of subarachnoid cisterns that may be mistaken
for subarachnoid hemorrhage on CT, but is
probably an artifact of partial volume averag-
ing.
14
In these instances, MRI helps rule out
subarachnoid hemorrhage.
In those circumstances where CT scan is not
readily available, a plain skull film can often
identify the fracture. Certainly, all patients with
head trauma should be cautioned that it is im-
portant to remain under the supervision of a
family member or friend for at least 24 hours;
the patient must be returned to the hospital
immediately if a lapse of consciousness occurs.
Careful follow-up is required even in patients
in whom the original CT was negative, as oc-
casionally the development of the hematoma is
delayed.
15
In comatose patients with epidural hemato-
mas, the treatment is surgical evacuation. The
surgery is an emergency, as the duration from
time of injury to treatment is an important
determinant of the prognosis.
16
Other factors
in determining outcome are age, depth of coma,
degree of midline shift, and size of the hema-
toma.
17
Most patients operated on promptly
recover, even those whose pupils are dilated
and fixed before surgery.
18
Rarely, acute epi-
dural hematomas resolve spontaneously, prob-
ably a result of tamponade of the bleeding
vessel by underlying edematous brain.
19
Subdural Hematoma
The unique anatomy of the subdural space also
can produce much slower, chronic subdural
hematomas in patients in whom the history of
head trauma is remote or trivial. The potential
space between the inner leaf of the dura mater
and the arachnoid membrane (subdural space)
is traversed by numerous small draining veins
that bring venous blood from the brain to the
dural sinus system that runs between the two
leaves of the dura. These veins can be dam-
aged with minimal head trauma, particularly
in elderly individuals with cerebral atrophy in
whom the veins are subject to considerable
movement of the hemisphere that may occur
with acceleration-deceleration injury. When
focal signs are absent, these cases can be quite
difficult to diagnose. A useful rule when faced
with a comatose patient is that ‘‘it could always
be a subdural,’’ and hence imaging is needed
even in cases where focal signs are absent.
Subdural bleeding is usually under low pres-
sure, and it typically tamponades early unless
there is a defect in coagulation. Acute subdural
bleeding is particularly dangerous in patients
who take anticoagulants for vascular throm-
botic disease. Continued venous leakage over
several hours can cause a mass large enough to
produce herniation. Warfarin inhibits the syn-
thesis of vitamin K-dependent clotting factors
II, VII, IX, and X and the anticoagulant pro-
teins C and S. The conventional treatment in-
cludes administering fresh frozen plasma and
vitamin K. However, these measures take hours
to days to become effective and are too slow
to stop subdural bleeding. Hence, in the case
of a subdural (or epidural) bleed in a patient on
warfarin, it is important to administer pooled
cryoprecipitate of factors II, VII, IX, and X
immediately. Recombinant factor VII has also
been used,
20
but data are lacking as to its ef-
fectiveness.
Acute subdural hematomas, which are usu-
ally the result of a severe head injury, are of-
ten associated with underlying cerebral contu-
sions. Rarely, acute subdural hematomas may
occur without substantial trauma, particularly
in patients on anticoagulants. Rupture of an
aneurysm into the subdural space, sparing the
subarachnoid space, can also cause an acute sub-
dural hematoma. The mass accumulates rapidly,
causing underlying brain edema and herniation.
Ischemic brain edema results when herniation
compresses the anterior or posterior cerebral
arteries and causes ischemic brain damage.
21
Patients with acute subdural hematomas usually
present with coma, and such cases are surgical
emergencies. Early evacuation of the mass pro-
bably improves outcome, but because of un-
derlying brain damage, mortality remains sig-
nificant. Prognostic factors include age, time
from injury to treatment, presence of pupillary
abnormalities, immediate and persisting coma
as opposed to the presence of a lucid interval,
and volume of the mass.
22
Chronic subdural hematomas usually occur
in elderly patients or those on anticoagulants.
