British Journal of Radiology (2007) 80, 488-498
© 2007 British Institute of Radiology
doi: 10.1259/bjr/56532933
Blood–fluid levels in the brain
B S Morris, MD
A M Nagar, DNB
A C Morani, MD, DNB
R K Chaudhary, MD, DNB
P A Garg, DMRD
P D Chudgar, DNB
and
A A Raut, MD
Department of Radiology, K E M Hospital, Acharya Dhonde Marg, Parel, Mumbai-400012, India
Correspondence: Dr Ajaykumar C Morani, Department of Radiology, Seth GS Medical College and KEM Hospital, Parel, Mumbai-400012, India. E-mail: ajaycmorani{at}yahoo.com
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Abstract
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17 cases reviewed prospectively over a period of 4 months highlight the varied appearance of blood–fluid levels in intracranial cystic lesions of different aetiologies; a finding which has not featured significantly in the medical literature. Four types of intracranial cysts demonstrating blood–fluid levels have been categorised according to the nature of the pathology, i.e. primary neoplasms of the brain, metastatic deposits to the brain in cases of extraneural malignancies, lesions of vascular aetiology and intraparenchymal bleeds secondary to trauma. The group of four primary intracranial neoplasms lists an oligodendroglioma, a recurrent tumour in a case of Von Hippel–Lindau syndrome, a Grade 3 astrocytoma and an acoustic schwannoma. Four cases of metastatic deposits to the brain were each secondary to primary malignant neoplasms of the breast, liver, ovary and lung. Of seven cases of a vascular aetiology, three resulted from arterial infarction, two from hypertension and one each from venous infarction and following anticoagulant therapy. Intracranial cysts within tumours have been postulated to occur secondary to a breakdown of the blood–brain barrier (BBB) rather than as a result of tumoural degeneration, as was thought probable earlier.
Fluid levels in the brain are not exceptional and are seen in a variety of intracranial pathologies. Gas–fluid levels are seen in brain abscesses [1] and fat–fluid levels have been described in intracerebral dermoids [2]. Zimmerman and Bilanuik in their description of intratumoural haemorrhages on CT in 1980 ascribe the formation of blood–fluid levels to sedimentation of particulate matter following the dissection of blood into a pre-existing fluid-filled space [3, 4].
Among cysts within the brain, those associated with tumours (
Figures 1–8) characteristically contain a proteinaceous fluid and are distinct from benign cysts such as arachnoid, neuroepithelial, leptomeningeal and porencephalic cysts which contain a cerebrospinal fluid (CSF)-like fluid [5]. Cerebral gliomatous cysts have been reported to occur in 20% of oligodendrogliomas, 40% of glioblastomas [6], 25–54% of supratentorial gliomas [7, 8] and over half to almost three quarters of paediatric astrocytomas [9]. They may also be found in cases of pleomorphic xanthoastrocytoma and in haemangioblastomas. Blood–fluid levels have been shown in cystic gliomas [3], cystic astrocytomas [4] and in cases of cystic cerebral metastatic melanomas [3]. Blurring of blood–fluid interfaces after contrast administration indicative of leakage of contrast into the cavity [3] was seen in a single case (Figure 2c) of a haemangioblastoma. This is thought to result from an increased permeability of the endothelium of the vessels in the tumour wall consequent to the opening of the junctions between the tumour cells [5]. Kaiser et al in 1983 thought that bleeding at several points within the tumour led to the formation of multiple cysts [10].
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Figure 1. CT and MRI images showing blood–fluid levels in cases of primary intracranial malignancies and metastases to the brain. (a) The preliminary CT of a 45-year-old man with frontal lobe signs and intractable seizures reveals a wedge-shaped hypodensity in the right fronto-parietal region with predominant involvement of the white matter. As erosion of the inner table of the skull was overlooked, the lesion was misdiagnosed as an arterial infarct. (b) A CT done 26 months later reveals a lesion of mixed attenuation with an enhancing solid and a larger septated cystic component in the fronto-parietal region, which extends across the midline along white matter tracts of the corpus callosum. Scalloped erosion of the inner skull table adjacent to the tumour and nodular calcification (seen on the higher sections) suggested an oligodendroglioma.
