The document discusses chronic subdural hematoma (CSDH), focusing on its pathophysiology, clinical presentation, imaging techniques, and treatment options. It outlines various theories about the initiation and propagation of CSDH, as well as highlighting advances in surgical and nonsurgical management. Key treatment methods include twist drill craniostomy and medical management strategies like the use of tranexamic acid.

1. CHRONIC SUBDURAL HEMATOMA
CONTROVERSIES AND RECENT ADVANCES
Presented By: Dr. Chirag Solanki

2. CHRONIC SUBDURAL HEMATOMA
CONTROVERSIAL
Its collection of blood within the
layers of dura of more than 2-3
weeks duration

3. Ultrastructural Anatomy of Dura and
Dura-Arachnoid Interface
 Continuum of cells from dura to arachnoid without naturally
occurring subdural space
 Layers:
Periosteal Dura Fibroblasts and extracellular intertwining collagen fibres
Meningeal Dura oriented in various directions giving strength
Dural Border Cell Layer (Light Cell Layer; Flake like cell Layer)
Arachnoid Barrier Cell Layer: formed by tightly bound cells by Tight
junctions, gap junctions, desmosomes with strong basement membrane
Neurosurgery 1993 Jan;32(1):111-20. Haines DE, Harkey HL, al-Mefty O

4. Devoid of collagen and has only
a few intercellular junctions
causing inherent weakness

5. Ultrastructural Anatomy of Dura and
Dura-Arachnoid Interface

6. EVOLUTION OF CHRONIC SDH
 Initiation
 Propogation
 Resolution

7. INITIATION
 Virchow (1857)- Due to Inflammation of dura termed
“Pachymeningitis Haemorrhagica”
 Trotter(1914)- Bleeding from bridging veins
 Yamashima and Friede (1984)- Areas of attenuation in cortical
bridging veins with wall consisting only of endothelium, a basement
membrane and thin sheet of collagen and single layer of dural cells
in the region of transit from subarachnoid space to dura as
compared to uniform thickness with thick surrounding trabecular
tissue

8. INITIATION
They also showed the relatively slow nature of collection of blood
and trivial- less severe and repetitive nature of trauma as compared
to Acute SDH resulting in chronic collection and less severe
symptoms
 McCormick and Weigel - 1% to 6% of patients with untreated acute
subdural hematoma experience transformation to CSDH, the latter
develops its own dynamics

9. THEORIES OF PROPOGATION
 Osmotic-oncotic theory
 Recurrent bleeding hypothesis
 Localized Coagulopathy

10. THEORIES OF PROPOGATION
Osmotic-oncotic theory
 Proposed by Gardner (1932)– supported by his
experiments in animals using cellophane paper
 Zollinger and Gross (1934)- modified it to incorporate
oncotic pressure
 However further studies could not support this as they
have failed to demonstrate significant difference between
hematoma fluid, plasma and CSF as demonstrated by Weir
B (1971; 1980)

11. THEORIES OF PROPOGATION
Recurrent bleeding Hypothesis
 Proposed by Putnam and Cushing in 1932
 Yamashima (1983)- extensive pathological studies of the
subdural outer neomembranes and showed
Capillaries with single layer of endothelium with indistinct
basement membrane with perivascular haemorrhage
Abnormal dilated sinusoids with gap junctions as large as 8 µm
resulting in leakage of plasma and RBCs in SDH cavity
 Ito (1976)- demonstrated bleeding % using 51Cr labelled
RBCs and showed daily hemorrhage accounted for a mean
of 10.2% of volume, with a range from 2% to 27%.

