Keywords
aneurysm rupture - anterior communicating aneurysm - intraventricular hemorrhage -
subarachnoid hemorrhage
Palavras-chave
aneurisma roto - aneurisma de artéria comunicante anterior - hemorragia intraventricular
- hemorragia subaracnóidea
Background
Subarachnoid hemorrhage (SAH) is a life-threatening condition and accounts for 5 to
10% of all strokes in the United States.[1] Vascular abnormalities are well documented causes of non-traumatic SAH, with aneurysm
rupture being the most common.[2]
[3]
Subarachnoid hemorrhage from intracranial aneurysm (IA) rupture is a leading cause
of stroke disability and death in young patients, with a high mortality rate (50%)
and up to 50% of morbidity in survivors.[4]
Intracranial aneurysm rupture causes SAH in 80% of the patients,[5] and it may be associated to intracerebral hemorrhage (ICH) and/or intraventricular
hemorrhage (IVH) in 34% and 17% of the patients, respectively.[6]
[7]
However, on infrequent occasions, aneurysm rupture may be present, causing isolate
ICH or IVH without SAH. Thai et al[7] reported a rate of only 1.6% of patients presenting with isolated ICH and/or IVH,
leading a poor prognosis.
We describe an unusual case of an anterior communicating aneurysm rupture presenting
with IVH, without t SAH.
Case Presentation
A 70-year-old male with a history of hypertension, type 2 diabetes, dyslipidemia,
and previous episode of ischemic stroke presented to the emergency department (ED)
of our institution with nausea, fatigue, and mild headache. His medications included
Aspirin (Bayer AG, Leverkusen, Germany), atorvastatin, and antihypertensive. The patient
denied the use of tobacco, drugs, or family history of a brain aneurysm. After an
initial assessment, he presented nausea, vomiting, and drowsiness. On physical examination,
his only significant finding was a Glasgow coma scale (GCS) score of 13, without any
focal deficits. His blood pressure was 185 × 100 mm Hg and returned to normal (< 140 × 90 mm
Hg) after treatment with sodium nitroprusside in 7 hours. The remainder of the neurological
examination was unremarkable.
A cranial computed tomography (CT) scan was initially performed and revealed a small
bleeding in the right occipital horn of the lateral ventricles, early hydrocephalus,
and a large ectatic basilar artery measuring 9 mm in diameter ([Fig. 1]). No parenchymal or SAH was present. The patient, therefore, underwent to computed
tomography angiography (CTA), showing a saccular aneurysm measuring ∼ 5.8 × 6.7 × 4.2 mm
in diameter arising from the anterior communicating artery (Acom) ([Fig. 2]).
Fig. 1 Computed tomography scan without contrast. Axial plane (A), in which a slightly hyperdense
lesion is seen in the occipital horn, without subarachnoid hemorrhage.
Fig. 2 Intracranial angiotomography. Axial plane (A) shows saccular dilation dependent on
the anterior communicating artery with anterior-superior direction. Multiplane reconstruction
of maximum intensity showing ectatic basilar trunk (B) and volumetric reconstructions
(C and D) showing the anterior communicating aneurysm.
Digital subtraction angiography (DSA) findings confirmed the diagnosis of Acom aneurysm
([Fig. 3]). Due to the size, morphology, and location of the aneurysm, we opted for treating
it with surgical clipping.
Fig. 3 Digital angiography oblique (A) and coronal (B) prior to surgical treatment. Volumetric
reconstruction of digital angiography prior to surgery (C) and volume reconstruction
of angiotomography (D) showing aneurysm clipped.
Three days after the diagnosis of a brain aneurysm and before treatment, the patient
presented deterioration of the level of consciousness and when the GCS got to 8, he
was intubated. Twenty-four hours later, the patient underwent surgery. The aneurysm
was clipped, and an extraventricular drainage was placed. Four days after the surgery,
the patient developed severe pneumonia, and, despite treatment, the patient died 2
weeks later of septic shock.
Discussion
Aneurysm rupture is more commonly seen as SAH in non-contrast CT scan, showing blood
filling the subarachnoid cisterns. It can also be associated to subdural hematoma,
ICH or IVH. Isolated IVH associated to aneurysm rupture is very rare, and it is related
to high morbidity and mortality, up to 40%.[8]
[9] Obstructive or communicating hydrocephalus occurs in 62% of patients, but only a
third require extraventricular drainage.[9] The development of early hydrocephalus is an independent factor to poor prognosis.
Although many cases of isolated subdural hematoma or ICH associated to aneurysmal
bleeding have been reported,[10]
[11] only few cases of pure IVH have been cited.[7]
[12]
[13] The two most common causes of isolated IVH are aneurysm rupture and arteriovenous
malformation, while moyamoya disease and dural arteriovenous fistula are rarer.[8]
The features and location of the anuerysm can predispose to direct hemorrhage into
the parenchyma or ventricular system. Considering the location of the Acom aneurysm
in this patient and its anterior superior projection, occipital horn hemorrhage could
be explained by direct rupture into the lamina terminalis and then into the ventricular
system.[14]
The diagnosis of IVH without SAH is even more challenging depending on the timing
when tests are performed. Computed tomography imaging is positive in over 90% of the
cases of SAH on the day the hemorrhage occurs,[15] and the sensitivity of the test subsequently declines with the passing of time,
reaching 50% by 5 to 7 days after the onset of symptoms.[16] Delay in performing a CT scan after bleeding might lead to false negative results
and increase poor prognosis outcome. Thai et al[7] reported 6 patients had a sentinel event on average of 6.3 days before admission
for head CT imaging. Due to the small amount of blood and an IVH without SAH in our
patient, the diagnosis of aneurysm rupture and its treatment were delayed. This might
have contributed to the decreased level of consciousness and poor prognosis of the
patient.
Flint et al[8] found that catheter angiogram was performed in 52% of the cases of IVH, with the
identification of the bleeding source in 56%. A causative lesion was identified in
44% of the patients, who were treated accordingly. The routine catheter angiography
in IVH is warranted to identify potentially treatable causes of hemorrhage. This has
direct implications in the management of these patients. Therefore, careful radiological
examination is necessary to evaluate cases of isolated ventricle hemorrhage.
Conclusions
This is a case of IVH without SAH caused by rupture of an Acom aneurysm. After extensive
neuroimaging investigation, an underlying aneurysm was discovered. Although isolated
IVH is rare, aneurysm rupture is a possible condition. Patients presenting with head
CT revealing IVH without SAH should be promptly investigated with contrasted image
exam to identify and treat possible causes, even in the absence of SAH.
