SDHs are blood clots that form between the dura and the brain.

Usually they are caused by

the movement of the brain relative to the skull, as seen in acceleration-deceleration injuries.
These hematomas are common in patients with brain atrophy, such as alcoholic or elder
patients. In these patients, the superficial bridging vessels traverse greater distances than in
patients with no atrophy. As a result, the vessels are more likely to rupture with rapid
movement of the head. Once they are ruptured, blood can fill the potential space between the
dura and arachnoid.
SDHs are more common than EDHs, occurring in up to 30% of patients with severe head
trauma.159 The slow bleeding of venous structures delays the development of clinical signs and
symptoms. As a result, the hematoma compresses the underlying brain tissue for prolonged
periods and can cause significant tissue ischemia and damage.
The patients clinical presentation depends on the amount of brain injury sustained at the
time of trauma and the rate of SDH expansion. If the patient with an SDH was rendered
unconscious at the time of trauma, the prognosis is poor; these patients often have
concurrent DAI. The signs and symptoms after injury that produces an SDH are initially related
to the other intracranial injuries that may have been sustained and then to the slow expan-
sion of the SDH.
SDHs are classified by the time to clinical presentation. Acute SDHs are symptomatic within
24 hours after trauma. Patients with acute SDHs often have a decreased level of
consciousness. Most patients with an SDH have a GCS score less than 8. Approximately 12 to
38% of patients will have a lucid period at some point in their presentation. The overall
mortality of patients who have an SDH and require surgical intervention is 40 to 60%.159
Because of associated brain injury caused by the SDH, the delay in clinical signs and
symptoms, and the more advanced mean age of the at-risk population, the mortality
associated with SDH is much higher than that associated with EDH. Pupil inequality, motor
deficit, and other signs consistent with increased brain swelling may be present on the initial
examination. If the patient is deeply comatose at presentation with flaccidity and without
signs of brainstem activity, supportive care should be considered in the ED. Subsequent
management decisions should be discussed with the patients family and the attending
neurosurgeon.
If the SDH is very small (only a few millimeters thick at its widest point on CT scan), some
neurosurgeons may choose careful observation for these patients. Even a small SDH may be
accompanied by extensive brain tissue damage that can cause an increase in ICP sufficient to
precipitate a herniation syndrome. Current consensus guidelines recommend that acute SDHs
with a thickness greater than 10 mm or a midline shift of more than 5 mm on CT should be
evacuated surgically, regardless of the patients GCS score. 159 Research indicates that the
longer the time between clinical worsening and operative treatment, the worse the patients
clinical outcome. In these cases, surgical evacuation should be performed as soon as
possible.159
Unlike EDHs, SDHs often extend beyond the suture lines (Fig. 41-11). An SDH may follow the
contour of the tentorium and be detected within the interhemispheric fissure (Fig. 41-12).
Many patients with an acute SDH also show CT evidence of intracerebral lesions contralateral
to the SDH.
A subacute SDH is symptomatic between 24 hours and 2 weeks after injury. It may appear
hypodense or isodense on CT scans. Contrast increases detection of isodense lesions. Patients
complain of a headache, altered mental status, or focal deficits. Most patients with subacute
SDH require surgical evacuation of the lesion.
A chronic SDH becomes symptomatic 2 weeks or more after trauma. The signs and
symptoms may be very subtle or nonspecific, but many patients demonstrate unilateral
weakness or hemiparesis.23 Most report an altered level of consciousness, but some patients
are unable to recall their head injury or describe only a minor injury. In 20% of cases, chronic
subdurals are bilateral. A chronic SDH may have initially been a small asymptomatic SDH that
eventually expanded owing to a combination of recurrent hemorrhage and escape of plasma
into the hematoma. At some point, a critical mass is reached and the chronic SDH becomes
symptomatic. On CT scan, a chronic SDH may appear isodense or hypodense to brain
parenchyma. In these cases, indirect evidence of the lesion includes a midline shift,
effacement of the ipsilateral cortical sulci, and ventricular compression. Contrast may
increase the likelihood of identifying a chronic SDH that has become isodense. On CT scan,
blood of various ages is seen as a mixed-density lesion. On MRI, a chronic SDH appears hyper-
dense. The treatment of chronic SDHs is controversial. If they become symptomatic, chronic
SDHs require surgical evacuation. Most patients have a good outcome after surgery. Overall,
the mortality from surgically drained chronic SDH approaches 4%, with decreased survival in
elders.23
 The prognosis of SDH does not entirely depend on the size of the hematoma but rather on
the degree of brain injury caused by the pressure of the expanding hematoma on underlying
tissue or by other intracranial injury caused by the initial impact. Mortality is highest in older
people, in patients who have a GCS score of 8 or less, and in those with signs of acute
herniation syndrome on initial ED presentation. Posterior fossa SDHs make up less than 1% of
all reported SDHs. They are caused by occipital trauma that tears bridging vessels or venous
sinuses. Clinical manifestations of posterior SDH vary but usually include nausea, vomiting,
headache, and decreased level of consciousness. Occasionally, CN palsies may be found, as
well as nuchal rigidity, cerebellar signs and symptoms, and papilledema. On a CT scan, a
posterior fossa SDH does not cross the midline or extend above the tentorium. The outcome
of a posterior SDH is very poor.
In children the presence of an SDH should prompt consideration of child abuse. Many types of
injury can produce SDH in children, but the infant who is repeatedly and forcibly shaken is
especially susceptible.130 Infants may have SDH because of birth trauma. In these cases the
initial clinical manifestation may be a generalized seizure within the first 6 months of life. On
examination the infant may have a bulging fontanel or an enlarged head circumference. A
careful history may elicit long-standing constitutional symptoms, such as failure to thrive or
lethargy. (

