Keywords
intracranial aneurysm - subarachnoid hemorrhage - subdural hematoma - intraventricular
bleed - intraparenchymal hematoma
Introduction
Subarachnoid hemorrhage (SAH) almost invariably develops following the rupture of
a cerebral aneurysm, and is often complicated by intracerebral hematoma (ICH) and
intraventricular hematoma. Subdural hematoma (SDH) can occur rarely. Reported incidence
of SDH associated with aneurysm bleed varies from 0.5 to 7.9%.[1]
[2] In most cases SDH is associated with SAH and/or ICH. Intracranial aneurysmal rupture
may cause acute SDH with or without radiologic evidences of SAH.[3]
[4] In this report, we are describing the pathophysiology and radiologic features of
SDH with aneurysm bleed.
Case Reports
First Case
An 18-year-old man presented with complaints of generalized seizure associated with
severe headache and weakness of all four limbs (power 4/5). There was no history suggestive
of trauma. Noncontrast computed tomography (NCCT) of the head on admission did not
reveal any abnormality ([Fig. 1A]). Magnetic resonance imaging (MRI) of the brain on admission was suggestive of features
of suspected posterior circulation stroke. The patient was evaluated and admitted
under neurology. Extensive vasculitis and coagulation workup failed to identify the
etiology. Repeat NCCT of the head done after 1 week revealed evidence of bilateral
thalamic ischemic changes ([Fig. 1B]).
Fig. 1 First case: Normal NCCT of the head on admission (A). NCCT of the head (after 1 week): B/L thalamic ischemic changes (B). NCCT of the head (after 2 weeks): Thin right frontoparietobasal SDH reaching till
falx and tentorium (C). Angiography shows anterior communicating artery aneurysm measuring 8.17 × 4.35 mm
filling from right side pointing anteroinferomedially with neck measuring 2.4 mm (D). NCCT of the head (postoperative): evidence of right lateral supraorbital craniotomy
and clip artifact. No evidence of EDH/hematoma/ventriculomegaly seen (E).
The patient had recurrence of seizure after 1 week with radiologic evidence of new
onset isolated thin right frontoparietal convexity acute SDH reaching till falx cerebri
and tentorium cerebelli with no evidence of subarachnoid or intracerebral hemorrhage
([Fig. 1C]). He also had intermittent fever spikes and vomiting subsequently. Fever workup
for malarial antigen and enteric fever were negative and blood culture was sterile.
Urine culture was positive for pseudomonas species, sensitive to piperacillin and
tazobactam. The patient was managed conservatively with antiepileptics, culture-based
antibiotics, and antipyretics. Inability to achieve a final diagnosis prompted to
obtain a six-vessel intra-arterial digital subtraction angiography (IADSA) that subsequently
revealed an 8.17- × 4.35-mm anterior communicating artery aneurysm (A-Comm), filling
from the right side and pointing anteroinferomedially with neck measuring 2.4 mm ([Fig. 1D]). There was no evidence of radiological vasospasm.
The patient was transferred under neurosurgery and was operated electively. Right
lateral supraorbital craniotomy was performed. Right frontotemporal SDH was evacuated
and A-Comm aneurysm was clipped ([Fig. 1E]). Organized subdural frontobasal and parietal hematoma was present on the right
side. He had an uneventful postoperative period and was discharged after 1 week with
no residual sensory-motor deficits. The patient was clinically asymptomatic on follow-up
after 6 weeks. Histopathologic examination revealed fibrocollagenous tissue with fresh
and old hemorrhage and infiltration by macrophages.
Second Case
A 49-year-old woman, with no history of head trauma, presented with 1 day episode
of left forehead heaviness followed by sudden headache and vomiting. The patient came
to our hospital in unconscious state. On neurologic examination, the Glasgow Coma
Scale (GCS) was E1V1M2; pupils were bilateral constricted and sluggish reacting to
light.
Neuroimaging showed right frontal extra-axial lesion suggestive of acute SDH with
right temporal hematoma and intraventricular bleed ([Fig. 2A]). A CT angiogram demonstrated right post communicating artery aneurysm ([Fig. 2B]).
Fig. 2 Second case: Axial CT images show right frontotemporal subdural hematoma with right
temporal hematoma with gross subarachnoid hemorrhage with intraventricular extension
with marked midline shift toward left (A). Right common carotid angiography shows a large aneurysm of the right posterior
communicating artery segment (B).
