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Pathophysiology
of subdural hematomas
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
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
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
Evolution of
chronic subdural hematomas
Evolution of
chronic subdural hematomas
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
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
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
Medical and Surgical Management
of Chronic Subdural Hematomas
Definition
• Fluid collection within the layers of dura matter
• DDx : subdural hygroma (subdural hydroma,
external hydrocephalus)
• Subdural hygroma can transform into CSDH
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
Patient history
• No pathognomonic sign and symptoms
• Asymptomatic
• Coma from increase ICP
• Refractory headache
• Lack of concentration
Imaging
• Preoperative CT scan
– sickle-shaped lesion
– midline shift
– High risk for recurrence : mixed-density or layer
type
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
Imaging
• MRI
– Hyperintense on T2 , proton-weightes image
– Variability in signal intensity on T1 : 50 %
hyperintense
– DDx : Subdural hygroma : Hypointense on
proton-weightes image
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
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
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
Surgical treatment
Surgical treatment
• Irrigation : remove
hematoma completely
• Drainage :
• Recurrence : BHC
Thank you

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037 Pathophysiology of subdural hematoma

  • 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
  • 10. Medical and Surgical Management of Chronic Subdural Hematomas
  • 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
  • 21. Surgical treatment • Irrigation : remove hematoma completely • Drainage : • Recurrence : BHC

Editor's Notes

  1. Microscopic exam พบ fresh erythrocyrte พบว่าเกิด progress leakage CSDH membrane เป้น source ของ rebleeding
  2. เกิดเส้นเลือดใหม่ขึ้นที่ด้านนอกของ CSDH Sinusoidal ขยาย เส้นเลือดทั้งสองมี endothelial cell Gap ที่กว้างทำให้ RBC และ plasma เข้าไปใน hematoma cavity
  3. Inflammatory mediator ทำให้ เกิด chronic bleeing เพราะทำให้ vessel fragile Eosinophil degranulation มี fibrinolytic and inflammatory เกิด local coagulopathe และ cell destruciton
  4. t-PA ไปกระตุ้นให้ plasminogen กายเป็น plasminplasmin ไปทำให้ fibrin factoe V VII XI กลายเป็น fibrin degraduatiob ตัว t- PA พบมากใน outer membrane ของ chroic subdural
  5. เริ่มจาก bleeding ทำใหเกิด defective clot formation เกิด fibrinolysis เกิด inflammation เกิด defective neovasularization
  6. A : isodense hematoma on Lt side asymmetrical of ventricle C : hypodentisy lesion
  7. GB, WW, BB
  8. สาเหตุการชัก เกิดขึ้นที่ cortical injury แต่ CSDH จะมี membrane ทำให้ epileptogenic ไม่ไปโดน cerebral cortex
  9. Mortality , cure rate ไม่มีความแตกต่างกัย Morbidity ใน Cranio จะเกิดมากที่สุด, Recurrence rate สูงที่สุดใน TDC, BHC และ craniotomy RR ต่ำ
  10. Irrigation ใน BHC not decrease recuurent rate แต้ใน TDC สามารถลดได้ Drainae : ลดการเกิด recurrence ได้ ถ้าเกิด Recurrence ให้ทำ BHC