoma, a chronic subdural hematoma is not always hyperdense; its density depends on the acuteness of the bleed, as well as the number of such prior episodes that the patient has sustained. Chronic subdural hematomas are seen more often in patients with cerebral atrophy and coagulation disorders.