= accumulation of blood in potential space between pia-arachnoid membrane (leptomeninges) + dura mater (= “epiarachnoid space”)
Incidence: in 5% of head trauma patients; in 15% of closed head injuries; in 65% of head injuries with prolonged interruption of consciousness
Age: accident-prone middle age; also in infants + elderly (large subarachnoid space with freedom to move in brain atrophy)
Cause: severe trauma, hemorrhagic diathesis
Source of blood:
- pial cortical arteries + veins: direct trauma = penetrating injury
- large contusions: direct / indirect trauma = “pulped brain”; occasionally in blood clotting disorder / during anticoagulation therapy
- torn bridging cortical veins (indirect force) ← sudden de-/acceleration; also with forceful coughing / sneezing / vomiting in elderly
Elderly predisposed: longer bridging veins in brain atrophy
- NO consistent relationship to skull fractures!
Pathogenesis:
differential movement of brain and adherent cortical veins with respect to skull + attached dural sinuses → tear of “bridging veins” (= subdural veins which connect cerebral cortex to dural sinuses + travel through subarachnoid and subdural space)
Location: hematoma freely extending across suture lines, limited only by interhemispheric fissure and tentorium
- nonspecific headaches, nonlocalizing signs; low-voltage EEG
- lethargy, confusion; usually negative lumbar puncture
CT:
- hyperdense 65–90 HU (<1 week) / isodense 20–40 HU (1–2 weeks) / hypodense 0–22 HU (3–4 weeks)
False-negative CT scan:- high-convexity location, beam-hardening artifact, volume averaging with high density of calvarium obscuring flat “en plaque” hematoma, too narrow window setting, isodense hematoma due to delay in imaging 10–20 days post injury / low hemoglobin content of blood / lack of clotting, dilution by CSF from associated arachnoid tear
- 38% of small subdural hematomas are missed!
- Aids in detection of acute subdural hematoma:
- perceived “thickening” of ipsilateral portion of skull (hematoma of similar pixel brightness as bone)
- “subdural window” setting = window level of 40 HU + window width of 400 HU
- effacement of adjacent sulci
- sulci not traceable to brain surface
- ipsilateral ventricular compression / distortion
- displacement of gray-white matter interface away from ipsilateral inner table
- midline shift (often greater than width of subdural hematoma due to underlying brain contusion)
- contrast enhancement of cortex but not of subdural hematoma
- Aids in detection of bilateral subdural hematomas:
- “parentheses” ventricles
- ventricles too small for patient's age
- high-convexity location, beam-hardening artifact, volume averaging with high density of calvarium obscuring flat “en plaque” hematoma, too narrow window setting, isodense hematoma due to delay in imaging 10–20 days post injury / low hemoglobin content of blood / lack of clotting, dilution by CSF from associated arachnoid tear
US (neonate):
- linear / elliptical space between cranial vault + brain
- flattened gyri + prominent sulci
- ± distortion of ventricles, extension into interhemispheric space
Limitations:
- convexity hematoma may be obscured by pie-shaped display + loss of near-field resolution
- Use contralateral transtemporal approach!
- small loculations may be missed
Prognosis: poor (due to association with other lesions)
DDx:
- Arachnoid cyst (extension into sylvian fissure)
- Subarachnoid hemorrhage (extension into sulci)
Cause: usually follows severe trauma, manifests within hours after injury
Time frame:<7 days old
Associated with: underlying brain injury (50%) with worse long-term prognosis than epidural hematoma, skull fracture (1%)
Location:
- over cerebral convexity, frequent extension into interhemispheric fissure, along tentorial margins, beneath temporal + occipital lobes; NO crossing of midline
- bilateral in 15–25% of adults (common in elderly) and in 80–85% of infants
- extraaxial peripheral crescentic / convex fluid collection between skull and cerebral hemisphere usually with:
- concave inner margin ← hematoma minimally pressing into brain substance
- convex outer margin ← following normal contour of cranial vault
- hyperdense collection of 65–100 HU
- Hematoma hypodense if hematocrit <29%!
