Emerg Radiol (2005) 12: 57–59 DOI 10.1007/s10140-005-0438-8
CASE REPORT
Ibrahim Adaletli . Akif Sirikci . Batuhan Kara . Sebuh Kurugoglu . Harun Ozer . Metin Bayram
Cerebral venous sinus thrombosis presenting with excessive subarachnoid hemorrhage in a 14-year-old boy Received: 15 June 2005 / Accepted: 1 July 2005 / Published online: 22 November 2005 # Am Soc Emergency Radiol 2005
Abstract Cerebral venous thrombosis presenting with subarachnoid hemorrhage (SAH) is very rare. We report a case of cerebral venous sinus thrombosis as an initial manifestation of SAH. A 14-year-old boy was admitted with progressive headache, nausea, vomiting, diplopia, and gait disturbance. Cerebral computed tomography scan showed a widely SAH in the basal cisterns, bilateral sylvian fissures, and anterior interhemispheric fissure. Cerebral angiography was performed to detect any aneurysm in intracranial vasculature as a cause of SAH; however, the totally thrombosed superior sagittal sinus, galenic vein, and straight sinus were the sole abnormal findings. Keywords Cerebral venous thrombosis . Superior sagittal sinus . Subarachnoid hemorrhage . Venous infarct
Introduction Cerebral venous thrombosis (CVT) has a wide spectrum of presentation. The clinical manifestation depends on the localization and the rate of progression of the thrombus and the extent of venous collateralization. More than one sinus involvement in one third of all cases causes a broad variety of symptoms, including headache, seizure, focal neurological deficit, lethargy, confusion, or even coma [1]. How-
I. Adaletli (*) . B. Kara . S. Kurugoglu . H. Ozer Department of Radiology, Cerrahpasa Medical Faculty, Istanbul University, 34300 Istanbul, Turkey e-mail:
[email protected] Tel.: +90-212-4143176 Fax: +90-212-4143167 A. Sirikci . M. Bayram Department of Radiology, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey
ever, the presentation of CVT with excessive subarachnoid hemorrhage (SAH) on computed tomography (CT) is very rare. In this report, we present the imaging findings of cerebral venous sinus thrombosis presenting with excessive SAH and discuss the mechanisms of SAH in CVT.
Case report A 14-year-old boy with progressive headache, nausea, vomiting, diplopia, and gait disturbance was admitted to an outside institution, where he got a diagnosis of typhus and received adequate antibiotic regimen. Five days after the admission, his general condition deteriorated, and the tests for meningeal irritation (Brudzinski, Kernig) were found to be positive. Bacterial meningitis was thought to be responsible for the clinical status. The cerebrospinal fluid (CSF) sample of lumbar puncture showed a bloody appearance but no biochemical abnormality. For further investigation of the subarachnoid bleeding, the patient was referred to our institution. During the physical examination, the patient was lethargic and was found to be presented with grade III SAH according to the Hunt–Hess classification [2]. The nonenhanced CT scan of the head revealed a diffuse SAH in the basal cisterns, bilateral sylvian fissures, and anterior interhemispheric fissure (Fig. 1). Considering the CT findings, cerebral angiography was performed to reveal possible etiologies of SAH. The angiography showed no aneurysm, which is the more likely and expected explanation for SAH, but revealed the totally thrombosed superior sagittal sinus, galenic vein, and straight sinus (Fig. 2). Also, the collateral venous drainage was detected on digital subtraction angiography (DSA). The magnetic resonance imaging (MRI) was ordered to check the thrombosis upon the persistence of the symptoms. Cerebral MRI showed subacute clot formation of the thrombus with hemorrhagic venous infarcted area in the bilateral frontal and parietal lobes (Fig. 3). The patient received systemic anticoagulations, and his symptoms and signs resolved completely.
