Keywords
magnetic resonance imaging - computed tomography - mucormycosis - COVID-19 - ROCM
- neuroimaging
Introduction
The coronavirus disease 2019 (COVID-19) pandemic continues to have an enormous impact
on the population of the world. Rhino-orbital-cerebral mucormycosis (ROCM) is a potentially
fatal angioinvasive secondary fungal infection which has shown a growing trend during
the COVID-19 pandemic, currently referred to as COVID-19-associated mucormycosis (CAM).[1]
[2] In all anatomical sites, tissue invasion and angioinvasion are the trademarks of
mucormycosis.[3]
[4] Central nervous system (CNS) affliction represents one of the most morbid manifestations
of mucormycosis and often governs the survival and functional outcome of the patient.[4] Prior to the pandemic, ROCM had a reported incidence of 0.005 to 1.7/million, which
has massively increased since 2021.[2] The main risk factors found for CAM were diabetes and steroid use.[2] Compared with non-COVID ROCM, patients most affected with CAM were middle-aged,
diabetic males with recent COVID-19 infection. New-onset upper jaw toothache and loosening
of teeth were striking symptoms and neurological manifestations, such as headache,
proptosis, vision loss, extraocular movement restriction, cavernous sinus, meningeal,
and parenchymal involvement were common in CAM. Also, stroke in CAM was found to follow
a definitive pattern with watershed infarction.[3] An aggressive diagnostic approach and timely initiation of antifungal therapy are
imperative to reduce morbidity and mortality.[5]
Pathophysiology
A multitude of factors, including pre-existing diseases, such as diabetes mellitus,
previous respiratory compromise, use of immunosuppressive therapy and steroids, and
systemic immune alterations of COVID-19 infection have been suggested in the etiopathogenesis
of this recent surge in cases.[6] A propensity of the virus to cause widespread lung involvement is found to raise
the risk of invasive fungal infections.[6] Another proposed mechanism is the alteration in innate immunity secondary to immune
dysregulation seen in COVID-19, with reduced numbers of T lymphocytes, CD4 + T, and
CD8 + T cells.[6]
Fungi of the genus Rhizopus account for the majority of the cases, followed by Lichtheimia
(formerly known as Absidia and Mycocladus), and Mucor.[7] Overall, Rhizopus oryzae is the most prevalent pathogen isolated from specimens.[7] The larger aseptate hyphae of Mucorales impede entry to the meningeal microcirculation
causing a more localized disease leading to cerebritis, abscess formation, or involvement
of larger vessels. The immune status and inflammatory response of the host determine
the degree of CNS involvement.[5]
Clinical Course of Rhino-Orbital-Cerebral Mucormycosis
Clinical Course of Rhino-Orbital-Cerebral Mucormycosis
In the head and neck location, mucor infection can be divided into isolated nasal,
rhino-orbital, or ROCM.[8] In the appropriate clinical settings, invasive fungal sinusitis is clinically detected
as a painless, necrotic ulcer (eschar) in the nasal septum and sinusitis, followed
by bony erosion and spread into adjacent structures like palate, orbit, and brain,
with a fulminant progression over a few days to weeks, usually leading to death.[9] Symptoms include fever, nasal congestion or discharge, facial pain or numbness,
and epistaxis. Intraorbital extension leads to proptosis and visual disturbances,
while intracranial spread results in headache, mental status changes, seizures, neurological
deficits, and coma.[9] Definitive diagnosis is by nasal biopsy and culture, which reveals broad aseptate
filamentous fungal hyphae.[6] Liposomal amphotericin B with sinus debridement using an endoscopic approach for
early disease and open surgery and exenteration for extensive disease is the preferred
management regime for ROCM.[4] Neurosurgical intervention is directed in raised intracranial pressure (e.g., hemispheric
stroke), obstructive hydrocephalus, and for lesions, compressing the spinal cord.[4]
Mechanism of Spread
Four main mechanisms proposed for the spread of ROCM are direct, perineural, perivascular,
and hematogenous spread ([Fig. 1]). The clinical manifestations and involved sites in each individual depend on the
mode(s) of spread and the extent of involvement by the disease process.[10]
Fig. 1 Methods of neuraxial spread of rhino-orbital-cerebral mucormycosis (ROCM).
