BrainTF14-Subdural Hematoma

Clinical Profile:

Alleged H/O head injury followed by left sided hemiparesis.

Findings:

There is evidence of a crescent shaped lesion overlying the right cerebral hemisphere with resultant compression on the underlying brain parenchyma. There is effacement of the right lateral ventricle with a shift of the midline to the contralateral side. It is hyperintense on all the pulse sequences. Multiple hypointensities within the lesion may represent membranes.

Discussion: 

Subdural hematomas (SDH) are located between the dura (attached to the inner table of the skull) and arachnoid covering the brain. There is stretching and tearing of the cortical bridging veins at the time of trauma leading to bleeding. The blood mixes with the CSF in the subdural space. Arterial SDH are less common.

• Acute - < 1-4 days

• Subacute - 2-20 days

• Chronic - > 10-20 days.

Patients may present with headache, mental alterations and sensory or motor deficits.  

Etiology:

• Trauma

• Dural vascular malformation

• Superficial intraparenchymal hemorrhage from any cause

• Dural-based metastases - renal cell or breast carcinoma or melanoma

• Meningioma

• Bleeding diathesis due to disease

• Iatrogenic coagulopathy

• Peripheral aneurysm - usually mycotic or traumatic

On MRI:

Subdural hematomas (SDH) are crescent like collections of blood between the inner table of the skull and brain. They are more extensive than  epidural hematomas (EDH) and cross sutures but not the dural attachments. They may spread diffusely over the cerebral hemispheres or may be seen in interhemispheric, supratentorial or infratentorial locations. 

Evolving SDH on MR usually exhibit similar signal characteristics to intraparenchymal hematomas in the acute and subacute phases. Hyperacute hematomas (oxyhemoglobin) are near isointense to brain parenchyma on the T1W and T2W images, whereas they are dark on the T2W and T2*W images in the acute phase (deoxyhemoglobin). In the early subacute stage (methemoglobin without cell lysis) they are hyperintense on the T1W images and dark on the T2W and T2*W images. In the late subacute stage (methemoglobin with cell lysis) they are hyperintense on the T1W images and also on the T2W and T2*W images. Subdural hematomas are easily identified on MRI due to the high contrast between the calvarium and blood. The problem of missing an isodense SDH like on CT does not arise, as these are seen to be hyperintense (subacute) on the MR.

Chronic SDH may be isodense to CSF on the CT but are usually hyperintense on the MR. On further evolution they are slightly hyperintense to CSF on the MR (due to low concentration of methemoglobin or high concentration of non paramagnetic protein). They may be separated from subdural hygromas (CSF collection) on the FLAIR or Proton Density images, as CSF signal is suppressed on these pulse sequences. Hypointense areas on the T2W and T2*W images due to hemosiderin are not seen commonly. Due to an absence of the blood-brain barrier in the dura it gets well absorbed into the blood stream. Rebleeding should be considered if irregular hypointense membranes leading to loculations of blood in different stages of evolution are seen or if debris-fluid levels are noted. Multiples sites of bleeds in different stages of evolution may be seen with child abuse.   

References:

1. Intracranial Hemorrhage. In: Atlas SW: Magnetic Resonance Imaging of the Brain and Spine, Lippincot-Raven, pp:818-830, Volume 1, Third Edition.