SUB-DURAL HAEMATOMA
Arachnoid cysts
A subdural hematoma (SDH) is classified by the amount of time
that has elapsed from the inciting event, if known, to the
diagnosis.
When the inciting event is unknown, the appearance of the
hematoma on CT scan or MRI can help date the hematoma.
1. Acute SDHs are less than 72 hours old and are hyperdense
compared to the brain on CT scan.
2. Subacute SDHs are 3-20 days old and are isodense or
hypodense compared to the brain.
3. Chronic SDHs are older than 20 days and are hypodense
compared to the brain.
 An acute SDH commonly is associated with extensive
primary brain injury. This diffuse parenchymal injury
correlates strongly with the outcome of the patient
 The presence of brain atrophy or loss of brain tissue due to
any cause, such as old age, alcoholism, or stroke, provides
a potential space between the dura and the brain surface
for a SDH to form
Pathophysiology:
Acute subdural hematoma
 The usual mechanism to produce an acute SDH is high-
speed impact to the skull. This causes brain tissue to
accelerate relative to a fixed dural structure, which, in turn,
tears bridging veins. This mechanism also leads to
associated contusions, brain edema, and diffuse axonal
injury.
 The ruptured blood vessel often is a vein connecting the
cortical surface to the dural sinuses.
 Alternatively, a cortical vessel can be damaged by direct
laceration. An acute SDH due to a ruptured cortical artery
may be associated with only minor head injury, and no
cerebral contusions may be associated.
Chronic subdural hematoma
 A higher incidence of chronic SDH exists in men. The male-
to-female ratio is 2:1. Most adults with chronic SDH are
older than 50 years.
 25-50% of chronic SDH pts have no identifiable history of
head trauma. If a patient does have a history of head
trauma, it usually is mild.
 The average time between head trauma and chronic SDH
diagnosis is 4-5 weeks.
 Most chronic SDHs are believed to be derived from
subdural hygroma(hygroma- A cystic swelling containing a
serous fluid)
 A subdural hygroma begins as a separation in the dura-
arachnoid interface, which then is filled by cerebrospinal
fluid (CSF).
 Dural border cells proliferate around this CSF collection to
produce a neomembrane. Then, fragile new vessels grow
into the membrane. These vessels can hemorrhage and
become the source of blood into the space, which results in
the growth of the chronic SDH.
 Chronic SDHs that form from acute SDHs have membranes
between the dura and hematoma at 1 week and between
the brain and hematoma at 3 weeks. As stated above, new
fragile vessels grow into these membranes.
 The hematoma liquefies at 1-3 weeks of age and becomes
hypodense on CT scan.
 If not resorbed, the vessels in the membranes surrounding
the hematoma can hemorrhage repeatedly, resulting in the
enlargement of the hematoma.
Risk factors for a chronic SDH
1.Chronic alcoholism
2.Epilepsy
3.Coagulopathy
JUDY WAWIRA GICHOYA yr 2007
4.
5.Anticoagulant therapy (including aspirin)
6.Cardiovascular disease (hypertension, arteriosclerosis),
7.Thrombocytopenia
8.Diabetes
9.Severe dehydration
10.Extremes of ages
 Clinical presentation often is insidious, with symptoms of
decreased level of consciousness, balance problems,
cognitive dysfunction and memory loss, motor deficit (such
as a hemiparesis), headache, or aphasia. Acute
presentation also is possible, as in the case of a patient
who presents with a seizure.
 Neurologic examination may demonstrate hemiparesis,
papilledema, hemianopsia, or third cranial nerve
dysfunction, such as an unreactive dilated pupil or a
laterally deviated eye of limited movement. In patients aged
60 years or older, hemiparesis and reflex asymmetry are
common presenting signs. In patients younger than 60
years, headache is a common presenting symptom.
 Chronic SDHs are observed bilaterally in 8.7-32% of cases.
Clinical presentation
Acute SDH
 Acute SDHs are most likely to occur after head injury from
a fall, motor vehicle accident, or an assault.
 More common in men compared to women with a ratio in
the range of 3:1.
 Patients found to have an acute SDH are on average older
than other trauma patients
 Thus older patients appear to be at greater risk for
developing an acute SDH after head injury. This is believed
to be due to older patients having more atrophy, which
allows more sheer force against bridging veins immediately
after impact.
 The clinical presentation of an acute SDH depends on the
size of the hematoma and the degree of any associated
parenchyma brain injury.
 All patients with traumatic brain injury should be evaluated
using the Glasgow Coma Score (GCS).
 Common neurological findings include
(1) altered level of consciousness
(2) dilated pupil ipsilateral to the hematoma
(3) failure of the ipsilateral pupil to react to light
(4) Hemiparesis contralateral to the hematoma.
Less commonly, the hemiparesis may be ipsilateral if caused by
direct parenchymal injury or by compression of the cerebral
peduncle (contralateral to the hematoma) against the edge of
the tentorium cerebelli (Kernohan notch)
(5) papilledema and unilateral or bilateral cranial nerve VI palsy.