1. Direct infiltration: Involvement of the CNS occurs most frequently (70%) due to contiguous spread from
the paranasal sinuses and orbits.[4] The disease process initially spreads via the dehiscent lamina papyracea, anterior
and posterior ethmoid orifices, involving the orbit, pterygopalatine fossa, periantral
fat, nasolacrimal duct, lacrimal sac, and rarely the nasopharynx.[11] Direct infiltration into frontal lobes (gyrus recti) may occur through the cribriform
plate or from frontal sinus,[10] while the extension to middle cranial fossa occurs through cavernous sinus.[3]
2. Perineural spread: Emerging studies have demonstrated the possible perineural spread of infection both
microscopically and macroscopically.[10] Sravani et al found perineural spread on biopsy specimens in 50% cases in a study
of 30 patients afflicted by ROCM, even for a substantial distance from the primary
focus of infection.[12] Direct spread through the cribriform plate into the anterior cranial fossa has been
suggested to represent perineural spread via olfactory nerves by some authors.[12] Galletta et al demonstrated V1 trigeminal branch division infiltration in a patient
with invasive mucormycosis.[10] V2 trigeminal root involvement, retrogradely via the infraorbital nerve to middle
cranial fossa through the inferior orbital fissure and foramen rotundum, and involvement
of intracisternal tract of the trigeminal nerve and Meckel's cave have also been reported.[10]
3. Perivascular spread: Vascular tropism is the hallmark of mucor infection. Fungal spores tend to invade
vessels and strongly adhere to endothelial cells. Also, R. oryzae produces an alkaline protease that cleaves elastin and separates the internal elastic
lamina from the media. Fungal hyphae extend along the internal elastic lamina and
further into the arterial lumen, obliterating it with intimal hyperplasia and thrombosis
and, thus, leading to infarction, vasculitis, and necrosis of involved tissues.[10]
4. Hematogenous dissemination: This may occur from a distant focus like the lung with predilection for gray–white
matter junction or via the valveless emissary veins draining the ethmoid sinus, traversing
the lamina papyracea, and facilitating fungal infiltration of periorbital tissue,
the orbital apex, and the cavernous sinus.[10]
Imaging of Rhino-Orbital-Cerebral Mucormycosis
Imaging of Rhino-Orbital-Cerebral Mucormycosis
Imaging plays a very important role in diagnosing and evaluating the extent of this
serious condition. Computed tomography depicts hypoattenuating mucosal thickening
of paranasal sinuses, and a tendency to involve ethmoid and sphenoid sinuses unilaterally
has been reported.[9] Bone erosion may be very subtle and suggested by obliteration of periantral fat
([Fig. 2]). Significant bony destruction of the sinus walls may occur rapidly with intraorbital
and intracranial extension of the inflammation.[9] On magnetic resonance (MR) imaging, the compacted fungal hyphae present low signal
intensity on T2-weighted sequences due to the presence of paramagnetic substances
and associated tissue necrosis from mucosal angioinvasion.[10] The “black turbinate sign” refers to nonenhancing portions in the turbinate on T1-weighted
post-contrast images owing to infarction from angioinvasion of the fungus ([Fig. 3]).[13]
Fig. 2 NCCT of paranasal sinuses in a 35-year-old male COVID-19 patient with sinonasal mucormycosis
shows bilateral maxillary and left ethmoid sinusitis with subtle erosion of the posterolateral
wall of the left maxillary sinus (black arrow) on axial (a) and coronal reformat (b) images in bone window, along with periantral fat obliteration with soft tissue (red arrow) on corresponding soft tissue window images respectively (c, d). COVID-19, coronavirus disease 2019; NCCT, noncontrast computed tomography.