12. THEORIES OF PROPOGATION
Recurrent bleeding Hypothesis
 Milo and associates (2011)- showed increased CCL2 and
CXCL8 angiogenic chemokines and also CXCL9 and 10 with
angiostatic activity within hematoma fluid.
 Kalamatianos (2013)- enhanced expression of PLGF in
hematoma fluid leading to inflammation and angiogenesis in
CSDH and reduced ratio of sVEGFR-1 to PLGF in hematoma
fluid is consistent with the proangiogenic capacity of CSDH
(The actions of PLGF and its related proangiogenic vascular endothelial
growth factor (VEGF) are antagonized by a high-affinity soluble receptor,
namely soluble VEGF receptor-1 (sVEGFR-1)

13. THEORIES OF PROPOGATION
Recurrent bleeding Hypothesis
 H. Fugisawa (1995)- activation of the kallikrein-kinin
system, by increasing vascular permeability, may cause
blood extravasation and plasma exudation from the
capillaries into both the outer membrane and the
hematoma cavity, resulting in enlargement of the
hematoma.

14. THEORIES OF PROPOGATION
Localized Coagulopathy
 Ito (1975; 1976; 1978)- Imbalance between fibrin formation
and fibrinolysis especially increased levels of t-PA.
 Kawakami et al (1991)-found excessive activation of
coagulation cascade & fibrinolytic systems
 Labadie and Glover (1975)- altered hemostatic and
fibrinolytic mechanisms with high levels of fibrin degradation
products (FDPs) and low mean plasminogen and FDPs inhibit
coagulation, platelet aggregation, and fibrin polymerization
and promote the activity of t-PA.

15. THEORIES OF PROPOGATION
Localized Coagulopathy
 Friede (1971) and Mullar (1998)- Degranulation of
abundant eosinophils in the outer as well as inner
membrane is the source of the fibrinolytic factors and
inflammatory mediators causing local coagulopathy
and cell destruction in the CSDH.

16. THEORIES OF PROPOGATION
VICIOUS CYCLE OF PROPOGATION

17. CONTRIBUTING FACTORS
 Cerebral atrophy – prevents tamponade effect
 Propensity for recurrent bleeding
 Intracranial hypotension- due to overshunting, especially in NPH
patients (Weiner showed 8% incidence); CSF leaks
 Alcoholism- Frequent falls, cerebral atrophy, coagulation
abnormality, increased estrogen (Goiffre in 1991 found increased ER
in outer membrane especially in males leading to increased t-PA),
increased fragility of vasculature due to avitaminosis, platelet
dysfunction
 Risk is doubled for each half unit increase in PT ratio >2
(Hylek & Singer)

18. RESOLUTION
 Not all CSDH progress.
 Reports of spontaneously resolved CSDH (Nagamuna et al
1986)
 Horikoshi et al (1998) reviewed a number of studies and
reported that 2.4%–18.0% of cases of CSDH resolved
spontaneously without surgical or medical intervention.
 When the balance is in favour of coagulation, the SDH
organizes----fibrosis----may even calcify.

19. CLINICAL PRESENTATION
 Onset usually insidious
 Mimics any other neurological disorder
 Types of presentations
◦ Raised ICP – commonest
◦ Focal deficits – may fluctuate
◦ Neurocognitive impairment – most liable to be missed
Atleast more than 90 ml of subdural hematoma is required to
produce symptoms.

20. CLINICAL PRESENTATION
 In elderly
◦ Insidious onset due to brain atrophy
◦ More liable for deficits (altered CBF)
◦ More cognitive defects
 In older children-headache s/o raised icp
 In infants
◦ Peak incidence – 6mths – 1 yr
◦ Suspect child abuse
◦ Acute (seizures/apnoea) or chronic (lethargy/irritability/failure to
thrive/macrocephaly)
◦ Post shunt cases may be asymptomatic

21. CLINICAL GRADING SYSTEMS
1 Fully alert and conscious, normal mental function, few or no focal signs
2 Drowsy or lethargic, organic mental syndrome, focal neurological signs
3 Very drowsy or stuporous, conspicuous organic mental syndrome,
pronounced focal signs
4 Coma or signs of herniation
Bender and Christoff

