1

Dr. Shahana Parveen

Oral & Maxillofacial Surgeon

Sushila Super Speciality Hospital & Trauma Centre

Narela, New Delhi

110040

drosshahana@gmail.com
2
Dr. Ruchi Agarwal

Associate Professor

Dept. Of Public Health Dentistry

Dr. D.Y. Patil Dental College and Hospital

Dr. D.Y. Patil Vidyapeeth , Pimpri,

Pune, 411018

Drmahi.009@gmail.com
3
Dr Minal M Kshirsagar

Assistant Professor

Dept. Of Public Health Dentistry

Bharati Vidyapeeth Dental College and Hospital Navi Mumbai

drminalkshirsagar12@gmail.com
4
Dr Dhiraj Bhambhani

MBBS

People’s College of Medical Sciences

Bhopal

dhirajbhambhani99@gmail.com
5
Dr Garima Bhambhani

Professor

Dept Of Public Health Dentistry

Peoples College of Dental Sciences and Research Centre ,

Bhopal

garima.bhambhani09@gmail.com
6
Dr Chandni Bharti

Professor

Department of Orthodontics

People’s Dental Academy

Madhya Pradesh

462037

drchandnibharti@gmail.com
POST-COVID ASSOCIATED MUCORMYCOSIS: AN OBSERVATIONAL STUDY WITH CLINICAL AND
RADIOGRAPHICAL PRESENTATION.

Introduction:

Mucormycosis also known as zygomycosis is an opportunistic infection

caused by a group of microorganisms belonging to the phylum glomeromycota. 1 Earlier
classified as a rare fungal disease, with increasing incidence in the last few years
mucormycosis is regrouped as an emerging pathogen. These groups of fungi are
ubiquitous and can be found in air, on soil and decaying organic matter, or in a
humidified atmosphere. The spread of these fungal spores is mainly through inhalation
followed by ingestion. Once entered the body either way they show the manifestation of
symptoms involving sinuses, orbital, cerebral and even pleura. The incidence of
mucormycosis globally varies from 0.005 to 1.7 per million population. In India,
prevalence is estimated as 140 per million population. 2

COVID-19 patient has a higher risk of mucormycosis due to several

factors and underlying diseases. India is known as the world’s diabetic capital. Diabetes
mellitus is the most common underlying cause of mucormycosis. In 54-76 % of cases, it
has been reported. Mucormycosis is associated with hematological malignancy in 1-9%
of cases. In India, solid-organ transplantation (SOT) is a contributing factor for
mucormycosis in 2.6-11% of patients. Chronic kidney disease (CKD), use of industrial
oxygen, pulmonary TB, chronic Obstructive pulmonary disease (COPD), neutropenia,
trauma, burns and deferoxamine medication in hemodialysis patients are all risk factors
causing mucormycosis. Other risk factors for mucormycosis include intravenous drug
use, autoimmune disease, HIV infection, immunosuppressant drugs, malnutrition and
prolonged ICU stay.3

Rhizopus Oryzae is the most common organism causing mucormycosis

and is responsible for around 70% of all cases of Mucormycosis. Unbound iron in the
blood plays a key role in predisposing Diabetic Ketoacidosis (DKA) patients to
mucormycosis. Patients with DKA have higher levels of free iron in their blood, which
encourages R.Oryzae growth at an acidic pH (7.3-6.88). Furthermore, adding
exogenous iron to serum caused R. Oryzae to grow rapidly in acidic environments and
simulated acidic conditions reduced serum’s iron-binding capacity, implying that
acidosis affects transferrin’s ability to bind iron. Desferrioxamine-treated patients are
also susceptible to mucormycosis. Deferoxamine removes ferric iron from bound
transferrin and binds to the mold through an inducible receptor, after which the iron is
transferred intracellularly by an active reduction of the ferric form to the more soluble
ferrous form. Mucormycosis is characterized by angioinvasion, resulting in vessel
thrombosis and extensive tissue necrosis. The angioinvasion leads to hematogenous
dissemination to other organs and ischemic necrosis. Damage to endothelial cells and
extracellular matrix cells causes angioinvasion. The glucose-regulated protein (GRP-78)
acts as a receptor to permit Mucorales to penetrate endothelial cells. GRP-78
expression is increased in patients with higher glucose and iron levels.