Fig. 3 MRI of sinonasal region done in a 42-year-old COVID-19 patient with culture proven
mucormycosis reveals non-enhancing areas within the left inferior turbinate (black
arrow) on T1W fat saturated postcontrast axial (a) and coronal (b) images, suggestive of “black turbinate sign.” COVID-19, coronavirus disease 2019;
MRI, magnetic resonance imaging.
Intraorbital invasion is suggested by thickening and lateral displacement of the medial
rectus muscle, orbital fat infiltration, preseptal or postseptal cellulitis, endophthalmitis,
and subperiosteal or intraorbital abscess. When proptosis from orbital cellulitis
is significant, the dorsal globe becomes deformed, with tenting of its posterior aspect,
and depicts the “guitar pick” sign ([Fig. 4]).[14] Orbital apex syndrome is a morbid manifestation, which leads to complete ophthalmoplegia
and rapid vision loss, due to the involvement of cranial nerves II, III, IV, V, and
VI.[6] Restricted diffusion may be the earliest detectable abnormality in acute ischemic
optic neuropathy due to rhinocerebral mucormycosis.[15]
Fig. 4 MRI of orbits in another 52-year old patient with similar history depicts right proptosis
and deformity of posterior globe or “guitar pick sign” (white arrow) secondary to
right orbital compartment syndrome on axial T2W fat saturated (a) and T1W fat saturated postcontrast (b) images. MRI, magnetic resonance imaging.
Neurological Manifestations
Neurological Manifestations
1. Cavernous sinus involvement—The cavernous sinus is often the first intracranial structure to be involved. Intracranial
extension of disease through sphenoid sinus or orbital apex often leads to cavernous
sinus thrombosis as evidenced by bulging walls of the sinus with nonenhancing internal
areas ([Fig. 5]). There can be associated carotid artery invasion/occlusion leading to brain infarction
or pseudoaneurysm formation with impairment of the function of cranial nerves III,
IV, VI, and trigeminal nerve branches V1 and V2 that traverse it.[9]
Fig. 5 MRI brain imaging done in a 22-year-old COVID-19 patient with culture-proven mucormycosis
demonstrates bilateral ethmoid sinusitis and contiguous left orbital spread of disease
on axial T1W fat suppressed postcontrast images (a, b). A focal non-enhancing region is seen in the left cavernous sinus (white arrow), causing mild lateral bulging of the wall of left cavernous sinus on axial (c) and coronal (d) contrast-enhanced images, suggesting cavernous sinus thrombosis. Flow void of cavernous
segment of left internal carotid artery is maintained and normal in caliber. Note
is made of sphenoid sinusitis as well. COVID-19, coronavirus disease 2019; MRI, magnetic
resonance imaging.
2. Infarcts—Strokes in CAM are primarily due to cavernous internal carotid artery (ICA) involvement
from intraluminal thrombosis, microscopic angioinvasion, vasospasm, or external compression.[3] The infarcts are majorly at external and internal watershed territories ([Fig. 6]) of anterior cerebral artery and middle cerebral artery (MCA) or MCA and posterior
cerebral artery, with or without hemorrhagic transformation.[3]
Fig. 6 NCCT of brain of a 42-year-old COVID-19 recovered gentleman with left hemiparesis
shows bilateral maxillary sinusitis with hyperdense internal contents on axial image
(a), which was culture proven to be mucormycosis. There is subtle asymmetric fusiform
enlargement of left cavernous internal carotid artery (red arrow) as compared with right side as seen on axial (b) and coronal reformat (c) images, suggesting mycotic aneurysm. Acute lacunar infarcts are also seen in left
gyrus rectus and left globus pallidus (black arrows) (d). COVID-19, coronavirus disease 2019; NCCT, noncontrast computed tomography.
