British Journal of Radiology (2005) 78, 646-650
© 2005 British Institute of Radiology
doi: 10.1259/bjr/60601877
Acute subdural haematoma without subarachnoid haemorrhage caused by rupture of an internal carotid artery bifurcation aneurysm: case report and review of literature
A Koerbel, MD
1
U Ernemann, MD
2 and
D Freudenstein, MD
1
Departments of 1 Neurosurgery and 2 Neuroradiology, University Hospital, Eberhard Karls University, Hoppe-Seyler-Strasse 3, D-72076, Tübingen, Germany
Correspondence: Dr Dirk Freudenstein
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Abstract
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Spontaneous pure acute subdural haematoma (ASDH) without intraparenchymal or subarachnoid haemorrhage caused by a ruptured cerebral aneurysm is extremely rare. To our knowledge, the present case is the first report of an internal carotid artery bifurcation aneurysm presenting as pure ASDH. Suitable diagnostic investigations and therapeutic strategies are discussed. Arterial origin of bleeding should be considered in all cases of non-traumatic ASDH and a vascular anomaly has to be excluded. The neurological status on admission dictates the appropriate timing and methodology of the neuroradiological investigations.
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Introduction
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In the majority of cases acute subdural haematomas (ASDH) are related to head trauma and are typically caused by disruption of superficial cerebral or cortical bridging veins.
Spontaneous ASDHs are uncommonly encountered. Arteriovenous malformations [1], cocaine abuse [2, 3], dural metastasis [4], coagulopathy [5, 6], falx meningioma [7] and rupture of a cortical artery located near the sylvian region [8, 9] have been cited as causes of their pathogenesis. Aneurysm rupture causing ASDH is rare and usually confined to subarachnoid haemorrhage (SAH) and intracerebral haemorrhage.
ASDHs constitute neurosurgical emergencies and immediate treatment must be conducted before neurological deficits become irreversible. Therefore, knowledge about the possibility of occurrence of spontaneous subdural haematoma and its mechanisms is mandatory to its prompt diagnosis and adequate management.
A case of a spontaneous pure ASDH without intraparenchymal haemorrhage or SAH due to rupture of an aneurysm of the internal carotid artery bifurcation is reported. Based on a thorough review of literature suitable diagnostic investigations and therapeutic strategies are discussed.
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Case report
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A 62-year-old woman presented to a peripheral hospital with a history of sudden onset of headache followed by reduction of the level of consciousness. There was no history of trauma or previous neurological disease. Her past history indicated hypertension and diabetes, with regular use of medication. The patient underwent CT that disclosed a high density holohemispheric subdural haematoma on the left side, without the presence of subarachnoid or intracerebral blood. There was moderate to marked mass effect with displacement of the ventricular structures to the right side (Figures 1 and 2
). On admission to our hospital she was somnolent and disoriented and underwent rapid and accentuated neurological deterioration. There was no evidence of head injury and general physical examination was unremarkable. The laboratory data including a coagulopathy screen were normal.
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Figure 1. CT scan showing an acute subdural haematoma over the left hemisphere with compression of the left ventricle.
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Owing to rapid clinical deterioration she was intubated, hyperventilated and taken immediately to the operating room. A large emergency frontotemporal craniotomy was performed and the haematoma evacuated. The underlying cortex was not damaged, typical signs of SAH on the surface of the brain were not present. A bleeding cortical artery or other abnormalities could not be identified.
On the first post-operative day she progressively recovered consciousness and was able to follow commands and to move all extremities. A post-operative CT showed reduction of mass effect without additional bleeding. Because of the spontaneous course of the ASDH she underwent cerebral angiography. This revealed a 5 mm diameter saccular aneurysm projecting from the bifurcation of the internal carotid artery (Figure 3). Three-dimensional (3D) angiography showed an irregular shape of the aneurysm with additional small outpouching indicating the point of rupture (Figure 4). The patient underwent successful coiling of the aneurysm (Figure 5). Her following hospital stay was uneventful, and she was discharged on the 14th post-operative day without neurological deficits, and able to return to her normal life.
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Figure 3. Left carotid angiography showing a 5 mm diameter saccular aneurysm projecting from the bifurcation of the internal carotid artery.
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Discussion
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ASDHs develop spontaneously in patients without history of trauma or coagulopathy and an arterial origin is responsible for the majority of such cases. Ruptures of aneurysms or of a small cortical artery located near the Sylvian fissure constitute the most frequently reported sources [1, 8–25].
The occurrence of SAH associated to ASDH due to cerebral aneurysms varies from 0.5% to 7.9% [21, 26, 27]. Several mechanisms have been proposed to explain the occurrence of ASDH after aneurysm rupture. Previous minor haemorrhages may fix an aneurysm to local arachnoid adhesions, resulting in bleeding directly into the subdural space when an arachnoid tear occurs after aneurysmal rupture [10]. A second mechanism may be due to a haemorrhage under high pressure, leading to pia-arachnoid rupture and extravasation of blood into the subdural space [10]. Theoretically, aneurysms located more superficially, such as distal anterior cerebral artery aneurysms or superficial branches of the middle cerebral artery may be more predisposed to bleed into a subdural location.