The reported incidence of Covid associated Mucormycosis during the

second wave of covid is 31-50 % showing a greater number of cases suffering from
diabetes mellitus or on prolonged corticosteroid therapy. 2 These reports suggested
faster growth of this infection and more lethal presentation in patients who were
immunocompromised. Clinically they are presented with eschar or blackening of skin
and thus, were also named black fungus (Figure 1). Patients suffering from COVID-
associated mucormycosis show symptoms ranging from a toothache, mobility of teeth,
multiple periodontal abscesses (Figure 2), sinus tract formation, bony erosion, mobility
of segmental or complete maxilla and palatal bone along with overlying soft tissue
necrosis involvement of sinus, orbit and cerebrum to death. The rapid spread of the
disease and extensive clinical manifestation of this disease is demanded through
understanding and prompt treatment.

FIGURE 1: Eschar (Blackened skin)

 Figure 2: Multiple periodontal abscesses

Thus, we designed a retrospective observational study with an objective to

document the clinical features, radiological extent and possible risk factors which might
be contributing to this illness in the context of the COVID-19 pandemic. This will help
the clinician with the early and prompt diagnosis of such cases for appropriate
management.

Methodology :

We carried out a Multi-center observational retrospective study. Patients

reported to our institute with complaints of Oro-Rhino-Orbito-Cerebral mucormycosis-
associated symptoms were included in the study. Through this study, we aimed to find
out the clinicoepidemiological profile of mucormycosis in patients with or without covid
19. The patient data repository was screened for patient files with diagnoses MM, fungal
sinusitis and COVID-19. Out of the 492 patient files screened, we found 70 patients with
suspected CAM. We included 47 patients who had confirmed MM with previously
treated or concurrent COVID-19.

INCLUSION CRITERIA:

1. Patients with a positive report of Real-Time Polymerase Chain Reaction (RT-

PCR) test, showed clinical features of COVID-19 and mucormycosis.
2. Patients with a positive report of RT-PCR showed clinical features of
mucormycosis but did not show clinical features of COVID-19 were
considered active covid patients.
3. Patients with a clinical presentation of COVID-19 and mucormycosis but with
negative RT-PCR report and showed clinical features of mucormycosis but
 showed no features of COVID-19 and with a negative report of RT-PCR were
considered as recent covid 19 patients.
4. Patients who were negative for symptoms of covid 19 but showed covid
positive tests and symptoms of mucormycosis.

EXCLUSION CRITERIA:

1. Patients with denial of admission and brought dead.

2. Patients with undiagnosed fungal infections.

Data collection:

A detailed data collection sheet was formulated. Information was collected from
the hospital records with an emphasis on the demographic profile, onset of CAM
symptoms and COVID-19 symptoms, clinical features of CAM (Table 2), detailed
comorbidities and risk factors of CAM, steroid usage details for COVID-19 (Table 1),
COVID-19 treatment received before CAM symptoms, arrival vitals, diagnostic
evaluations [ radiological (Table 3), and microbiological (Table 4) ] medical treatment
given and final disposition with the surgical plan.

Table 1:Summarizes the demographic data and associated risk factors in the study
group.

Variable Characteristic Percentage n=47

Age Median years 44
Gender Male 31 (65.95%)
Female 16(34%)
Covid status Present 35
Recent Covid history 08
Active Covid 23
Absent 12
Onset of symptoms Early phase 15
Late phase 32
Comorbidities Diabetes Mellitus 40 (85%)
Hypertension 05(10.63%)
Chronic Kidney 02(4.25%)
Patients on steroid therapy Parenteral route 22
Inhalational route 07
Duration of Steroid therapy Mean duration 10 days
Patients receiving Oxygen Number of patients 16
therapy
Mean Duration 07 days

Table 2: Shows the extraoral and intraoral clinical features

CLINICAL FEATURE EARLY PHASE LATE PHASE

EXTRAORAL FINDINGS (N) (N)

