2. Pathophysiology of
the development of CSDH
• Clear yellow to dark, thin liquid to semisolid
• Gardner 1932,Osmotic gradient theory
– Increase protein content increase oncotic
pressure
• Weir
– CSDH fluid to be isosmotic to blood and CSF
• Microscopic examination of fluid from CSDHs of
any age reveals fresh erythrocytes
• CSDH membrane
3. Pathophysiology of
the development of CSDH
• Neovasculature at outer membrane of CSDH
• Abnormal sinusoidal dilate
• Both vessel types are composed of
endothelial cells
• Erythrocytes and platelets found in perivascular
space
• Gap junction 8 um leakage of plasma and RBC
into hematoma cavity
4. Pathophysiology of
the development of CSDH
• Kallikrein, bradykinin, and platelet-activating factor
(PAF) vasodilatation, increase vascular
permeability, prolong the clotting time, release t-PA
• Eosinophil degranulation in the outer membrane
fibrinolytic factor, inflammatory mediator local
coagulopathy and cell destruction
7. Surgical Treatment of
chronic subdural hematomas
• 1925, Putnam and Cushing : craniotomy with
complete removal of the outer membrane and
hematoma contents
• 1964, Svien and Gelety : bur hole better outcome
than craniotomy (lower reoperation)
• 1977, Tabaddor and Shulmon : study comparing
craniotomy had the highest mortality rate
8. Surgical Treatment of
chronic subdural hematomas
• Suzuki and associates : closed system drainage
without irrigation to be as effective as closed system
drainage with irrigation
• Smely and coauthors : twist drill drainage without
irrigation was superior to bur hole drainage with
irrigation
9. Medical Treatment of
chronic subdural hematomas
• Corticosteroid : decreases leukocyte chemotaxis,
inhibits degranulation, inhibit neomembrane
formation, prevent clot enlargement
• Bender and Christoff : more rapid neurologic
improvement after introducing corticosteroids to the
treatment regimen, thereby allowing shorter
hospitalization
• ACEI : interrupt neovascularization by inhibiting
endothelial vascular growth factor
11. Definition
• Fluid collection within the layers of dura matter
• DDx : subdural hygroma (subdural hydroma,
external hydrocephalus)
• Subdural hygroma can transform into CSDH
12. Epidemiology
• Peak incidence , 80th
• Male
• Trauma most important risk factor
• Postsurgical communication of the subarachnoid
space
• CSF shunting
• Primart coagulopathy in children
• Anticoagulant treatment in adult
• Chronic alcoholism
13. Patient history
• No pathognomonic sign and symptoms
• Asymptomatic
• Coma from increase ICP
• Refractory headache
• Lack of concentration
14. Imaging
• Preoperative CT scan
– sickle-shaped lesion
– midline shift
– High risk for recurrence : mixed-density or layer
type
15. Imaging
• Postoperative CT scan
– Recurrence : BHC 29 %, TDC 76 %
– Residual fluid : 78% of case on day 10, 15% in
the 6th
week
– Intracranial air : tension pneumocephalus
– Bilateral CSDH : Mount Fuji sign
16. Imaging
• MRI
– Hyperintense on T2 , proton-weightes image
– Variability in signal intensity on T1 : 50 %
hyperintense
– DDx : Subdural hygroma : Hypointense on
proton-weightes image
17. Contemporary treatment
• Corticosteroid : anti-inflammatory, antiangiogenic
• Mannitol
• ACEI : antiangiogenic
• Anticonvulsant : posttraumatic and postoperative
epilepsy have low incidence in Pt c CSDH
• Patient posture after surgey : RDCT,flat position in
the first 3 day after surgery for reduce recurrence
• Hydration : increase brain volume
• Postoperative hyperemia
18. Surgical treatment
• Gold standard
• TDC : up to diameter 5 mm
• BHC : 5-30 mm diameter
• Craniotomay : larger than 30 mm diameter
• Hematoma cavity be filled with 100% Oxygen or
carbon dioxide
19. Twist drill craniotomy : TDC
• Decompress brain slowly and avoid the presume
rapid pressure shift that occur ICH
• 0.5 cm incision
• Twist drill hole is place 45 angle,aim direction in
longitudinal axis of the collection
• Ventricular catherter insert to subdural space