3. Fungal meningitis—Leptomeningeal enhancement due to fungal meningitis may be smooth or thick, nodular
and irregular, long and continuous, poorly demarcated or asymmetric ([Fig. 7]).[5] Enhancement (characteristically focal) of anterior and medial temporal poles was
most common followed by frontal lobes in a study.[3]
Fig. 7 MRI of brain in a 52- year-old patient with rhino-orbital cerebral mucormycosis post-COVID-19
infection presented with left hemiparesis. T2W coronal images (a, b) demonstrate bilateral maxillary and ethmoid sinusitis with right orbital involvement
and right cavernous sinus thrombosis with loss of flow void of cavernous and clinoid
segments of right internal carotid artery (ICA) (black arrow). Axial FLAIR image (c) depicts hyperintense areas in right internal and external watershed territories,
which appear hyperintense on diffusion weighted image (d) with corresponding hypointensity on ADC map (e), suggesting acute- early subacute infarct. Maximum intensity projection TOF (time-of-flight)
MR angiography image shows non-visualization of intracranial part of right ICA, consistent
with thrombosis. COVID-19, coronavirus disease 2019; FLAIR, fluid-attenuated inversion
recovery; MRI, magnetic resonance imaging.
4. Intracranial granulomas—Granulomas consist of lymphocytes, plasma cells, and fungal hyphae. Intracranial
granulomas are typically hypointense on T1- and T2-weighted images with minimal postcontrast
enhancement and mild perilesional edema ([Fig. 8]).[9]
Fig. 8 A 47-year-old COVID-19 in-patient treated with intravenous steroids developed nasal
discharge and sudden right- sided loss of vision. Postcontrast T1W fat saturated axial
(a, b) images reveal mild bilateral ethmoid sinusitis and right optic neuritis as suggested
by bulky, enhancing right optic nerve with perineural enhancement (white arrow). The inflammation is extending along right optic nerve into the optic canal and
orbital apex. Coronal T1W fat saturated postcontrast images (c, d) show further extension of infection to the right cavernous sinus, causing perivascular
enhancement around right internal carotid artery (arrowhead). There is focal leptomeningitis in the right frontal lobe (black arrow) and involvement of right medial rectus and superior oblique muscle due to focal
erosion of the cribriform plate and lamina papyracea respectively. Culture from sinonasal
contents revealed mucormycosis. COVID-19, coronavirus disease 2019.
5. Cerebritis—On T1WI, fungal cerebritis appears as an iso- or hypointense area involving gray
matter with subtle mass effect and minimal to no enhancement ([Fig. 9]).[5] On T2WI and fluid-attenuated inversion recovery, they appear as hyperintense lesion,
with areas of decreased signal intensity within the lesion due to the paramagnetic
effects of metal ions.[5] These lesions usually present with restricted diffusion on diffusion-weighted imaging
(DWI).[5]
Fig. 9 Coronal T1W postcontrast images (a, b) in a culture-proven case of invasive fungal sinusitis in a COVID-19 patient treated
with antivirals and oral steroids demonstrate right cavernous sinus thrombosis (white arrow) with complete thrombosis of cavernous and clinoid segments of right internal carotid
artery. Focal cerebritis is seen in the right frontal lobe (arrowhead). Conglomerated fungal granulomas showing peripheral enhancement is seen in left
posterior parietal cerebral parenchyma (black arrow) and few tiny disk-enhancing fungal granulomas are also seen in bilateral parietal,
temporo-occipital parenchyma and in right temporal lobe abutting right cavernous sinus
on axial T1W postcontrast sequences (c, d). COVID-19, coronavirus disease 2019.
6. Brain abscess—Fungal abscesses tend to be numerous and can involve the deep gray matter and basal
ganglia.[5] On DWI, fungal abscesses demonstrate restricted diffusion in the abscess wall and
intracavitary projections, with central core sparing ([Fig. 10]).[5] On MR, the core appears hypointense on T1W and hyperintense on T2W images, with
a surrounding isomildly hyperintense rim on T1WI, which appears hypointense on T2WI.