Facial edema/Erythema 10 28
Extraoral gangrene 12 20
Extraoral eschar 8 15
Periorbital Edema 7 17
Proptosis of eye 12 21
Chemosis 10 25
Restricted eye movements 14 21
Dilated Pupil 10 12
Vision loss/ diminution 7 15
Heaviness of the ipsilateral jaw 15 27
Heaviness of whole jaw 9 18
Extraoral sinus/ fistula 0 0
Obliteration of Nasolabial Fold 21 29
Nasal Congestion/Blockage 7 18
Nasal Discharge (Blood) 8 17
Nasal Discharge (Blackish/Brown) 5 11
Hyposmia/Anosmia 4 10
Preseptal edema 18 20
Sinus Pain 6 12
Headache 3 9
Altered Mental Status 0 8
Hemiplegia 0 2
Dysarthria 0 4
INTRA-ORAL FINDINGS
Toothache 18 25
Single Sinus tract 18 25
Multiple Sinus tracts 21 30
History of Tooth Extraction 10 18
History of Microtrauma 15 26
Mobility of teeth 14 23
Mobility of ipsilateral maxilla 10 15
Mobility of whole maxilla 8 12
Mucosal Ulceration 19 30
Palatal Ulceration 9 19
Bone exposure/Necrotic Bone 21 27
Fistula 10 11
Palatal swelling 14 21
Palatal Necrosis 10 25
Erythematous Nasal Mucosa 9 14
Necrotic eschars on nasal Mucosa 6 10

Table 3 : Shows radiographic features in patients with CAM

RADIOGRAPHIC FINDINGS N(%)

Infratemporal Fossa 5
Temporal Fossa 10
Maxillary sinus involvement (Unilateral) 22(55%)
Maxillary Sinus Involvement (Bilateral) 29
Ethmoid sinus involvement 19(47.5%)
Sphenoid Sinus Involvement 16
Combination of maxillary, Sphenoid sinus 20 (50%)
ethmoidal sinuses
Frontal sinus 18(45%)
Combination of all sinuses 10(25%)
Orbital involvement 15(37.5%)
Cavernous Venous Sinus Thrombosis 01(2.5%)
Brain Infaction 01(2.5%)
Internal Carotid Artery Occlusion 01(2.5%)
Mucosal thickening 26(65%)
Palatal and alveolar wall erosion 20(50%)
Table 4: Shows Variation in Blood investigations (N= 47%).

TEST NAME INCREASED DECREASED NORMAL

Platelet 33 (70.2%) 8 (17%) 6 (12.7%)
ESR 28 (59.57%) 12(25.53%) 7(14.89%)
CRP 32 (68%) 10(21.27%) 5(10.63%)
D-Dimer 19(40.4%) 7(14.89%) 21(44.68%)
LDH 31(65.9%) 6(12.7%) 10(21.2%)
TLC 29(61.7%) 8(17%) 10(21.2%)
DLC 31(65.9%) 7(14.89%) 9(19.1%)
Fasting Blood 35(74.46%) 4(8.5%) 8(17%)
Sugar (FBS)
Post-Prandial (PP) 38 (80.85%) 3(6.38%) 6(12.7%)
HbA1c 40(85.1%) 2(4.25%) 5(10.63%)
RBS 31(65.9%) 5(10.63%) 11(23.4%)
LFT 18(38.29%) 10(21.27%) 19(40.42%)
KFT 24(51%) 8(17%) 15(31.9%)

Statistical analysis:

Counts and percentages were used to summarize categorical data. Mean and
standard deviation was used to summarize normally distributed data, whereas median,
range and interquartile range (IQR) were used to summarize non-normal continuous
data. Normality of data was tested by Kolmogorov– Smirnov test. A total of 47
diagnosed CAM were included in the analysis (Table 1). These patients presented to
our institute between June 2020 and November 2021. Thirty-five out of 47 patients
(74.46%) were active with COVID-19, whereas twelve patients (25.53%) were with
recent COVID-19 infection (COVID-19 negative during ED presentation). Among the
active COVID-19 cases, 7 patients (10%) presented primarily with CAM symptoms but
were incidentally detected to have COVID-19, i.e. they were asymptomatic for COVID-
19. The median age of the included patients was 44.5 years, with an IQR of 38–55.5
years, with 60% (n ¼ 42) males. Overall, a lag period was observed between the onset
of COVID-19 symptoms and the onset of CAM symptoms, with the median duration
being 20 days (IQR: 13.5–25)

RESULTS
Demographic profile:

Total of fifteen patients reported in the early phase while thirty- two patients
reported in the late phase (TABLE 1).