22. CLINICAL GRADING SYSTEMS
Markwalder and Reulen
0 Patient neurologically normal
1 Patient alert and oriented, mild symptoms such as headache, absent
or mild neurological deficits such as reflex asymmetry
2 Patient drowsy or disoriented with variable neurological deficits such
as hemiparesis
3 Patient stuporous but responding appropriately to noxious stimuli,
severe focal signs such as hemiplegia
4 Patient comatose with absent motor responses to painful stimuli,
decerebrate or decorticate posturing

23. MECHANISM OF NEUROLOGICAL
DEFICITS
 Local pressure
 Alterations in regional cerebral blood flow
◦Locally
◦Distant effects

24. ALTERED REGIONAL CBF AND
METABOLISM
 Ikeda et al – Used 133Xe inhalation system and found reduced CBF
in frontal, superior temporal and Rolandic areas in with
proportionately greater decrease in Rolandic area in patients with
hemiparesis
 Ishikawa et al – reduced CBF and CMRO2 in deep white matter.
 Tanaka et al – documented reduction in CBF, reversible with
acetazolamide implying that vasospasm and not mechanical
compression that causes ischemia

25. ALTERED REGIONAL CBF AND
METABOLISM
 Alterations in CBF in deeper structures causes deficits
 This alteration is reversible and hence deficits are not
permanent.
 However causal association not proved

26. IMAGING: CT
 Acute SDH-60 to 80 HU
 Subacute SDH-25 to 45 HU
 Chronic SDH-0 to 25 HU
 Kawakami et al (1989)- in acute subdural hematoma, a midline shift
is regularly correlated with signs of elevated intracranial pressure, it
is not uncommon in CSDH that shifts of greater than 1 cm are
compensated for without neurological deficit. In one study, an
average of 90 mL of hematoma fluid was compensated for without a
detrimental rise in intracranial pressure

27. IMAGING: CT CLASSIFICATION SYSTEMS
1 Hyperdensity
2 Isodensity
3 Hypodensity
4 Mixed density
5 Layering type
Nomura and colleagues
- Layering type is characterized by a high
hyperfibrinolytic activity.
- The mixed-density type has a lower
hyperfibrinolytic activity than the layering type
- The hypodense hematoma has the lowest
fibrinolytic activity

28. IMAGING: CT CLASSIFICATION SYSTEMS
1 Homogeneous density
2 Laminar type
3 Layering or separated type
4 Trabecular density type
Naganuma and colleagues
- separated type of CSDH had a higher recurrence
rate (36%) compared to the laminar (19%) and
homogeneous (15%) types.
- Stanisic et al- confirmed the high recurrence rate
of the separated (29%) and laminar (27%) types

29. IMAGING: MRI
 More sensitive (espspecially isodense CSDH)
 Exact age
 Complexity of SDH (septae, Multicomparmetnal cSDH etc)
 DD from empyema
Duration T1 T2
Acute(<3 d) Hyper Hypo
Early subacute (3d-2wks) Hypo/iso Hyper
Late subacute (2wks-2mths) Hyper Hyper
Chronic (>2mths) Hyper Hyper with
iso ring

30. IMAGING: MRI CLASSIFICATION
 They showed that the recurrence rate of
CSDHs that exhibited homogeneous high
intensity on T1-weighted images was
significantly lower (3.4%) than that in the
non–high-intensity groups (11.6%).
 Tanikawa and colleagues found that
subdural hematomas divided into multiple
layers by an intrahematomal membrane (as
demonstrated on T2-weighted MRI) are
more effectively treated with craniotomy
1 Hyperintense
2 Mixed Hyper/isointense
3 Isointense
4 Mixed Iso/hypointense
5 Hypointense
Tsutsumi and colleagues
(Based on T1 sequences)

31. TREATMENT OPTIONS
Nonsurgical
Surgical
◦ Twist drill craniostomy ( upto 5 mm)
◦ SEPS (Subdural Evacuation Port System)
◦ Replacing hematoma with O2
◦ Burr hole evacuation (6 mm to 30 mm)
◦ Endoscopic evacuation
◦ Trephine/ craniotomy with membranectomy (>30 mm)
◦ MMA Embolisation
◦ Needle aspiration
◦ Reservoir placement
◦ Subduro-peritoneal shunt/Subduropleural Shunt
◦ Reduction cranioplasty

