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CT & MRI Imaging features of Rhinocerebral mucormycosis
Poster No.: C-2072
Congress: ECR 2012
Type: Educational Exhibit
Authors: P. K. Mondel1, A. S. Udare1, A. A. Raut2; 1Mumbai, Maharastra/IN,2Mumbai, MH/IN
Keywords: Inflammation, Infection, Diagnostic procedure, MR, CT, Head andneck
DOI: 10.1594/ecr2012/C-2072
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Learning objectives
1. To describe the normal anatomy of paranasal sinuses highlighting the routes of spread.
2. To describe the role of CT and MRI in rhinocerebral mucormycosis.
3. To review and illustrate the importance of clinico-radiological correlation in therapeuticdecision making.
Background
Mucormycosis are infections produced by fungi of the class phycomycetes [1]. There aresix forms of mucormycosis namely rhinocerebral, pulmonary, gastrointestinal, cutaneous,disseminated or uncommon [2&3]. The most commonly isolated species were Rhizopusfollowed by Mucor & Cunninghamella [3]. Rhinocerebral mucormycosis clinically presentwith rhinosinusitis, pansinusitis, and rhino-orbital or rhinocerebral manifestations [3].Rhinocerebral mucormycosis is the most common form of mucormycosis & present asacute infections of the nose and paranasal sinuses. It may cause death by occlusion,rupture, thrombosis of arteries or invasion of the brain [4]. These fungi are ubiquitousand are considered non - pathogenic. However, patients with debilitating diseases likediabetic acidosis & those on steroids or immunosuppressive drugs are highly susceptibleto infection with these fungi [5]. One of the first description of rhinocerebral mucormycosiswas by Baum et. al [6]. The fungal hyphae enters the nasal cavity and paranasal sinusesvia inhaled dust particles. It sporulates in tissues & the hyphae then enter the blood vesselwalls & also into the veins & lymphatics causing arteritis, with thrombosis & infarction ofthe organ supplied by these vessels [7]. Direct spread through the cribriform plate into theanterior cranial fossa may also occur via perineural spread. Treatment strategies includeaggressive surgical debridement, intravenous amphotericin B therapy, and control ofblood glucose.Central nervous system involvement is associated with dismal survivalrates of 20% to 60% [8].
Imaging findings OR Procedure details
The radiographic findings of mucormycosis of the sinuses were first described by Greenet al. [9], who noted three typical signs:
nodular thickening of sinus linings, absence of fluid levels, and spotty destruction of bonywalls of the sinuses.
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Addlestone and Baylin [10] reported similar findings, but noted that sinus wall destructioncould be extensive rather than spotty, that sclerosis of the osseous walls of sinuses couldbe seen in chronic cases, and that the typical mucosal thickening in the sinus was smoothrather than nodular.
Infiltration of the periantral fat planes with rim of soft-tissue attenuation of variablethickness along the walls of the sinuses represent the earliest imaging finding inrhinocerebral mucormycosis [fig. 1] & should suggest the possibility of invasive fungalsinusitis.
Areas of increased density, with well defined, markedly hyperdense foci are seen withinthe inflammatory reaction. This hyperdensity is attributed to calcium phosphate andcalcium sulfate deposits in necrotic areas of the mycetoma [3] Fungal disease of thesinuses is demonstrated radiologically as a nodular mucoperiosteal inflammation leadingto homogeneous opacification of the sinus cavity & bony erosion [fig.2].
Soft-tissue infiltration of the deep face is characterized by obliteration of the normal fatplanes in the infratemporal fossa, pterygopalatine fossa & pterygomaxillary fissure [fig. 3].
Thickening and lateral displacement of the medial rectus muscle are characteristicof orbital invasion. Proptosis occurs because of enhancing soft-tissue mass at theorbital apex and the cavernous sinuses. Orbital involvement can result in cellulitis,subperiosteal abscess, orbital abscess or cavernous sinus thrombosis[fig. 4].