Chronic alcoholism, hemodialysis, and intra-
cranial hypotension are also risk factors. A his-
tory of trauma can be elicited in only about one-
half of patients, and then the trauma is usually
minor. The pathogenesis of chronic subdural
hematomas is controversial. One hypothesis is
that minor trauma to an atrophic brain causes a
small amount of bleeding. A membrane forms
Specific Causes of Structural Coma
123
around the blood. Vessels of the membrane
are quite friable and this, plus an increase of fi-
brinolytic products in the fluid, leads to repet-
itive bleeding, causing an enlarging hema-
toma.
23
Another hypothesis is that minor trauma
leads to the accumulation of either serum or ce-
rebrospinal fluid (CSF) in the subdural space.
This subdural hygroma also causes membrane
formation that leads to repetitive bleeding and
an eventual mass lesion.
24
If the hemorrhage is
small and no additional bleeding occurs, the
hematoma may resorb spontaneously. How-
ever, if the hematoma is larger or it is enlarged
gradually by recurrent bleeds, it may swell as
the breakdown of the blood into small mole-
cules causes the hematoma to take on additional
water, thus further compressing the adjacent
brain.
24
In addition, the membrane surrounding
the hematoma contains luxuriant neovascular-
ization that lacks a blood-brain barrier and may
cause additional edema in the underlying brain.
Chronic subdural hematomas are usually uni-
lateral, overlying the lateral cerebral cortex, but
may be subtemporal. They are bilateral in about
20% of patients, and occasionally are interhemi-
spheric (i.e., within the falx cerebri), sometimes
causing bilateral leg weakness by compression
of the medial frontal lobes.
Table 4–2 lists the clinical features of the
typical patient with a chronic subdural hema-
toma who presents with a fluctuating level of
consciousness.
A majority of patients, but no more than
70%, complain of headache. A fluctuating level
of consciousness is common.
23,25,26
There may
be tenderness to percussion of the skull at the
site of the hematoma. About 15% to 30% of
patients present with parenchymal signs such
as seizures, hemiparesis, or visual field defects.
Unusual focal signs such as parkinsonism, dy-
stonia,
27
or chorea occasionally confuse the
clinical picture. Focal signs such as hemipare-
sis or aphasia may fluctuate, giving an appear-
ance similar to transient ischemic attacks.
28
Occasionally patients may have unilateral as-
terixis. Because subdural hematoma can ap-
pear identical to a metabolic encephalopathy
(Chapter 5), imaging is required in any patient
without an obvious cause of the impairment of
consciousness.
The symptoms of subdural hematoma have
a remarkable tendency to fluctuate from day
to day or even from hour to hour, which may
suggest the diagnosis. The pathophysiology of
fluctuations is not clear. Some may reflect in-
creases in ICP associated with plateau waves,
29
and careful clinical observations suggest that
the level of consciousness reflects the patient
moving in and out of diencephalic or uncal
herniation. Given the breakdown in the blood-
brain barrier along the margin of the hema-
toma, this fluctuation may be due to fluid shifts
into and out of the brain, a situation from which
the brain is normally protected. When the brain
is critically balanced on the edge of herniation,
such fluid shifts may rapidly make the difference
between full consciousness and an obtunded
state. Cerebral blood flow in the hemisphere
underlying a subdural hematoma is reduced,
perhaps accounting for some of the unusual cli-
nical symptoms.
30
In favor of the vasogenic edema hypothesis
is the observation that oral administration of
corticosteroids rapidly and effectively reverses
the symptoms in subdural hematoma.
31
Cor-
ticosteroids reduce the leakage of fluid from
capillaries,
32
and they are quite effective in mini-
mizing the cerebral edema associated with sub-
dural hematomas.
Table 4–2 Diagnostic Features
of 73 Patients With Fluctuating Level
of Consciousness Due to Subdural
Hematoma
Unilateral hematoma
62
Bilateral hematomas
11
Mortality
14
(3 unoperated)
Number of patients
in stupor or coma
27
Principal clinical diagnosis before
hematoma discovered
Intracranial mass lesion
or subdural hematoma
24
Cerebral vascular disease, but
subdural hematoma possible
17
Cerebral infarction
or arteriosclerosis
12
Cerebral atrophy
5
Encephalitis
8
Meningitis
3
Metabolic encephalopathy
secondary to systemic illness
3
Psychosis
1
124
Plum and Posner’s Diagnosis of Stupor and Coma