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Figure 2. CT and MRI images showing blood–fluid levels in cases of primary intracranial malignancies and metastases to the brain. (a) A post-contrast axial T1 weighted image through the posterior fossa of an 18-year-old woman reveals a cystic lesion with a small mural nodule displacing the fourth ventricle. A smaller unencapsulated cyst in the right cerebellum shows enhancement of the dependent component creating an uneven interface within the lesion. At histopathology the lesion was found to be a haemangioblastoma which was part of a larger spectrum of findings in a case of Von Hippel–Lindau syndrome. (b,c) CT following resection of the midline tumour reveals a persistence of the smaller right cerebellar cyst. Enhancement of the dependent isodense solid component of the lesion by contrast creates an interface, which simulates leakage of contrast into a cyst thereby exemplifying a spurious fluid level within an intracranial lesion.
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Figure 3. CT and MRI images showing blood–fluid levels in cases of primary intracranial malignancies and metastases to the brain. A contrast enhanced CT of a 40-year-old man with a history of seizures for the past 4 years reveals an ill-defined grade 3 glioma which crosses the midline along white matter tracts with distortion of the lateral ventricles. A cystic component with a fluid level is seen within the tumour.
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Figure 4. CT and MRI images showing blood–fluid levels in cases of primary intracranial malignancies and metastases to the brain. (a) Plain and (b) post-contrast images of the posterior fossa in a 21-year-old man reveal a heterogeneously enhancing mass centred at the right cerebello-pontine angle. Intense and homogeneous enhancement of the solid component of the tumour is seen following contrast administration. The thin-walled peripherally enhancing cystic component has a blood–fluid level and shows no appreciable enhancement of its contents. Sections at a more caudal level reveal gross widening of the ipsilateral internal acoustic canal (not shown) typical of an acoustic schwannoma.
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Figure 5. CT and MRI images showing blood–fluid levels in cases of primary intracranial malignancies and metastases to the brain. A plain CT reveals a fluid interface within a cystic lesion in the frontal cortex of a 65-year-old woman with carcinoma of the breast. There was no enhancement of the wall or contents of the cyst, which was thought to be a secondary deposit.
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Figure 6. CT and MRI images showing blood–fluid levels in cases of primary intracranial malignancies and metastases to the brain. On a plain CT metastatic cysts with fluid interfaces are seen in the (a) basifrontal and (b) medial temporal regions of a 70-year-old woman with hepatocellular carcinoma. The cause of subarachnoid haemorrhage was not established.
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Figure 7. CT and MRI images showing blood–fluid levels in cases of primary intracranial malignancies and metastases to the brain. Cystic secondary deposits from an ovarian malignancy in a 46-year-old woman are widely seeded throughout the brain on (a) a pre-contrast CT. The cystic lesions have imperceptible walls and show fluid interfaces. (b) Lower attenuation values of the dependent components of two of these lesions (one in the midline posterior fossa; the other in the high parietal deep white matter on the right side) suggest sedimentation of particulate matter rather than the presence of frank blood.
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Figure 8. CT and MRI images showing blood–fluid levels in cases of primary intracranial malignancies and metastases to the brain. On a post-contrast CT of a 35-year-old man diagnosed with bronchogenic carcinoma, two of four cystic lesions in the high parietal region demonstrate fluid levels. Differential levels are seen in the largest cyst located posteriorly on the left side.
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Lohle et al in their 1998 study on 35 patients, and later in 2000 in their volumetric study of tumour, oedema and cysts, hypothesized on the pathogenesis of cysts accompanying gliomatous tumours and metastases in the central nervous system (CNS) linking it to a disruption of the blood–brain barrier (BBB) [11, 12]. This was established by a comparative chemical analysis of the levels of different protein fractions in cyst fluid, blood plasma and CSF which were found to be highly similar in all three locations. Plasma proteins were found to exceed 95% of the total protein fraction while endogenous cerebral proteins constituted only a minor proportion of cyst fluid proteins. This suggested the probable mechanism of cyst formation as being triggered by BBB disruption followed by exudation of plasma proteins into brain parenchyma which in turn led to oedema [11, 12]. Cysts form later as a result of an imbalance between oedema formation and resolution. The confluence of microcysts which leads to the formation of larger cysts retards the process of CSF resorption on which the resolution of oedema depends [5]. This is because fluid reabsorption is a surface related process and the surface/volume ratio of a globular structure is known to fall with an increase in its volume.