Risk factors :

Out of the total forty-seven patients, forty patients were having diabetes mellitus
regardless of the presence of Covid 19 or not. While twenty-nine patients with a history
of covid were on corticosteroids. The Majority (Twenty-Two patients) received
parenteral corticosteroids while seven patients were on inhalational therapy. The mean
duration of steroid therapy for all the patients was 10 days. Ten patients in the positive
group required oxygen supply during their hospital stay. Other comorbidities like
hypertension (found in five patients) and chronic kidney disease (two patients) were not
statistically significant (TABLE 1).

TABLE 1: Summarizes the demographic data and associated risk factors.

Variable Category n %
Age (n=47) Mean 43.83 ± 7.89 --
Male 31 66%
Gender (n=47)
Female 16 34%
Present 33 70.2%
Covid status (n=47)
Absent 14 29.8%
Recent history 22 46.8%
Covid history (n=47) Active covid 11 23.4%
No history 14 29.8%
Early phase 15 31.9%
Onset of symptoms
Late phase 32 68.1%
Diabetes Mellitus 38 80.9%
Co-morbidities Hypertension 30 63.8%
Chronic Kidney 10 21.3%
No steroids 27 57.4%
Steroid therapy Parenteral route 15 31.9%
Inhalational route 5 10.6%
Yes 16 35%
Oxygen therapy
No 31 66%
Note: Cumulative % of co-morbidities may go higher than 100% as some patients were having more
than one co-morbidity

Clinical features:

The clinical presentation of the patients ranged from simple extraoral swelling
(Figure 3), intraoral sinus tract involvement, and segmental mobility to loss of vision.
Extraoral swelling with facial pain was the commonest feature and was seen amongst a
total of thirty patients accounting for 80.85%. Symptoms showing ischaemic changes
like the presence of eschar and gangrene were observed in thirty -two patients mainly
contributed by patients in the late phase. With more patients showing facial gangrene
(n=32) (Figure 4) than eschar(n=23). While no patient was reported with extraoral sinus
tract or fistula or facial nerve palsy. While one patient presented with hemiplegia
signifying intracranial involvement. The ophthalmic symptoms were diminution of vision
(n=7, Early phase; n=15, Late phase), Proptosis (Early phase n=12, Late phase n=21)
and dilated pupil (n=22) (Figure 5). Almost all patients showed the presence of sinus
tract intraorally (n=43) and mobility of teeth (n=37). While segmental mobility was seen
in 53.12% of patients (n=25). The disease showed an erosive pattern and erosion of the
associated part of the palate and maxilla which was initially presented as intraoral
mucosal and palatal swelling (Figure 6). Details of each extraoral & intraoral features
are tabulated in (TABLE 2) & (Table 3).
Figure 3: Extra-oral Periorbital region swelling

Figure 4: Facial Gangrene

Figure 5: Dilated Pupil (Left Eye)

Figure 6: Palatal Swelling

TABLE 2: Details of Extra-oral findings among subjects

Total
Early phase Late phase
present p
Condition (n=15) (n=32)
(n=47) value
N % N % N %
Facial edema/Erythema 4 26.7 20 62.5 24 51.1 0.030*
Extraoral gangrene 0 0 13 40.6 13 27.7 0.004*
Extraoral eschar 1 6.7 6 18.8 7 14.9 0.404
Periorbital Edema 0 0 11 34.4 11 23.4 0.009*
Proptosis of eye 0 0 5 15.6 5 10.6 0.162
Chemosis 1 6.9 9 28.1 10 21.3 0.135
Restricted eye movements 0 0 7 21.9 7 14.9 0.080
Dilated Pupil 0 0 8 25 8 17.0 0.042*
Vision loss/ diminution 0 0 6 18.8 6 12.8 0.157
Heaviness of the ipsilateral 17
9 60 8 25 0.027*
jaw 36.2
Heaviness of whole jaw 2 13.3 9 28.1 11 23.4 0.461
Extraoral sinus/ fistula 0 0 0 0 0 0.0 --
Obliteration of Nasolabial Fold 3 20 4 12.5 7 14.9 0.664
Nasal Congestion/Blockage 6 40 8 25 14 29.8 0.324
Nasal Discharge (Blood) 0 0 3 9.4 3 6.4 0.541
Nasal Discharge 12
6 40 6 18.8 0.158
(Blackish/Brown) 25.5
Hyposmia/Anosmia 1 6.7 2 6.3 3 6.4 1.000
Preseptal edema 4 26.7 2 6.3 6 12.8 0.072
Sinus Pain 5 33.3 4 12.5 9 19.1 0.121
Headache 1 6.7 8 25 9 19.1 0.236
Altered Mental Status 0 0 5 15.6 5 10.6 0.162
Hemiplegia 0 0 2 6.3 2 4.3 1.000
Dysarthria 0 0 1 3.1 1 2.1 1.000
Chi-square test; * indicates significant difference at p≤0.05

