Subdural hemorrhage (SDH) (also commonly called a subdural hematoma) is a collection of blood accumulating in the subdural space, the potential space between the dura and arachnoid mater of the meninges around the brain. SDH can happen in any age group, is mainly due to head trauma and CT scans are usually sufficient to make the diagnosis. Prognosis varies widely depending on the size and chronicity of the hemorrhage.
Subdural hematomas are seen in all age-groups although etiology will vary 4,5:
- infants: non-accidental injury
- young adults: motor vehicle accidents
- elderly: falls (although a definite history of trauma may be lacking)
They are present in ~15% (range 10-20%) of all head trauma cases and occur in up to 30% of fatal injuries.
Acute subdural hemorrhages usually present in the setting of head trauma. This is especially the case in young patients, where they commonly co-exist with cerebral contusions.
Most patients (65-80%) present with a severely depressed conscious state, and pupillary abnormalities are seen in ~40% (range 30-50%) of cases 5.
Occasionally spontaneous acute subdural hematomas are seen with an underlying bleeding disorder (e.g. anticoagulation medication, thrombocytopenia) or structural abnormality (e.g. dural arteriovenous fistula).
Clinical presentation of subacute/chronic subdural in the elderly is often vague and is one of the classic causes of a pseudodementia. A history of head trauma is often absent or very minor.
See the article: EDH vs SDH
Subdural hemorrhages are believed to be due to stretching and tearing of bridging cortical veins as they cross the subdural space to drain into an adjacent dural sinus. These veins rupture due to shearing forces when there is a sudden change in the velocity of the head. The arachnoid may also be torn, creating a mixture of blood and CSF in the subdural space.
10 to 30% of chronic subdural hematomas show evidence of repeated hemorrhage. Rebleeding usually occurs from the rupture of stretched cortical veins as they cross the enlarged fluid-filled subdural space or from the vascularized neomembrane on the outer (calvarial) side of the fluid collection.
Subdural hematomas are interposed between the dura and arachnoid. Typically crescent-shaped, they are usually more extensive than extradural hematomas. In contrast to extradural hemorrhage, SDH is not limited by sutures but are limited by dural reflections, such as the falx cerebri, tentorium, and falx cerebelli.
Some controversy, albeit of academic interest only, exists as to the exact location of a subdural hematoma. Classical teaching is that it is located in the potential space between the arachnoid layer and inner layer of the dura; however, no such space really exists. Rather the arachnoid-dura junction is composed of "avascular tissue with flake-like [...] cells stacked in several layers with narrow intercellular clefts" 10. Bleeding occurs within this multicellular layer, with these cells located on both sides of the hematoma 9,10. This possibly accounts for why some acute hematomas appear to have multiple compartments, usually ascribed to intermittent bleeding ref required.
Overall 85% of subdural hematomas are unilateral in adults. However, 75-85% are bilateral in infants. Common sites for subdural hematomas are frontoparietal convexities and the middle cranial fossa. Isolated interhemispheric/parafalcine subdural hematomas are seen more frequently in children and are common in cases of non-accidental trauma.
In the vast majority of cases, CT scans are sufficient to make the diagnosis and manage these patients. Contrast is sometimes helpful if there is the concern of a subdural empyema, of the presence of a small isodense subdural, or to try and distinguish enlargement of the extra-axial CSF space from a chronic subdural hematoma.
The appearance of SDHs on CT varies with clot age and organization.
In most instances, patients are not imaged in the hyperacute phase (first hour or so), but on occasion when this is performed they appear relatively isodense to the adjacent cortex, with a swirled appearance due to a mixture of the clot, serum and ongoing unclotted blood 4. There is often a degree of underlying cerebral swelling (especially in young patients where head trauma is often more severe) which accentuates the mass-effect created by the collection 4.
The classic appearance of an acute subdural hematoma is a crescent-shaped homogeneously hyperdense extra-axial collection that spreads diffusely over the affected hemisphere. As the clot starts to retract the density increases typically to >50-60 HU and is thus hyperdense relative to the cortex 4.
Up to 40% of SDHs have mixed hyper- or hypodense areas that reflect unclotted blood, serum extruded during clot retraction or CSF within the subdural hematoma due to an arachnoid laceration.
Rarely, acute SDHs may be nearly isodense with the adjacent cerebral cortex. This occurs with anticoagulation, coagulopathies or severe anemia when the hemoglobin concentration drops to 8 to 10 g/dL. Patients with a deficient coagulation can also demonstrate a hematocrit fluid-fluid level as the blood does not form a clot and red cells have time to drift dependently 4.