32. NONSURGICAL MANAGEMENT
 Masterly inactivity:
 For asymptomatic and incidentally detected cases
Horikoshi et al (1998) reviewed a number of studies and reported that 2.4%–
18.0% of cases of CSDH resolved spontaneously without surgical or medical
intervention
 Medical management:
Mannitol and rest:
Jiro Suzuki (1970) showed significant decrease in size or disappearance in21
out of 20 patients; Duration of treatment was 12 to 106 days

33. NONSURGICAL MANAGEMENT
 Medical management:
Steroids and rest:
P.D. Delgado Lopez (2009)- Favourable outcome was obtained in 96% and
93.9% of those treated with dexamethasone and surgical drain respectively.
Medical complications occurred in 34 patients (27.8%), mainly mild
hyperglycemic impairments.
He used 4 mg of dexamethasone every eight hours, either oral or
intravenously. Those who did not respond within 48 hours were subjected to
surgery (21.8%). Rest were discharged on dexamethasone and it was slowly
tapered (reducing 1 mg per day every three days) until complete withdrawal.
BUT FURTHER STUDIES FAILED TO PRODUCE CONSISTANT RESULTS

34. NONSURGICAL MANAGEMENT
 Medical management:
Role of Tranexamic Acid:
Hiroshi Kageyama (2013)- He studied 21 patients with primary medical
therapy with tranexa in 18 patients and in 3 patients postop BHC. Clinical
symptoms improved before the hematomas were fully reduced. None of the
hematomas recurred or progressed. Among all study patients, no adverse
events occurred over the follow-up of 21-127 days with 750 mg of Tranexamic
Acid per day.
Tranexamic acid is a specific antifibrinolytic drug that inhibits plasminogen
activation and plasmin activity.

35. NONSURGICAL MANAGEMENT
Mechanism of action
of
Tranexamic Acid

36. NONSURGICAL MANAGEMENT
Role of Tranexamic AcidDay1ofstartingTranexa
4monthsafterstartingTranexa

37. NONSURGICAL MANAGEMENT
Role of Tranexamic Acid

38. ANTIEPILEPTIC PROPHYLAXIS
 Ohno K. et al (1993)- Out of 129 patients, NONE out of 73 patients with AED prophylaxis and
only 2 out of 56 who were not given AED prophylaxis developed seizures. So AEDs not
recommended in cSDH due to very low incidence of seizures.
 Bartosz C. et al(2009)- Out of 88 bur hole–treated CSDH patients Eleven (12.5%) suffered at
least 1 seizure between hemorrhage onset and discharge from their treatment hospital
admission. Seizures were more frequent in women than men (p = 0.030) and least frequent in
patients with right-sided lesions (p = 0.030). Preoperative initiation of AED prophylaxis was the
only significant predictor of the lower incidence of postoperative seizures (OR 0.10, p = 0.013).
However, preoperative initiation of AED prophylaxis did not significantly affect outcome at
discharge.
 Cochrane review- No recommendation due to controversial findings in retrospective studies
 Still AEDs can be considered in high risk groups
 Accidental opening of inner membrane during surgery
 Alcohol abuse Frey L. C. et al(2003)
 Age more than 65 years

39. TWIST DRILL CRANIOSTOMY (TDC)
 Placement of a hole in the skull using a hand-held drill.
 1966- Dr William Cone , first used it diagnostically.
 Tabaddor & Schulman (1977) suggested the use of a drain to decrease recurrence
rates—good results, 10% rec, 2weeks stay, no infection (21 patients); demonstrated that
the subdural pressure dropped to zero after the initial 20% of the subdural collection
was removed. This initial 20% was usually enough to lead to marked clinical
improvement
 Hubschmann (1980)-22 pts age >60 or coexisting illness.mortality-23%
 Burchiel and Taylor (1985)- without drain found 73% improvement, 23% required
additional surgical procedure and stay of 23 days.
 Camel & Grubb (1986)-114 cases ,93% improved