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Fig. 1 An axial nonenhanced CT scan shows a diffuse subarachnoid hemorrhage in the basal cisterns, bilateral sylvian fissures, and anterior interhemispheric fissure
Discussion The broad variety of signs and symptoms of CVT makes the clinical diagnosis difficult. The patients may be presented with signs of elevated intracranial pressure such as headache, papilledema, cranial nerve palsies, confusion, seizure, or focal neurological deficits [1]. There are many causes of CVT, although the precise mechanism is not always identified in one third of the cases [1, 3]. The most common causes are pregnancy and puerperium, oral contraceptives, and intracranial infections. Other causes include hematologic disorders such as protein S or protein C deficiency, antithrombin III deficiency, diffuse intravascular coagulation and anticardiolipin syndrome, neoplasm or by direct compression or invasion of a dural sinus, dehydration, trauma, and underlying inflammatory condi-
Fig. 2 Venous phase of a left internal carotid angiogram, lateral view, shows totally thrombosed superior sagittal sinus (arrows) and engorgement of the superficial veins
tions such as ulcerative colitis or Behçet’s disease, the medical conditions increasing the risk of deep venous thrombosis such as surgical, gynecologic-obstetrics cases [3]. After a complete clinical and laboratory evaluation of our patient, we decided that dehydration was the reason for the CVT. Nontraumatic SAH develops usually due to the rupture of an intracranial aneurysm. Arteriovenous malformations, tumors, vasculitides, amyloid angiopathy, and coagulopathies are other causes of SAH. CVT in itself is a rare cause of SAH. Up to now, only a few authors mentioned about CVT presented with SAH. Ohta et al. [4] reported a patient with aplastic anemia presenting as an SAH with thrombosis of the superior sagittal sinus. Oshiro et al. [5] described an SAH induced by the rupture of cortical venous thrombosis in a patient with systemic lupus erythematosus. Sztajzel et al. [6] reported one patient who presented with right cerebellar SAH associated with thrombosis of the right transverse or sigmoid sinus. Widjaja et al. [7] reported a case of superior sagittal sinus thrombosis accompanied by SAH seen in interhemispheric fissure and sulci. Recently, Chang and Friedman reported three patients with isolated cortical venous thrombosis presenting as an SAH [8]. Different explanations are proposed for SAH observed in CVT. These are (a) oozing of blood through inflammed and thrombosed superficial vein into the subarachnoid space, (b) rupturing of venous parenchymal hemorrhagic infarct to subarachnoid space, and (c) extension of the dural sinus thrombosis into the superficial veins causes their rupture, which usually bridges the subarachnoid space near their site of entrance into the sinuses [6, 7]. The superficial veins bridging the subarachnoid and subdural spaces have thin walls, no smooth muscle fibers, and no valves, which enable an important capacitance of cerebral veins and reversal of the direction of blood flow if the sinus into which they drain is occluded. These anatomical features explain why the rupture of the superficial veins in subarachnoid space and consecutive clinical symptoms and radiological appearance of SAH occurs so rarely [6, 9]. To the best of our knowledge, our patient is different from all of the reported cases of CVT with SAH. Because SAH in our case was widely extended, including basal cisterns, bilateral sylvian fissures, and anterior interhemispheric fissure on nonenhanced CT scans. The diffuse involvement of subarachnoid spaces in our case was remarkable and different from other reported cases, possibly because of the delay in diagnosis. In our case, the possible pathological mechanism seemed to be the rupture of superficial vein or veins since the admission CT showed only extensive SAH findings and no infarcts. Nonetheless, CVT rarely mimics SAH due to an aneurysmal rupture. The differential diagnosis of SAH should include CVT, especially if the predisposing factors are present, since the management of the aneurysm and the CVT are absolutely different.
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Fig. 3 a–c Control cerebral MRI obtained. An axial T2-WI (a) (TR/ TE:4464/100) shows hyperintense subacute clot formation of the thrombus (arrows) with venous infarcts (*) in the bilateral frontal and parietal lobes. An axial nonenhanced T1-WI (b) (TR/ TE:583/15) shows hyperintense thrombus (arrows) and increased
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signal intensity at the venous infarct areas (*) due to the hemorrhagic character. A sagittal T1-WI (c) (TR/TE:583/15) shows hyperintense thrombus (arrows) extending from superior sagittal sinus to torcular Herophili
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