William G. Heegaard)

Subdural Hematoma
Subdural hematoma occurs when blood accumulates between the dura mater and
arachnoid layer. Most commonly, subdural hematoma occurs in the setting of trauma.
This can occur following either major or minor trauma, with the latter often occurring in
older patients with cerebral atrophy, a condition that lends itself to stretching and
rupture of bridging veins that run in the subdural space. Patients taking anticoagulants
and antiplatelet drugs are at greatest risk. As with epidural hematomas, early evacuation
of the hematoma is associated with better outcome.
Signs and symptoms of a subdural hematoma may evolve gradually over several days (in
contrast to epidural hematomas) because the hematoma is due to slow venous bleeding.
Headache is a universal complaint. Drowsiness and obtundation are characteristic
findings, but the magnitude of these changes may fluctuate from hour to hour.
Lateralizing neurologic signs eventually occur, manifesting as hemiparesis, hemianopsia,
or language disturbances. Elderly patients may have unexplained signs of progressive
cognitive decline or dementia.
Conservative medical management of subdural hematomas may be acceptable for
patients whose condition stabilizes, but surgical evacuation of the clot is desirable in
most patients. Most subdural hematomas can be drained via burr holes; the procedure
can be performed under general anesthesia, local anesthesia, or monitored anesthesia
care. If the subdural hematoma is particularly large, is chronic, or consists of clotted
blood, removal may require craniotomy. Because a subdural hematoma is usually caused
by venous bleeding, normocapnia is desirable following evacuation of the hematoma to
allow for a larger brain volume, which may help tamponade any sites of venous bleeding.
(

JEFFREY J. PASTERNAK)