Well-circumscribed multiple fluid–blood interfaces were seen in all cases of cerebral metastases (
Figures 6a, 7a,b and 8), in two cases of arterial infarct (Figures 10 and 13) and a single case each of a patient on anticoagulant therapy (Figure 14) and trauma to the skull (Figure 17).
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Figure 10. CT and MRI images of lesions of a vascular aetiology. A 35-year-old man with rheumatic heart disease had undergone an open mitral commisurotomy 20 years earlier. A CT done for right-sided paresis of recent origin revealed multiple fluid levels within an amorphous focus of haemorrhage in the left parietal region. In the light of these findings, the bleed was thought to represent a haemorrhagic arterial infarct.
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Figure 13. CT and MRI images of lesions of a vascular aetiology. There are multiple fluid levels within the haemorrhagic component of an arterial infarct in a 75-year-old woman. Gross subfalcine herniation was thought to result from an accompanying subdural bleed, the presence of which could not be explained.
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Figure 14. CT and MRI images of lesions of a vascular aetiology. The CT brain of a 75-year-old man with deep vein thrombosis of the lower limb reveals multiple fluid levels within a large focus of haemorrhage in the right cerebral hemisphere. Extension into the ventricles has led to obstructive hydrocephalus. The bleed was attributed to anticoagulants that were given as a prophylaxis against pulmonary thrombo-embolism.
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Figure 17. CT in traumatic brain lesions. A fluid level is seen in the largest focus of bleed in a case of traumatic bifrontal haematomas. Similar to the previous image, there is evidence of sedimentation of particulate matter within the bleed in the left frontal region.
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Intracranial haemorrhage in anticoagulated patients may be associated with minor trauma, but often there is no antecedent event recorded [1]. The bleed can be subdural or intraventricular, but a solitary intracerebral haematoma seems to be the most common event [13–15]. Livoni and McGahan in 1983 discussed two cases of multiple intracerebral bleeds in patients who were on anticoagulant therapy [16]. The single such case featured in this review is of multiple blood–fluid levels in a large solitary intraparenchymal focus of bleed (Figure 14).
The pathogenesis of cyst fluid has been the subject of much speculation as it was believed that cyst fluid originated from necrobiosis of tumour tissue. This line of thinking was supported by a supposed predominance of endogenic cerebral proteins in the cyst fluid [17–20]. Subsequent studies have, however, established a vasogenic origin of cyst formation and rendered the earlier premise of cyst formation by tissue necrosis untenable [11, 12].
In conclusion, a majority of blood–fluid levels in cystic lesions in the brain (15 of 17 patients, 88%) were found to be of malignant (47%) (Figures 1–8) and vascular (41%) (Figures 9–15) origin. A history of head injury was elicited in two cases (Figures 16 and 17). In cases of extraneural malignancy (Figures 5–8) and of trauma, the diagnosis can be more easily reached. In the absence of head injury, blood–fluid levels within cystic lesions in the brain are likely to be of either a malignant or vascular aetiology.
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Figure 9. CT and MRI images in lesions of a vascular aetiology. A haemorrhagic venous infarct presents as a thin-walled cystic lesion with a blood–fluid level in the deep right cerebral hemisphere. There is subfalcine herniation with gross distortion of a blood-filled ventricular system. A CT venogram of a 23-year-old man revealed evidence of thrombosis of the superior sagittal sinus (not shown).
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Figure 11. CT and MRI images of lesions of a vascular aetiology. The CT brain of a 13-year-old boy with a haemolytic uraemic syndrome reveals a circumscribed but unencapsulated haemorrhagic focus in the posterior parietal region. Components of the lesion with different attenuation values have linear demarcations and did not show appreciable enhancement on the post-contrast scan (not shown).
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Figure 12. CT and MRI images of lesions of a vascular aetiology. In a 65-year-old man a haemorrhagic infarct in the territory of the middle cerebral artery shows hyperperfusion of the gyri and a focus of haemorrhage in the parietal region with a horizontal anterior margin which appears gravity dependent but without a frank fluid-fluid level.
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Figure 15. CT and MRI images of lesions of a vascular aetiology. CT brain of a 67-year-old woman who was a known hypertensive reveals a cerebellar and vermian bleed with an isodense component on the right side. The horizontal anterior margin of this component of the bleed suggests a probable gravity-dependent level. (a) T1 weighted and (b) T2 weighted images of an MR done 3 days later show a large cerebellar and vermian bleed. A fluid level and varying signal intensities within the bleed indicate blood products at different stages of degradation.
