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Neuroradiology Case of the Week

Case 212

Brady Huang, MD and Per-Lennart Westesson, MD, PhD, DDS

Clinical Presentation: An 84-year-old male who presents with confusion, urinary incontinence, and shuffling gait. A head CT examination was requested to evaluate for possible hydrocephalus. No history of trauma is given.

Radiological Findings: Two axial images from a non-contrast enhanced CT (NECT) at the level of the basal ganglia (Fig. 1) and the centrum semiovale (Fig. 2) demonstrate extra-axial fluid collections seen along the bilateral cerebral convexities, left greater than right, with layer densities, representing bilateral subdural hematomas. There are focal areas of hyperdensity within the left subdural hematoma along the frontal lobe anteriorly as well as posteriorly (arrows), consistent with acute subdural hemorrhage.  There is mass effect on the left cerebral hemisphere and left lateral ventricle, with approximately 8 mm of midline shift to the right.

Diagnosis: Acute and subacute subdural hematoma

Differential Diagnosis: Epidural Hematoma, Subdural Hygroma / Effusion / Empyema, Pachymeningiopathies.

Discussion: Subdural hematomas (SDHs) are due to stretching and tearing of the bridging cortical veins which cross the subdural space to drain into the adjacent dural venous sinuses. The subdural space is a potential space between the inner layer of the dura mater and arachnoid mater. The rupture is due to a sudden change in head velocity. SDHs can cross sutures, but not the dural attachments, where as the opposite is true in epidural hematoma. Therefore the location is important in differentiating the two. In addition, the arachnoid mater may be torn, which can create a mixture of blood and CSF in the subdural space. SDHs are categorized into acute, subacute, and chronic forms.
     Acute SDH is defined as an acute hemorrhagic collection in the subdural space, ranging in time from 6 hours to 3 days. Key imaging findings for acute SDH on NECT is a crescent-shaped, hyperdense, extra-axial collection spreading diffusely over one hemisphere and can extend along the falx and tentorium. As in this case, it compresses and displaces the underlying brain, and cortical sulci do not reach the inner calvarial table. Hyperacute SDH is mostly hypodense on NECT, as fresh hemorrhage is unclotted. 40% acute SDHs are mixed hyper/hypodense and demonstrate the "swirl" sign of active bleeding as in this case. Generally, the density decreases by approximately 1.5 Hounsfield units per day as the SDH evolves. A contrast-enhanced CT (CECT) will demonstrate inward displacement of cortical vessels. The MRI findings will show the same anatomical relationship as in the CT findings, however the signal characteristics on T1/T2 will depend on the acuity of the hemorrhage (e.g. hyperacute oxyhemoglobin vs. acute deoxyhemoglobin).
     As SDHs undergo clot lysis and organization, they being to form neomembranes composed of granulation tissue and are rich in capillaries. Subacute SDH is defined by its age, ranging from 3 days to 3 weeks. NECT findings demonstrate isodense to hypodense (see Neurocase187) extra-axial fluid collection, that may be the same density as the underlying cortex. CECT demonstrates enhancing dura and membranes, in addition to displaced cortical vessels. MR imaging will demonstrate T1 hyperintensity due to methemoglobin and variable T2 intensity (usually hyperintense). Post contrast T1 images may demonstrate enhancing membranes. This case demonstrates more of an acute process with variable densities of blood, however there are probably components of subacute hemorrhage as there is evidence of rebleeding.
     Chronic SDH is defined as a collection of blood products in the subdural space for more than 3 weeks. Further organization of a subacute SDH leads to a crescent-shaped, multiseptated, extra-axial collection with enhancing membranes. NECT demonstrates that the collection is hypodense, compared to acute and subacute SDH. If there is increased density or size of the collection, this suggests rebleeding, from friable neocapillaries. Resorption of most SDHs occurs after three months as the outer membrane stabilizes. If there is no rebleeding, most SDHs will follow CSF signal on MR imaging. Also, 1% to 2% of old SDHs calcify or ossify, having been present for months to years and can be seen on plain radiographs.
     Clinically, SDHs are seen in 10 to 20% of all head trauma. Acute traumatic subdural hematoma has an estimated morality rate ranging from 50% to 85%. They are common in the elderly as brain atrophy is a contributing factor, however a definite history of trauma may not be present as in this case. SDHs can also be seen in children, and bilateral SDHs or mixed-age hemorrhages should raise the suspicion for nonaccidental trauma. Most patients with acute SDHs present with a Low Glasgow Coma Score, although some patients may be asymptomatic with an initial "lucid" interval. It is also common to see other lesions, such as traumatic subarachnoid hemorrhage in greater than 70% of cases. 10% to 30% of chronic SDHs rebleed, as cortical veins are stretched by the SDH itself in addition to the formation of friable vascular neomembranes. Treatment is surgical drainage if the SDH is growing or symptomatic, although they can spontaneously resolve.

References:

1. Osborn AG, Blaser S, Salzman K. Diagnostic Imaging: Brain. W.B. Saunders Company 2004; i:2:10-21.
2. Osborn AG. Diagnostic Neuroradiology. Mosby 1994;205-211