Peripheral enhancement is seen on T1W postcontrast enhancement sequence. Fungal abscesses
may demonstrate lipids (1.2–1.3 ppm), lactate (1.3 ppm), alanine (1.5 ppm), acetate
(1.9 ppm), succinate (2.4 ppm), and choline (3.2 ppm) on MR spectroscopy. A distinctive
feature of fungal infections is the presence of disaccharide trehalose (3.6 ppm) in
the abscess wall ([Fig. 10]).[5]
Fig. 10 MRI brain in a 48-year-old patient with rhino-orbital-cerebral mucormycosis demonstrates
a well-defined fungal abscess in left frontal parenchyma. On axial T1W image (a), the core of the lesion shows few hyperintense areas, while the wall appears hypointense
to gray matter. T2W (b), FLAIR (c) images reveal heterogeneously hyperintense internal contents and T2W/ FLAIR hypointense
wall. Note made of extensive perilesional edema, mild midline shift to right and effacement
of frontal horns of bilateral lateral ventricles. Axial T2* GRE image (d) shows focal internal blooming areas (black arrow), suggestive of bleed. There is diffusion restriction of wall of the abscess (white arrow) on axial DWI (e) and smooth rim enhancement on T1W fat saturated postcontrast coronal image (f). There is evidence of left maxillary and ethmoid invasive fungal sinusitis with
involvement of left orbit. FLAIR, fluid-attenuated inversion recovery; GRE, gradient
echo sequences; MR, magnetic resonance;
7. Obstructive hydrocephalus—This may occur due to meningeal and cisternal exudates or infiltration of the cisterns/ventricular
lining ([Fig. 11]).[4]
Fig. 11 Single voxel proton MR spectroscopy was done by placing the ROI along the wall of
the abscess in the same patient as in [Fig.10]. Spectroscopy reveals a significant lipid-lactate peak at 1.2–1.3 ppm, small choline
peak at 3.2 ppm and another peak at 3–4–3.6 ppm (white arrow), suggestive of substrate trehalose found in wall of fungal abscesses. MR, magnetic
resonance; ROI, region of interest.
8. Mycotic aneurysms—The elastic laminae of the vessel wall may get disrupted causing focal dilatation
of artery and development of mycotic aneurysms, which can rupture resulting in intracranial
bleed ([Fig. 12]). Mycotic aneurysms are commonly seen within the anterior circulation, affecting
long portions of proximal segments of the large cerebral vessels such as anterior,
middle, or posterior cerebral arteries.[5]
Fig. 12 MRI in a 42-year-old COVID-19 patient who had developed culture-proven invasive sinonasal
mucormycosis following a course of intravenous steroids are shown. T2W axial image
(a) reveals heterogeneously hyperintense areas in suprasellar cistern, left parasagittal
frontal cerebral region, and left medial temporal lobe, involving gray and white matter.
Mild white matter edema is also seen in the right frontal lobe. T2W FLAIR axial image
(b) shows hyperintensity in the adjoining left ganglio-capsulo-thalamic region with
mild hydrocephalus and periventricular ooze. Diffusion weighted image (c, d) showed patchy diffusion restriction in the above-mentioned areas (black arrows). Postcontrast T1W axial images at the level of basal cisterns (e, f) reveal minimally enhancing exudates contiguously extending into the left basifrontal
and temporal lobes, causing compression of anterior and left middle cerebral artery
flow voids as well as extraventricular obstructive hydrocephalus. The diffusion restriction
may be attributed to fungal cerebritis. COVID-19, coronavirus disease 2019; FLAIR,
fluid-attenuated inversion recovery; MRI, magnetic resonance imaging.