The patient could not be taken up for operative procedure because of deranged coagulation
profile and very poor clinical status. Ideally, endovascular treatment should have
been done in view of inability to clip the aneurysm because of deranged coagulation
profile, but the patient's relatives did not agree for endovascular treatment of the
aneurysm (because of financial restrictions), so he was managed conservatively.
Discussion
Only very few cases (< 20 cases so far) have been documented in literature for isolated
SDH presentation of aneurysm rupture.[5]
[6]
[7]
[8]
[9]
[10]
[11]
The three mechanisms are postulated for isolated. First, an aneurysm adherent to the
arachnoid may bleed directly into the subdural space. The previous minor bleeds may
cause localized arachnoid adhesions to aneurysm dome. Second, aneurysm rupture with
hemorrhage under significant pressure may lead to pia-arachnoid rupture and subsequent
SDH. Third, aneurysms arising from part of carotid lying in subdural space will eventually
cause SDH after rupture.[3]
[8]
Barton and Tudor[3] studied various aneurysm locations contributing to SDH associated with aneurysmal
bleed and SAH; 34.4% of SDH were due to anterior cerebral/A-Comm aneurysm bleeds.
Although previous reports by Strang et al[2] in 1961 showed 17% of such cases associated with A-Comm/anterior cerebral artery
aneurysmal bleeds, the present cases exemplify the significance of aneurysmal etiology
of nontraumatic SDH.
Weir et al, in 1982,[12] proposed the following CT criteria to differentiate SDH caused by ruptured aneurysms
or trauma: (1) SDH of aneurysmal origin is unilateral, hyperdense, and crescentic
in convexity or triangular over the lower Sylvian fissure, whereas traumatic SDH is
more likely to be mixed, iso- or hypodense, may be bilateral or lentiform as well
as crescentic; (2) SDH due to ruptured aneurysms is frequently associated with SAH,
intracerebral hemorrhage, or intraventricular hemorrhage, whereas traumatic SDH may
be pure SDH or associated with hemorrhagic contusions with further evidence of scalp
or bone injury ([Table 1]).
Table 1
Differentiation of aneurysmal and traumatic subdural hematoma
|
S no.
|
Feature
|
Traumatic SDH
|
Spontaneous acute SDH (aneurysmal)
|
|
1.
|
History of trauma
|
Present
|
Absent
|
|
2.
|
CT characteristics
|
• Mixed, iso- or hypodense
• May be bilateral
• Lentiform as well as crescentic
|
• Hyperdense
• Unilateral
• Crescentic in convexity or triangular over the lower Sylvian fissure
|
|
3.
|
Associated CT findings
|
Pure SDH or associated with hemorrhagic contusions with further evidence of scalp/bone
injury
|
Frequent association with SAH, ICH, or intraventricular hemorrhage
|
Abbreviation: CT, computed tomography; ICH, intracerebral hematoma; SAH, subarachnoid
hemorrhage; SDH, subdural hematoma.
The first case was admitted and managed initially in Neurology Department for about
1 week. Then neurosurgery consultation was sought, and then repeat CT of the head
and IADSA were planned and then after confirming aneurysm definitive steps taken.
A CT angiogram could also be obtained if IADSA was not feasible. In first case, the
patient initially did not reveal SDH on CT scan, which later became prominent after
second seizure. This suggests possibility of earlier minor bleed causing arachnoid
adhesions and later on manifesting as SDH on rebleed. Although the scans did not show
all the characteristics of either aneurysmal or traumatic SDH, but a high index of
suspicion is necessary for arriving at the right diagnosis and early management. This
case report also reinforces the pitfalls associated with CT in diagnosing SDH caused
by ruptured aneurysms and potentially emphasizing on the role of angiography in selected
cases with high index on clinical suspicion.[13]
[14]
Multicompartmental hemorrhage may support the theories that high pressure emanating
from the ruptured aneurysm or massive hemorrhage causes an aneurysmal SDH. Three-dimensional
CT angiography is regarded as the best investigative technique for differentiating
aneurysmal SDH if the patient is in poor clinical condition.[15]
[16] The conventional four-vessel angiography is the gold standard for detecting the
presence of an aneurysm; however, it is time consuming and not safer than 3D CT angiography,
particularly in poor-grade patients.[17]
Conclusion
Clinicians should be aware of the possibility of aneurysmal SDH to avoid misdiagnosis
and mismanagement. Characteristic CT findings and clinical history may be helpful
for differential diagnosis. For early detection of aneurysm even in the patient with
poor clinical grade, 3D CT angiography is a very useful tool.
