Subdural hematoma (SDH) is a blood accumulation between the skull and brain caused by high-speed impact, with varying incidence and gender ratios. Diagnosis typically involves CT or MRI scans to determine the type and stage of the hematoma, while treatment options include conservative management and surgical interventions. Complications may include increased intracranial pressure and recurrence, with prognosis varying based on the type of SDH and initial clinical state.

2. Dr:Faizyab Ahmed

3. Acute SDH
 Subdural hematoma is a collection of blood
that accumulates inside the skull but outside
the brain.
 It collects under the dura so the blood is then
described as being sub (under)dural.
 Incidence 5-22 %
 Male : female ratio 3:1

4. SDH
ACUTE
48-72 hrs
CHRONIC
3 weeks to
months
SUB ACUTE
3-20 days
HYPERACUTE
Within 24 hrs

5. Pathogenesis
 Caused by high speed impact that accelerates the
brain relative to fix dural structures ,tearing bridging
veins
 Injury to surface of brain with bleeding from cortical
vessels
 SDH is often associated with diffuse brain injury

7. Clinical Findings & Diagnosis
 Altered level of consciousness
 Pupillary inequality(ipsilateral dialated pupil)
 Contralateral Motor deficits
 Kernohan’s notch
 Ipsilateral(false localizing) motor deficits may be
present that result from cerebral parenchymal injury
on the side opposite to SDH or from compression of
contralateral cerebral peduncle against the edge of
tentorium

9. Specialized diagnosed evaluation
 X ray skull
 CT Scan
 First diagnostic test
 The classic appearance of an acute subdural haematoma is a crescent shaped
homogeneously hyperdense extra axial collection
 Isodense in case of low HB
 MRI
 More sensitive & specifiec than CT scan

10. MRI
 Can distinguish between acute ,chronic & subacute subdural hematoma
 MRI
 The appearance of a haematoma varies with the biochemical state of
haemoglobin which varies with the age of the haematoma. The most
sensitive standard sequence is FLAIR.
 Hyperacute
 T1: isointense to grey matter
 T2: iso to hyperintense
 FLAIR: hyperintense to CSF
 Acute
 T1: iso- to hypointense to grey matter
 T2: hypointense to grey matter
 FLAIR: hyperintense to CSF


11.  Subacute
 T1: typically hyperintense
 T2: variable appearance usually hyperintense
 FLAIR: hyperintense

13. Treatment
 Conservative management
 Surgical procedure
 Decompressive craniectomy
 Craniotomy plus evacuation of hematoma

18. Complications
 Increase in ICP due to brain swelling due parenchymal
damage
 ICP >45 mm Hg indicates poor outcome
 Recurrent or residual hematoma
 Traumatic fits
 Focal deficits

19. Outcome
 Prognosis is dependent intial & postresuscitative GCS
 Overall mortality rate is >50 %

20. Chronic subdural hematoma
 Incidence is 1-2 per 1 lac people
 Risk factors include
Patients on heparin,warferrin,clopidogrel,aspirin
Drug addicts
Substance abuse eg alcohol

21. Pathogenesis

22.  Asymptomatic small subdural hematoma is covered by
another membrane beneath the dura and by 3 weeks
an inner membrane forms between hematoma &
arachnoid surface over brain.
 Chronic SDH is enlarged with time because capsule
acts as osmotic membrane & csf diffuse into
hematoma
 They may ultimately either resolve or enlarge

23. Clinical features


24. Diagnostic evaluation
 CT scan is initial investigation of choice
 After 2 weeks it will appear as isodense
 After 3 weeks it will assume a lenticular shape &
hypodense in relation to brain
 In case acute on chronic SDH ,it may appear as mixture of
hypodense & hyperdense material
 Sometimes its difficult to distinguish between brain
parenchyma & chronic SDH ,in this case contrast
material 300 ml of 30 % diatrizoate meglumine is
used which cause membranes of isodense hematoma to
opacify.

26.  Chronic SDH
 T1: if the haematoma is stable it appears isointense to
CSF, it can appear hyperintense to CSF if there is a
rebleed or infection.
 T2: if haematoma is stable it appears isointense to CSF
if there is rebleed the haematoma appears hypointense
 FLAIR: hyperintense to CSF
 Rarely, the periphery of the SDH may calcify,
see calcified chronic subdural haematomafor an in-
depth discussion regarding the MRI signal
characteristics of this entity.

29. Treatment
 Conservative
Bed rest
Osmotic diuresis
Corticosteroids
 Surgical
Craniotomy
Burrhole
Twist drill aspiration
Most common treatment of chronic SDH is evacuation
using burrholes at the site maximim hematoma thickness
Single burrhole is sufficient , 2 burrholes are preferred
Subdural placement of drain for 24 hrs

30.  Twist drill craniost omy for chronic subdurals
 This method is thought to decompress the brain more
slowly and avoids the presumed rapid pressure shifts
 A 0.5 cm in cision is made in the scalp in th e rostral
portion of the h ematoma, and then a twist drill hole is
placed at a 45° angle to the skull, aimed in the direction of
the longitudinal axis of the collection
 A ventricular catheter is inserted into the subdural space,
and is drained to a standard ventriculostomy
 drainage bag maintained 20 cm below the level of the
craniostomy site

33. Complications
 Reoccurrence is common
 Infectious complications include subdural empyema,brain
abscess,meningitis
 Fits in 10 %
 Tension pneumocephalus
 Prognosis
 Better than acute subdural hematoma
 Mortility is <10 %