9. Garcin syndrome—It is the unilateral cranial nerve palsies without the involvement of sensory and
motor tracts due to mycelial growth along the cranial nerves ([Fig. 13]).[16]
Fig. 13 Contrast-enhanced MR angiography (a) in the same patient as in [Fig 12] reveals mycotic aneurysm of the terminal part of left internal carotid artery (black arrow). Axial T2W gradient images (b–d) show low signal bleed lining bilateral Sylvian fissures, suprasellar cistern, right
fronto-parieto-temporal dura, with a thin subdural hematoma in the fronto-parietal
region (arrowhead). Note the bleed in occipital horn of left lateral ventricle and third ventricle
(white arrow). Features are consistent with rupture of mycotic aneurysm with subarachnoid hemorrhage,
intraventricular hemorrhage, and subdural hematoma. MR, magnetic resonance.
10. Skull base osteomyelitis—Contiguous extension of pathology from the paranasal sinuses into the skull base
is common and holds prognostic significance with involvement of pterygopalatine fossa,
pterygoid wedge, vidian canal often requiring bone drilling ([Fig. 14]).[17]
[18]
Fig. 14 3-D contrast enhanced MR scan in a 50-year-old male with COVID-19 associated mucormycosis
reveals skull base osteomyelitis in the form of enhancement of left petrous apex (red arrow) (a), pneumatization of sphenoid sinus into pterygoid pates with mucosal thickening of
left pterygoid plate (white arrow), with soft tissue in left pterygomaxillary fissure (white arrowhead) (b), along with hypoenhancing soft tissue in the left vidian canal (black arrow) (c). There is also involvement of the left lateral pterygoid muscle (white asterisk) by the disease process with enhancement of the left pterygoid wedge (curved white arrow) at the site of attachment of pterygoid muscles as compared with right side (d). COVID-19, coronavirus disease 2019; MR, magnetic resonance.
11. Uncommon manifestations of cranial invasion include sagittal sinus thrombosis,
epidural, subdural, or suprasellar abscess ([Fig. 15]).[4]
Fig. 15 Axial short tau inversion recovery (STIR) image (a) of skull base in the same patient as in [Figs.12] and [13] demonstrates bilateral maxillary sinusitis with extensive inflammation of left preantral,
prezygomatic soft tissue and left infratemporal fossa. There is abnormal hyperintensity
in left jugular fossa as compared with right side, suggesting perineural involvement
(black arrow). Axial heavily T2W sequence (b) reveals extension of exudates from prepontine cistern to left internal auditory
canal, with perineural spread of infection (curved white arrow). Coronal T1W postcontrast image (c) shows sphenoid sinusitis and perivascular spread of disease along cavernous segment
of left internal carotid artery, causing its luminal narrowing (white arrowhead). Postcontrast T1W fat saturated sagittal sequence (d) depicts pituitary involvement as well as a suprasellar peripherally enhancing abscess
(white arrow).
The imaging correlates along with the pathophysiology of various manifestations seen
in neuraxial involvement by CAM are elaborated in [Table 1].
Table 1
Imaging correlates for various neurological manifestations of COVID-19 associated
mucormycosis
|
Manifestations
|
Pathophysiology
|
Imaging correlate
|
|
Headache
|
Involvement of pain sensitive structures in brain like meninges, large pial arteries,
venous sinuses, and trigeminal nerve. Extracranial pain may arise from scalp.
|
Invasive sinusitis extending to superior orbital apex and
cavernous sinus, meningitis, venous sinus thrombosis, vasculitis, and trigeminal neuritis.
|
|
Proptosis and retroorbital pain
|
Results from increase in intraorbital content from
invasion, extraocular muscle infiltration, or sequelae of
vascular or neural involvement.
|
Retroocular soft tissue, optic neuritis or perineuritis, ophthalmic artery thrombosis/
vasculitis, cavernous sinus thrombosis.
|
|
Ptosis/diplopia
|
Occurs from myogenic, neurogenic or mechanical cause
|
Signal intensity changes and swelling of extraocular muscles, third nerve involvement
at the level of superior orbital apex or cavernous sinus
|
|
Diminution of vision
|
Optic nerve involvement
|
Optic nerve or optic nerve sheath intensity changes with enhancement, or compression
of optic nerve by damaged soft tissue in retro-orbital space.