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Figure 16. CT in traumatic brain lesions. CT in a 42-year-old man who sustained a traumatic injury to the skull reveals a contusion in the frontal and parietal regions. A fluid level within the bleed with graded attenuation levels suggests sedimentation of erythrocytes. There is a shift of the midline to the right despite an epidural haematoma in the contralateral parietal region.
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Received for publication December 16, 2004.
Revision received June 30, 2005.
Accepted for publication November 24, 2005.
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References
|
|---|
- Stevens EA, Norman D, Kramer RA, Messina AB, Newton TH. Computed tomographic brain scanning in intraparenchymal pyogenic abscesses. AJR Am J Roentgenol 1978;130:111–14.[Abstract]
- Cornell SH, Graf CJ, Dolan KD. Fat–fluid level in intracranial epidermoid cyst. AJR Am J Roentgenol 1977;128:502–3.[Medline]
- Dublin AB, Norman D. Fluid–fluid level in cystic cerebral metastatic melanoma. J Comput Assist Tomogr 1979;3:650–2.[Medline]
- Zimmerman RA, Bilaniuk LT. Computed tomography of acute intracranial haemorrhage. Radiology 1980;135:355–9.[Abstract/Free Full Text]
- Lohle PN, Verhagen IT, Teelken AW, Blaauw EH, Go KG. The pathogenesis of cerebral gliomatous cysts. Neurosurgery 1992;30:180–5.[Medline]
- Frankel SA, German WJ. Glioblastoma multiforme; review of 219 cases with regard to natural history, pathology, diagnostic methods and treatment. J Neurosurg 1958;15:489–503.[Medline]
- Hood TW, McKeever PE. Stereotactic management of cystic gliomas of the brain stem. Neurosurgery 1989;24:373–8.[Medline]
- Mercuri S, Russo A, Palma L. Hemispheric supratentorial astrocytomas in children. Long term results in 29 cases. J Neurosurg 1981;55:170–3.[Medline]
- Tomita T, McLone DG, Naidich TP. Mural tumors with cysts in the cerebral hemispheres of children. Neurosurgery 1986;19:998–1005.[Medline]
- Kaiser MC, Rodesch G, Capesius P. Blood–fluid levels in multiloculated cystic brain metastasis of hypernephroma. A case report. Neuroradiology 1983;25:339–41.[CrossRef][Medline]
- Lohle PN, Wurzer HA, Seelen PJ, Kingma LM, Go KG. The pathogenesis of cysts accompanying intra-axial primary and metastatic tumors of the central nervous system. J Neurooncol 1998;40:277–85.[CrossRef][Medline]
- Lohle PN, van Mameren H, Zwinderman KH, Teepen HL, Go KG, Wilmink JT. On the pathogenesis of brain tumour cysts: a volumetric study of tumour, oedema and cyst. Neuroradiology 2000;42:639–42.[CrossRef][Medline]
- Kinney TR, Zimmerman RA, Butler RB, Gill FM. Computerized tomography in the management of intracranial bleeding in hemophilia. J Pediatr 1977;91:31–5.[CrossRef][Medline]
- Banna M, Sengupta RP. Multiple cerebral hematomas. Clin Radiol 1972;23:415–16.[CrossRef][Medline]
- McCormick WF, Rosenfield DB. Massive brain haemorrhage: a review of 144 cases and an examination of their causes. Stroke 1973;4:946–54.[Abstract/Free Full Text]
- Livoni JP, McGahan JP. Intracranial fluid–blood levels in the anticoagulated patient. J Neuroradiol 1983;25:335–7.[CrossRef]
- Vivekanandan S, Rao AP, Sampathkumar MM, Kanaka TS. Presence of immunoreactive beta-endorphin in human brain tumor cyst fluids. J Neurol Sci 1983;59:13–19.[CrossRef][Medline]
- Szymas J, Morkowski S, Tokarz F. Determination of the glial fibrillary acidic protein in human cerebrospinal fluid and in cyst fluid of brain tumors. Acta Neurochir (Wien) 1986;83:144–50.[CrossRef][Medline]
- Hirano A, Matsui T. Vascular structures in brain tumors. Hum Pathol 1975;6:611–21.[Medline]
- Persson L, Boethius J, Gronowitz JS, Kallander C, Lindgren L. Thymidine kinase in brain-tumor cysts. J Neurosurg 1985;63:568–72.[Medline]
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