Subdural Hematoma
SDHs are located between the dura and arachnoid layer and may result from arterial or venous
hemorrhage. Classically, SDHs are caused by tearing of bridging veins that span the subdural
space to drain cortical blood directly into dural sinuses. Many SDHs, however, result from bleeding
from other structures adjacent to the subdural space, such as superficial cortical vessels. SDH can
be classified as acute, subacute, or chronic, although there is no uniformity of nomenclature. 65,105,106
Pathologically, an acute SDH is composed of clot and blood (within 48 hours), a subacute SDH
represents a mixture of clotted blood and fluid (2-14 days), and a chronic SDH is one that is in fluid
phase (>14 days; Table 346-6). 65 Clinically, an acute SDH becomes evident within 3 days of injury,
subacute between 3 and 21 days, and chronic if more than 21 days elapse between injury and
clinical presentation. Radiographically, acute SDHs are hyperdense on CT scan, subacute SDHs are
hyperdense to isodense, and chronic SDHs are hypodense relative to adjacent brain.

Acute Subdural Hematoma. Acute SDHs account for 50% to 60% of all SDHs. They are most
common after sudden head movements that occur with assaults or falls. 73 In a review of patients
with acute SDH, 72% had sustained falls or assaults, whereas only 24% experienced motor vehicle
crash.30 Rarely, acute SDH may occur spontaneously (or after minor trauma) in patients receiving
chronic anticoagulation therapy 107,108 or after rupture of a posterior communicating artery aneurysm
(n = 4 in the 30+-year career of the senior author [J.P.M.]).
Most acute SDHs result from venous vascular injury at the brain surface, resulting in two distinct
pathologies.109 The first type of hematoma, produced by contact forces and associated with
contusions or lacerations, results from cortical bleeding into the adjacent subdural space and is
most common at the temporal pole. This complex of SDH and damaged and necrotic brain is
termed burst lobe. The second type of SDH is located over the cerebral convexity and is produced
by inertial forces that tear bridging veins.30,109 The underlying brain damage in this type of injury is
usually milder, and primarily caused by local ischemia from mass effect or compromised venous
outflow. Rapid deterioration, as in the case of classic EDH, may accompany these lesions,
especially if cortical arteries are ruptured. Despite the often relatively minor underlying brain
damage, prognosis is generally poor in these patients unless the hematoma is rapidly evacuated. 110
Cerebral ischemia plays a critical role in the pathology of SDH and has been demonstrated both
experimentally111 and in postmortem studies. 112 The mechanisms responsible for ischemia following
SDH are poorly understood, but are likely related to compressive effects of the hematoma and
elevated ICP with resultant compromised CPP. Evidence of brain compression resulting in ischemia
was reported by Schroder and colleagues 113; in two patients with acute SDHs, preoperative cerebral
blood flow (CBF) was in the ischemic range (<18 mL/100 g per minute), and cerebral blood volume
(CBV) was approximately half of normal. These values normalized immediately after surgical evac-
uation. In a small series of five patients with acute SDHs and low GCS scores (5), Verweij and
colleagues found ICP between 40 and 80 mm Hg, CPP between 10 and 60 mm Hg, low jugular
venous oxygen saturation (40%-60%), and low CBF measured with laser Doppler immediately
before hematoma evacuation.114 Values began to normalize with elevation of the bone flap, opening
of the dura, and subsequent hematoma removal.
Timely clot evacuation (within 4 hours) generally results in significantly improved neurological
outcome.115 Patients with initial CT evidence of significant hemispheric or generalized brain swelling
have extremely poor outcome with or without early surgery. 116 The prognosis of SDH is still poor in
many cases. It is thought that the coexisting brain damage (DAI, contusion, laceration) is
responsible for poor neurological function after injury. In a subset of patients, compression of the
microcirculation and resultant low CBF may explain the poor clinical condition and outcome.
Patients who deteriorate after a lucid interval (i.e., patients who talk and die) may be the subset
of patients who experience this type of insult.113 (
Kiarash Shahlaie)