40. TWIST DRILL CRANIOSTOMY (TDC)
 Smely(1991) – 33 pts-compared twist drill with drain and burr hole with drain –
same results with a decreased hospital stay in the former
 Many other studies have produced same results
Role :
◦ as an emergency temporizing modality.
◦ Definitive treatment especially for high risk cases
◦ Hence if to be used as definitive therapy, use with
drain due to better results with drain

41. TWIST DRILL CRANIOSTOMY (TDC)
 Sun-Chul Hwang (2009)-
 recommended Safe entry point- on Superior Temporal Line 1 cm anterior to coronal suture as
all the branches of the middle meningeal artery ran posterior to the coronal suture and the
vascular grooves were also located posterior to the coronal suture at the level of the STL.
 The mean thickness of the skull and the CSDH at the proposed point was 8 mm (range 5–13
mm) and 20 mm (range 10–28 mm), respectively.
 45° angle to the surface of the bone to prevent the catheter from entering the cortex. The
typical direction of the drill was postero-inferior toward the auricle
 drainage bag was kept 90 cm below head level so that gravity aided in the drainage from the
subdural cavity
 hydrated in the first 24 hours postoperatively using 2000 ml of normal saline to help reexpand
the brain

42. TWIST DRILL CRANIOSTOMY (TDC)
 S. K. Suku (2007)-
 entry point posterior to the parietal
eminence with angle required must be
40 degrees or less to prevent injury to
brain with either drill or drain
 The increase in the inner diameter of
the catheter from 1.3 to 2.8mm
enlarged the cross sectional area from
1.69 to 7.84mm2.
 size of the holes of the catheter is more
important than the number of holes
because even a small piece of blood
clot or other debris can obstruct the
holes.

43. REPLACING HEMATOMA WITH O2
WITHOUT IRRIGATION OR DRAIN IN TDC
 N. Takeda et al (2006):
 Perforating point is always at the parietal eminence except for unusually localized
hematoma. The parietal eminence is not only an easy landmark, but also a suitable
position for the complete hematoma evacuation
 After perforation of the skull, a needle device consisting of outer and inner parts is
placed, and the outer needle is left in site (19-gauge, Muraishi Iryoki, Tokyo). After
measuring the pressure of the hematoma cavity with an extension tube, 10ml of
oxygen in a syringe is slowly injected into the hematoma cavity, and an equal volume
of the hematoma is aspirated with the syringe
 repeated until no more hematoma can be obtained.
 An average amount of replaced hematoma was 96.1ml, ranging from 5 to 280ml. An
initial hematoma pressure ranged from 0 to 200mm H2O (average: 92.1mm H2O).
 clinical recurrence was noted in 10% of patients

44. REPLACING HEMATOMA WITH O2
WITHOUT IRRIGATION OR DRAIN IN TDC
Pre Post 10 days 60 dyas

45. SEPS (SUBDURAL EVACUATION PORT
SYSTEM)
 a variation of twist-drill craniostomy,
adds the advantage of an airtight seal
while allowing gentle vacuum suction to
the subdural space
 This device is called the SEPS
(Medtronic) and consists of a 6-mm
stainless steel port that is threaded
through a 5.8-mm twist-drill craniostomy
with its tip in the diploic space, which is
then attached to a Jackson-Pratt bulb .
 Negative pressure (2.5 cm Hg) is applied
by using a bulb for a variable time period,
typically 24–48 hours, but until drainage
of subdural fluid has ceased

46. SEPS (SUBDURAL EVACUATION PORT
SYSTEM)
 Anand Rughani (2010)- Decrease in size of cSDH post procedure,
recurrence, need for subsequent procedure and mortality similar as
compared to BHC with drainage but the advantage being less
invasive and bedside feasibility
 Amit Singla (2011) and Mina Safain (2013)- similar result to earlier
study showing SEPS as an effective and less invasive alternative to
BHC
 Further RCTs are required to recommend

47. BURR HOLE CRANIOSTOMY (BHC)
 Involves placement of one or more burr holes under LA/GA with irrigation of
subdural space
 Markwalder (1981)
◦ compared various modalities and concluded that twist drill/burr hole with
drain was best for adults and children after infancy.
◦ 32 cases of BH+drain. No mortality, low morbidity and good results.
◦ Identified brain re-expansion as most imp determinant of recurrence.(it
depends intraop on subdural pressure and postop on restoration of CBF)
◦ No need for membranectomy.