Chronic subdural hematoma
 A higher incidence of chronic SDH exists in men. The male-
to-female ratio is 2:1.
 Most adults with chronic SDH are older than 50 years.
 25-50% patients with chronic SDH have no identifiable
history of head trauma. If a patient does have a history of
head trauma, it usually is mild.
Indications for surgery
 Emergent surgical evacuation should occur in patients with
an acute SDH larger than 5 mm in thickness (as measured
by axial CT scan) and causing any neurological signs, such
as lethargy, unresponsiveness (coma), or focal neurological
deterioration.
 Surgery for chronic SDH is indicated if SDH is symptomatic
or producing significant mass effect on imaging studies
Lab Studies:
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 To determine whether defective coagulation was involved in
the formation of the acute SDH and to correct any
coagulation abnormalities a prothrombin time (PT),
activated partial thromboplastin time (aPTT), and a platelet
count should be performed. A bleeding time may detect
platelet dysfunction.
 Routine trauma lab studies that aid in the initial assessment
include hemoglobin, electrolytes, and a drug/alcohol
screen. Obviously, the drug and alcohol screens are
important in correlating the neurological examination with
the imaging studies.
Imaging Studies:
a) Computed tomography scan of the head without contrast
 Acute SDH appears on CT scan as a crescent-shaped
hyperdense area between the inner table of the skull and
the surface of the cerebral hemisphere
 The characteristic evolution of an SDH appearance on CT
scan is as follows: In the first week, the SDH is hyperdense
to brain tissue. In the second and third weeks, the SDH
appears isodense to brain tissue After the third week; the
SDH is hypodense to brain tissue.
 Often, a chronic SDH will appear as a heterogeneously
dense lesion indicative of recurrent bleeding with a fluid
level between the acute (hyperdense) and chronic
(hypodense) components of the hematoma
 Typical signs of mass effect may be observed, such as
midline shift and ventricular compression.
b).MRI
MRI may be particularly helpful in diagnosing bilateral chronic
SDH because a midline shift may not be apparent.
Pick the acute hemorrhages earlier than CT-scan.
Medical therapy:
Acute subdural hematoma
 Small acute SDHs less than 5 mm thick on axial CT
images, without sufficient mass effect to cause midline shift
or neurological signs, can be followed clinically .
 Hematoma resolution should be documented by serial
imaging because an acute SDH that is treated
conservatively can evolve into a chronic hematoma.
 Emergent medical treatment of an acute SDH causing
impending transtentorial herniation is the bolus
administration of mannitol (in the patient who is adequately
fluid resuscitated with an adequate blood pressure).
 Surgical evacuation of the lesion is the definitive treatment
and should not be delayed.
Chronic subdural hematoma
 Without mass effect on imaging studies and no neurological
symptoms or signs except mild headache, a chronic SDH
can be followed with serial scans and may resolve.
 No medical therapy has been shown to be effective in
expediting rapid resolution of acute or chronic SDHs
Surgical therapy:
Acute subdural hematoma
 Surgery for acute SDH consists of a large craniotomy
(centered over the thickest portion of the clot) to
decompress the brain, stop any active subdural bleeding,
and evacuate any intraparenchymal hematomas in the
immediate vicinity of the acute SDH.
 The craniotomy exposure should include the sylvian fissure
because this can be a likely source of a ruptured cortical
vessel. If brain injury and edema are associated, an
intracranial pressure (ICP) monitor should be placed.
Chronic subdural hematoma
JUDY WAWIRA GICHOYA yr 2007
 Liquefied chronic SDHs commonly can be treated with
drainage through 1-2 burr holes. Burr holes are placed so
that conversion to a craniotomy is possible if needed. A
closed drainage system sometimes is left in the subdural
space for 24-72 hours postoperatively. Small catheter
drainage via twist drill craniotomy at the bedside also has
been described as adequate treatment.
 A nonliquified chronic SDH cannot be decompressed
adequately by burr holes and must be removed by
craniotomy.
 Bilateral chronic hematomas must be drained from both
sides, usually during the same operation through burr holes
placed on each side of the head.
Preoperative details:
 Phenytoin (Dilantin) is administered to decrease the risk of
developing early posttraumatic seizures (within the first 7 d
after the injury).
 Patients have an estimated risk of greater than 20% for
developing posttraumatic epilepsy after an acute SDH.
 Phenytoin only should be continued for 7 days after the
injury because it is not effective in preventing late
posttraumatic seizures (beginning 1 wk or more after the
injury).
Acute subdural hematoma
 After the evacuation of an acute SDH, medical treatment is
aimed at controlling the ICP below 20 mm Hg and
maintaining the cerebral perfusion pressure above 60-70
mm Hg. These parameters are vital to maintain during the
perioperative period.
 Within 24 hours of removing an acute SDH, a follow-up CT
scan should be obtained routinely
Complications
1.absess formation
2.Raised ICP
3.Permanent neurological deficits
4.Rebleeding
5.Meningitis
6.Convulsive disorders
7.Hydrocephalus
8.Surgical complications, including acute SDH formation,
intraparenchymal hematoma, or tension pneumocephalus
postoperatively
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