The document discusses various types of subdural hemorrhages including acute, chronic, spontaneous, and those occurring in infants. Acute subdural hematomas are often associated with underlying brain injury and symptoms may include depressed consciousness, pupillary abnormalities, and focal signs. Surgery is usually indicated for acute subdural hematomas over 10mm thick or with a midline shift over 5mm. Chronic subdural hematomas typically occur in older patients and present with headaches, confusion, weakness, and seizures. Spontaneous subdural hematomas can occur with no identifiable trauma and risk factors include hypertension, vascular abnormalities, and coagulopathies.

1. Subdural hemorrhage
Acute, Chronic & Spontaneous
Momen Ali Khan
Neurosurgery Resident
Department Of Neurosurgery
Dhaka Medical College Hospital

2. Acute subdural hematoma
[Handbook of Neurosurgery 10th Greenberg 1076]
 Acute subdural hematoma (ASDH) often associated underlying brain injury, which
may be less common with EDH.
 Receiving anticoagulation therapy increases the risk of ASDH 7-fold in males and
26-fold in females
 Symptoms may be due to compression of the underlying brain with midline shift, in
addition to parenchymal brain injury and possibly cerebral edema
o Most patients (65-80%) present with a severely depressed conscious state
o Pupillary abnormalities are seen in ~40% (range 30-50%)

3. Two common causes of traumatic ASDH
 Accumulation around parenchymal laceration (usually frontal or temporal lobe). There is
usually severe underlying primary brain injury. Focal signs usually occur later and are
less prominent than with EDH
 Surface or bridging vessel torn from cerebral acceleration-deceleration during violent
head motion. With this etiology

4. Locations of ASDH
1. Convexity (the most common). Usually appears as a crescentic mass of increased
density adjacent to inner table
2. Interhemispheric
3. Layering on the tentorium
4. In p-fossa
[Handbook of Neurosurgery 10th Greenberg 1076]

5. Tentorial subdural hematoma
Acute (convexity) subdural hematoma
Interhemispheric subdural hematoma
Right-sided posterior fossa subdural hematoma

6. CT scan in ASDH
1. Acute subdurals are usually hyperdense compared to brain (possible exceptions: patients with
low hematocrit.
2. Edema in the adjacent brain may be present.
3. Differences in convexity EDH from SDH. SDH is typically
a. More diffuse
b. Less uniform
c. Usually crescentic over brain surface
d. Often less dense (possibly from mixing with CSF).
e. SDH cannot cross intradural barriers such as the falx and tentorium, whereas an EDH can.
[Handbook of Neurosurgery 10th Greenberg 1076]

7. SDH changes with time on CT
The density of subdural hematomas on CT scans changes with time as blood breaks down
and transforms from thick coagulum to low viscosity fluid
Category Time frame Density on CT relative to brain
Acute 1 to 3 days Hyperdense
Subacute 4 days to 2 or 3 wks. ≈ Isodense
Chronic Usually > 3 wks and < 3–4 mos Hypodense (approaching density of CSF)
After about 1–2 months May become lenticular shaped (similar to epidural
hematoma) with density > CSF, < fresh blood
[Handbook of Neurosurgery 10th Greenberg 1078]

8. Indications for surgery
1. ASDH with thickness > 10mm or midline shift (MLS) > 5mm (on CT) should be
evacuated regardless of GCS
2. ASDH with thickness < 10mm and MLS < 5mm (see text regarding the evacuation
of ASDH < 10
3. Mm thick) should undergo surgical evacuation if:
a) GCS drops by ≥ 2 points from injury to admission
b) And/or the pupils are asymmetric
c) Fixed and dilated
d) And/or ICP is > 20mm Hg
4. Monitor ICP in all patients with ASDH and GCS < 9
[Handbook of Neurosurgery 10th Greenberg 1078]