- “swirl” sign = mixture of clotted and unclotted blood
- occasionally with blood-fluid level
- after surgical evacuation → underlying parenchymal injury becomes more obvious
- after healing → ventricular + sulcal enlargement
Cx: Arteriovenous fistula ← meningeal artery + vein caught in fracture line
Prognosis: may progress to subacute + chronic stage / may disappear spontaneously
Rx: evacuation, but with poor response ← high uncontrollable intracranial pressure from associated injuries
Mortality: 35–50% (higher number due to associated brain injury, mass effect, old age, bilateral lesions, rapid rate of hematoma accumulation, surgical evacuation >4 hours)
Interhemispheric Subdural Hematoma
Most common acute finding in child abuse ← whiplash forces on large head + weak neck muscles
- predominance for posterior portion of interhemispheric fissure
- crescentic shape with flat medial border
- unilateral increased attenuation with extension along course of tentorium
- anterior extension to level of genu of corpus callosum
Subdural Hemorrhage in Newborn
Cause: mechanical trauma during delivery (excessive vertical molding of head)
- Posterior fossa hemorrhage
- tentorial laceration with rupture of vein of Galen / straight sinus / transverse sinus
- occipital osteodiastasis = separation of squamous portion from exoccipital portion of occipital bone
- high-density “thickening” of affected tentorial leaf extending down posterior to cerebellar hemisphere (better seen on coronal view)
- mildly echogenic subtentorial collection
Cx: death from compression of brainstem → acute hydrocephalus - Supratentorial hemorrhage
- laceration of falx near junction with tentorium ← rupture of inferior sagittal sinus (less common than tentorial laceration)
- hematoma over corpus callosum in inferior aspect of interhemispheric fissure
- convexity hematoma ← rupture of superficial cortical veins
- usually unilateral subdural convexity hematoma accompanied by subarachnoid blood
- underlying cerebral contusion
- sonographic visualization of convexities difficult
- laceration of falx near junction with tentorium ← rupture of inferior sagittal sinus (less common than tentorial laceration)
Time frame: 7–22 days
CT:
- isodense hematoma of 25–45 HU (during 1st–3rd week), may be recognizable by mass effect:
- effacement of cortical sulci
- deviation of lateral ventricle
- midline shift
- white matter buckling
- displacement of gray-white matter junction
- contrast enhancement of inner membrane
Aid in Dx: contrast enhancement defines cortical-subdural interface
MR (modality of choice in subacute stage):
- high sensitivity for Met-Hb on T1WI (superior to CT during isodense phase concerning small subdural hematomas + for hematomas oriented in the CT scan plane, eg, tentorial subdural hematoma):
- hyperintense on T1WI
Time frame:>22 days old
Cause: mild unremembered head trauma ?
Pathogenesis: vessel fragility accounts for repeated episodes of rebleeding (in 10–30%) following minor injuries that tear a fragile capillary bed within neomembrane surrounding subdural hematoma
Predisposing factors:
- alcoholism, increased age, epilepsy, coagulopathy, prior placement of ventricular shunt
- >75% occur in patients >50 years of age!
Histo: hematoma enclosed by thick + vascular membrane, which forms after 3–6 weeks
- history of antecedent trauma often absent (25–48%)
- ill-defined neurologic signs + symptoms: cognitive deficit, behavioral abnormality, nonspecific headache
- progressive neurologic deficit; low-voltage EEG, normal CSF
- often biconvex lenticular = medially concave configuration, esp. after compartmentalization ← formation of fibrous septa
- low-density lesion of 0–25 HU (= intermediate attenuation between CSF + brain):
- different attenuations within different compartments
- sometimes as low as CSF
- high-density components of collection (after common rebleeding)
- fluid-sediment levels (= sedimented fresh blood with proteinaceous fluid layered above)
- displacement / absence of sulci, displacement of ventricles and parenchyma
- No midline shift if bilateral (25%)
- absent “cortical vein” sign = cortical veins seen along periphery of fluid collection without passing through it (1–4 weeks after injury)
DDx: Acute epidural hematoma (similar biconvex shape)