|
|
Facial numbness
|
Trigeminal nerve involvement at cavernous sinus, brain stem,
subarachnoid space or at the level of terminal small facial branches involvement.
|
Trigeminal nerve enhancement with abnormal signal intensity
|
|
Facial deviation
|
Facial nerve involvement, either lower motor neuron (LMN) or upper motor neuron (UMN)
type. UMN type palsies are associated with infarction. LMN type facial nerve palsies
from peripheral involvement by invasive mucormycosis either at the level of parotid
gland or due to vasa nervosum angioinvasion by mucor causing infarction of facial
nerve at the level of parotid or when it emerges through the parotid gland.
|
Brain stem infarction in UMN palsies,
Parotid gland signal intensity changes and enhancement, extensive involvement of soft
tissue of cheek in LMN palsies.
|
|
Bulbar symptoms
|
Palatal and pharyngeal muscle weakness
|
Abnormal signal intensity of palatal and pharyngeal muscles with surrounding soft
tissue, representing direct invasion of fungus
|
|
Stroke
|
Involvement of cavernous segment of internal carotid artery
|
Superficial and deep watershed infarcts with or without hemorrhagic transformation
|
|
Seizure/disorientation
|
Brain parenchymal or meningeal involvement most commonly by direct infiltration into
frontal and temporal lobes
|
Cerebritis or brain parenchymal invasion, meningitis.
|
Abbreviation: COVID-19, coronavirus disease 2019.
Source: Adapted from Dubey et al.[3]
Conclusion
Patients with COVID-19 may develop a wide range of neurological symptoms, some of
which may be attributed to CAM, which is now a well-established entity with the predominant
risk factors being diabetes, immunodepletion, and steroid therapy in COVID-19 pneumonia.[2] Imaging helps in the early detection of neurological involvement of this serious
condition, delineating the extent of intracranial infection and ruling out postsurgical
residual disease ([Figs. 16] and [17]). Due to the changing trends in the COVID-19 pandemic, it is an absolute necessity
for all radiologists to have a high index of suspicion and be aware of the imaging
features of ROCM and its possible complications, as prompt diagnosis and treatment
with antifungal medication and surgical debridement can halt the progression of the
infection. More effective prevention and treatment of severe COVID-19 infection through
widespread vaccination, social distancing, and more efficacious antiviral therapy
would positively decrease the incidence of CAM in the near future.[2]
Fig. 16 Follow-up MRI done in a 38-year-old patient who had undergone treatment with antifungal
medication, endoscopic sinus surgery and left sided exenteration for post-COVID-19
rhino-orbital-cerebral mucormycosis reveals residual disease in left orbital apex
and cavernous sinus (black arrow) as evidenced by enhancing soft tissue on 3-D isotropic T1W fat saturated postcontrast
axial (a) and coronal (b) sequences. Note made of residual left ethmoidal sinusitis and air-fluid level in
left orbit. Follow-up MRI scan in another 54-year-old female with similar history
and management is shown. 3-D isotropic T1W fat saturated postcontrast axial (c) and coronal (d) images demonstrate residual enhancing inflammatory tissue in left orbit (white arrow) with extension of disease process into orbital apex, cavernous sinus, and periorbital
soft tissue. There is leptomeningeal enhancement in left frontal lobe (arrowhead) suggesting residual meningitis. COVID-19, coronavirus disease 2019; MRI, magnetic
resonance imaging.
Fig. 17 Postoperative NCCT scan of paranasal sinuses in a 63-year-old female COVID-19 recovered
patient with invasive mucormycosis reveals extensive erosive destruction of all walls
of left maxillary sinus on coronal reformatted bone window image (a) with associated residual hyperdense soft tissue extending into the left orbital
extraocular fat (red arrow) on soft tissue window (b). Left inferior and middle turbinates are missing suggesting postoperative changes.
COVID-19, coronavirus disease 2019; NCCT, noncontrast computed tomography.