In patients with a history of no or inadequate head trauma presenting with a disproportionately massive subdural haematoma and SAH on CT scans, a ruptured aneurysm should be considered as possible source of bleeding [15].
Comparison between cases of aneurysmal SAH with and without subdural haematoma demonstrated that a dominance of worse neurological status, higher rate of pre-hospitalization re-bleeding, higher rate of intraparenchymal haematoma and a poorer prognosis were found in the patients with subdural haematoma [20].
The incidence of pure ASDH, without associated intraparenchymal haemorrhage or SAH, due to a ruptured aneurysm is extremely rare. The reported cases in the literature are summarized in Table 1. The most frequent site of aneurysm causing pure ASDH was at the origin of the posterior communicating artery from the internal carotid artery (IC-PC) (58.3% of the cases), followed by the distal anterior cerebral artery (ACA) (16.7%) and middle cerebral artery (12.5%). To our knowledge, the present case is the first report of an internal carotid artery bifurcation aneurysm presenting as pure acute subdural haematoma.
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Table 1. Cases of pure subdural haematoma (without subarachnoid haemorrhage and without intraparenchymal haematoma) caused by rupture of intracranial aneurysm
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Internal carotid artery bifurcation aneurysms arise at the apex of the T-shaped bifurcation. They point upward along the axis of the pre-bifurcation segment of the artery toward the anterior perforated substance [28].
The anterior incisural space, where the supraclinoidal portion of the internal carotid artery is found, extends upward around the optic chiasm to the subcallosal area [29]. This space opens laterally into the part of the Sylvian fissure situated below the anterior perforated substance. Anatomical studies show that the chiasmatic and carotid cisterns communicate laterally with the Sylvian fissure as well [29]. Thus, the most plausible explanation for the occurrence of a subdural haematoma following internal carotid bifurcation aneurysm rupture in the present case could be related to previous minor bleedings and secondary arachnoid adhesions. Thus, a new haemorrhage under high pressure could lead to extravasation of blood in a lateral direction toward the Sylvian fissure. Rupture of arachnoid or pia around or in this fissure could allow open communication between the anterior incisural and the subdural spaces.
Regarding the location of the ASDH and the aneurysm, all cases of tentorial haematoma, except one were related to IC-PC aneurysms. In the majority of cases, interhemispheric haematomas were related to distal ACA aneurysms.
Pure ASDH following rupture of intracranial aneurysm carried a poor prognosis in 42% (10 of 24) of the reported cases in the literature. 21% (5 of 24) of the patients were disabled in the follow-up and 21% (5 of 24) died due to the bleeding. The mortality rate of 21% in this group of patients is high and is similar to the mortality rate of simple traumatic subdural haematomas (reported to be also 21%) [30]. The simple traumatic acute subdural haematomas are distinguished from the complicated traumatic subdural haematomas by the absence of parenchymal damage [30].
This high mortality rate may be due to the initial elevated intracranial pressure caused by the subdural haematoma or by re-bleeding of the aneurysm before its occlusion. Therefore, adequate diagnostic investigations and respective prompt treatment are essential for a better outcome.
The choice of initial neuroradiological investigation in patients with spontaneous pure acute subdural haematoma should be based on the neurological status of the patient. If the patient presents with a stable neurological condition, angiography should be performed prior to surgery to dictate the best strategy. In the presence of an aneurysm or an arteriovenous malformation, the patient should undergo emergency surgery to evacuate the haematoma and obliterate or extirpate the lesion. Angiographic extravasation of contrast medium can be visualized in some cases of bleeding from rupture of a cortical artery near the Sylvian fissure [9]. In such cases, a prompt removal of the haematoma and obliteration of the bleeding point is also indicated. If the angiography does not demonstrate the source of bleeding, the patient can be managed conservatively or surgically according to the subsequent evolution of the neurological status. If necessary, additional investigation with contrast enhanced CT or MRI can be performed to rule out dural tumours.
In cases of patients presenting with rapid neurological deterioration, immediate decompression surgery should be performed before performing angiography. In the absence of intraoperative identification of a cortical arterial rupture or other source of bleeding, complementary post-operative arteriography is required, as performed in our case. If pre-operative CT angiography is available, it can be performed without delaying surgery and may demonstrate the source of bleeding, allowing clipping of an aneurysm at the same surgical session.
In summary, pure acute spontaneous subdural haematoma can follow rupture of aneurysm of the bifurcation of the internal carotid artery, as demonstrated in the present case. A high level of suspicion for bleeding of arterial origin should be maintained in all cases of acute subdural haematoma without history of trauma. The presence of a vascular anomaly should be excluded by angiography. However, the pre-operative neurological status of the patient should dictate the best management concerning the appropriate time and choice of neuroradiological investigation.
Received for publication July 28, 2004.
Revision received January 4, 2005.
Accepted for publication February 14, 2005.
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Abstract
Introduction