48. BURR HOLE CRANIOSTOMY (BHC)
SINGLE V/S DOUBLE BURR HOLES
 Taussky et al- Single burr hole drainage (without drain) was associated with
statistically significant higher recurrence rate, longer average hospitalization
length and higher wound infection rate.
 Kansal et al- (without drain) (267 patients) no statistically significant difference
between the two procedures. The recurrence rate of double burr hole drainage
was 8.33 %, whereas patients with a single burr hole had a 13.33 % recurrence
rate
 Han et al- (with drain) (180 patients) CSDH treated with two burr holes had
higher recurrence rate; however, the difference was not statistically significant

49. BURR HOLE CRANIOSTOMY (BHC)
SINGLE V/S DOUBLE BURR HOLES
 Lee et al- studied the results of treatment of CSDH with one burr-hole
craniostomy with closed-system drainage with or without irrigation, two burr-
hole craniostomy with closed-system drainage with irrigation and small
craniotomy with irrigation and closed-system drainage in a small series of 87
patients. small craniotomy was associated with significantly lower complications
and recurrence rate
 Dimitrios Pahatouridis (2012)- When a single burr hole was used, the size was
enlarged up to a diameter of 30 mm enlarged single or double burr hole with
postop drainage has the same efficacy for the treatment of CSDH

50. BURR HOLE CRANIOSTOMY (BHC)
SINGLE V/S DOUBLE BURR HOLES
CONCLUSION
With postop drainage, there is no difference between
single and double burr hole techniques

51. BURR HOLE CRANIOSTOMY (BHC)
RINSING VOLUME AND LMWH PROPHYLAXIS
 Yasemin Tahsim-Oglou (2012)- Copious (atleast 1500 ml)
intraoperative irrigation and avoidance of postoperative low-
molecular-weight heparin thromboprophylaxis may reduce the
recurrence rate of cSDH.

52. BURR HOLE CRANIOSTOMY (BHC)
SUBDURAL DRAIN V/S NO DRAIN
 Thomas Santarius (2009)- Recurrence occurred in ten of 108 (9·3%) people with
a drain, and 26 of 107 (24%) without (p=0·003; 95% CI). At 6 months mortality
was nine of 105 (8·6%) and 19 of 105 (18·1%), respectively (p=0·042; 95% CI).
Medical and surgical complications were much the same between the study
groups.
 Use of a drain after burr-hole drainage of chronic subdural haematoma (for an
average period of 48 hours and dependant on drainage volume) is safe and
associated with reduced recurrence and mortality at 6 months.

53. BURR HOLE CRANIOSTOMY (BHC)
SUBDURAL DRAIN PLACEMENT
 Hiroshi Nakaguchi (2000)
Patients with parietal or occipital drainage had a higher rate of CSDH
recurrence and much more subdural air than those with frontal drainage.
Patients with residual subdural air demonstrated on CT scans obtained 7 days
postsurgery also had a higher recurrence rate than those without subdural air
collections.
Patients with a subdural space wider than 10 mm on CT scans obtained 7 days
postsurgery had a higher recurrence rate than those with a space measuring
10 mm or less.
Incidence of postoperative fluid re-accumulation seems to be reduced by
placing the tip of the drainage catheter in the frontal convexity and by
removing subdural air during or after surgery.