9. Timing of surgery
[Handbook of Neurosurgery 10th Greenberg 1078]
Timing of surgery for ASDH is a matter of controversy. As a general principle, when surgery for ASDH is
indicated it should be done as soon as possible.
“Four-hour rule”
1. Patients operated within 4 hrs of injury had 30% mortality, compared to 90% mortality if surgery was
delayed > 4 hrs
2. Functional survival (Glasgow outcome scale ≥ 4,) rate of 65% could be achieved with surgery within 4 hrs
Other factors related to outcome in this series included:
1. Post-op icp: 79% of patients with functional recovery had post-op ICPs that didn’t exceed 20mm hg,
whereas only 30% of patients who died had icp < 20mm hg
2. Initial neuro exam
3. Age was not a factor in this study (ASDH tend to occur in older patients than EDH)

10. Outcome as related to admission GCS

11. Interhemispheric subdural hematoma
Subdural hematoma along the falx between the two cerebral hemispheres (older term:
interhemispheric scissure
Cause
1. May occur in children,31 possibly associated with child abuse
2. In adults, may be the consequence of33:
a. Head trauma in 79–91%
b. Ruptured aneurysm34 in ≈ 12%
c. Surgery in the vicinity of the corpus callosum
d. Spontaneously: Spontaneous cases should be investigated for possible underlying
aneurysm.
[Handbook of Neurosurgery 10th Greenberg 1078-79]

12. Clinical features
1. Most often are asymptomatic
2. May present with the so-called “falx syndrome
a. Paresis
b. Focal seizures contralateral to the hematoma.
3. Other presentations
a. Gait ataxia
b. Dementia,
c. Language disturbance
d. Oculomotor palsies.
[Handbook of Neurosurgery 10th Greenberg 1079]

13. Treatment
1. Small asymptomatic cases may be managed expectantly.
2. Surgery should be considered for progressive neurological deterioration with larger lesions.
Outcome
Reported mortality: 25–42%. Mortality is higher in the presence of altered levels of
consciousness. Mortality rate may actually be lower (24%) than with all-comers.33 This is
significantly lower than SDH in other sites (see above).
[Handbook of Neurosurgery 10th Greenberg 1079-80]

14. Infantile acute subdural hematoma
Definition
An acute SDH in an infant due to minor head trauma without initial loss of consciousness or
cerebral contusion possibly due to rupture of a bridging vein.
General information
 The most common trauma is a fall backwards from sitting or standing.
 These clots are rarely pure blood, and are often mixed with fluid. 75% are bilateral or have
contralateral subdural fluid collections.
 It is speculated that IASDH may represent acute bleeding into a preexisting fluid collection
 Skull fractures are rare
[Handbook of Neurosurgery 10th Greenberg 1081]

15. Clinical features
[Handbook of Neurosurgery 10th Greenberg 1081]
1. Patients are usually < 2 yrs old (most are 6–12 mos)
2. The infants will often cry immediately
3. Then (usually within minutes to 1 hour) develop a generalized seizure.

16. Treatment
[Handbook of Neurosurgery 10th Greenberg 1081]
 Treatment is guided by clinical condition and size of hematoma.
 Minimally symptomatic cases (vomiting, irritability, no altered level of consciousness and no motor
disturbance) with liquefied hematoma may be treated with percutaneous subdural tap, which may be
repeated several times as needed.
 Chronically persistent cases may require a subduroperitoneal shunt.
 More symptomatic cases with high density clot on CT require craniotomy. A subdural membrane
similar to those seen in adult chronic SDH is not unusual.36 Caution: these patients are at risk of
developing intraoperative hypovolemic shock.

17. Chronic subdural hematoma
General information
 Originally termed “Pachymeningitis Hemorrhagica Interna” by Virchow37 in 1857.
 Chronic subdural hematomas (CSDH) generally occur in the elderly, with an average
age of ≈ 63 yrs; exception: subdural collections of infancy
 CSDHs are bilateral in ≈ 20–25% of cases
 Classically CSDHs contain dark “motor oil” fluid which does not clot.
 When the subdural fluid is clear (CSF), the collection is termed a subdural hygroma.
[Handbook of Neurosurgery 10th Greenberg 1081]

18. Aetiology and Risk factor
1. Head trauma is identified in < 50%
2. Coagulopathies (including therapeutic anticoagulation)
3. Patients at risk for falls (e.g., with hemiplegia from previous stroke).
4. Seizures
5. CSF shunts
6. Alcohol abuse
[Handbook of Neurosurgery 10th Greenberg 1081]