Subdural Hematoma
Subdural hematoma (SDH) is found in 10% to 20% of all patients with TBI and is characterized by
blood beneath the dura. SDHs usually are caused by bleeding from torn bridging veins in the sub-
dural space and frequently are associated with parenchymal lesions. On head CT, they classically
appear as crescent-shaped collections that cross sutures lines and layer along the falx (Figure 2).
An acute SDH should be evacuated, regardless of the patients GCS, if the hematoma is more than
10 mm thick or if there is midline shift greater than 5 mm. In a patient with a SDH and a GCS of 8
or less, surgical evacuation also should occur if the patients GCS has dropped by 2 or more points
since the time of injury, the patient has anisocoria or fixed pupils, or the ICP is greater than 20 mm
Hg. Depending on the size and location of the SDH, there are multiple surgical approaches ranging
from craniotomy to hemicraniectomy with or without a dural patch to allow for swelling.
Patients with a GCS of 8 of less who do not meet the criteria for surgery can be managed
nonoperatively but must have an ICP monitor, close observation in an ICU setting, and serial head
CTs as recommended by the neurosurgery department. (

Carrie Sims, MD)

Subdural Hematoma
The SDH develops within the potential subdural space between the arachnoid mater and the inner
layer of the dura. Subdural hematomas most commonly result from tearing of cortical bridging
veins, which extend from the surface of the brain, traverse the subarachnoid space, penetrate the
dura mater, and travel a variable distance within the dura before draining into a venous sinus. Less
commonly, subdural hematomas can result from disruption of penetrating branches of superficial
cerebral arteries, pial vessels, or arachnoid granulations. 50
On neuroimaging, SDH most commonly appears as a crescent-shaped extra-axial collection
overlying a cerebral convexity (Fig. 344-10A). Unlike the firm attachment between outer periosteal
dural layer and the inner table of the skull, the dura and arachnoid mater are only loosely attached
to each other through an intervening, thin, delicate fibroblast layer that is easily disrupted. 56 Thus,
despite usually originating from venous bleeding, SDH may thus be extensive and spread over
most or all of a cerebral convexity. SDH also frequently extends along the anterior or posterior falx,
where it is recognized as a thickened shaggy falx (Fig. 344-10B). The tentorial SDH is also
common; it appears as high CT density along the tentorium cerebelli, either bilaterally asymmetric
or bilaterally symmetric, but unusually prominent or thickened in appearance (Fig. 344-10C). This
should not be confused with traumatic subarachnoid hemorrhage.
Unlike EDH, which does not cross most suture lines because of the tight attachment of the outer
periosteal layer of dura to most of the cranial sutures (with exception of the sagittal suture near
the vertex), the SDH freely crosses suture lines. Unlike the EDH, SDH cannot cross the thick dural
reflections formed by the falx cerebri and tentorium cerebelli. Also unlike EDH, there is no known
consistent association between SDH and skull fracture. Finally, unlike EDH, the SDH is more often
located at the contrecoup site than at the coup site.50
As with hyperacute EDH, the hyperacute SDH, as well as SDH in patients with coagulopathies,
may demonstrate heterogeneous high and low CT density, similar to the aforementioned
hyperacute mixed-density EDH. In the absence of an underlying coagulopathy, most acute SDHs
become uniformly hyperdense on CT within the first hour or two after formation. Over the initial
several days to 1 week after formation, the SDH progressively decreases in CT density, by an
estimated 0.7 to 1.5 HU per day on average because of the chemical breakdown of globin
molecules.57 Of subacute SDHs between 1 and 3 weeks of age, approximately 50% are isodense to
the brain, and 50% are hypodense. At 3 weeks of age, 10% are isodense and 90% are hypodense. 58
Rebleeding into a chronic SDH can result in a laminated appearance, with alternating hyperdense
and hypodense layers or internal septations (Fig. 344-11A). Such acute-on-chronic SDHs can also
appear as a heterogeneous collection with a fluid-fluid level with high CT density fluid layering
below and low-density fluid layering above (Fig. 344-11B). Calcifications occur after months to
years in an estimated 0.3% to 2.7% of chronic SDHs.57 (

Esther L. Yuh)