In patients with underlying low hemoglobin and platelets conditions such as sickle cell anemia, acute subdural hemorrhage may be hypodense even in the acute phase 11.
As the clot ages and protein degradation occurs, the density starts to drop. At some point between 3 and 21 days (typically 10-14 days), the density will drop to ~ 35-40 HU and become isodense to the adjacent cortex, making identification potentially tricky, especially if subdural collections are bilateral 4. Contrast-enhanced CT is often useful in this instance if MRI is unavailable. The key to identification is visualizing a number of indirect signs, including:
- CSF-filled sulci do not reach the skull but rather fade out into the subdural
- mass-effect including sulcal effacement (distortion) and midline shift
- apparent thickening of the cortex
By definition, it is at least 3 weeks old.
The subdural collection becomes hypodense and can reach ~0 HU and be isodense to CSF, and mimic a subdural hygroma.
A crescentic shape may change to a biconvex one.
Rarely, the periphery of the SDH may calcify, see calcified chronic subdural hematoma for an in-depth discussion regarding the CT appearance of this entity.
Acute on chronic
Acute on chronic subdural hematomas refers to a second episode of acute hemorrhage into a pre-existing chronic subdural hematoma. It typically appears as a hypodense collection with a hematocrit level (located posteriorly). A similar appearance can be seen in patients with clotting disorders or on anticoagulants 4.
The appearance of a hematoma varies with the biochemical state of hemoglobin which varies with the age of the hematoma. The most sensitive standard sequence is FLAIR.
- T1: isointense to grey matter
- T2: iso- to hyperintense
- FLAIR: hyperintense to CSF
- T1: iso- to hypointense to grey matter
- T2: hypointense to grey matter
- FLAIR: hyperintense to CSF
It may appear biconvex-shaped on the coronal plane rather than crescent-shaped which is a typical appearance on the axial plane
- T1: typically hyperintense due to the presence of methemoglobin
- T2: variable appearance usually hyperintense
- FLAIR: hyperintense
- T1: if the hematoma is stable it appears isointense to CSF, it can appear hyperintense to CSF if there is a rebleed or infection.
- T2: if the hematoma is stable it appears isointense to CSF if there is rebleed the hematoma appears hypointense
- FLAIR: hyperintense to CSF
Rarely, the periphery of the SDH may calcify, see calcified chronic subdural hematoma for an in-depth discussion regarding the MRI signal characteristics of this entity.
Treatment and prognosis
Treatment depends primarily on the amount of mass-effect and neurological impairment caused by the collection, and thus correlates with the size of the subdural hemorrhage.
Small collections – so-called 'smear subdurals' – especially those which are chronic and are not causing symptoms can be observed with serial CT scans.
Symptomatic collections need to be surgically evacuated. In the acute setting, this should be performed rapidly (within 4 hours) 3 and usually requires a craniotomy as the clot is not easily evacuated via burr holes.
Symptomatic subacute/chronic subdural hematomas are often treated via one or more burr holes as the blood clot has liquefied and can be washed out more easily. The compressed brain can take some time to re-expand, and subdural collections may re-accumulate.
Although subdural hematomas are often thought of as relatively benign entities it should be noted that the mortality in acute subdural hematomas requiring surgery is very high (50-90%), particularly in patients who are anticoagulated, and that only 20% fully recover 2,3,5.