19. Pathophysiology of CSDH
Blood within the subdural
space evokes an
inflammatory response.
Fibroblasts invade the
clot and form
neomembranes on the
inner (cortical) and
outer (dural) surface.
This is followed by
ingrowth of
neocapillaries,
enzymatic fibrinolysis
Liquefaction of blood
clot.
Fibrin degradation
products are
reincorporated into
new clots
Inhibit hemostasis.
Rebleeding from the
neomembranes on the
one hand and
reabsorption of fluid.
Formation of CSDH

20. Presentation of CSDH
1. Headache
2. Confusion
3. Language difficulties (e.g., wordfinding difficulties or speech arrest, usually with
dominant hemisphere lesions)
4. TIA-like symptoms
5. Coma
6. Hemiplegia
7. Seizures (focal, or less often generalized).
[Handbook of Neurosurgery 10th Greenberg 1082]

21. Markwalder neurologic grading scale for CSDH

22. Treatment
1. Seizure prophylaxis
2. Coagulopathies (including anticoagulation & antiplatelet therapy) should be reversed
Treatment indications of the hematoma
1. Symptomatic lesions (usually > 1cm maximal thickness). Symptoms include: focal deficit, mental
status changes, seizures, severe h/a…
2. Or progressive increase in size on serial imaging (CT or MRI scans)
Treatment options
1. Surgical evacuation of the hematoma: numerous methods employed (see below)
2. Endovascular embolization of the middle meningeal artery (p.1935)
[Handbook of Neurosurgery 10th Greenberg 1082]

23. Surgical options
1. Placing two burr holes, and irrigating through and through with tepid saline
until the fluid runs clear
2. Single “large” burr hole with irrigation and aspiration
3. Single burr hole drainage with placement of a subdural drain, maintained for
24–48 hrs (removed when output becomes negligible)
4. Twist drill craniostomy
[Handbook of Neurosurgery 10th Greenberg 1082]

24. Spontaneous subdural hematoma
Occasionally patients with no identifiable trauma will present with severe
headache with or without associated findings (nausea, seizures, lethargy, focal
findings including possible ipsilateral hemiparesis)
CT or MRI discloses a subdural hematoma that may be acute, subacute or chronic
in appearance.
The onset of symptoms is often sudden.
[Handbook of Neurosurgery 10th Greenberg 1084]

25. Risk factors
1. Hypertension
2. Vascular abnormalities: arteriovenous malformation (AVM), aneurysm
3. Neoplasm
4. Infection: including meningitis, tuberculosis
5. Substance abuse: alcoholism, cocaine61
6. Hypovitaminosis: especially vitamin c deficiency
7. Coagulopathies
8. Seemingly innocuous insults (e.g., bending over) or injuries resulting in no direct
trauma to the head (e.g., whiplash injuries)
9. Intracranial hypotension: spontaneous or following epidural anesthesia, lumbar
puncture, or VP shunt.
[Handbook of Neurosurgery 10th Greenberg 1085]

26. Etiology
The bleeding site was determined in 14 of the 21 cases, and was arterial in each, typically involving a
cortical branch of the MCA in the area of the Sylvian fissure
Possible mechanisms for arterial rupture in idiopathic acute subdural hematoma (ASDH) include tears
occurring secondary to sudden head movements or trivial head trauma of the following-
1. Small artery at perpendicular branch point off a cortical artery
2. Small artery connecting the dura and cortex
3. Adhesions between cortical artery and dura
[Handbook of Neurosurgery 10th Greenberg 1085]

27. Treatment
 Same as for traumatic SDH.
 If symptomatic and/or > ≈ 1cm thick, surgical evacuation is the treatment of choice.
 For subacute to chronic subdurals, burr hole evacuation is usually adequate
 For acute SDH, a craniotomy is usually required, and should expose the Sylvian fissure
to identify bleeding point. Microsurgical repair of arterial wall has been described.
[Handbook of Neurosurgery 10th Greenberg 1085]