Imaging of Mucormycosis

1. By
Dr Shaik Asma
Second year post graduate

2.  Mucormycosis is a life threatening infection caused by member of
mucoraceal family , including Absidia,Mucor,Rhizopus.
 It is a not a pigmented fungi,it is called black fungus due to
development of black crusts
 Black necrotic eschars that are formed on the nasal or palatine
mucosa,characteristic feature of mucormycosis.

3.  Diagnosis of mucormycosis requires thorough clinical history and
evaluation of underlying risk factors.
 Presence of nasal or palatal necrosis should raise the suspicion of this
condition.
 Necrotizing and angio invasive pathogen.

5.  COVID 19 worsens pre existing diabetes in normal individuals
 Steroid use
 Decreased immunity
 Elevated ferritin and elevated cytokines
 Vasculopathy
 Use of combination of various antibiotics
 Steam inhalation leading to mucosal burns
 Contaminated masks and oxygen cylinders

7.  RhinoCerebral
 Rhino Orbito Cerebral
 Pulmonary
 Gastrointestinal
 Cutaneous
 Disseminated

11.  Invasive- presence of fungal hyphae within the
mucosa,submucosa,bone,blood vesselsof the paranasal sinuses
 Non invasive-Absence of fungal hyphae within the mucosa and other
structures of paranasal sinuses.

13.  Nasal stuffiness, nasal crusting and obstruction, epistaxis ,headache
 Facial pain
 Proptosis, chemosis, ophthalmoplegia
 Fever and confusion
 Discolouration of skin of face
 Ulceration of palate and loosening of the teeth.
Black necrotic eschar over the turbinates and palate-Very characteristic

16.  Radiographs
 CT scan
 MRI
 CE-MRI
Investigation of choice is CE MRI Brain and PNS –better for evaluating
intracranial and intraorbital extension,it can access cavernous sinus
involvement, invasion into internal carotid artery, involvement of
meninges and brain parenchyma, anatomical extent of disease.

17.  Opacification of sinuses with air fluid level and bony erosions is best
seen on radiographs
 It does not allow assessment of extent of inflammation and its
complications.

18.  First understand the normal anatomical areas through which spread of
infection occurs in mucormycosis.
 The fungus reach the nasal cavity and may spread to paranasal sinuses
and subsequently to the orbit and brain.
 Orbital involvement results from spread through nasolacrimal duct
and medial orbital wall(lamina papyracea).
 Spread to the brain occurs via the orbital apex, orbital vessels and via
the cribriform plate.

20. The pterygopalatine fossa/Sphenopalatine fossa is an important pathway for
the spread of neoplastic and infectious processes:
 medially: communicates with the nasal cavity via the sphenopalatine
foramen, which transmits the sphenopalatine artery.
 laterally: communicates with the infratemporal fossa via
the pterygomaxillary fissure
 anteriorly: communicates with the orbit via the inferior orbital
fissure (superiorly)
 posteriorly and superiorly: communicates with the Meckel
cave and cavernous sinus (of the middle cranial fossa) via the foramen
rotundum
 posteriorly and inferiorly: communicates with the middle cranial fossa via
the vidian canal
 inferiorly: communicates with the palate via the greater and lesser palatine
canals

22. Greater palatine canal
Foramen
rotundum
inferior orbital fissure
PPF

24.  The radiographic findings of mucormycosis of the sinuses three typical
signs: nodular thickening of sinus linings, absence of fluid levels, and
spotty destruction of bony walls of the sinuses.
 Fungal disease of the sinuses is demonstrated as a nodular
mucoperiosteal inflammation leading to homogeneous opacification of
the sinus cavity & bony erosion.

25.  Infiltration of the periantral fat planes with rim of soft-tissue
attenuation of variable thickness along the walls of the sinuses
represent the earliest imaging finding in rhinocerebral mucormycosis &
should suggest the possibility of invasive fungal sinusitis.
 Areas of isodense mucosal thickening, with markedly hyperdense foci
are seen within the inflammatory reaction. This hyperdensity is
attributed to calcium phosphate and calcium sulfate deposits in necrotic
areas of the mycetoma
 Soft-tissue infiltration of the deep face is characterized by obliteration
of the normal fat planes in the infratemporal fossa, pterygopalatine
fossa & pterygomaxillary fissure .

36.  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 of calcium concretions, air & ferromagnetic
elements like manganese, iron & magnesium.
 DWI showed hyperintense signal intensity in the distribution of
infiltrating lesion in sinuses,turbinates,subcutaneous soft
tissue,orbit,caernous sinus.Restricted diffusion was evident in the form
of hypointense signal intensity on ADC.

37.  Thickening and lateral displacement of the medial rectus muscle are
characteristic of orbital invasion. Proptosis occurs because of
enhancing soft-tissue mass at the orbital apex and the cavernous
sinuses. Orbital involvement can result in cellulitis,subperiosteal
abscess, orbital abscess or cavernous sinus thrombosis.
 Intracranial findings include infarcts related to vascular thrombosis,
mycotic emboli, and frontal lobe abscesses. Intracranial involvement
would result in epidural and subdural abscesses and cavernous and
sagittal sinus thrombosis
 Lack of enhancement of the superior ophthalmic vein or ophthalmic
and internal carotid arteries is related to vasculitis and thrombosis.

38.  The black turbinate sign refers to the non-enhancement of nasal
turbinates in a patient with acute invasive fungal rhinosinusitis.
 Angioinvasive fungal infection involves the nasal mucosa and causes
infarction of the surrounding tissue. The infarcted tissue is non-
enhancing on contrast-enhanced MRI and may show diffusion
restriction. In comparison, non-infarcted inflamed mucosa shows
contrast enhancement.
 This sign is important for the early detection of invasive fungal
rhinosinusitis .

58.  CT-Isodense mucosal thickening and bone erosions
 MRI –T2 hypointense fungal elements
 CE MRI-Nonenhncing infarcted areas and turbinates-Black turbinate
sign

59.  Cavernous sinus thrombosis – can cause infarcts
 Multiple cranial nerve palsies
 Optic neuritis-Visual loss
 Frontal lobe abscess
 Carotid and jugular vein thrombosis

63. On CT scan-
 Perivascular ground glass opacities progressing to large
nodules,consolidations.
 Reverse halo sign
 Halo sign
 Cavitation
 Angioinvasion causing pulmonary infarction.
On MRI scan-
 T2 hypointense rim(because of hemorrhage,iron deposition)
 On CE MRI –BLACK HOLE sign-Central nonenhancement of
necrotized infarcted lung parenchyma.

71. Pulmonary Mucormycosis Invasive Aspergillosis
>10 nodules Lesser nodules
Reverse halo sign Halo sign
Aseptate,broad based obtuse branching fungi Septate,acute branching fungi
Resistant to Voriconazole Responds to Voriconazole

72.  Nasal aspirate and soft tissue biopsy specimen revealed aseptate hyphae
with right angle branching on KOH smear and culture,which confirmed
as mucormycosis.

73. Involvement Surgery
Only sinus involvement Endoscopic sinus surgery
Only palate and alveolar arch Intra oral approach and partial maxillectomy
Orbital involvement with vision Endoscopic sinus surgery with orbital decompression
Orbital involvement without vision Maxillectomy with orbital exenteration
Rhino cerebral involvement Debridement with neurosurgeon
MEDICAL MANAGEMENT
Control diabetes
Reduce steroids
Discontinue immuno modulating drugs
IV Amphotericin B under supervision and other antifungals