Workup
Laboratory Studies
- Initial blood tests
- To determine if defective coagulation was involved in the formation of the subdural hematoma (SDH) and to guide correction of any coagulation abnormalities, a prothrombin time (PT), activated partial thromboplastin time (aPTT), and a platelet count are typically performed. A bleeding time assessment may reveal platelet dysfunction.
- Routine trauma laboratory studies that aid in the initial patient assessment may include hemoglobin or hematocrit, electrolytes, and a drug and alcohol screening. The drug and alcohol screenings may be important for correlating the neurological examination with the imaging studies.
Imaging Studies
- CT scan of the head (without contrast)
- An emergent head CT scan needs to be performed when an acute subdural hematoma (SDH) is suspected and should be obtained immediately after the patient is stabilized using standard advanced trauma life support (ATLS) guidelines.
- An acute SDH appears on the noncontrast head CT scan as a crescent-shaped hyperdense area between the inner table of the skull and the surface of the cerebral hemisphere (see Image 7). Acute SDHs are usually unilateral.
- A small acute SDH may be difficult to appreciate because of the appearance of the overlying skull. Use of the bone window setting may aid in discrimination.
- An SDH may also be located along the falx (ie, interhemispheric), along the tentorium, or in the posterior fossa. Interhemispheric SDHs are among the findings identified in some abused children. Rarely, a SDH appears –lens shaped (ie, more like an epidural hematoma).
- All or part of an acute SDH may appear hypodense or isodense to brain if the patient’s hematocrit is low, if the clot is hyperacute (eg, <1 hour old), if the subdural space contains active bleeding, if coagulopathy is present, or if the CSF if creating a dilutional effect. Detection of an isodense SDH may require a high index of suspicion; subtle changes in the appearance or position of the cortical sulci may be found. Contrast-enhanced CT or MRI may help to better define the lesion. Interestingly, isodense SDHs may be either hypointense or hyperintense on T2-weighted MRI; this may be a clue to the underlying pathophysiology.14
- The characteristic evolution of an SDH appearance on CT scan is as follows: In the first week, the SDH is hyperdense to brain tissue. In the second and third weeks, the SDH appears isodense to brain tissue (see Images 3-4). After the third week, the SDH is hypodense to brain tissue.
- Often, a chronic SDH appears as a heterogeneously dense lesion indicative of recurrent bleeding with a fluid level between the acute (hyperdense) and chronic (hypodense) components of the hematoma (see Image 2).
- On a contrast-enhanced CT scan, the chronic SDH membrane enhances to varying degrees, depending on numerous factors. Sometimes, a contrast-enhanced scan shows evidence of an underlying cause, such as a tumor or vascular lesion (eg, in patients with acute but nontraumatic SDH).
- Typical signs of mass effect, such as midline shift and ventricular compression, may be observed.
- Magnetic resonance imaging
- MRI is less useful than CT in diagnosing an acute SDH because of the increased time needed to obtain the study and the inability to use metallic objects that are needed to resuscitate patients with trauma (eg, most ventilators) in the scanning environment.
- MRI can be a useful study to evaluate associated parenchymal brain injury and predict prognosis, but only after stabilizing and treating any life-threatening lesions. MRI is more sensitive for detecting nonhemorrhagic brain lesions, contusions, and diffuse axonal injury.15
- An MRI is helpful in imaging chronic SDH when CT scans are difficult to interpret (eg, when suspecting an isodense hematoma). MRI may be particularly helpful in diagnosing bilateral chronic SDH because a midline shift may not be apparent on CT scan.
Histologic Findings
Acute subdural hematomas (SDHs) usually contain both liquid and clotted blood. Intact erythrocytes are usually found within the clot. Associated skull fractures and underlying focal traumatic parenchymal damage are often present.
Fibroblastic membranes form on the dural side and arachnoid side of the chronic SDH, with the dural neomembrane being more vascular. The neomembrane consists of many capillaries, intact and lysed erythrocytes, hemosiderin-laden macrophages, and granulation tissue.
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References
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Further Reading
Clinical guidelines
Bullock MR, Chesnut R, Ghajar J, Gordon D, Hartl R, Newell DW, Servadei F, Walters BC, Wilberger JE, Surgical Management of Traumatic Brain Injury Author Group. Surgical management of acute subdural hematomas. Neurosurgery 2006 Mar;58(3 Suppl):S2-16-S2-24. 13
Davis PC, Seidenwurm DJ, Brunberg JA, De La Paz RL, Dormont PD, Hackney DB, Jordan JE, Karis JP, Mukherji SK, Turski PA, Wippold FJ, Zimmermam RD, McDermot MW, Sloan MA, Expert Panel on Neurologic Imaging. Head trauma. ACR Appropriateness Criteria® head trauma [online publication]. Reston (VA): American College of Radiology (ACR); 2006. 12 p.
Keywords
subdural hematoma, SDH, subdural hematomas, subdural hemorrhage, subdural hemorrhages, acute subdural hematoma, ASDH, subacute subdural hematoma, chronic subdural hematoma, CSDH, intracranial hemorrhage, brain bleed, brain bleeding, contralateral hematoma, subdural hygroma, dementia
Workup: Subdural Hematoma