TABLE 3: Details of Intra-oral findings among subjects

Early Total
Late phase
phase present p
Condition (n=32)
(n=15) (n=47) value
N % N % N %
Toothache 3 20 8 25 11 23.4 1.000
Single Sinus tract 6 40.0 7 21.9 13 27.7 0.295
Multiple Sinus tracts 4 26.7 10 31.3 14 29.8 1.000
History of Tooth Extraction 3 20 3 9.4 6 12.8 0.367
History of Microtrauma 6 40 14 43.8 20 42.6 1.000
Mobility of teeth 6 40 16 50 22 46.8 0.550
Mobility of ipsilateral maxilla 2 13.3 4 12.5 6 12.8 1.000
Mobility of whole maxilla 0 0 6 18.8 6 12.8 0.157
Mucosal Ulceration 8 53.3 11 34.4 19 40.4 0.339
Palatal Ulceration (Figure 10) 4 26.7 10 31.3 14 29.8 1.000
Bone exposure/Necrotic Bone
3 20 19 59.4 0.015*
(Figure 8) (Figure 9) 22 46.8
Fistula (Figure 7) 1 6.4 4 12.5 5 10.6 1.000
Palatal swelling 7 46.7 3 9.4 10 21.3 0.007*
Palatal Necrosis 1 6.7 14 43.8 15 31.9 0.017*
Erythematous Nasal Mucosa 4 26.7 6 18.8 10 21.3 0.704
Necrotic eschars on nasal
2 13.3 6 18.8 8 17.0 1.000
Mucosa
Chi-square test; * indicates significant difference at p≤0.05
Figure 7: Fistula Formation in Palate.

Figure 8 : Sloughing in hard Palate

Figure 9: Necrosis of Alveolar bone

Figure 10: Ulceration & hemorrhage in palate

Vital Signs:

The vital signs of respective patients are ranged from severely to moderately deranged to
normal vitals. Most patients reported with their vital signs noticed were increased
Respiratory rate, Decreased Oxygen Saturation, normal baseline to low Blood pressure and
increased body temperature. (Table 4)

TABLE 4: Details of vital signs

Vital Signs Increased Decreased Normal Total

Blood Pressure 19 (40.4) 0 28 (59.6) 47 (100%)
Respiratory Rate 3 (6.4) 3 (6.4) 41 (87.2) 47 (100%)
Oxygen Saturation 0 13 (27.7) 34 (72.3) 47 (100%)
Temperature 9 (19.1) 0 38 (80.9) 47 (100%)

Radiographic features:

All the patients included in the study were subjected to CT scans on admission
(Table 5). Sections of 1mm were evaluated to identify the disease extent through the
palate, maxilla, floor of the orbit, the orbit, sinuses and cranium (Figure 11) (Figure 12).
The presence of hyper density along the sinuses was recorded as sinus lining
thickening. Sinus lining thickening was the primary radiographic feature found showing
minimal clinical characteristics with or without bony involvement. The most commonly
affected sinus was the maxillary sinus followed by the ethmoidal sinus and then the
frontal sinus. About 20 % of cases showed a combination of sinus involvement. The
patients with erosion of bone clinically showed bone exposure, mobility of teeth or
segmental mobility. There was no significant difference found amongst unilateral or
bilateral involvement cases. One patient showed cranial involvement with extension into
the cavernous sinus which was seen as a hyperdense image along the cavernous
sinus. An Infarction involving the anterior part of the cerebrum was seen in one patient.
(Figure 13)

Figure 11: Bilateral Maxillary sinus Involvement

Figure 12: Lateral wall of orbital ,maxillary, ethmoid

& sphenoid sinuses involvement

Figure 13: Involvement of half Cerebrum (Right side)