54. BURR HOLE CRANIOSTOMY (BHC)
SUBGALEAL DRAIN PLACEMENT
 R. Gazzeri (2007)
After evacuation of the hematoma through a single burr hole, we inserted a
Jackson Pratt drain into the subgaleal space, with suction facing the burr hole,
allowing for continuous drainage of the remaining hematoma
Out of 224 patients 17 patients (7.6%) needed a second operation for a
recurrence of the hematoma no patient required a third operation.
Postoperative complications developed in 3 patients with mortality rate of
0.9%.
 The use of suction assisted evacuation, is followed by results that compare
satisfactorily to reports of previous methods, with a low rate of recurrence and
complications. It is relatively less invasive and can be used in high risk patients.

55. BURR HOLE CRANIOSTOMY (BHC)
SUBGALEAL DRAIN PLACEMENT
 A burr hole is performed over the thickest portion of the hematoma,
generally the parietal bulge, and subsequently enlarged up to a diameter of
3cm.
 A 7mm Jackson Pratt drainage tube is positioned in the subgaleal space,
with the tip of the catheter over the burr hole and exteriorised through a
separate incision. After suturing the primary wound, the drainage tube is
connected to a closed drainage system under suction.
The patient is kept in the supine position until the drainage catheter is
removed 48–72 hours after surgery. The patient receives parenteral fluids
and antibiotics for the first 3 postoperative days.

56. BURR HOLE CRANIOSTOMY (BHC)
SUBGALEAL DRAIN PLACEMENT

57. BURR HOLE CRANIOSTOMY (BHC)
SIGNIFICANCE OF POSTOP DRAINAGE VOLUME
 Taek-Hyun Koan (2000)
175 cases were investigated between 1991 and 1997.
The mean drainage volume over 5 days was 320 ml, with the largest volume
(413 ml) seen in the low-density type and the smallest (151 ml) in the mixed-
density type of CSDH.
The mixed-density type had the highest recurrence rate (8.6%), whereas there
was no recurrence for the low-density type.
There were no recurrences in 81 patients in whom the total drainage volumes
for 5 days were more than 200 ml. There were recurrences in six of 94
patients in whom the total drainage volume was less than 200 ml.
Patients with CSDH in whom there is less postoperative drainage than
expected should be carefully observed, with special attention paid to the
possibility of recurrence.

58. NEUROENDOSCOPY
 Hellwig et al (1991) used for recurrent & loculated cases
 Flexible steerable endoscpes used
 Allows visualization of the subdural space and breaking of loculi.
 Minimally invasive technique done through burr hole
 Not recommended for acute SDH
 However comparative studies not available

59. NEUROENDOSCOPY

60. CRANIECTOMY
 Involves a formal craniotomy with evacuation of hematoma and
membranectomy
 Cushing and Putnam(1925)-procedure of choice
 Subsequently fell out of favour because of high morbidity and mortality rates-
Sven & Gelety (1964); Tabaddor & Shulman (1977)
 Revived by Hamilton(1993)
 Role (Markwalder)
◦ Hyperdense SDH
◦ Recurrent CSDH
◦ Loculated CSDH

61. CRANIECTOMY
SUBTEMPORALIS MARSUPIALIZATION
Modification by Sambasivan (1978)
Involves temporal craniectomy with wide opening of dura and hitching of dura
to temporalis muscle
Provides alternate route of absorption of hematoma
Results in 2255 cases-
◦ Resolution in 7-10 days
◦ Mortality 0.5%
◦ Recurrence 0.35%

62. MIDDLE MENINGEAL ARTERY
EMBOLISATION
 Shinya Mandai (2000)- a Case Report
In a 59 years old male, initially BHC with drainage done for
right frontoparietal chronic SDH. Later twice needle
aspiration through burr site and then continuous
requirement of aspiration through Ommaya reservoir
placement, Middle meningeal artery was embolised.