Intracranial findings include infarcts related to vascular thrombosis, mycotic emboli, andfrontal lobe abscesses. Intracranial involvement would result in epidural and subduralabscesses and cavernous and sagittal sinus thrombosis [fig. 5].
Lack of enhancement of the superior ophthalmic vein or ophthalmic and internal carotidarteries is related to vasculitis and thrombosis [fig. 6].
MR imaging may be used in the initial evaluation of complicated sinusitis because of itsability to better depict advanced disease involving the orbit [fig.7&8]or brain, extraaxialspace and meninges,and the cavernous sinuses [figs. 9].
MR imaging, especially the nonenhanced T1 weighted images are sensitive to minorpathologic abnormalities in the skull base[fig. 10]. The characteristic finding is lost T1signal hyperintensity of skull base marrow fat.
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In mucormycosis the affected sinuses appear profoundly hypointense on T2 weighted& iso to hypo intense on T1 weighted images . This is attributed to the presence ofcalcium concretions, air & ferromagnetic elements like manganese, iron & magnesium.
Images for this section:
Fig. 1: Fig. 1 Infiltration of the right periantral fat planes with rim of soft-tissue attenuation
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Fig. 2: Fig.2 Areas of increased density within the nasal cavities and maxillary antrum
Fig. 4: Fig.4 Intraorbital spread through the left infraorbital foramen
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Fig. 5: Fig.5 Intracranial extension with right frontal lobe abscess.
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Fig. 6: Fig.6 : Right ICA occlusion by invasive mucormycosis & resultant acute right MCAterritory infarct.
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Fig. 10: Fig 10. Skull base involvement
Fig. 3: Fig. 3 Spread of mucormycosis
Fig. 7: Fig.7 Involvement of the left orbital apex by mucor.Also note the meningealenhancement.
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Fig. 9: Fig.9 Right cavernous sinus and intracranial extension by mucormycosis.Alsonote the intense loss of signal on T2w images.
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Fig. 8: Fig. 8 Intraocular muscle involvement by mucormycoses
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Conclusion
1. Cross-sectional imaging plays a vital role in detection and delineating the spread ofmucormycosis which is vital to therapeutic decision making.
2. CT scan helps in the delineation of extent of bony involvement.
3. MRI has an edge over CT scan in detecting base of skull, perineural, intraorbital andintracranial extension.
Personal Information
email: [email protected]
References
1.Mikhael MA: Case report: cerebral phycomycosis. Journal of Computer AssistedTomography 3:417-420, Jun 1979.
2. Yanagisawa E, Friedman 5, Kundargi RS, et al. Rhinocerebral phycomycosis.Laryngoscope 87:1319-1335, Aug 1977.
3. RodenMM, Zaoutis TE, Buchanan WL, et al. Epidemiology and outcome ofzygomycosis:
a review of 929 reported cases. Clin Infect Dis 2005;41(5):634-53.
4. Ricardo S. Centeno et. al. CT Scanning in Rhinocerebral Mucormycosis andAspergillosis. Radiology 140:383-389, August 1981.
5. Ajit Auluck. Maxillary necrosis by mucormycosis. A case report and literature review.Med Oral Patol Oral Cir Bucal 2007;12:E360-4.
6. Baum JL. Rhino-orbital mucormycosis. American journal of Ophthalmology63:335-339,
Feb1967.
7. Bergstrom L, Hemenway WG, Barnhart RA: Rhinocerebral and otoloogicmucormycosis. Annals of Otology 79:70-81, Feb 1970.
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8.Jorge L. Gamba et. al. Craniofacial Mucormycosis: Assessment with CT. Radiology1986; 160:207-212.
9. Green WH, Goldberg HI, Wohi GT: Mucormycosis infection of the craniofaclalstructures. Am J Roentgenol 101:802-806,Dec 1967.
10. Addlestone RB, Baylin GJ. Rhinocerebral mucormycosis.Radiology1975;115:113-117