TABLE 5: Details of radiographic findings

RADIOGRAPHIC FINDINGS N %
Infratemporal Fossa 5 10.6
Temporal Fossa 5 10.6
Maxillary sinus involvement (Unilateral) 23 48.9
Maxillary Sinus Involvement (Bilateral) 17 36.2
Ethmoid sinus involvement 31 66.0
Sphenoid Sinus Involvement 26 55.3
Combination of maxillary, Sphenoid sinus ethmoidal sinuses 14 29.8
Frontal sinus 7 14.9
Combination of all sinuses 7 14.9
Orbital involvement 11 23.4
Cavernous Venous Sinus Thrombosis 5 10.6
Brain Infarction 3 6.4
Internal Carotid Artery Occlusion 1 2.1
Mucosal thickening 29 61.7
Palatal and alveolar wall erosion 9 19.1

BLOOD INVESTIGATIONS:

All the patients included in the study were advised of various blood
investigations. This included Platelet Count, Erythrocyte Sedimentation Rate (ESR), C-
Reactive Protein (CRP), D-dimer, Lactate Dehydrogenase (LDH),Total Leukocyte Count
(TLC), Differential Leukocyte Count (DLC), Diabetic Profile (Fasting FBS), Post Prandial
(PP), HbA1c, Random Blood Sugar (RBS), Liver Function Test (LFT), Kidney Function
Test (KFT), (Table 4). Common deranged blood levels included increased blood sugar
(FBS-74.46%, PP-80.85%, HbA1c- 85.1% and RBS- 65.9%) followed by increased CRP
(68%), DLC (65.9%). TLC (61.7%), ESR (59.57%), KFT (51%), LFT (38.29%), D-dimer
Test (40.4%) and CBC (21.27%).

TABLE 6: Details of outcome of blood investigations

Test Increased Derranged Normal Total

Platelet 17 (36.2) 0 30 (63.8) 47 (100%)
ESR 20 (42.6) 0 27 (57.4) 47 (100%)
CRP 8 (17) 0 39 (83) 47 (100%)
D-Dimer 5 (10.6) 0 42 (89.4) 47 (100%)
LDH 8 (17) 0 39 (83) 47 (100%)
TLC 23 (48.9) 0 24 (51.1) 47 (100%)
DLC 17 (36.2) 0 30 (63.8) 47 (100%)
Fasting Blood Sugar (FBS) 31 (66) 0 16 (34) 47 (100%)
Post-Prandial (PP) 33 (70.2) 0 14 (29.8) 47 (100%)
HbA1c 33 (70.2) 0 14 (29.8) 47 (100%)
RBS 30 (63.8) 0 17 (36.2) 47 (100%)
LFT 0 9 (19.1) 38 (80.9) 47 (100%)
KFT 0 17 (36.2) 30 (63.8) 47 (100%)

Discussion:

We conducted a Multi-center, retrospective study of 47 patients with CAM

who presented to our institute in the setting of acute or recent COVID-19. Our study
aimed to provide clinic-epidemiological data of Covid associated Mucormycosis. As per
our study, out of forty patients, twenty-five patients with the covid history presented with
mucormycosis symptoms while fifteen patients did not have any significant evidence of
Covid history and were considered covid negative. Chander et al 4 reported 82
mucormycosis patients of which two third patients were male and aged between 31-60
years. It has been hypothesized that the effect of estrogen might be protective in
systemic fungal infection, which could have led to a lower incidence in females.
Similarly in our study majority of patients were middle-aged and nearly 60 % of patients
were male.
 Immunocompromised patients, corticosteroid therapy, use of industrial oxygen
and rate of oxygen flow are the possible cause of increased incidence of Mucormycosis
in the 2nd wave of COVID-19. Lack of facility in the rural areas, late diagnosis and
medically compromised status was the possible cause of death in post-Covid
Mucormycosis. Many experts believe that the combination of high-dose steroids and
uncontrolled diabetes has led to this epidemic of MM in COVID-19 patients. 5,6,7 Diabetes
mellitus as a predisposing factor for the development of mucormycosis is not a new
phenomenon and is recognized way before pre covid era. as a study by Prakash and
Chakrabarti DM was reported as a predisposing factor in 17-88% cases globally while in
India it was 50%.8 In the setting of COVID-19, the case series by Sharma et al 9
described diabetes as a risk factor in 90% of cases of which 52% had the uncontrolled
disease. Our results are in accordance with the above findings with about 70 % of
patients having DM. out of patients with negative symptoms of Covid 19, three patients
showed a chronic history of diabetes mellitus. Prolonged use of corticosteroids is a
known cause of immunosuppression long. Recently, Ribes et al proposed that acute or
chronic use of steroids in such patients predisposes them to fungal infection. 10 Sooner
understood by WHO, as a need for an hour, the international guidelines recommended
limiting the use of corticosteroids to patients supplemented by oxygen therapy. Despite
these guidelines In India, there were many reports suggesting indiscriminate use of
steroids even in mild COVID-19 patients. 11 Increased number of cases, and lesser
infrastructure, adverse use of social media and homemade tutorials pushed people to
use steroids injudiciously. Improper and unmonitored use of steroids for a long time was
in itself a major risk factor for the development of opportunistic infections like
mucormycosis. In their retrospective analysis of 287 Indian CAM patients during the
first wave, they found 32% with COVID-19 as the only underlying disease among which
78% had received steroid therapy. 12 Our study had 25 patients who received steroid
therapy, 20 patients were on systemic steroids as part of COVID-19 management.
Among this group, 57% had non-hypoxic disease and steroids were not indicated as per
guidelines. Other comorbid conditions identified include hypertension and chronic
kidney disease.
Patients with Covid 19 presented with respiratory distress and
fibrosis in the lungs thus necessitating the use of oxygen therapy. In a developing
country like India, due to unavailability of beds and proper oxygen system, led to an
unhygienic oxygen supply. the humidifier used for oxygen was found to have stagnant
water for a long time. Thus, acting as the potential to the harbor and grow fungus.
Microtrauma due to multiple swab tests for diagnosis of COVID-19, steam inhalation
and burn injuries may have had a role in this substantial rise of CAM.13
 This observational study showed a correlation between risk factors,
clinical features and radiographic features. In our study, depending on the onset of
symptoms patients were divided into early phase and late phase. Patients with risk
factors were prone to the development of disease. Early phase patients showed facial
pain, heaviness, edema, presence of intraoral minute sinus tract and slight mobility of
teeth which was correlated with thickening of the mucosal lining of the sinus and erosion
of underlying bone. Moderately severe cases showed bone necrosis with exposure of
bone, segmental mobility, ulceration and erosion of greater extent of bone. rapidly
spreading disease led to ischemic changes giving rise of eschar and gangrene extra
orally. Late phase disease showed orbital and cranial involvement with cavernous sinus
thrombosis and ischaemic changes in cerebrum and disease extending to orbit
radiographically that led to hemiplegia. As per earlier reports, the presence of
associated facial erythema, perinasal swelling, nasal ulcers or eschar serves as early
pointers.14 Palatal necrosis is a hallmark sign which may be seen in 38% of patients. 15
Satish et al.16 reported that 48% of patients in their case series had rhino-orbital disease
followed by rhino-orbito-cerebral form.
The role of Dental surgeons, Oral and Maxillofacial Surgeons can
not be overlooked because most patients were reported at a late stage and were
incubated, due to which adequate and thorough clinical examination as well as
treatment strategy could not be assessed and done.

As with any other disease, the treatment modality of this Covid-associated

mucormycosis is varied depending upon the symptoms. Identification of potential risk
factors and their prevention, and thorough assessment of clinical features are the
mainstay.17 The overall prognosis of MM is poor and the outcome may drastically
change based on the initial treatment trajectory. Sending appropriate investigations,
early administration of systemic antifungals, avoiding unnecessary antibiotics and
systemic steroids, and prompting for early multidisciplinary surgical debridement
including performing lateral canthotomy in ED are the learning points for an emergency
physician.18 It is also imperative for the ED physician to exercise caution during the
management of acute COVID-19. This includes strict control of hyperglycemia, titration
of oxygen therapy only as per patient need and proper cleaning and maintenance of
oxygen delivery devices within hospital settings.

Conclusion:
Mucormycosis is a rapidly spreading debilitating disease and has
affected a huge population suffering from Covid 19. Long-term use of corticosteroids,
leading to immunosuppression, and associated comorbidities like diabetes mellitus are
predisposing risk factors for the development of covid-associated mucormycosis. To
limit this rapid spread of disease one should have a thorough knowledge of the clinical
and radiographic presentation of this disease. This article presents patients in both early
and late phases of disease thus giving an overview of all the symptoms and radiological
findings. We suggest a multicentric study with a larger sample size for confirmatory
results.

References-
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