SUBDURAL HEMATOMA

SUBDURAL HEMATOMA
Acute SDHs are less than 72 hours old and are
hyperdense compared to the brain on CT scan.
Subacute SDHs are 3-20 days old and are isodense
or hypodense compared to the brain. 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. In
one study, 82% of comatose patients with acute SDH
had parenchymal contusions (Kotwica,1993)

Most chronic SDHs are believed to be derived

from SDG (Subdural hygroma). 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 SDG to
form.
SDG may occur after head trauma and
frequently is asymptomatic.
The minority of chronic SDH cases are
derived from acute SDH cases that have
matured for lack of treatment.

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 blood
vessels. 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. Bridging veins commonly are

found along the sagittal sinus and around

the anterior tip of the temporal lobe.
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

Most chronic SDHs begin as SDG. An SDG 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 13 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.
Kawakami (1989) discovered that the coagulation
and fibrinolysis systems both were excessively
activated in chronic SDH. This results in defective clot
formation and recurrent hemorrhage.

CLINICAL :
Acute subdural hematoma

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.

Neurological

findings :
(1) altered level of consciousness
(2) a 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).
Less common findings include papilledema and
unilateral or bilateral cranial nerve VI palsy.

 Chronic subdural hematoma

Most adults with chronic SDH are older than 50 years.

One quarter to one half of 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.
The average time between head trauma and chronic SDH
diagnosis is 4-5 weeks.
Risk factors for a chronic SDH include chronic alcoholism,
epilepsy, coagulopathy, arachnoid cysts, anticoagulant
therapy
(including
aspirin),
cardiovascular
disease
(hypertension, arteriosclerosis),
thrombocytopenia, and
diabetes.

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 unreactive dilated pupil.
In patients younger than 60 years, headache is a
common presenting symptom.

Workup
Lab Studies :
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

Imaging Studies :
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. Acute SDHs usually are
unilateral.

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.
Typical signs of mass effect may be
observed, such as midline shift and
ventricular compression.

Head CT

Acute subdural
hematoma. Note the
bright (white) image
properties of the
blood on this
noncontrast cranial
CT scan.

Head CT
Subacute subdural
hematoma. The
crescent-shaped clot is
less white than on CT
scan of acute subdural
hematoma. In spite of
the large clot volume,
this patient was awake
and ambulatory.

Treatment
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.

INDICATIONS of surgery
Emergent surgical evacuation should occur in
patients with an acute SDH larger than 5mm 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.