63. MIDDLE MENINGEAL ARTERY
EMBOLISATION

64. TREATMENT IN CHILDREN
 Subdural needle aspiration – both as immediate life saving
and definitive treatment as closed external drainage.
 Internal Subdural shunt – subduroperitoneal &
subduropleural shunting or Reservoir placement
◦For recurrent cases especially hygromas
 Reduction cranioplasty with duroplasty
◦For refractory cases, as a last resort

65. TREATMENT OF RECURRENT CHRONIC
SDH
 No definitive consensus
 Search for underlying cause (including tumours- Histopathological fluid analysis )
 Common procedures in sequence of preference
◦ Reexploration of Burr hole
◦ Craniotomy
 Other options
◦ Reservoir placement
◦ Subdural shunt (Subduropleural shunt can be considered for highly
proteinacious SDH fluids)
◦ Endoscopy
◦ Subtemporalis marsupialization

66. BEST TREATMENT OPTIONS FOR cSDH
 Bradley C. and colleagues (2010): Published a decision analysis of 32 articles from
1966 to 2006
 Bur-hole craniostomy is the most efficient choice for surgical drainage of
uncomplicated CSDH. Bur-hole craniostomy balances a low recurrence rate with a
low incidence of highly morbid complications.
 Andrew Ducruet (2012) Meta-analysis of 45 Studies from 1983 to 2010
 AED prophylaxis in patients who are likely to be at a higher risk for seizures, such
as alcoholics and those with a history of significant TBI
 Primary TDC drainage at the bedside for cSDH patients who are high-risk surgical
candidates with unseptated hematomas and craniotomy in the setting of cSDH
with significant membranes. If burr-hole evacuation of cSDH is performed,
available literature supports the placement of a closed drainage system.

67. BEST TREATMENT OPTIONS FOR cSDH
 Weigel, Schmeidek and Krauss (2003)- Reviewed major surgical
series 1981-2001 (total 48)
Classified levels of evidence --1,2,3
None class 1, 6 class 2 and 42 class 3
Mortality same across all series
Morbidity
Craniotomy – 12.3%
Burr hole – 3.8%
Twist drill – 3%

68. BEST TREATMENT OPTIONS FOR cSDH
 Classes of evidence
◦ Class I: Evidence provided by one or more well designed randomized controlled clinical
studies.
◦ Class II: Evidence provided by one or more well designed clinical studies such as prospective
open, case-control studies, etc
◦ Class III: Evidence provided by expert opinion, non-randomized historical controls, or case
reports of one or more patients
 Recommendation
◦ TYPE A: Strong recommendation, based on class I evidence or overwhelming class II evidence
when circumstances precludes randomized clinical trials
◦ TYPE B: Recommendation based on class II evidence
◦ TYPE C: Recommendation based on strong consensus of class III evidence.

69. BEST TREATMENT OPTIONS FOR cSDH
Surgical approach
Type C – TD & BH safest
-- BH & CR most effective
--BH best cure-complication ratio
Irrigation
Type C – irrigation decreases risk of rec after TD
-- no rise in infection
Drain
Type B – decreases rec in BH
-- frontal position of drain better
Type C – decreases rec in TD
-- no rise in infection
Treatment of recurrence
Type C –BH more effective than TD
-- CR as a last resort

70. NIMHANS EXPERIENCE
Ramnarayan et al (1999)
 Analysis of 647 cases.
 M:F = 534:113
 Majority in the 5th to 7th decade
 Most common C/F - cognitive dysfunction, headache, limb
weakness
 14% alcoholics, 56% history of trauma
 CT- 47% hypo, 33% mixed, 20% isodense on CT

71. NIMHANS EXPERIENCE
Ramnarayan et al (1999)
 Surgery – 93% two burr hole evacuation, 5 twist drill, 1 craniotomy
 Subdural drain used in 165 cases
 Subdural membrane in 58%, brain re-expansion in 31%
 Outcome
◦ 65% improved at time of discharge
◦ 91% by the time of suture removal
 Recurrence – 21%
◦ Related to age, presence of enhancing membrane and brain re-
expansion.
◦ Use of drain recommended.
 Mortality – 5%
◦ Related to age, GCS<8 and associated illnesses

72. THANK YOU