General imaging differential considerations include 1-4:
- prominent subarachnoid space due to cerebral atrophy or benign enlargement of the subarachnoid space in infancy
- can look similar
- lack of mass effect
- vessels course through space rather than displaced towards the brain
- CT contrast, therefore, helps (in adults) by delineating the vessels (cortical vein sign) as well as demonstrating an enhancing 'capsule' of a subdural hematoma/empyema
- ultrasound and MRI are useful in infancy
- similar appearance on non-contrast scans
- different clinical context (patients usually unwell and febrile)
- prominent marginal enhancement
- associated cerebral abscess/infarction
- sometimes difficult to differentiate if small
- biconvex in shape (lentiform) rather than crescentic
- limited by sutures
- may displace dural venous sinuses
- usually associated with fractures
- on CT can be indistinguishable from a chronic subdural hematoma
- exactly CSF density
- no evidence of prior hemorrhage
- motion artefact
- cortical veins
- 1. Osborn AG. Diagnostic neuroradiology. Mosby Inc. (1994) ISBN:0801674867. Read it at Google Books - Find it at Amazon
- 2. Gunderman RB. Essential radiology, clinical presentation, pathophysiology, imaging. Thieme Medical Pub. (2006) ISBN:1588900827. Read it at Google Books - Find it at Amazon
- 3. Greenberg MS. Handbook of Neurosurgery. Thieme Medical Pub. (2010) ISBN:1604063262. Read it at Google Books - Find it at Amazon
- 4. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology. Lippincott Williams & Wilkins. (2007) ISBN:0781761352. Read it at Google Books - Find it at Amazon
- 5. Jallo J, Loftus CM. Neurotrauma and Critical Care of the Brain. Thieme Medical Pub. (2009) ISBN:1604060328. Read it at Google Books - Find it at Amazon
- 6. Fobben ES, Grossman RI, Atlas SW et-al. MR characteristics of subdural hematomas and hygromas at 1.5 T. AJR Am J Roentgenol. 1989;153 (3): 589-95. AJR Am J Roentgenol (abstract) - Pubmed citation
- 7. Brant WE, Helms CA. Fundamentals of Diagnostic Radiology. Lippincott Williams & Wilkins. (2007) ISBN:0781761352. Read it at Google Books - Find it at Amazon
- 8. Osborn AG. Diagnostic neuroradiology. Mosby. ISBN:0801674867. Read it at Google Books - Find it at Amazon
- 9. Chung CK, Kim YM, Chi JG. Intralaminar dural haematoma developing in the contralateral convexity after temporal lobectomy. J. Neurol. Neurosurg. Psychiatr. 1999;66 (2): 248-9. doi:10.1136/jnnp.66.2.248 - Free text at pubmed - Pubmed citation
- 10. Orlin JR, Osen KK, Hovig T. Subdural compartment in pig: a morphologic study with blood and horseradish peroxidase infused subdurally. Anat. Rec. 1991;230 (1): 22-37. doi:10.1002/ar.1092300104 - Pubmed citation
- 11. Thust SC, Burke C, Siddiqui A. Neuroimaging findings in sickle cell disease. The British journal of radiology. 87 (1040): 20130699. doi:10.1259/bjr.20130699 - Pubmed
Related Radiopaedia articles
Stroke and intracranial haemorrhage
stroke and intracranial hemorrhage
- general discussions
- scoring and classification systems
- Alberta stroke program early CT score (ASPECTS)
- Canadian Neurological Scale
- NIH Stroke Scale
- Mathew Stroke Scale
- modified Rankin scale
- Orgogozo Stroke Scale
- Scandinavian Stroke Scale
- thrombolysis in cerebral infarction (TICI)
- TOAST classification
- by region
- hemispheric infarcts
- frontal lobe infarct
- parietal lobe infarct
- temporal lobe infarct
- occipital lobe infarct
- internal capsule infarct
- ataxic hemiparesis syndrome: MCA perforators or basilar artery perforators
- lacunar infarct
- thalamic infarct
- striatocapsular infarct
- cerebellar infarct
- midbrain infarct
- pontine infarct
- Brissaud-Sicard syndrome
- facial colliculus syndrome
- Gasperini syndrome: basilar artery or AICA
- inferior medial pontine syndrome (Foville syndrome): basilar artery
- lateral pontine syndrome (Marie-Foix syndrome): basilar artery or AICA
- locked-in syndrome: basilar artery
- Millard-Gubler syndrome: basilar artery
- Raymond syndrome: basilar artery
- medullary infarct
- acute spinal cord ischemia syndrome
- hemispheric infarcts
- by vascular territory
- anterior cerebral artery infarct
- anterior choroidal artery infarct
- anterior inferior cerebellar artery infarct
- basilar artery infarct
- middle cerebral artery infarct
- posterior cerebral artery infarct
- posterior inferior cerebellar artery infarct
- superior cerebellar artery infarct
- treatment options
- by region or type
- basal ganglia hemorrhage
- cerebellar hemorrhage
- cerebral contusions
- cerebral microhemorrhage
- hemorrhagic venous infarct
- hemorrhagic transformation of an ischemic infarct
- hypertensive intracranial hemorrhage
- intraventricular hemorrhage (IVH)
- lobar hemorrhage
- pontine hemorrhage
- jet hematoma
- extra-axial hemorrhage
- extradural versus subdural hemorrhage
- extradural hemorrhage (EDH)
- intralaminar dural hemorrhage
- subdural hemorrhage (SDH)
subarachnoid hemorrhage (SAH)
- vasospasm following SAH
- grading systems
- intra-axial hemorrhage
- ischemic stroke